gro‘lnfl In. «In.» p fezro’vh . r199!!! :-:f.l.5r::«.&vl l r Aha-1.. . » oliorvtov.In.II¥I ¢ v0! 31 p I. 1.1.: If (IllrrYtrvIIUIIv .‘ 7.31.: r. Q31Alt‘. . .. . i... .. ii ’15., . Nl.‘..u§!§ . ”3.2.11 {1.4.1 ’3’}! 5.3L. . .3. L . 1. J. .‘L J! ?o 2r trink ». V I . . w: l r I... I e. 5!. it...» ,1» 52!...13 »-b . .1 .IL 7.3.1.! {1.1 . If! x lA!tI5..}E9. 5!, . fr....v?-.;V.Ju!). .. is . {It I II 1 9“! A P .6... if»! . 'cfzfti‘rrtt. .01 . . (ti-ll!!! u :I; '4‘ , 1. w 7...... . llvcivlr: ‘ T #3.»: ;rr.... . 1.... I! THES'S SITY LIBRARI ISE |\\|\\\\\|\‘i\|l\“liiliillihill | || Hi This is to certify that the thesis entitled RELATIONSHIPS BETWEEN ENDOCRINE FACTORS AND RATE, EFFICIENCY AND COMPOSITION OF GAIN OF BEEF FROM FOUR BIOLOGICAL TYPES presented by Scott Patrick Greiner has been accepted towards fulfillment of the requirements for M. S . degree in Animal Science Major professor Date March 29, 1993 0-7639 MS U is an Affirmative Action/Equal Opportunity Institution LIBRARY Mlchlgan State Unherslty k PLACE IN RETURN BOX to remove this checkout from your record. TO AVOID FINES return on or before date due. ‘W L L % igfi L____J ’7 I L________ ’T‘T usu Is An Affirmative ActiorVEqueI Opportunity Institution emu-banana.- RELATIONSHIPS BETWEEN ENDOCRINE FACTORS AND RATE, EFFICIENCY AND COMPOSITION OF GAIN OF BEEF FROM FOUR BIOLOGICAL TYPES BY Scott Patrick Greiner A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department of Animal Science 1993 ABSTRACT RELATIONSHIPS BETWEEN ENDOCRINE FACTORS AND RATE, EFFICIENCY AND COMPOSITION OF GAIN OF BEEF FROM FOUR BIOLOGICAL TYPES BY Scott Patrick Greiner One hundred fifty nine steers from four breed groups were used in a two year study to evaluate the relationship among hormones and rate, efficiency, and composition of gain. Breed groups consisted of unselected Herefords, Herefords selected for growth, Shorthorn x Angus x Hereford and Gelbvieh x Simmental x Holstein. Cattle within a breed group were subdivided into three pens and slaughtered after 225, 247, and 260 days on feed. Ninety days prior to slaughter, blood was collected on each animal every .5 hours for an 8-hour period for hormone analysis. Routine carcass measurements were taken 24 hours post-slaughter. A 9-10-11 rib section from each animal was dissected to estimate carcass composition. Selection for growth resulted in larger framed, heavier, faster growing, leaner cattle that had significantly lower percentages of carcass fat and higher percentages of carcass protein (P < .01) . Selection for growth did not increase growth hormone or insulin-like growth factor I concentrations. There were significant (P < .01) differences in concentrations of growth hormone, insulin-like growth factor I, and insulin between the breed groups. Hormone concentrations were correlated with carcass traits and carcass composition. ACKNOWLEDGEMENTS Without the help and guidance of numerous people, the research reported in this thesis would not have been possible. I am grateful to all who provided assistance. My appreciation is expressed to Dr. Steven Rust for his guidance throughout my M.S. program. Dr. Rust was very supportive of my efforts not only with this research but with my teaching and coaching responsibilities as well. His encouragement and advice are tremendously appreciated. Dr. Harlan Ritchie and Dr. David Hawkins both deserve thanks for their help with this project. My most sincere thanks are expressed to them for bringing me to Michigan State University and giving me the opportunity to be involved in teaching and coaching. Their advice and guidance on many other issues are appreciated. Dr. Robert Merkel and Dr. Kent Refsal deserve thanks for their part in designing, conducting, and interpreting this research. Their expertise in their respective fields was invaluable, and their review of this manuscript is sincerely appreciated. Numerous faculty, staff and students have contributed to the completion of this study. I am indebted to Dr. H. Allen Tucker, Dr. Mike VandeHaar, and Dr. Kent Refsal for use of their laboratories. Special thanks are extended to Larry Chapin, Geoff Dahl, and Balkrisha Sharma for their instruction and assistance in hormone analysis. My appreciation goes to all those who assisted in sample collection. Included in this group are Mike Schlegel, Tadd Dawson, Terri Stroman, Doug Cook, Matt Doumit, Al Jordan, Scott Kramer, Lisa Lutchka, Stacy Moore, Sharon DeBar and Tom Forton and the meat lab employees. Without the help of these people, this project would not have been possible. I am also indebted to Dan Jennings and Brett Barber for their help and friendship. I will always be thankful to my parents, Nick and Georgie Greiner, and to the rest of my family. My accomplishments are largely a result of the values they have instilled. Their love and support are treasured. I am also grateful for the love, help, and encouragement provided by my fiance Lori Nixon. Her support of all my endeavors is appreciated. iii TABLE OF List of Tables . . . . . . . . Introduction . . . . . . . . . Literature Review. . . . . . . Effects of Selection. . . CONTENTS 0 . . o . . . . . . . . . . V . . . . . . . . . . . . . . 1 . . . . . . . . . . . . . . 4 . . . . . . . . . . . . . . 5 Differences Among Breeds and Biological Types . . . . 8 Endocrine Influence on Growth . . . . . . . . . . . . 12 Growth Hormone . . . O O O O O O O O O O O O O O 13 Insulin-Like Growth Factor I . . . . . . . . J . 20 Insulin. . . . . . . Thyroid Hormones . . Objectives . . . . . . . .'. . Materials and Methods. . . . . Results. . . . . . . . . . . . Discussion . . . . . . . . . . Conclusions. . . . . . . . . . Literature Cited . . . . . . . Appendix . . . . . . . . . . . . . . . . . . . . . . . . . 27 . . . . . . . . . . . . . . 33 . . . . . . . . . . . . . . 41 . . . . . . . . . . . . . . 43 . . . . . . . . . . . . . . 52 . . . . . . . . . . . . . . 74 . . . . . . . . . . . . . . 90 . . . . . . . . . . . . . . 92 O O O O O O O O O O O O O .106 iv LIST OF TABLES TABLE 1. Description of different breed groups. . . 2. Effect of breed group and year on initial of cattle in slaughter groups. . . . . . . 3. Diet composition . . . . . . . . . . . . . 4. Blood collection and slaughter schedule. . 5. Feedlot performance of breed groups. . . . 6. Feedlot performance of slaughter groups. . 7. Carcass measurements of breed groups . . . 8. Carcass measurements of slaughter groups . 9. Carcass composition of breed groups. . . . 10. Carcass composition of slaughter groups. . 11. Influence of breed group and year on selected carcass characteristics . . . . . 12. Influence of slaughter group and year on selected carcass characteristics. . . . 13. Serum hormone concentrations for breed groups. 14. Serum hormone concentrations for bleed groups. 15. Influence of breed group and bleed group on growth hormone concentration. . . . . . 16. Growth hormone analysis of breed groups. . 17. Growth hormone analysis of bleed groups. . 18. Serum hormone relationships for breed groups . 19 . Serum hormone'relationships for bleed groups . V IQGE . 44 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. Correlations between GH, IGF-I and insulin and carcass characteristics. . .... . . . . . . . . Correlations between serum hormone relationships and carcass characteristics. . . . . . . . . . . . . Individual performance and carcass characteristics of Lake City steers born in 1989 . . . . . . . . . . Individual performance and carcass characteristics of Lake City steers born in 1990 . . . . . . . . . . Individual hormone parameters of Lake City steers born in 1989 . . . . . . . . . . Individual hormone parameters of Lake City steers born in 1990 . . . . . . . . . . Metabolism room performance and intakes of Lake City steers born in 1989 . . . . . . . . . . Metabolism room performance and intakes of Lake City steers born in 1990 . . . . . . . . . . Pen intakes and gains by period of Lake City steers born in 1989 . . . . . . . . . . Pen intakes and gains by period of Lake City steers born in 1990 . . . . . . . . . . vi . 72 . 73 .108 .111 .114 .118 .121 .123 .125 .126 INTRODUCTION In recent years, the beef industry has seen a decline in market share relative to other suppliers of protein in the American diet. Although some decline can be attributed to changing lifestyles and consumer perceptions, many of today's challenges may be resolved by animal scientists and beef producers. Results of the 1991 National Beef Quality Audit identified three major factors that contributed to the decline in market share of beef products: excessive fat, low overall uniformity, and price. These problems are the result of several factors, one of which is the diverse genetic pool of beef cattle in the United States. Although this diverse population has contributed to the current problems facing the beef industry, it also has great potential for improving its consistency and competitiveness. Although selection in the beef cattle industry has occurred since its inception, only recently have predictable genetic evaluations of breeding stock been available for wide-spread use throughout the industry. For the beef industry to become more competitive, production of a lean product is imperative. This is further emphasized by industry movement towards value-based marketing. Production of -a leaner product may be accomplished through 1 2 available genetic resources and management techniques or through new technologies. One such technology is the administration of exogenous hormones. It is known that the complex process of growth is mediated by several factors, including environment, nutrition, and hormones. Hormones are the mediators between the environment and the biological systems involved with growth and metabolism. Although the environment places limits on growth in practical situations, the other factors previously mentioned are limited by the genetics of the animal. Little research has been conducted to study differences in hormone concentrations between cattle of known genetic variation and what relationship exists between those endocrine factors and rate, efficiency, and composition of gain. The Lake City Experiment Station breeding project offers a unique opportunity to investigate the differences in endocrine mediators in groups of cattle with diverse genetic genomes. The relationships between live-weight gain, feed efficiency or carcass composition and the endocrine mediators may identify a new phenotypic trait to enhance selection for superior livestock. Secondly, establishment of the relationships between endocrine factors and rate, efficiency, and composition of gain will enhance our understanding of the ‘underlying tenets of animal growth. The results of this research project will assist the :tndustry in production of a leaner, more consumer-appealing product. For the industry to compete with other suppliers of 3 protein in human diets, a lean beef product must be made available. This may be accomplished by genetic selection or by exogenous manipulation with hormones. Before either of these factors can be approached, the basic relationships between genetic selection, animal performance, carcass characteristics, and endocrine factors must be established. LITERATURE REVIEW Several tools are available to the beef industry to accomplish changes in cattle growth and development. The loss of market share to other protein sources in recent years has underlined the importance of utilizing these tools to make all segments of the industry more competitive and profitable. The shift toward value-based marketing by the feedlot and packer segments in response to consumer demands will feedback on cow- calf and seedstock producers. Selection programs will become increasingly important as the beef industry attempts to produce a more consumer acceptable product. Technological development in the last twenty years has greatly enhanced the ability of producers to make fast and predictable genetic improvement. The initiation of National Sire Evaluation programs in the early 1970's led to increased selection intensity and accuracy and made expected progeny differences (EPD's) available. The shift to National Cattle Evaluation beginning in 1984 made across-herd prediction possible for all breeding animals and provided a performance link across all segments of the industry for traits of interest (Middleton and Gibb, 1991) . The importation of continental European beef breeds in the late 1960's and early 1970's has resulted in a large 4 5 genetic base of breeds and biological types from which to select. Studies have clearly indicated that there are significant differences between breeds and biological types for growth, efficiency, and carcass traits. These breed differences and different mating systems are resources available to change the growth and development of cattle to meet the needs of health-conscious consumers (Willham, 1982) . Effects of Selection During the past 25 years, numerous studies have been conducted to quantify phenotypic response to selection in beef cattle. Hough et a1. (1985) designed a study to determine the response to yearling weight selection in Hereford cattle using nationally evaluated sires. The six year study (1978-1983) utilized sires from the top 1% of the Hereford breed for yearling weight EPD. The genetic trend in yearling weight was +6.2 kg/year and resulted in an indirect increase in weaning weight of 5.0 kg/year when compared to controls. There was also an increase in yearling hip height (.75 cm/year), indicating that frame size in selected cattle increased as weight increased. There were no significant responses in post-weaning average daily gain or fat thickness, although the selected line tended to grow faster and possess more lean tissue. The authors concluded that selection for yearling weight preferentially increased lean tissue mass as compared to fat. Australian workers studied the effects of long-term, 6 single-trait selection for yearling weight in Angus cattle. Closed-line selection (utilizing sires produced within the herd) was based on weight gain from birth to one year of age. Three lines were utilized: high yearling weight, low yearling weight, and control. Responses in yearling weight were +15% and ~14% for the high and low lines compared to controls, respectively. Similar trends were reported for weaning weight. At a constant age endpoint, there were no significant differences in feed efficiency or carcass traits, except the high yearling weight line of cattle were heavier. At a constant weight endpoint, selection for heavier yearling weights resulted in 10-15% less feed consumption, 2 mm less backfat and required 20 days less time on feed to reach a specified body weight than controls (Parnell, 1992). Newman et al. (1973) summarized ten years of selection for yearling weight in two replicate Shorthorn herds. Yearling weight increased by 4.8 and 4.1 kg/year in males and 3.3 and 2.3 kg/year in females due to selection in the two herds. Furthermore, in a Nebraska study, progeny sired by Angus and Hereford bulls born in the early 1980's had 13 to 15% heavier weaning weights than those born in the late 1960's (Cundiff et al., 1991). Since many traits are positively correlated, single-trait selection may result in increases in other traits. For example, Koch et al. (1974) used three lines of Hereford cattle and practiced selection for weaning weight, yearling weight, or an index of yearling weight and muscle thickness. 1 Growth traits increased similarly in all three selected lines. Andersen et al. (1974) investigated the response of intensive selection for yearling weight on growth and carcass characteristics. Cumulative selection responses of 41.5 and 46.2 kg in yearling weight over the five year study were observed. Associated with this response were increases in weaning weight and daily weight gain from birth to 10 months of age. The indirect effects on carcass merit were a higher percentage of bone and a trend for a decreased amount of weight and age adjusted fat thickness. Koch (1978) found changes in composition associated with selection for growth rate and muscling score to be in a positive direction. Phenotypic trends indicated that at a constant weight endpoint, percentage of retail product increased while trimmable fat decreased as rate of weight gain increased. The author suggested that dual-trait selection for weaning or yearling weight combined with measures of fatness or’muscling would lead to increased carcass weight at a given age and a higher proportion of edible product (Koch, 1978). Ohio workers (Bishop et al., 1991) examined response to selection for post-weaning feed conversion and correlated effects on. post-weaning growth and carcass traits. No differences were found between high and low feed conversion progeny for feed intake although the high feed conversion (lower feed/gain) progeny gained significantly faster during the post-weaning test. Consequently, feed conversion efficiency was increased slightly. Progeny from the more 8 efficient feed conversion group had greater subcutaneous fat at slaughter, indicating the advantage in average daily gain resulted in accretion of more fat rather than lean. Differences Among Breeds and Biological Types Identification of a breed or biological type that is optimum for specific nutritional or management systems has been studied for decades. With the introduction of continental European breeds,‘ crossbreeding has become an accepted method to utilize heterosis to match breed characteristics to market specifications and environment. Due to the large number and diversity of breeds contributing to the available genetic pool, vast differences in performance and carcass traits exist both between and within breeds and biological types. Advantages in rate of gain and feed efficiency common to large, late maturing breeds have been well documented (Byers and Rompala, 1979; Crouse et al., 1985: Schmidt et al., 1987). Thonney et al. (1981) found larger framed Holstein steers consumed more dry’matter, required one unit less feed.per'unit of gain, and grew .2 kg/day faster than small-framed Angus steers when compared at similar weights. However, within a breed type, only 2 to 19% of the variation in daily dry matter :tntake was explained by weight. The authors concluded that among cattle with a similar mature size, increasing weight has a dramatic effect on growth rate and feed efficiency as both variables decrease with increasing weight and maturity. 9 In most studies, the variations in growth rate, feed efficiency, and carcass composition between various cattle types have been compared either at a constant weight or after a constant time on feed. Smith et a1. (1976) reported Simmental and Charolais sired steers grew faster than Hereford and Angus crossbred steers. Faster growing cattle were more efficient on an age and weight constant basis. Evaluation of feed efficiency' over an age constant interval gives an advantage to breed groups that gain rapidly relative to weight being maintained whereas feed efficiency measured over weight constant intervals is increased by rapid growth rate because fewer days of maintenance are required. Additionally, the authors suggest that weight constant evaluation of efficiency favors breeds that are less mature because of their leaner composition of gain (Smith et al., 1976). One would expect larger, later maturing cattle to have an advantage as they would be younger physiologically; thus, would be depositing a lower'proportion of fat.in.gain (Ferrell and Crouse, 1978). In an effort to address this problem, Ferrell and Crouse (1978) compared growth rate, feed efficiency and carcass characteristics of various types of steers at a constant carcass fat end-point. Larger framed Gelbvieh and Chianina steers had higher average daily gains than Red Poll steers. Gelbvieh crossbred steers consumed more dry matter which was not attributable to a difference in metabolic body size. The authors suggested a difference in net efficiency of energy utilization for maintenance of gain 10 due to steer type, with Gelbvieh sired steers being the least efficient. The effects of larger framed, faster growing breeds can be complemented by crossbreeding. Long (1980) has summarized several studies utilizing straightbred and crossbred breed groups to estimate breed effects and.heterosis across varying sexes and management systems. Post-weaning daily gains had an average heterosis effect of 6% in Shorthorn, Angus, and Hereford cattle. Similarly, yearling weight exhibited an average heterosis effect of 4%. The importance of sire breed within a crossbreeding system was made evident by Marshall et a1. (1990) who found post-weaning average daily gain to decline for generations within rotations for which Hereford was the sire breed. Reported effects of breed or biological type on carcass characteristics are variable because many are confounded with slaughter endpoints and feeding systems. Dikeman et al. (1985) reported larger, faster growing Simmental-Charolais steers were heavier, leaner, and more muscular with less marbling than conventional Hereford-Angus steers. Similarly, Marshall et a1. (1990) found Simmental-Hereford calves produced heavier carcasses with less backfat, larger ribeyes, and a higher cutability than Angus-Hereford steers. However, the -Angus-Hereford steers excelled in marbling and quality grade. Similar data have been reported by Crouse et al. (1985). Martin et al. (1980) found that at the same amount of ll marbling, carcasses from Simmental and Chianina-sired crossbreds were much leaner than carcasses from Angus sired steers. However, these effects were confounded with heavier carcass weights. In support of this observation, Smith et al. (1976) reported Charolais and Simmental sired steers have heavier weights and required more days on feed to reach 5% longissimus fat than Angus, Hereford, or Angus-Hereford steers. At a constant percentage fat in carcass soft tissues; larger framed Chianina and Gelbvieh cattle have heavier carcass weights, larger ribeye areas, and less internal fat with a correspondingly lower yield grade than Red Poll cattle. Conversely, the larger breeds had less marbling and more external fat. Simmental steers have been reported to have increased weight, higher percent lean and less fat trim in the hindquarter and flank compared to Polled Hereford steers. Polled Hereford steers had increased flank weights which contain a large fat component thereby making the flank more reflective of total fat rather than lean (Arnold et al., 1990). Koch et al. (1976) found a positive association between growth rate of breed groups and percentage of retail product or bone. A negative association was observed between growth rate of breed groups and percentage of fat trim. Because of this negative association, breed groups attaining the same percentage of fat in the longissimus may have significantly different carcass weights. Crouse et al. (1985) suggested that increasing the rate of fattening through breed selection 12 reduces carcass weights and muscling. W The complex process of growth includes increased cell number, size and the deposition of substances within these cells. Many factors are involved in these processes including hormones, diet, environment, age, and sex. The hyperplasia and hypertrophy of skeletal muscle, adipose tissue, and bone are of primary concern in meat-producing animals. The homeostatic and. homeorhetic control of ‘these 'tissues is regulated by hormones and hormone receptors. The process of tissue growth and metabolism may not be attributed to a single endocrine influence as one hormone may have multiple actions and multiple hormones may perform one function. The relationships between hormones and their receptors regulate growth and nutrient deposition within tissues. Although the endocrine system regulates short and long term growth, it is theigenetic ability of the animal that sets the upper limits to animal growth. The maximum growth potential of meat animals is not clear, nor are the rate limiting steps which cause individual animals to gain at varied rates, utilize nutrients more efficiently, or partition nutrients into specific tissues. It is not clear if genetic selection for growth and efficiency has altered the endocrine status of meat animals. Current research in animal growth includes the use of exogenous hormones to alter growth rate 13 and composition. Insight as to influences of physiological hormone concentrations on growth may result from the administration of these substances. Future research will also clarify tissue sensitivity, receptors, and clearance rates of hormones. Growth Hormone Growth hormone (GH; somatotropin) is a peptide hormone which is stored and secreted from the somatotropic cells of the anterior pituitary. In humans, several forms of GH differing in molecular weight are secreted (Lewis et al., 1978). These epitopes vary in immunoreactivity. Differing forms of GH have not been confirmed in the bovine species. However, results from research in primates suggest the possibility that different epitopes are produced and may have different biological activities (Baumann et al., 1985). Control of GH secretion from the anterior pituitary is controlled.primarily by two hypothalamic hormones (Martin and Millard, 1986; BuonomouandiBaile, 1990; Frohman, 1991), growth hormone releasing factor (GRF; also called growth hormone releasing hormone, GHRH) and somatostatin (somatotroph release-inhibiting factor, SRIF) . Growth hormone secretion in the ruminant is pulsatile and variable among animals (McAtee and Trenkle, 1971a; Breier et al., 1986; Anderson, 1987; Laurentie et al., 1989). Fluctuations in GRF and somatostatin are thought to cause GH pulses (Davis, 1988). In male rats, GH is secreted in peaks with higher amplitude and baseline 14 values than females. Similarly, bulls have higher peak amplitudes than steers (Afinson et al., 1975) and young bulls have higher GH concentrations than heifers (Keller et al., 1979). Neonatally secreted androgens imprint the high amplitude pulses in males and sexually dimorphic patterns in GH secretion may explain growth rate and body size differences between males and females (Gluckman et al., 1987). Control of GH secretion also involves negative feedback. Growth hormone and insulin-like growth factor-I (IGF-I; somatomedin-C, SM-C) stimulate somatostatin release from the hypothalamus (Berelowitz et al., 1981), thereby inhibiting pituitary release of GH. Somatostatin inhibits GH response to GRF. Berelowitz et al. (1981) reported that IGF-I participates in the negative feedback loop with an immediate effect on hypothalamic somatostatin and a delayed effect on the anterior pituitary. Nutritional status plays a role in determining the circulating GH concentration in cattle. Growth hormone concentrations are elevated during nutritional deficit in sheep and cattle (Ellenberger et al., 1989). Breier et a1. (1986) observed a three-fold increase in GH pulse amplitude of Angus steers fed 1% versus 3% of live weight on a dry matter basis. There was no change in GH pulse frequency or baseline concentration. Fasting increases the half-life, and reduces the turnover and metabolic clearance rates of GH in calves (Trenkle, 1976). In lactating dairy cows, energy balance is negatively associated.with concentrations of GH (Villa-Godoy, 15 1987). It is postulated that increased levels of GH at lower planes of nutrition are an adaptation to mobilize energy from adipose tissue to maintain basal metabolism (Bauman et al., 1982; Gluckman et al., 1987). However, under optimum planes of nutrition fed for maximum growth, there is little evidence to suggest that GH concentrations are significantly affected by nutritional status. A decline in circulating GH with advancing age has been observed by several workers (Stern et al., 1971; Trenkle, 1971; Trenkle and Topel, 1978; Keller et al., 1979; Anderson, 1987). Early investigators attributed the decline in growth rate from birth to market weight to lowered serum GH concentrations (Baird et al., 1952; Baker et al., 1956). Purchas et al. (1970) reported a decrease in pituitary GH content and a decline in the ratio of pituitary weight to body weight 'with increasing age. Declines in rate of gain exhibited by cattle have coincided with decreases in circulating GH and a dilution of GH concentration on a per unit of body weight basis (Trenkle and Topel, 1978; Anderson, 1987). Although the primary effects of GH on bone growth are mediated by the somatomedins (Spencer, 1985), it has been demonstrated that GH can directly stimulate bone growth. Isaksson et al. (1982) demonstrated a direct effect of GH on epiphyseal cartilage growth by injecting human GH locally into the growth plate of hypophysectomized rats. Width of the cartilage growth plate was increased after 4 days of GH 16 treatment in a similar study (Isaksson et al., as cited in Isaksson et al., 1986). Growth hormone binds to receptors on chondrocytes isolated from rabbit ear cartilage (Eden et al., 1983) and stimulates DNA synthesis in the same tissue (Madsen et al., 1983). Isaksson et al. (1986) suggests that GH directly stimulates chondrocyte differentiation in the growth plate. Local growth factors (IGF-I), produced in the growth plate, are responsible for subsequent clonal expansion. The finding that GH specifically binds to cells in the proximal part of the growth plate (Isaksson et al., 1986) would support this "dual effector" theory. Growth hormone does not appear to have direct effects on growth of muscle cells in culture (Florini, 1985). Growth hormone had little effect on proliferation or amino acid uptake of rat myoblasts or myotubes in vitro (Florini et al., 1977; Ewton and Florini, 1980). Allen et al. (1983) found no effect of GH on actin synthesis in cultured satellite cell myotubes. Similarly, exogenous GH at physiological concentrations showed no effect on rat muscle satellite cell proliferation in vivo (Beermann et al., 1983). Harper et al. (1987) reported no effect of GH on protein synthesis and degradation in cultured ovine muscle cells. In contrast to studies on individual muscle cells, GH has been found to be anabolic in isolated muscles. Growth hormone stimulates amino acid incorporation in diaphragm muscle from hypophysectomized (Kostyo and Engel, 1960; Kostyo and Schmidt, 1961) and normal (Albertsson-Wikland et al., 1980) rats. 17 Increased activity of the ribosomes was also found in the same tissues (Kostyo and Rillema, 1971). The effect of GH on proliferation of non-muscle cells may explain the results found when GH is added to isolated muscles as compared to cells in culture (Florini, 1985). It has been suggested that the actions of GH on skeletal muscle are mediated by IGF-I (Florini, 1985: Davis, 1988). The effects of GH on adipose tissue metabolism are thought to be diabetogenic and lypolytic. Eisemann et al. (1986) showed fatty acid (FA) turnover rates are increased in dairy and beef cattle treated with highly purified bovine GH, coupled with an irreversible loss of FA from the plasma pool. The authors attributed the results to an enhanced release of FA from adipose tissue (lipolysis). In vitro studies with ruminant adipose tissue have not shown conclusive evidence that GH is lipolytic (Duquette et al., 1984; Etherton and Walton, 1986). Positive lipolytic responses to exogenous GH in vivo but not in vitro may suggest that the GH molecule needs to undergo in vivo modification or may activate a lipolytic intermediate (Hart, 1984a; Hart et al., 1984b: Etherton and Walton, 1986; Gluckman, 1987). In support of this theory, Hart et al. (1984b) found that recombinant GH increased FA concentrations in vivo but did not stimulate glycerol release in vitro. In hypophysectomized rats, glucose transport occurs at maximum rate and cannot be stimulated by insulin. Administration of GH to the same rats decreased glucose 3 18 transport and increased sensitivity to insulin (Schoenle et al., 1979). The ability of GH to alter tissue response to insulin has also been demonstrated in bovine adipose tissue (Etherton et al., 1987). No effects of GH on insulin- stimulated lipogenesis were observed with short-term incubations of swine adipose tissue (Etherton and Walton, 1986). However, chronic exposure of the tissue to- physiological concentrations of GH showed a strong antagonisitic effect of insulin action on lipogenesis, suggesting that GH is acting to divert nutrients away from lipid synthesis. Adipocyte differentiation has been shown to be affected by GH in vitro. Nixon and Green (1984) and Green et al. (1985) showed that GH stimulates the differentiation of 3T3 preadipose cells to adipocytes, and that IGF-I was not involved in differentiation. The "dual effector" theory states that GH directly stimulates cells to differentiate, and IGF-I acts on the differentiated cells to promote clonal expansion (Green et al., 1985). These results are in conflict with in vivo data, as increases in cell number would lead to an increase in lipid accretion (Boyd and Bauman, 1989). Several workers have attempted to relate GH status of animals to growth rate. Larger breeds of beef cattle have higher mean GH serum concentrations than smaller breeds (Ohlson et al., 1981; Verde and Trenkle, 1982; Grigsby and Trenkle, 1986). Grigsby and Trenkle (1986) found Simmental steers to have higher GH concentrations, less frequent release 19 of GH, and secretory spikes of greater magnitude than Angus steers. Higher GH concentrations have been reported in rams selected for increased rate and efficiency of gain (Dodson et al., 1983) and in Hereford bulls selected for heavier body weight and muscling (Davis et al., 1983). Contrastingly, elevated GH concentrations have been reported in slow growth strains of chickens (Goodard et al., 1988), dwarf chickens (Hoshino et al., 1982), and swine (Norton et al., 1989). Dev and Lasley (1969) reported that dwarf Hereford cattle possessed a normal amount of GH. Purchas et al. (1970), Trenkle (1970), Irvin and.Trenkle (1971), Keller et al. (1979) and Klindt et al. (1985) all found GH was not related to measurements of growth rate in ruminants while Hafs et al. (1971), Purchas et al. (1971), Trenkle and Topel (1978), Wheaton et al. (1986), and Verde and Trenkle (1987) obtained negative correlations. The contradictory reports of the correlation between GH and growth in the literature suggests other molecules or levels of regulatory control are involved. Growth hormone has been found to be negatively related to carcass fatness (Purchas et al., 1970; Trenkle, 1970; Purchas et al., 1971; Trenkle and Topel, 1978; Keller et al., 1979; JKlindt et al., 1985). Wangsness et al. (1977) reported lower GH levels in obese versus lean pigs. Trenkle and Topel ( 1978) found positive correlations between percent carcass muscle and GH status. Eversole et al. (1981)‘ reported both average daily protein and fat gain to be negatively related to serum GH. The complexity of factors involved in the development of 20 the various tissues involved in body growth and the possibility that many of the actions of GH are mediated by IGF-I, does not make it surprising to find inconsistent relationships between GH, growth and carcass traits. Measurement of circulating concentrations of GH does not provide insight into other factors involved in growth such as hormone receptors, tissue refractoriness‘ or other steps involved in the secretion and metabolism of the hormone. Infrequent sampling technique to accurately assess GH status was also a problem in many early studies. Further research is needed to define the biological significance and the parameters involved in the episodic secretion of GH. Thus, correlations between endogenous GH secretion and growth or carcass composition as a selection tool in the animal industry have yet to be demonstrated. Insulin-Like Growth Factor I The insulin-like growth factors (IGF; somatomedins) are a family of circulating polypeptides derived from several tissues. The early study of Salmon and Daughaday (1957) described a factor in normal serum that stimulated the incorporation of labeled sulfate into cartilage explants. Serum from hypophysectomized rats failed to stimulate sulfate incorporation. However, serum from hypophysectomized rats treated with GH stimulated sulfate uptake. Direct addition of GH to the explant media failed to stimulate sulfate incorporation either in the presence or absence of 21 hypophysectomized rat serum. The "sulfation factor” found in serum that mediated the growth promoting actions of GH was later termed somatomedin (Daughaday et al., 1972). Somatomedins are one of a variety of growth promoting factors found in serum that originate from different sources. Somatomedin-C is homologous to IGF-I and has structural similarity to proinsulin. Somatomedin-A and IGF-II are the same peptide. Insulin-like growth factor I is a basic, 70 amino acid single chain peptide and IGF-II is a neutral peptide consisting of 67 amino acids (Gluckman et al., 1987). Insulin-like growth factor II is primarily involved in fetal growth, while IGF-I is associated with postnatal growth and development. Insulin-like growth factors are bound to large molecular weight proteins in blood (Spencer, 1987). Half-life of IGF is increased when bound to the transport protein. Transport proteins. render IGF inactive, preventing insulin-like effects. Activity is restored upon release from the transport protein. The transport protein provides short term storage and transports IGF to target tissues (Spencer, 1987). Liver is the major source of circulating IGF (D'Ercole et al., 1984). Schwander et al. (1983) showed that IGF is produced and secreted by the perfused rat liver. Many other tissues also synthesize IGF (D'Ercole et al., 1984), suggesting that IGF may exert its biological influence in an autocrine, paracrine, or endocrine manner. However, it has been estimated that over 90% of the total IGF is secreted by 22 the liver (Froesch et al., 1986). Concentrations of IGF in serum. are related. to» GH. Concentrations are lower in hypopituitary states and elevated in GH excess (Clemmons et al., 1987; Gluckman et al., 1987). Administration of GH to humans resulted in an increase in plasma IGF-I concentration (Copeland et al., 1980 cited in Clemmons et al., 1987). Underwood et al. (1982) reported.a 5- fold increase in IGF concentration in intact compared to hypophysectomized ewes. In chickens (Hoshino et al., 1982) and sheep (Roberts et al., 1990) , IGF concentrations are greater in males than females. Bishop et al. (1989) showed a similar trend in beef cattle. Insulin-like growth factor I concentrations rise after birth and then remain constant from 6‘to 18 weeks of age in rams (Olsen et al., 1981). Lund-Larsen et al. (1977) reported an increase in IGF-I concentration from 6 to 10 months of age in Red Danish bulls. Hoshino et al. (1982) showed a decline in IGF-I concentrations over time in chickens. Limited data are available on the effects of time or age on IGF-I concentrations; however, a decline in GH over time should result in a corresponding decrease in IGF-I. Indeed, Davis and Bishop (1991) reported circulating IGF-I concentrations to decline with age in heifers; and Hammond et al. (1990) reported a negative correlation between IGF-I concentration and days on feed. Nutritional status plays a dominant role in regulating IGF-I concentrations. Gluckman et al. ( 1987) showed a 50 23 percent decrease in plasma IGF-I in Angus steers fed below maintenance compared with steers at higher intakes. Upon realimentation, IGF-I concentrations returned to normal (Ellenberger et al. , 1989) . Similarly, low energy diets have been associated with reduced IGF-I concentrations in steers (Elsasser et al., 1987; Houseknecht et al., 1988; Ellenberger et al., 1989; Elsasser et al., 1989; Hammond et al., 1990). Elsasser et al. (1989) reported lower IGF-I concentrations in a state of low or negative nitrogen balance and diminished response of IGF-I to exogenous GH. Concentrations of IGF-I increased with added protein in isocaloric diets. The authors speculate that protein may be the primary nutritional determinant of basal IGF-I in cattle and that undernutrition can uncouple the regulation of IGF-I by GH (Elsasser et al., 1989). Similar trends have been reported in humans (Clemmons et al., 1987). Insulin-like growth factors have been identified in all tissues; including adipocytes, skeletal muscle and cartilage (Gluckman et al., 1987). The stimulatory effects of IGF-I on cartilage growth was first demonstrated by Simon and Daughaday (1957). More recent evidence suggests the growth promoting effects of GH may be attributed to IGF-I (Schoenle et al., 1982). These workers infused IGF-I into hypophysectomized rats and showed that tibial cartilage growth was restored to rates similar to GH treatment. In an effort to demonstrate paracrine function of locally produced IGF-I, Schlecter et al. (1986, cited in Davis, 1988) demonstrated inhibited tibia 24 growth in rats infused with anti-IGF-I antibody. In similar studies, exogenous IGF-I administration to hypophysectomized and.normal rats.has resulted in increases in tibial width, but not to the same degree as with GH treatment (Guler et al., 1986; Hizuka et al., 1986 cited in Clemmons et al., 1987). The primary functions associated with IGF are stimulation of mitosis in cell culture, stimulation of growth in hypophysectomized animals and insulin-like effects (Gluckman et al., 1987). Rate of growth in both normal and hypophysectomized rats has been shown to increase with IGF-I administration (Froesch et al., 1986; Davis, 1988). Insulin- like growth factor I is active in istimulating‘ anabolic processes in muscle (Florini,1985) . Insulin-like growth factor I has been shown to stimulate proliferation, amino acid uptake and differentiation in cultured myogenic cells (Ewton et al., 1987). Harper et al. (1987) demonstrated the ability of IGF-I to stimulate muscle protein synthesis and decrease protein degradation in ovine myotubes. Dodson et al. (1987) reported IGF-I increased proliferation of satellite cells. However, Greene and.Allen (1991) found IGF-I to have no effect on proliferation but rather to stimulate differentiation of bovine satellite cells in vitro. The effects of IGF-I on adipose tissue are less clear than with muscle and bone. Insulin-like growth factor I elicits classical insulin-like effects on the target tissues of insulin. Increased glucose metabolismL and lipid synthesis (Froesch et al., 1986); and decreased lipolysis in adipose 25 tissue (Gluckman et al., 1987) are associated with higher concentrations of IGF-I. Compared with adipose tissue, the rat heart muscle is 20 times more sensitive to IGF than adipose tissue. It is likely that IGF affects glucose metabolism in muscle through an IGF receptor (Froesch et al. , 1986) , whereas it has been postulated that IGF exerts insulin- like function in adipose tissue through the insulin receptor (Gluckman et al., 1987). Incorporation of labeled glucose into diaphragm muscle is stimulated at IGF concentrations lower than those necessary to produce insulin-like effects on adipose tissue. From these results, Froesch et al. (1986) have suggested IGF infusion would lead to an insulin-like effect on muscle before lipolysis is inhibited and glucose metabolism of adipose tissue is stimulated. Further studies combining in vivo and in vitro approaches are necessary to understand how IGF-I affects adipose tissue. Correlations between IGF-I concentration and animal performance have been variable. Eigenmann et al. ( 1984) studied IGF-I concentrations in lines of Poodles bred for different mature body sizes. Larger breeds of Poodles have significantly higher concentrations of IGF-I, whereas normal growth hormone concentrations were found in all groups. Selection for high lean tissue in mice resulted in increased body weight and higher basal IGF-I concentrations. Selection for fatness had no effect on IGF-I status in the same study (McKnight and Goddard, 1989) . Similarly, Blair et al. (1988) reported increases in 6-week and mature body weights after 7 26 generations of selection for elevated IGF-I in mice. In cattle, Davis et al. (1992) reported a low IGF-I selection line tended to have higher weaning weights, daily gains, and yearling weights than the high IGF-I line. Limited data are available in cattle using IGF-I concentrations as a selection tool. Lund-Larsen et al. (1977) found circulating IGF-I to be positively related with rate of gain and growth, and negatively related to feed conversion efficiency in Red Danish bulls. Insulin-like growth factor I concentrations were also found to be positively correlated with body weight and hip height in sets of identical twin heifers (Davis and Bishop, 1991). Goddard et a1. (1988) reported IGF-I was not related to growth rate between lines of chickens, although higher IGF- I was positively correlated with an increase in body weight. Olsen et al. (1981) measured IGF-I concentrations in Dorset lambs from 2 to 18 weeks of age. Insulin-like growth factor I was positively correlated with relative weight gain (gain as.a percentage of body weight) but not absolute body weight gain over the period. Faster growing Suffolk sired lambs were found to have higher IGF-I than Finnsheep by the same workers (Wangsness et al., 1981). Hammond et al. (1990) found IGF-I concentration to be positively related to estimated percentage of Brahman breeding and inversely related to estimated percentage of English breeding. However, the specific design of the study was to evaluate the effects of nutritional levels on IGF-I concentration and not breed of 2'7 cattle. These same workers found IGF-I to be significantly correlated with empty body weight (r= -.60), empty body water (rs -.59) and empty body protein (r= -.60). Davis et al. (1992) reported a positive relationship between ribeye area, carcass weight, marbling, and quality grade with IGF-I. In the same study, IGF-I was positively related to backfat, percentage kidney, pelvic and heart fat, and yield grade; however, the authors attribute these findings due to a corresponding increase in carcass weight. In contrast, Anderson (1987) reported negative correlations (P < .05) between IGF-I concentrations and percentage carcass fat (r8 - .60), carcass fat accretion rate (r= -.57), total carcass fat (r= -.52), fat thickness (r-- -.73) and percentage carcass protein (r= .60). Insulin Insulin is a peptide hormone secreted from the beta cells of the pancreatic Islets of Langerhans. In coordination with other anabolic and catabolic hormones, insulin controls partitioning of available nutrients during growth. Insulin has pronounced effects on carbohydrate and protein metabolism by regulating entry of glucose and amino acids into tissues. Due to differences in metabolism between ruminant and nonruminant species, insulin may exert dissimilar functions in different species. As a result of microbial fermentation in the rumen, ruminants utilize acetate instead of glucose as a 28 major substrate for energy storage and oxidation and are almost totally dependent on gluconeogenic pathways for the supply of needed glucose in both the fed and fasted state (Prior and Smith, 1982). McAtee and Trenkle (1971b) found a biphasic secretory pattern of insulin after a meal in growing cattle. There is a rapid increase of circulating insulin followed by a second rise of insulin which lasts between 2 and 6 hours, coinciding with absorption of the products of digestion and peripheral tissue anabolism (Weekes, 1986). Because carbohydrates are fermented in the rumen, concentration of insulin in the blood is not correlated with blood glucose (Trenkle, 1981). Products of digestion that induce release of insulin from the pancreas are not clearly defined in the ruminant. Intravenous injection of propionate or butyrate stimulate release of insulin, .Amino acid infusion also causes a release of insulin (McAtee and Trenkle, 1971b). However, the authors point out that there is not a marked increase in concentrations of propionate, butyrate, or free amino acids in the blood of ruminants after feeding. Contrastingly, Stern et al. (1971) found intravenous glucose administration to elevate insulin concentrations in suckling, weanling, and mature ruminants. Heifers fasted for intervals of two to eight days had lower concentrations of circulating insulin than during the fed state (McAtee and Trenkle, 1971b). An increased proportion of concentrate in diets enhanced the magnitude of 29 post-feeding rise of insulin in sheep (Weekes, 1986) and cattle (Trenkle, 1970). Growing lambs fed a fixed amount of feed per unit of metabolic weight had an increased secretion of insulin as age and body weight increased (Weekes, 1986). Trenkle (1970) , Trenkle and Topel (1978) , and Verde and Trenkle (1987) reported insulin concentrations were lowest in young cattle and gradually increased with age and weight. The increased insulin response to feeding with age may be associated with the increase in deposition of body fat (Weekes, 1986). Insulin is generally thought to stimulate lipogenesis (Prior and Smith, 1982). The effects of insulin on fat metabolism in the man and rat are well established. Insulin increases adipocyte uptake of fatty acids by stimulation of lipoprotein lipase activity. Lipogenesis is stimulated by increased glucose uptake and increased activities of pyruvate dehydrogenase, acetyl-CoA carboxylase and fatty acid synthesis (Weekes, 1986) . Insulin is also thought to decrease the mobilization of stored triglyceride (Martin et al., 1984; Weekes, 1986). Insulin receptors have been found on adipocytes from cattle (Vernon et al., 1985). Incubation with physiological concentrations of insulin for 24 hours stimulated glucose and acetate utilization by sheep adipose tissue (Vernon et al., 1985) . Yang and Baldwin (1973) found a combination of insulin and glucose increased acetate utilization by isolated bovine adipocytes. Insulin treatment of diabetic steers 30 significantly decreased plasma glucose, lactate, free fatty acid and triglyceride concentrations. Further results from these studies suggested that insulin was necessary to reestablish rates of acetate and lactate incorporation into fatty acids in adipose tissue in vitro (Prior and Smith, 1982) . Prior and Smith (1982) have suggested that the primary effects of insulin on ruminant adipose tissue are to increase the uptake of glucose and to stimulate lipoprotein lipase with an overall effect of increasing triglyceride deposition. Insulin is thought to be one of the major regulators of muscle protein metabolism (Etherton, 1982) . Cattle hind-limb studies have been used to study the effect of insulin to increase uptake of amino acids. The work of Brockman et al. (1975) showed insulin had no effect on hepatic removal of amino acids, suggesting skeletal muscle would account for a major portion of these effects. Indeed, Prior and Smith (1983) reported that insulin treatment of diabetic steers reversed an increase in plasma amino acid concentrations. Similar results have been obtained in sheep (Prior and Smith, 1982). Airhart et al. (as cited in Florini, 1985) demonstrated stimulation of protein synthesis in chick myoblasts with physiological concentrations of insulin. Muscle cell DNA, RNA, and protein synthesis are decreased in insulin deficient rats and these effects are reversed by insulin administration (Martin et al., 1984) . Florini (1985) suggested that insulin plays an essential role in maintaining cells in a viable condition, thus allowing 31. cells to grow rather than a direct stimulatory effect. The basis for this theory originates from the crossreactivity of insulin and IGF-I receptors. The IGF type 1 receptor binds IGF-I and.has a*weak.crossreactivity with insulin, Both IGF-I and IGF-II have a weak affinity to the insulin receptor (Gluckman et al., 1987). The close homology of the IGF type 1 and insulin receptors and the corresponding crossreactivity of the two hormones may explain the anabolic effects of insulin on muscle when added at high concentrations (Florini,' 1985). The mode of action of IGF and insulin in any tissue may depend on.the-distribution of insulin and IGF receptors in that tissue (Gluckman et al., 1987). Direct action of insulin on cell growth remains inconclusive and further research is needed to define the effects of insulin in the ruminant and its synergism with other hormones controlling tissue metabolism. Etherton and Kensinger (1984) propose that measurements of insulin receptor sensitivity, secretion and metabolic clearance rate may provide a better understanding of the physiological role of insulin on growth. The importance of insulin in the regulation of growth is made apparent by the effects of diabetes. Romsos et al. (1971) was able to reverse chronic tissue wasting and weight loss in diabetic pigs with insulin administration. However, circulating insulin concentrations appear to be unrelated to growth rate (Irvin and Trenkle, 1971; Trenkle and Topel, 1978; Etherton, 1982). Wangsness et al. (1977) reported a line of pigs selected for slow growth and obesity had higher insulin 32 concentrations than the faster growing, lean control line. Contrastingly, Norton et al. (1989) found elevated insulin concentrations in gilt‘s selected for rapid versus slow growth. Iowa workers have also reported conflicting evidence with respect to cattle breed and insulin concentration. Irvin and Trenkle (1971) originally reported no differences in circulating concentrations among breeds. Grigsby and Trenkle (1986) found earlier maturing Angus steers have significantly higher insulin concentrations than Simmental steers. In a later study, large frame steers had higher blood insulin concentrations compared to medium or small frame steers (Verde and Trenkle, 1987). The authors attribute the latter finding to an increased level of feed intake in the large frame steers. Similarly, it has been suggested that a positive relationship between growth rate and insulin could not be demonstrated due to the variation in insulin concentration throughout the day in response to feeding (Etherton and Kensinger, 1984). However, Eversole et al. (1981) reported insulin concentration to be positively related to average daily gain. Despite the inability of workers to relate insulin with growth, insulin has been shown to be strongly correlated with carcass fatness. In growing cattle, Trenkle and Topel ( 1978) found that circulating insulin concentrations were positively correlated with percentage of carcass fat and negatively related with carcass muscle. These correlations are opposite those reported for GH (Purchas et al., 1970; Keller et al., 33 1979; Klindt et al., 1985). Elevated GH and low insulin concentrations in. larger, leaner' breeds. of cattle favor increased and more prolonged growth of skeletal muscle rather than shifting energy to adipose tissue. Smaller breeds of cattle have more insulin and is associated with increased fat deposition at an earlier age (Trenkle, 1981). Although this hypothesis has yet to be confirmed, it would support the. theory that a number of hormones and their interactions are involved in the complex process of growth and ultimately carcass composition. Thyroid Hormones Triiodothyronine (T3) and thyroxine (T4) are amine hormones produced, stored, and secreted by the thyroid gland. Thyroid hormones are iodinated derivatives of the amino acid tyrosine, with the subscripts denoting the number of iodine atoms in the molecule. Of the two iodinated thyronines, thyroxine is predominant; accounting for approximately one- third of the total iodine in the thyroid, with less than ten percent in the form of T3. Thyroid hormones are found in the bloodstream primarily bound to thyroxine binding globulin. A very low percentage of hormone circulates unbound. The concentration of T4 in plasma is much greater than T3 due to its greater affinity for the binding protein. Conversion of T4 to T3 by peripheral deiodination of the T4 molecule suggests that T4 may serve as a storage form of the more biologically active T3. 34 Secretion of thyroid hormone is under control of the. hypothalamic-pituitary axis. The hypothalamic releasing hormone, thyrotropin releasing hormone (TRH), stimulates secretion of thyroid stimulating hormone (TSH, thyrotropin) from the anterior pituitary. Thyroid stimulating hormone stimulates release of T3 and T4 (thyroid hormone) from the thyroid gland. Thyroid hormone exerts a negative feedback on the anterior pituitary to decrease the sensitivity of TSH secreting cells to the stimulatory effects of TRH. Hammond et al. (1984) used Hereford steers to investigate the rhythmicity of circulating T3 and T4. Time series analysis suggested 12 and 24 hour cyclical trends for T3, which may have been related to feeding period. Thyroxine demonstrated a 24 hour cyclical pattern and relatively larger values were found in the early afternoon and decreasing values through the morning hours. However, day and time had no significant effect on T3 or T4 as concentrations over a 48 hour period varied only 8 and 0.3 ng/ml for T4 and T3, respectively. There was a tendency to increase concentrations of both hormones at or shortly after feeding. Thyroid hormones do not seem to be strongly influenced by cattle age. Irvin and Trenkle (1971) studied the effects of age, breed, and sex on the concentration of protein-bound iodine (PBI, thyroid hormone index) in cattle from 18 to 371 days of age. No differences were found although 18 day old cattle tended to have higher average concentrations of PBI. Similar findings were reported by Trenkle (1970) who found no 35 variation in PBI concentration over a 142 day feeding period with older cattle. Blood samples taken for 12 months in cattle from 5 to 17 months of age revealed concentrations of T3 increased during the first 4 months of the experiment and T4 concentrations decreased slightly during the same period (Verde and.Trenkle, 1987). For’the remainder of the study, T3 remained steady while T4 increased. Patterns of the concentrations of thyroid hormones were similar for all groups of cattle studied. Work in Belgium would support the findings of a slight increase in T4 concentrations with age (Fabry, 1983). Advancing age has no effect on the secretory pattern of TSH or the clearance and secretion rates of TRH in rams (Morrison et al., 1981). Little research has been conducted to study the relationship between sex and thyroid hormones. Kahl and Bitman (1983) found bulls to have higher T3 and T4 concentrations than heifers between 1 and 4 months of age. Over a longer time period, Irvin and Trenkle (1971) saw no differences in PBI related to sex. Similarly,.Anderson et al. (1973) found no differences in growing Jersey heifers and bulls. Ellenberger et al. (1989) investigated thyroid hormone status in steers during compensatory and normal growth and dietary restriction. During restricted growth, mean serum concentrations of T4 were lower and T3 concentrations remained unchanged. Upon realimentation T4 concentrations increased. Reductions in T3 and T4 concentrations have been associated 36 with calorie-restricted diets in the rat (Schalch and Cree, 1985). In periparturient cows, elevated T3 and T4 concentrations were associated with diets exceeding NRC energy requirements versus those fed at NRC recommendations (Pethes et al., 1985). The authors also noted that T3 paralleled T4 throughout the experiment. Hammond et al . (1984) reported plasma T4, but not T3, concentration increased with increasing nitrogen level in the diets However, this increase could.have been related to a trend toward higher digestible energy intake with the higher nitrogen diets. The same workers failed to show differences in thyroid hormone concentrations in steers fed on two winter nutritional levels or during‘ grazing (Hammond et al., 1990). Thyroid hormones are important in bone growth as hypothyroidism results in decreased bone growth. Hyperthyroidism increases bone resorption but has no effect on net bone growth (Spencer, 1989). Mundy et al. (1976) showed thyroid hormone can directly stimulate bone resorption. Receptors for T3 have been found on chondrocytes in the growth plate and thyroid hormone administration to hypothyroid animals increases the size of the growth plate (Spencer, 1989). The finding that dwarf chickens,have lower circulating T3 concentrations would support the theory that normal growth is dependent on a euthyroid state (Bowen et al., 1987). Skeletal muscle protein synthesis and degradation are affected by thyroid hormone status. Reduced growth is associated with hypothyroidism and hyperthyroidism. A minimal 37 amount of T3 is essential for normal muscle growth and suboptimal concentrations lead to dwarfism (Goldberg et al., 1980) as seen in the chicken (Lilburn et al., 1986; Bowen et al., 1987). Thyrotoxicosis is accompanied by weight loss and severe muscle wasting. Goldberg et al. (1980) attempted to clarify the effects of high and low doses of thyroid hormones on muscle. The authors compared the effects of catabolic (high) and anabolic (low) doses of T4 on muscle protein synthesis and breakdown in hypophysectomized rats. Rates of protein synthesis did not differ in the two groups. However, rates of protein degradation were 50 to 75 percent greater in the high dose group suggesting increased protein catabolism was responsible for severe muscle wasting associated with hyperthyroidism. Thyroidectomized animals have reductions in both protein synthesis and degradation causing growth to cease (Goldberg, 1980). In a sex-linked abnormality causing dwarfism in chickens, Bowen et al. (1987) observed that T3 supplementation could increase growth. The same treatment decreased growth in normal strains (normal T3 concentrations) which agrees with the adverse effects of excess thyroid hormone. Triiodothyronine may influence GH and IGF production and activities in tissue. Thyroidectomized rats have depressed hypothalamic GRF and rats treated with an antithyroid drug have reduced pituitary and plasma GH concentrations (Cabello and Wrutniak, 1989). In the dwarf mouse or hypophysectomized rat, administration of thyroid hormone and GH increased or 38 restored concentrations of IGF (Cabello and Wrutniak, 1989). Froesch et al. (1976) indicated that T3 is needed for maximum stimulation of chick cartilage by IGF. Thyroid hormones have been found to be positively related to IGF concentrations in backgrounded but not feedlot steers (Hammond et al., 1990). Hoshino et a1. (1982) reported reduced T3 and IGF-I concentrations in dwarf chickens. Thyroid hormones may be positively related to insulin (Weekes, 1986; Verde and Trenkle, 1987). Relationships between thyroid hormones and other classical hormones (GH, IGF-I, insulin) need further clarification. Efforts to relate circulating concentrations of thyroid hormones to different cattle types and weight gains have generally been unsuccessful and difficult to interpret. Irvin and Trenkle (1971) found FBI to be similar between various purebred and crossbred British breeds. Similar results have been obtained in three frame sizes of cattle with differing propensities to deposit fat (Grigsby and Trenkle, 1986) and in strains of chickens selected for growth (Goddard et al. , 1988). In contrast, Verde and Trenkle (1987) reported large framed, fast growing steers (Simmental cross) had higher’mean T4 concentration than small framed, slower growing steers (Angus-Hereford cross). No difference was observed in T3 concentration. ThyrotrOpin secretion was similar between breeds (Ohlson et al., 1981) and.did.not change with selection for growth (Davis et al., 1983) in cattle. IHowever, Dodson et al. (1983) indicated higher overall means and baseline values 39 for TSH in Targhee rams selected for rate and efficiency of gain. Trenkle (1970) found no relationship between FBI and weight gain in steers while Kahl and Bitman (1983) indicated ‘a positive correlation between thyroid hormones and weight gain in Holstein calves. variability in the relationships between thyroid hormones and daily gain in cattle are best demonstrated by the results of Fabry (1983). A significant positive correlation existed between daily gains over a 12 month period and T4 concentrations measured at 8 to 10 and 15 to 20 days of age. However, in a separate experiment, significant negative correlations existed between daily gains during a 1 year period and T4 sampled at the end of the first month of life. Verde and Trenkle (1987) reported positive correlations between T4 and dry matter intake or body weight of both small and large frame steers during a 12 month period. Standal et al. (1987) indicated correlations between thyroid hormones and production traits (feed intake, growth rate, feed conversion efficiency) in growing heifers were low. Measures of thyroid hormones have not been found to be related to carcass traits (Purchas et al., 1971). It is not surprising that attempts by several workers to relate thyroid status to growth have been unsuccessful. Growth of various tissues may be dependent on the euthyroid state as growth is slowed above or below an optimal concentration. A number of clinical or experimental 4O observations underline the importance of thyroid hormones in the regulation of growth. However, further research is needed to allow a more complete understanding of the relationships between T3 and T4 with other hormones and growth. OBJECTIVES The changes in cattle type that have occurred in the last two decades have been well documented. These changes have resulted in larger framed, later maturing animals that are able to attain heavier. weights while maintaining carcass traits that are acceptable to consumers. Most of these changes have been the result of genetics through the introduction of new breeds and through the advancement of selection practices and technologies. The process of growth and development is generally thought to be primarily under the control of the endocrine system. Several groups of workers have conducted studies to relate differences in serum hormone concentrations with differences in growth rate and carcass composition of cattle. The primary objective of this study was to evaluate differences of critical hormones among four distinct biological types of cattle. These populations of cattle offer a unique opportunity to evaluate changes in hormone parameters that have occurred as a result of selection. Assessment of the relationship of these hormones to various measures of rate and composition of gain was also intended. Recent research with administration of exogenous hormone, in conjunction with in vitro techniques, has greatly enhanced 41 42 our understanding of how hormones affect growth and development. However, specific roles of individual hormones, and how hormones interact to influence biological systems have yet to be determined. With these thoughts in mind, this experiment was designed with the following null hypotheses: 1. Circulating hormone concentrations of growing beef steers will be unaffected by breed, biological type, or selection for growth. 2. Circulating hormone concentrations of growing beef steers will be unrelated to growth rate, carcass traits, and measures of carcass composition. MATERIALS AND METHODS Cattle and Management One hundred fifty nine steers from four breed groups were utilized in a two year experiment to evaluate the relationship among various hormones and rate, efficiency, and composition of gain. The steers utilized were obtained from the herds assigned to a breeding project at the Lake City Experiment Station, Lake City, Michigan. Group 1, an unselected Hereford (UH) herd, had no selection practiced since the initiation of the project in 1966. Group 2 (selected Hereford) steers came from the same original parentage as group 1. Cows in group 2 were artificially inseminated to superior growth (yearling weight) sires within the Hereford breed. Groups 3 and 4 were rotational crossbreeding herds. Moderate sized, moderate milk production breeds (Shorthorn, Angus, Hereford; SAH) comprised group 3. Group 4 consisted of three large sized, high milk production breeds (Gelbvieh, Simmental, Holstein; GSH). Selection in both crossbred groups was for yearling weight. In both years, Shorthorn and Gelbvieh served as sire breeds for groups 3 and 4, respectively. A summary of breed groups and estimated frame scores is given in Table 1. After weaning, cattle were weighed and transported 220 km to the test facility. Initial weight was determined by the 43 Table1. Dewfffntinodierentbreedfcm-r h f a p i f i if a f _ Selection Frame Group criteria score 1 Unselected Herefords (UH) None 1.6a 2 Selected Herefords (SH) Growth 5.3b 3 Shorthom x Angus x Hereford (SAH) Growth 6.06 4 Gelbvieh x Simmental x Holstein (GSH) Growth 6.3d , a,b,c,d Means within a column lacking a common superscript differ (P < .01). 45 average of weights taken on two consecutive days upon arrival. At weaning, all calves were vaccinated for clostridial and respiratory diseases, treated for internal and external parasites and given a growth-promotant implant containing estradiol and progesterone‘. Cattle within a breed group were allotted to pens to equalize age and randomly assigned into three slaughter groups (Table 2). Each slaughter group consisted of one pen of steers from each breed group. Cattle were housed on the south side of a covered, open sided slatted floor facility. Cattle were allowed a minimum of 1.86 square meters per animal. Steers were adjusted to an 80% concentrate.diet (Table 3) within 21 d after arrival at the test facility. Steers were given ad libitum access to diets and fresh feed added once daily. Pen feed refusals were collected and weighed weekly. Cattle were weighed prior to feeding at 28 d intervals. Feedstuffs were collected at two week intervals and analyzed for dry matter and protein content (AOAC, 1984). Carcass Composition Cattle were weighed on two consecutive days immediately prior to slaughter and the average recorded as final weight. Hip heights were taken on all steers approximately one week prior to the first slaughter. Cattle were transported 114 km to a commercial slaughter facility and slaughtered within one 1Synovex-S. Syntex Animal Health Inc., West Des Moines, IA. 2- Efim ' - Slaughter W group Year UH SH SAH GSH 1 1 1951 8.9 19817.5 20117.5 19417.0 2 1 200 1 8.9 198 1 7.0 207 1 7.5 191 1 7.5 3 1 200 1 8.9 20017.0 20217.5" 19517.0 1 2 1921100 16717.0 19117.0 18417.5 2 2 1961 8.9 16818.1 19117.5 19418.9 3 2 1951 8.9 16917.5 18917.0 18517.5 47 Table 3. Diet como . itiona Component Percentage of dry matter High moisture corn 85.0 Corn silage 10.0 Supplementb 5.0 a Diet was formulated to provide 11.0% crude protein and contained 2.4 Mcal NErn/kg and 1.48 Mcal NEg/kg of dry matter. 9 Supplement in redients (as-fed basis): soybean meal, 50.1%; calcium carbonate. 20.9%; trace rn neral salt, 9.5%; urea, 7.1%; potassium chloride, 5.3%; dicalcium phos hate 2.1%; ground corn, 3.5%; Selenium 200, 1.0%; vitamin A, .15%, Rumensin 60, . 5%. The total diet was formulated to contain: Ca. .5%; P. .35%; K, .6%; Se. .02 mg/kg; vitamin A, 454 lU/kg; Monensin, 4.54 mg/kg. 48 hour. Approximately 24 h postmortem, carcasses were ribbed and carcass characteristics measured. Fat thickness, ribeye area, . maturity, marbling score, adjusted fat thickness, and percentage kidney, pelvic, and heart fat were determined by trained university personnel. Yield grades were calculated and quality grades assessed. A five rib section (ribs 9 to 13) was removed from each carcass and transported to the Michigan State University Meats Laboratory. The 9-10-11 rib section was prepared according to procedures described by Hankins and Howe (1946). The 9-10-11 rib section was deboned, bone and soft tissue weights recorded, and.the soft tissue ground three times“ Soft tissue was mixed by hand between grindings to assure a representative sample. Approximately 450 g of sample was collected and stored in a Whirlpack bag at -30 degrees C until further preparation. Samples were thoroughly homogenized.with liquid nitrogen in a large, industrial strength Waring blender prior to dry matter, protein, and ether extract analysis. Triplicate samples were dried in aluminum pans for 48 h at 60 degrees C to determine dry matter content (AOAC, 1984). Crude protein content of duplicate samples was calculated from total nitrogen as determined by the Kjeldahl procedure using a Technicon auto-analyzer system (AOAC, 1984) . Fat content of each sample was determined in triplicate by ether extraction for 12 h in a Soxhlet apparatus. Percentage carcass moisture, fat and protein were estimated from rib fat and protein using 49' the equations of Crouse and Dikeman (1974). Estimations of percentage carcass bone were made using the equation developed by Hankins and Howe (1946). Blood Collection and Hormone Assays One pen of cattle from each breed group was assigned a bleeding date corresponding with slaughter group (Table 4). Approximately 21 d prior to blood collection, cattle were placed in individual stalls in the metabolism room at the MSU Beef Cattle Research Center. Diets and feeding regimen remained consistent with cattle in pens. Dry matter intake was measured on individual animals while in the metabolism stalls. Over the 21 d adaption period, steers were adapted to halters to facilitate blood collection. Under veterinary supervision, steers were fitted with a polyvinyl cannula in the jugular vein the day prior to blood collection. The next day, beginning at 0900 h, blood samples were taken from each steer every 30 min for 8 h. Blood samples were stored at room temperature for 2 to 4 h and stored overnight at 4 degrees C. Serum was obtained by centrifugation at 2000 x g for 25 min. Serum was decanted and stored at -20 degrees C until further analysis. Steers were returned to original pens the day following blood collection. Serum bovine growth hormone was quantified using a double antibody radioimmunoassay (Zinn et al., 1989). Analysis of pulsatile GH secretion was performed using PULSAR (Merriam and Wachter, 1982). Binding proteins for IGF-I were removed by Table 4. Blood collection and sla ohter seduchle _ _. - 5 Slaughter 230 251 265 220 243 51 formic acid/ethanol extraction as reported by Bruce et al. (1991). The international IGF-I reference standard (Bristow et al., 1990) was used as the standard. Insulin-like growth factor I concentration of serum extracts was measured by radioimmunoassay using rabbit anti-hIGF-I (L. ‘Underwood, University of North Carolina-Chapel Hill, personal communication). The antisera is specific for IGF-I and had less than .5% cross-reactivity with IGF-II. After overnight incubation of samples and standards with first antibody, labeled IGF-I was added and samples were incubated for an additional 48 h. Bound IGF-I was precipitated with Staphloccocus aureus protein (Sigma Chemical Company, St. Louis, MO) and the resulting pellet was counted, Commercially prepared radioimmunoassay kits were used to quantitate serum insulin, T4 (Corning Medical, Medfield, MA), and T3 (Refsal et al., 1984). Statistical Analysis Data were analyzed by analysis of variance with breed group, slaughter group, and year as the main effects. All interactions were included in. the model. Analysis 'was performed using the General Linear Models Subroutine of SAS (SAS, 1987). Initial age was included as a covariate due to the young age of SH steers in year two (Table 2). least square means with standard errors are presented in the tables. RESULTS Feedlot Performance Feedlot performance reported on an animal basis for breed groups (BG) and slaughter groups (SG) is shown in Tables 5 and 6, respectively. unselected Hereford steers were lightest initially and at slaughter (P < .01). Initial and final weights increased (P < .01) as frame score increased among BG. Final weights increased.with.time on feed (P < .01). Selected Hereford steers gained the fastest and UH steers the slowest across all SG (P < .01). Crossbred steers (SAH and GSH) were intermediate to UH and SH, but not different from each other for ADG. Average daily gains were similar across SG. Feed intakes and feed conversion efficiencies are reported on a pen basis over the entire feeding period. Daily feed intake paralleled live weight for UH, SH, and GSH steers. Daily feed intake was highest for SAH steers (P < .01) . Steers in SG 3 consumed more feed on.a daily basis than steers in SG 1 and SG 2 (P < .01). Unselected and selected Hereford steers required less feed per unit of gain than SAH or GSH steers (P < .01) over the entire trial, with UH steers having the most desirable feed conversion numerically. Feed conversion efficiency tended to decrease with time on feed (Table 6). 52 53 Table 5. Feedlot . rformance of breed erouu - mm Item UH SH SAH GSH Initial wt. kg 15258148 21408139 25650139 277.38 14.0 Finalwt. kg 40318181 53938168 55768166 58468168 ADG. kg 1.0381 .02 1.336102 1.248102 1.268102 DMI, kg/steer/d 56981.09 75481.09 8.2081.09 7.9801.09 Feed conversion 55381.14 5.6681 .14 6.60bzl: .14 6.3481 .14 efficiency, feed/gain a,b,c,d Means within a row lacking a common superscript differ (P < -01)- 54 Table 6. Feedlot . rformance of Slau hter ermiu 7 - SW Item 1 2 3 initial wt. kg 21958135 22178136 233013135 Final wt, kg 49478161 52268162 54618160 ADG. kg 1221.02 121.02 1.201 .02 DMI, kg/steer/d 7.218108 7.328108 7.528108 1299:3923 "argon eflbiency' 5.86 1 .12 5.99 1 .12 6.24 1 .12 8.88 Means within a row lacking a common superscript differ (P < .01 ). 55 Carcass Characteristics Differences in carcass characteristics among BG reflect the diversity of cattle types used in this study. Carcass measurements of BG are shown in Table 7. Carcass weights paralleled live weights and there were no differences in dressing percentage due to BG. As frame size and slaughter weight increased among BG, fat thickness decreased while carcass weight and ribeye area (REA) increased (P < .01) . Across all SG (Table 8), UH carcasses had the highest REA/carcass weight (P < .01), marbling score (P < .05), and corresponding quality grade (P < .10). Carcass weights and final weights increased as time on feed (SG) increased. Fat thickness (P < .05), REA and marbling score (P < .01) were lowest for SG 1. Slaughter group 3 carcasses had the smallest REA on a carcass weight basis (P < .01) . Significant SG x year interactions existed for marbling score (P < .01) and quality grade (P < .10) . Least squares means of the slaughter group x year interactions are listed in Table 12. Carcass Composition Proportions of carcass fat, protein, moisture, and bone for BG and SG are given in Tables 9 and 10, respectively. Unselected Hereford carcasses had the highest percentages of carcass fat, and GSH carcasses were the leanest across all BG (P < .01) . Estimates of carcass protein and moisture were inversely related to carcass fat. Carcass fat increased with SG, while carcass protein and moisture decreased (P < .01) . 56 Table 7. Carcass measurements of breed oorou f accustom Item UH SH SAH GSH Carcasswt. kg 244.18 15.3 329.58 14.4 346.68 14.3 364.4f 14.5 Fat thickness, mm 12.68 1.62 10.48 1.52 8.58 1.51 7.2f 1.52 Adjusted fat thickness, mm 15.48 1.66 12.38 1.55 10.18 1.54 83'155 Fiibeye area, cm2 67.08 11.4 77.68 11.2 80.78 11.3 90.9f 11.2 REA/carcass wt; cm2/kg .2768 1.004 2368 1.003 .2348 1.003 .2508 1.003 Yield grade 3.298 1.10 3.048 1.09 2.918 1.09 2.348 1.09 Marbling score8 5489 111.3 507h 19.3 521'1 19.2 504h 19.4 Quality gradeb 12.1i 1.16 118 1.14 11.7i 1.13 11.51 1.14 a 400 = Slight 0; 500 = Small 0. b 11.0 = high Select; 12.0 = low Choice. c,d,e,f Means within a row lacking a common superscript differ (P < .01 ). 93“ Means within a row lacking a common superscript differ (P < .05). hi Means within a row lacking a common superscript differ (P < .10). .__ .__ __‘, .-.___._.—.__ _ _—__._._~___———_—_..___ _ _ _ _.#_____- #__ ‘i__._. 4 . _ if 57 T8888 8- 88W88 8'8 88 888°: , - - - SlammLomup item 1 2 3 Carcass wt, kg 305.48 14.0 321.38 14.1 335.88 13.9 Fat thickness, mm 8.6f 1.46 10.09 1.48 10.49 1.45 Adjustedfatthickness. mm 10.8 1.49 11.9 150 11.9 1.48 Ribeye area. cm2 75.88 11.1 80.98 11.1 80.58 11.1 REA/carcass wt; crn2/kg 2518 1.003 .2558I 1.003 .2418 1.003 Yield grade 2.86 1.08 2.84 1.08 3.00 1.08 Marbling score8 4988 18.4 5318 18.6 5328 18.2 Quality gradeb 11.5 1.12 11.8 1.13 11.8 1.12 a 400 = Slight 0; 500 = Small 0. b 11.0 = high Select; 12.0 = low Choice. c,d,e Means within a row lacking a common superscript differ (P < .01). 7.9 Means within a row lacking a common superscript differ (P < .05). 58 Table 9. Carcass comusltion ofbr f...i f ,1 ,, , , W m UH SH SAH Carcass fat, % 36.581.53 34281.44 33581.43 Carcass protein, 91. 13.58 1.16 13.98 1.13 1438 1 .13 Carcass moisture, % 49281 .37 50.78 1 .31 51.28 1 .30 Carcass bone, 8/. 13.88 1 .16 14.58 1 .14 14.88 1 .13 a.b,c,d Means within a row lacking a common superscript differ (P < .01). 59 enumerate-in Item 2 Carcass fat. 8/. 32281.40 33381.41 35.181.39 Carcass protein, 8/. 14.38 1 .12 14.58 1 .12 13.78 1 .12 Carcass moisture. 8/. 52.08 1 .28 51.28 1 28 5038 1 27 Carcass bone. % 14.51.12 14.51.13 14.51.12 a,b,c Means within a row lacking a common superscript differ (P < .01). 60 Table 11. Influence of breed crouo and ear on selected carcass cararihctestcs _ XQRLJ. Quality gradeab Carcass fat, %b Carcass protein, %b Carcass moisture, %b Carcass protein, % r Carcass moisture, % 12.1 1 .23 37.2 1 .73 13.1 1 .22 48.6 1 .51 12.1 1 .24 35.7 1 .76 13.8 1 .23 49.8 1 .53 11.11 .19 35.41.60 13.61.18 49.8 1 .42 12.0 1 .21 32.9 1 .68 14.1 1 .20 51.6 1 .48 11.8 1 .20 33.61.63 14.51.19 51.11.44 11.7 1 .18 33.41 .59 14.21.18 51.21 .41 11.3 1 .18 29.51.59 15.0 1.18 54.0 1 .41 11.7 1 .20 30.5 1 .66 15.1 1 .20 r 53.3 1 .46 (a 11.0 = high Select; 12.0 = low Choice. Breed group x year interaction (P<.10). ltern 61 Table 12. Influence of slau -_ hter _._ . and e on selected carcasscarahcteristics _- leaLl Marbling scoreac Quality gradebd Carcass fat, "'led Carcass moisture. %d W Marbling score Quality grade Carcass fat, % . Carcass moisture, % 4881118 11.41 .17 33.31 .55 51.01 .39 5071122 11.61 .18 31.01 .57 52.91 .40 4941119 11.41 .17 33.41 .56 51.11 .39 569112] 12.21 .19 33.11 .60 51.21 .42 a 400 = Slight 0. 500 = Small 0. b 11.0 = high Select. 12.0 = low Choice. ° Slaughter group x year interaction (P < .01). ‘3 Slaughter group x year interaction (P < .10). 62 Year x BG interactions (P < .10) existed for carcass fat, protein, and.moisture. Significant SG x year interactions (P < .10) existed for carcass fat and moisture. Least squares means for selected carcass characteristics are given in Tables 11 and 12. Hormone Parameters Serum hormone concentrations for each breed group are reported in Table 13. Each GH value shown represents the mean of 17 serum samples analyzed on each steer. Hourly serum samples from each steer’were pooled for quantification of IGF- I, insulin, T3 and T4. Across all bleed groups, UH and GSH steers had higher (P < .01) GH concentrations than SH and SAH steers. A bleed group x breed group interaction (P < .01) existed for GH. Least squares means are reported in Table 15. Insulin-like growth factor I concentrations paralleled. GH. Unselected Hereford steers had higher IGF-I concentrations than other BG (P < .01), with SH and GSH steers not different from each other but.higher than SAH steers. Purebred steers (UH and SH) had higher (P < .01) insulin concentrations than crossbred steers. Triiodothyronine (P < .10) and thyroxine (P < .01) concentrations were lower in SH steers than other BG. Thyroxine concentrations were found to be higher in UH steers than SH or SAH steers. The effects of sampling date on serum hormone means are shown in Table 14. Growth hormone and IGF-I means declined 63 Table 13. Serum hormone concentrations for breed . rou-s W item UH SH SAH GSH !Growth hormone. rig/ml 3.708 1 .17 3.318 1 .14 3.238 1 .14 3.898 1 .14 IGF-l, 11ng 880.58 1 28.3 795.38 1 23.5 724.18 1 23.1 808.48 1 23.6 Insulin, uU/ml 35.1 b 1 1.9 33.98 1 1.6 27.28 1 1.6 27.48 1 1.6 13, ng/ml 2.408 1 .06 2.21 d 1 .05 2.368 1 .05 2.358 1 .05 T4, 11ng 102.48 1 2.8 87.38 1 2.3 95.08 1 2.3 98.988 1 2.4 a,b,c Means within a row lacking a common superscript differ (P < .01). 00 Means within a row lacking a common superscript differ (P < .10). 57...-.. 7 l . if ‘__1 Table 14. Serum hormone concentrations forbleed corous Item Growth hormone. ng/ml 4.068 1.13 3.428 1.13 3.128 1.13 lGF-l,ng/ml 898.68 121.1 797.38 1 21.7 710.48 120.7 Insulin, nU/mi 30.8 11.4 32.6 11.5 29.2 11.4 T3. ng/ml 2.36b 1.05 2.44b 1.05 2.208 1.05 98.2 12.1 95.2 12.2 94.3 12.1 a,b,c Means within a row lacking a common superscript differ (P < .01). 65 Table 15. Influence of breed group and bleed group or growth hormone concentration . ml a W Bleed group ' UH SH SAH GSH 1 4.111.31 421124 3.451 .24 4.461 24 2 4.001 .29 2.851 25 3291 25 3.531 27 3 2.991.29 2.871 .24 2.951 24 3.681 .24 a Breed group x bleed group interaction (P < .01). 66 over time (P < .01). Concentrations of T3 were lowest for bleed group 3 (P < .01). Analysis of growth hormone secretion for breed and bleed groups are shown in Tables 16 and 17, respectively. Baseline GH concentration was highest (P < .05) for Gelbvieh-sired crossbred steers. Ranking of breed groups by growth hormone concentration for the eight hour sampling period was similar whether measured by area under the curve or mean GH concentration. No differences were detected for peak number or time between peaks (inter-peak interval), although UH steers had numerically fewer peaks and a longer interspeak interval than other BG. The lowest (P < .01) peak amplitude was calculated for SAH steers. Growth hormone secretion patterns across all BG over time are reported in Table 17. Higher (P < .01) baseline GH concentrations were found in steers in bleed group 1. Growth hormone area under the curve declined over time (P < .01). Steers in bleed group 1 had.a higher peak number and frequency (P < .01), along with a longer inter-peak interval (P < .10) than steers in bleed groups 2 and 3. Lower (P < .01) peak amplitudes were reported for bleed group 3. Serum hormone relationships for breed groups are presented in Table 18. Purebred Hereford steers had higher ratios of IGF-I/GH and insulin/GH than GSH steers. Shorthorn- sired crossbred steers had less (P < .01) IGF-I and insulin per unit of GH than SH steers. GSH steers had the lowest (P < .01) insulin/CH ratio when compared to all BG. Both 67 _able 16. Growth hormone anal o e 90”“. y _ 7 f __ W SAH SH GSH Item UH Baseline GH, rig/ml 2.77a 1.12 2.62a 1.10 2.77a 1.10 3.07b 1.10 GH area under curve, 17748 181.1 15938 1673 15568 166.1 18538 167.6 rig x min/ml Peak no. 1.18 1.16 1.69 1.13 1.54 1.13 1.66 1.13 Peakamplitude,ng/ml 6068 1.73 5.728 1.60 f 3.968 1.59 5.908 1.61 lnter-peakinterval, min 158 123.9 109 119.8 109 119.5 82 119.9 a,b Means within a row lacking a common superscript differ (P < .05). C.d Means within a row lacking a common superscript differ (P < .01). 68 Table 17. Growth hormone anal sis of bl gr_u_-~_ __ _ . __ _ W item 1 2 3 Baseline GH, ng/ml 3.128 1.08 l 2.678 1.09 2.628 1.09 GH area under curve, 19528 1 60.6 16518 1 62.2 14798 1 59.3 ng x min/ml Peak no. 1.99b 1.12 1.508 1.12 1.548 1.12 Peak amplitude, 11ng 6.578 1.54 5.595 156 4.068 1.53 Peak frequency, 00428 1.0002 00318 1.0003 00328 1.0002 peaks/min lnter-peakinterval, min 15008 117.9 97.18 1183 97.281175 a,b Means within a row lacking a common superscript differ (P < .01). c,d Means within a row lacking a common superscript differ (P < .10). 69 Table18. Serumhormone rnelatioshio for breed .g.. - 1 - -1 f 1 We item UH SH SAH GSH lGF-l/GH 253.488 112.2 264.08 110.1 231.788 110.0 218.88 110.2 lnsulin/GH 10.288 1.76 11.38 1.63 9.08 1 .62 7.78 1 .63 Insulin/IGF-l .0418 1.003 .0448 1.002 .040d8 1.002 .0358 1.002 a,b,c Means within a row lacking a common superscript differ (P < .01). (1:9 Means within row lackin- a common su- --rscrit differ P < .10 . 70 Hereford breed groups had higher (P < .10) ratios of insulin/IGF-I than GSH steers. Table 19 illustrates the effects of bleed group on relationships of serum hormones. Steers sampled in bleed group 1 had significantly (P < .01) lower ratios of insulin/GH than steers in later bleed groups. The same response was noted for the relationship of insulin/IGF-I (P < .10). Correlations between GH, IGF-I and insulin and selected carcass traits and estimates of carcass composition are given in Table 20. Growth hormone was negatively correlated with measures of fatness and positively correlated with estimates of carcass muscle. Similar correlations existed for IGF-I and certain carcass characteristics. Insulin concentration was positively correlated with carcass fat measures while being negatively related to carcass protein and moisture. Correlations between serum hormone relationships and carcass characteristics are listed in Table 21. Ratios of insulin to GH and IGF-I were positively correlated with measures of fat in the carcass. Negative relationships existed between estimated carcass protein and moisture and insulin:GH and insulin:IGF-I ratios. 71 Table 19. Senim hormone relationshi. for bleed 1°" . 1 ' W m 2 insulin/GH 8.18 156 10.58 1.58 lnsulin/lGF-l .0358 1.002 0428 1.002 a,b Means within a row lacking a common superscript differ (P < .01). Cd Means within a row lacking a common superscript differ (P < .10). 72 Table 20. Correlations between GH. IGFI and insulin and carcasscharacteristics ,1 f GH Probability lGF-l Probability Insulin Probability Fat thickness -.22 .006 .06 .45 .29 REA/carcass wt 20 .01 .20 . .04 Yield grade -.17 .03 .08 Marbling score -.27 . .06 Carcass fat -.28 . -.17 Carcass protein 25 . .11 Carcass moisture .25 . .15 Carcass bone .08 . -.08 73 99'9 1w C°"9'9m°"9 99“”99" 99”" h°"“°9 '9"_fi° W. W939 . IGF-ll lnsulin/ lnsulin/ GH Probability GH Probability IGF-l Probability Fat thickness .17 .03 .33 .001 .25 .001 Yield graie .08 .30 .25 .001 .25 .001 Marbling score .17 .03 .28 .001 .22 .007 Carcass fat .08 .32 .29 .001 .32 .001 Carcass protein -.11 .17 -.26 .001 -.26 .001 Carcass moisture —.07 .37 -.28 .001 -.30 .001 Carcass bone -.09 .26 -.24 .003 .22 .004 DISCUSSION Differences in feedlot performance and carcass characteristics of the four breed groups reflect the effects of selection and diversity among breeds and biological types, as all steers were raised and managed at the same location and under the same conditions throughout the entire trial. The dramatically higher initial weight, final weight, frame score and ADG of SH, SAH, and GSH steers versus UH steers demonstrate the effects of long-term selection for yearling growth. These expected results are in agreement with similar growth performance reported by Newman et al. (1973), Cundiff et al. (1991) and Parnell (1992). The corresponding increase in frame size with selection for growth was also reported by Hough et al. (1985) . Presumably because of heavier weights throughout the feeding period and higher maintenance requirements, the two crossbred genotypes were less efficient in the conversion of feed to live animal gain. Carcass results further magnify the effects of selection for growth observed in this study. One would expect the larger, later maturing cattle (SH,SAH, and GSH) to have an advantage in carcass composition as they would be younger physiologically; and therefore, would be depositing a lower proportion of fat. in carcass gain. The superior marbling 74 75 scores and quality’ grades attained. by ‘UH carcasses are reflective of higher percentages of carcass fat. The ability of smaller, earlier maturing cattle types to attain acceptable quality grades with fewer days on feed is well documented (Crouse et al., 1985; Dikeman et al., 1985; Marshall et al., 1990). Although UH carcasses had the smallest absolute REA, due to lighter carcass weights, UH steers had the largest REA per kg carcass weight. This muscling advantage on a carcass weight basis existed despite the increased subcutaneous fat and higher percentage of carcass fat associated with UH carcasses. The observed differences in carcass traits and measures of carcass composition are expected when comparing straightbred English-type steers with continental European crossbred steers (Smith.et al., 1976). As expected, SAH and GSH steers had heavier carcasses, less backfat, larger REA, and lower yield grades than SH steers when slaughtered at a similar age. Estimates of percentage carcass fat, protein, and moisture demonstrate the same trends. Across slaughter groups, estimated carcass fat did not account for differences observed in marbling score among the three selected breed groups. Adthough not statistically different, the highest marbling scores were observed in SAH carcasses which were intermediate to SH and GSH in carcass fat, indicating differences in carcass fat depots among breeds or biological types (Smith et al., 1976; Arnold et al., 1990). Carcass characteristics reported for the three selected breed groups 76 are reflective of traits associated with the breed of sire for each respective cattle type (Smith et al., 1976; Crouse et al., 1985; Dikeman et al., 1985; Arnold et al., 1990). Decreases in ADG and feed conversion efficiency with time on feed have been frequently reported (Smith et al., 1976; Thonney et al., 1981). The heavier body weights associated with each successive slaughter group may have resulted in higher maintenance requirements and reduced ADG. The increases in carcass weight, backfat, and REA in each successive slaughter group were expected (Smith et al., 1976; Thonney et al., 1981). The decrease in REA/carcass weight in slaughter group 3 would be expected as muscle deposition decreases in relation to fat deposition as the animal matures. Estimated carcass fat closely paralleled the differences in marbling score observed in successive slaughter groups. Carcass protein and moisture were inversely related to carcass fat (R = -.78 and -.99, respectively; P < .01). Breed group x year least squares means for quality grade and estimated carcass composition illustrate variation in carcass characteristics between years for cattle treated alike. Unselected Hereford steers required 1.5% less carcass fat in year 2 to attain the same quality grade. Shorthorn- sired steer carcasses increased one-third of a quality grade with a decrease of 2.5% in carcass fat and crossbred Gelbvieh carcasses increased quality grades with increased carcass fatness. These results further indicate that quality grades are influenced by a number of factors, including breed and 77 genetics, and external fat or percentage carcass fat. A. single indicator appears to be a poor predictor of carcass quality. This observation is critical to the current discussions about changing the quality grading system. Slaughter group x year interaction means also revealed an increase in marbling and quality grade with a decrease in percentage carcass fat for slaughter'groups 1 and 2 in year 2. The complexity of factors involved in the development of the various tissues involved in body growth. make interpretation of hormone data in this study difficult. Due to the design of this study, hormone data are only available over a short window in each steer's life. Despite these complications, hormone data from this study are in general agreement with the literature in regard to the role of specific hormones and their interactions in the control and regulation of meat animal growth and development. The nutritional status of the steers utilized in this study should not have had an effect on reported GH concentrations. Level of intake, fasting, and energy balance can all play a role in determining GH concentrations in the bovine animal (Trenkle, 1976; Villa-Godoy, 1987; Ellenberger et al., 1989). Although the cattle were subject to stress while in the metabolism stalls and during the sampling period, there is no evidence to suggest that malnutrition affected circulating GH concentration. Growth hormone concentrations declined over time in this study as evidenced by a significant correlation between GH and 78 bleed group (R = -.35, P < .01). A decline in circulation GH over time has been observed by several workers using cattle of the same age (Trenkle, 1971; Trenkle and Topel, 1978; Keller et al. , 1979; Anderson, 1987) . Trenkle and Topel (1978) ‘attributed the decline in ADG as cattle approach slaughter weight to decreases in circulating concentrations of GH. The significant decrease in GR across bleed groups in this study did coincide with an observed decrease in rate of gain over the same time period. Larger breeds of beef cattle have been reported to have higher mean GH concentrations than smaller breeds (Ohlson et al. , 1981; Verde and Trenkle, 1982; Grigsby and Trenkle, 1986). The fact that GSH steers had higher GH concentrations than either SH or SAH steers in this study would support these observations. Grigsby and Trenkle (1986) also found Simmental steers to have higher GH concentrations than British-bred steers, which is in agreement with the differences observed between the Gelbvieh-crossbred steers and straightbred Herefords in this study. In contrast to what has been previously reported, the larger cattle with higher GH concentrations did not demonstrate an advantage in rate of gain in this study. The reasons for higher concentrations of GH in UH steers is not apparent to the authors. Elevated GH concentrations have been reported in slow growth strains of chickens (Goodard et al., 1988) and normal concentrations have been measured in dwarf Hereford cattle (Dev and Lasley, 1969). Selection for 79 growth has been shown to increase GH concentrations (Davis et al., 1983; Dodson et al., 1983). Growth hormone concentrations of the UH in this study do not support these findings. However, the possibility that many of the actions of GH are mediated by IGF-I does not make it surprising to find inconsistent relationships between GH values reported both in this study and in the literature. In addition, measurement of circulating concentrations of any hormone does not provide insight into other factors such as receptors and interaction with other hormones involved in growth and development. Breed group x bleed group interaction means may provide insight as to the differences found in GH concentration between cattle type. All breed groups declined in GH concentration over time (P < .01). Unselected Hereford and SAH steers exhibited the sharpest decline in bleed group 3, while SH and GSH steer GH concentrations declined the most from bleed group 1 to bleed group 2. The influence these declines in GH concentration have on cattle performance and composition are unknown; but may have a role, in combination with other hormones, in partitioning of nutrients into specific tissues. Patterns of GH secretion have been implicated as explanations for differences in growth rate and body size between sexes (Afinson et al., 1975; Keller et al., 1979; Gluckman et al., 1987). Higher peak amplitudes and baseline values are found in males which are known to have a larger 80 body size and later maturity pattern than females. The largest framed, latestumaturing'steers in this study (GSH) had numerically higher baseline GH concentrations and higher peak amplitude than other breeds, although these differences were not statistically significant. Of more importance may be the analysis of GH secretory patterns over time and relationships to growth and development. Baseline GH concentrations, peak number, peak amplitude, and peak frequency all declined over time. Higher baseline concentrations and a greater number of peaks with higher amplitudes have been associated with increased growth rate and higher lean:fat ratios (Afinson et al., 1975; Keller et al., 1979). The pattern of GH secretion over time observed in this study would coincide with growth and compositional changes that occurred during the same period, as the steers declined in growth rate while fat deposition increased. Insulin-like growth factor I concentrations paralleled GH, and declined over time in this study; Insulin-like.growth factor I was negatively correlated with bleed group (R = -.43, P < .01). One would expect IGF-I concentrations to decline over time as concentrations of IGF-I in serum are directly related to GH (Clemmons et al., 1987; Gluckman et al., 1987). Davis and Bishop (1991) and Hammond et al. (1990) also reported IGF-I concentrations to decline with age in cattle. The close relationship between GH and IGF-I concentrations is also influenced. by the role of IGF-I in GH secretion. Insulin-like growth factor I inhibits GH release from the 81 anterior pituitary through negative feedback (Berelowitz et al., 1981) . Consequently, GH release from the anterior pituitary‘ is inhibited by elevated IGF-I concentrations. Analysis of IGF-I concentrations for breed groups shows an association between IGF-I and GH concentrations. Those breed groups with higher serum concentrations of GH also had higher IGF-I concentrations. Insulin-like growth factor I concentrations would be expected to parallel GH since many of the biological actions of GH are mediated by IGF-I. Administration of GH to humans (Clemmons et al., 1987) and sheep (Underwood et al., 1982) resulted in increased blood concentrations of IGF-I. Growth hormone may directly stimulate release of IGF-I from the liver and other tissues, thus explaining the tight relationship between concentrations of the two hormones in this study and others. Correlation analysis in this study revealed. a positive relationship between.GH and IGF-I (R.= .24, Pr< .01). However, it explained only a small proportion of the variation. Care should be exercised when interpreting the IGF-I results. The assay used is specific for IGF-I, but measures total immunoreactive IGF-I, including the large portion bound to transport proteins in serum. These transport proteins provide short term storage and transport IGF-I to target tissue. The transport proteins also render IGF-I inactive. Since the transport proteins were removed prior to hormone determination, the values reported in this study represent 82 total IGF-I and not necessarily the activity or use of the hormone. This may partially explain why GSH steers had significantly lower concentrations of IGF-I than UH steers when. GH concentrations were similar; The. higher concentrations of circulating IGF-I in UH steers may reflect a lower uptake of IGF-I from the circulatory system and more storage of the hormone compared to GSH steers. The association between serum IGF-I concentrations and metabolic utilization of the hormone by the animal requires further research. The ratio of IGF-I:GHI may give insight as to the utilization of IGF-I. A lower IGF-I/GH ratio would indicate a lower concentration of circulating IGF-I if GH concentrations were comparable. Therefore, a lower ratio may indicate greater tissue utilization with less of the hormone being stored bound to transport proteins. Insulin-like growth factor I is thought to have positive effects on bone and lean tissue deposition, with little influence on adipose tissue development. A high ratio of IGF-I/GH was found in the UH steers, and a low ratio was demonstrated in the GSH steers, who were larger framed and physiologically less mature at the time of sample collection. Advantages in carcass composition demonstrated in the GSH steers may have been partially attributed to increased utilization of IGF-I. Circulating concentrations of insulin in the bloodstream are largely a function of the fed state of the animal (McAtee and.Trenkle, 1971b; Weekes, 1986). Due to the great variation 83 in.eating patterns of the steers in this study, hourly samples from each animal were pooled for determination of insulin. The pooled sample would minimize the secretory increase of insulin that occurs after a meal in cattle. No significant differences were recorded in insulin concentration over time in this study. Insulin concentrations are lowest in young cattle and.gradually increase with age and weight (Trenkle, 1970; Trenkle and Topel, 1978; Verde and Trenkle, 1987). However, these researchers measured concentrations of the hormone over a longer time period than used in this study. Consequently, the age of the steers in this study may not have been sufficiently variable to detect differences. Serum insulin concentrations of breed groups revealed that straightbred Hereford steers had higher concentrations of insulin than the Shorthorn and Gelbvieh-sired crossbred steers. Grigsby and Trenkle (1986) reported similar results in Angus versus Simmental steers. Insulin is thought to be one of the major regulatory hormones in determining body composition (Prior and Smith, 1982). The importance of insulin in the regulation of growth is made apparent by the effects of diabetes (Romsos et al., 1971). Although insulin is important in normal growth and development of muscle tissue, insulin has its greatest effects on adipose tissue through stimulation of lipogenesis (Prior and Smith, 1982; Weekes, 1986). The differences observed in carcass fat between breed groups may be partially attributed 84 to differences in insulin concentration. Of major interest and importance may be the relationship between GH and insulin, as the two hormones are thought to have opposite effects on adipose tissue. Growth hormone is thought to be lipolytic (Eisemann et al. ,1986) whereas insulin is generally thought to be lipogenic (Prior and Smith, 1982). How these two hormones interact may influence tissue deposition and ultimately carcass composition in the animal. Elevated concentrations of GH and low insulin concentrations in larger, leaner breeds of cattle may favor increased and more prolonged growth of skeletal muscle rather than shifting energy to adipose tissue. In addition, smaller breeds of cattle have higher insulin concentrations which is associated with increased fat deposition at an earlier age (Trenkle, 1981). Relationships between insulin and GH in this study would generally confirm these observations. Across all slaughter groups, the larger framed, leaner GSH steers had a significantly lower ratio of insulin/GH than other breed groups. However, the small framed, early maturing UH steers did not differ in insulin/GH ratio when compared to SH or SAH steers due to their high conCentrations of GH. Although the role of IGF-I in fat deposition is less clear than for GH, one would expect the ratio of insulin:IGF-I to be similar to that of insulin/GH since IGF-I and.GH are tightly coupled. Indeed, ranking of breed groups was the same for insulin/GH and insulin/IGF-I. Serum hormone relationships over time may also explain 85 compositional changes over the same period. Steers in bleed group 1 had a significantly lower ratio of insulin:GH than those sampled in bleed groups 2 and 3. The correlation between insulin/GH and bleed group was positive (R.- .18, P < .05). Since insulin did not change over time, the higher ratios associated with bleed groups 2 and 3 are a function of lower GH concentrations in each successive bleed group. The ratio of insulin: IGF-I exhibited the same trend. The increase in these ratios over time coincides with a shift away from lean tissue deposition towards fattening as steers across all breed groups became physiologically more mature. Results of this study indicate a breed group effect on triiodothyronine and thyroxine. Thyroid hormones are primarily involved in the control of metabolic rate and are important in permitting normal growth, as reduced growth is associated with hypothyroidism and hyperthyroidism (Goldberg et al., 1980; Bowen et al., 1987). Optimal bone and muscle growth are dependent on a euthyroid state. Efforts to relate differences in circulating concentrations of thyroid hormones to different cattle types have been unsuccessful, making interpretation of results from this study difficult. Across breed groups, T3 and.T4 values appear to be normal for the age and type of cattle evaluated (Davis et al., 1983; Grigsby and Trenkle, 1986). Relationships between thyroid hormones and other hormones, and resulting influence on growth and development need further clarification. Significant negative correlations existed between GH 86 concentration and fat thickness, yield grade, marbling score, and percentage carcass fat. These results are consistent with research done by several workers (Purchas et al. , 1970, Trenkle, 1970; Purchas et al., 1971; Trenkle and Topel, 1978; Keller et al., 1979; Klindt et al., 1985). In this study, growth hormone was also found to be positively correlated with REA/carcass weight, and estimates of carcass protein and moisture. These results are in agreement with the generally accepted role of GH in stimulating protein synthesis and decreasing the amount of adipose tissue. Although the effects of GH are thought to be mediated by IGF-I, correlations between IGF-I and carcass characteristics did not reflect these assumptions. Insulin-like growth factor I was found to be correlated with REA/carcass weight, carcass fat, and carcass moisture. These correlations were not as strong as those observed for the same traits when correlated with GH. As many of the anabolic actions of GH on muscle are mediated by IGF-I, one would expect IGF-I to be positively related to carcass protein content. There is little evidence to suggest that GH affects adipose tissue via IGF-I or that IGF-I has a direct effect on adipose tissue. Thus, the negative correlation between IGF-I and carcass fat may not indicate existence of a true relationship. Correlations reported between insulin and carcass characteristics are opposite those reported for GH. Insulin has been shown to be strongly correlated with carcass fatness (Trenkle and Topel, 1978). In agreement with these findings, 87 ‘ insulin was positively associated with fat thickness, yield grade, marbling score, and carcass fat in this study. Insulin favors lipogenesis and is thought to decrease the breakdown and.mobilization of stored fat (Prior and Smith, 1982; Martin et al., 1984; Weekes, 1986). Since insulin has these strong effects on adipose tissue, positive correlations between concentrations of the hormone and carcass fat measurements are likely. Likewise, negative correlations between insulin and carcass. protein would be. expected given the negative association among the estimates of carcass composition. Correlations between insulin and IGF-I with carcass characteristics support earlier discussion on the relationships of these hormones and different effects across breed type and time. The theory that the interaction of hormones play a vital role in determining composition are supported by these correlations. Higher ratios of insulin:GH and insulin:IGF-I would favor fattening in relation to protein deposition when estimated on a carcass basis. Indeed, the ratios of insulin to GH and IGF-I were positive with fat thickness, yield grade, marbling score and carcass fat; while being negatively correlated with percentage carcass protein and moisture. The correlations for insulin:GH and insulin:IGF-I ratios are similar to those reported for insulin concentration alone for the same carcass characteristics. This may imply that insulin concentration has the most effect on determining the compositional traits evaluated. However, insulin ratio 88 correlations are slightly stronger suggesting that the relationship between insulin and other hormones explains more of the variation in carcass characteristics. No significant correlations were found between thyroid hormones and carcass characteristics. Similar reports can be found in the literature (Purchas et al., 1971) . Although thyroid hormones are undoubtedly involved in the regulation of animal growth, they may have much less of a direct effect when compared to the hormones previously discussed. Thyroid hormones may be more involved in permission of animal growth and also influence production and activity of other hormones. These roles are made evident as maximum growth of various tissues is dependent on a euthyroid state. Serum hormone concentrations were not significantly correlated with ADG which is in agreement with other studies (Purchas et al., 1970; Irvin and Trenkle, 1970; Etherton and Kensinger, 1984) . Attempts were made to relate hormone status to both ADG over the entire trial as well as current ADG in the metabolism room when serum samples were taken. Serum hormone concentrations were related to neither and a high correlation existed between the two measurements of ADG (R = .84, P < .01). With the exception of the UH steers, little ‘variation in. ADG 'was observed among the cattle, ‘making significant correlations between ADG and hormone concentrations difficult to obtain. Due to the design of this study, serum hormone concentrations were only measured during a short period in 89 each steer's growth curve. This small window may or may not be reflective of hormone' concentrations from birth to slaughter. If the concentration of hormones early in life sets the stage for rate and composition of growth, measuring hormones later in life may not be related to variables of interest. Therefore, correlations between hormone concentration and.their relationships with growth and carcass measurements are difficult to interpret. Since hormones were measured.approximately'90 days prior to slaughter, the time at which hormone data were taken may not be most appropriate for drawing conclusions of how these hormones affected carcass composition. This may explain why stronger correlations between GH, IGF-I and insulin and carcass characteristics have been reported in the literature. Despite these complications, the hormone concentrations, relationships, and correlations reported in this study are inigeneral agreement with.the roles each hormone is thought to have in influencing growth and development and with.what has been previously reported in the literature in similarly designed studies. CONCLUSIONS Resultsfrom this study provide support for the changes in cattle type that have occurred in the past three decades. These changes in type have been accomplished by intense selection for growth. This study confirms that selection for growth is effective, and that changes in carcass conformation have been primarily associated with slaughtering cattle that are physiologicallyless mature. Selection for growth has resulted in larger framed, faster growing cattle that are heavier throughout their life span. Decreased carcass fat thickness, marbling scores, and.quality'grades are realized in the carcass along ‘with increased. percentages of’ carcass protein and moisture and decreased carcass fat. Differences in growth hormone, IGF-I, and insulin concentrations were noted for biological types and selection for growth in this study. The correlation coefficients calculated in this study indicate relationships between the measured parameters as cattle grow and do not necessarily indicate the specific metabolic functions of any of the hormones. However, the correlations between the measurements of growth, carcass characteristics and hormone concentrations are in general agreement with accepted roles of the hormones in the regulation of growth and development. 90 91 Measurements of hormone concentrations over the entire growth curve for the diverse population of cattle utilized in this study may provide a clearer understanding of the effects of biological type and selection on the endocrine system. In this study, the relationships reported support our previous understanding of how these hormones and their relationships interact with growth, carcass traits, and.measures of carcass composition. Growth and development of meat animals is a complex process. This process is under the influence of hormones and one hormone may have multiple actions while one function is likely under the control of multiple hormones. For these reasons, relating one hormone to a specific growth or carcass trait may be over-simplified. 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APPENDIX APPENDIX Witt ADG - average daily gain over entire feeding period, kg ADJ BF - adjusted 12th rib fat thickness, mm AND - animal days BEG NT - initial weight, kg BEG AGE - initial age, d BF - 12th rib fat thickness, mm BG - breed group; 1 . UH, 2 - SH, 3 - SAH, 4 . GSH BL AGE - age at blood collection, d DMI - dry matter intake, kg FIN HT - final weight, kg FS - frame score GH - growth hormone, ng/ml GH BS LN a baseline GH, ng/ml GH AUC - GH area under curve, ng x min/ml GH PK INT - GH inter-peak interval (time between peaks), min GH PK LN - GH peak length, min GH PK AMP - GH peak amplitude, ng/ml GH PK NO - GH peak number GH PK FREQ - GH peak frequency, peaks/min HCH - hot carcass weight IGF-I - insulin-like growth factor 1, ng/ml 106 107 rev i ’ INS - insulin, uU/ml KPH - kidney, pelvic and heart fat, 1 MR IADG - average daily gain for entire feeding period prior to blood collection MR ADG - metabolism room average daily gain, kg MR HT - metabolism room weight, kg MR ADFI - metabolism room average daily feed intake, kg dry matter NS - marbling score; 400 - Slight 0, 500 - Small 0 N0 - individual steer identification number PN - Beef Cattle Research Center pen number 06 - quality grade; 11 . high Select, 12 - low Choice REA - ribeye area, cm2 RIB H20 - 9-10-11 rib moisture, % RIB BONE - 9-10-11 rib bone, % RIB PROT - 9-10-11 rib protein, % RIB EE - 9-10-11 rib ether extract, % SG - slaughter group SL AGE . slaughter age, d T3 - triiodothyronine, ng/ml T4 - thyroxine, ng/ml UH - weaning weight, kg YG - yield grade 1.08 HN.mH No.NH om.H¢ om.m¢ oH oov Hm.N m.H N.Nm m.m w.N a.mH¢ ese m¢.m NH¢.H Now NNN «ON omN on m N mcH mm.mH om.¢H mo.oe Nm.vv NH can He.» m.N o.ow N.NH ¢.HH N.mNm ans mo.¢ ONv.H mNm HoN NON mON on H m meH mo.mH cm.mH mo.mm mo.~¢ HH ome Nm.N m.N ¢.aN N.NH o.N o.HHm one m¢.e amN.H NHm amH moN mmH em N N oeH mH.mH we.mH oN.mN om.mm HH owe Hc.N m.N m.mm m.N v.9 o.m¢m use mm.m NNN.H omm cmN mHN moN No H e me ¢N.mH mm.NH mN.N¢ ¢H.m¢ NH cvm ma.N o.m N.o¢ m.m o.N o.mov mse mo.o omm.H one ouN NON NNN NN m m HeH os.¢H Na.mH mm.sm ma.sv NH com mN.N m.N o.Hu N.oH o.N m.omm Nee em.m moo.H onm omN oHN moN on N m ceH om.oH NH.mH mN.mm No.Hm HH ome a¢.H m.N m.moH H.m H.m m.omm use aN.N mom.H aNo moN HHN mmN ON m e NmH am.mH mm.NH om.¢c m¢.N¢ HH cos mm.m m.m m.mm H.aH N.NH N.MN¢ mmc mN.o mom.H emu mom HHN NHm mm N e mmH me.¢H om.oH Hm.cm oo.wm NH on Nv.¢ o.N M.Hm «.NN m.ON N.mmm NN¢ mo.¢ ¢m¢.H one emN HHN NeN co m N mmH Nm.mH mo.NH cN.ov mn.mv NH omm mo.N o.N N.vm N.oH N.oH e.mmm Nee mH.v oeH.H mam NNN HHN omN N@ H a smH on.mH NN.NH mm.¢e oa.m¢ oH oee me.” o.N m.mo N.NH N.oH ¢.mmN nee em.¢ NNN.H va aaH NHN ooN mm H N mmH mo.mH m¢.NH mc.H¢ NN.mv NH com mm.m o.N H.NN m.oH N.mH o.mNm owe Hm.e moo.H mHm NmN vHN moN on m N omH mm.oH m¢.mH mm.¢m mm.me HH owe m¢.N m.N N.mm o.N ¢.o m.N¢m Noe NH.o scN.H mmm NvN mHN ch em N m mNH No.mH os.vH m¢.on mm.mm NH ONm mo.H m.H o.ooH H.m m.m N.moc Hmc mN.N mam.H mmo mmN mHN NHm cu m c mNH mo.¢H om.¢H vm.am Nm.¢v a oem cH.m o.N o.HN e.HH o.~ m.eHm owe Ho.e coH.H mom HvN mHN HmN mm H N mNH a¢.NH mm.oH NN.o¢ m¢.Nv NH cam ¢0.m o.m m.o~ m.ON m.ON «.moN ewe mH.H Heo.H Nme omH wHN HmH Nm m H oNH o¢.mH om.NH H¢.om oo.m¢ oH ch ¢N.N m.H o.om o.m ¢.o e.me ose mm.¢ NNN.H mHm NmH wHN HON em N N mHH mm.mH om.HH Hm.Nv eo.m¢ vH ocs Nm.N m.N ¢.NN o.N H.m o.HHm mme ou.m oom.o mac nmN mHN moN NN m m wHH oH.mH No.mH oN.oc vm.o¢ oH occ Nm.N o.N ¢.mn N.NH v.HH m.NNm Hsv Hm.¢ osm.H NNm omH mHN mmH em N N NHH m~.mH co.NH HH.o¢ N¢.m¢ mH coo wN.N m.N v.wo K.NH N.NH o.m¢m was ev.m coH.H mmm NeN oNN N¢N NN m m eHH mN.mH NN.mH Nm.mv ¢N.H¢ NH osm om.¢ m.m 9.9m «.NH o.¢H m.moc NN¢ Hm.m mwN.H NNo com ONN NHm co N m mHH mH.mH om.oH NH.N¢ om.Hv eH cHN Nm.m o.m ¢.mn H.aH N.NH N.mmN mmv NN.H mNN.H one NmH NNN HoH Nm m H HHH so.oH on.mH Ho.¢m «N.om NH com em.H m.N o.coH m.o a.» H.Hom mus mN.m esN.H Nam NoN NNN oNN an N e oHH mH.mH H¢.mH mm.om oo.mm oH cow mm.N m.N m.¢m o.N o.» o.¢mm omv NN.m mmm.H mmo HmN vNN mmN as n v moH Nm.vH mm.mH mc.am oa.o¢ NH cam mm.m m.N N.¢N m.NH c.¢H v.mom wmc mm.m N¢N.H Nom NmH NNN mmH mm H N NcH om.NH NN.¢H mH.¢m mm.cm HH cmv ¢N.H m.H o.Nm H.m m.m m.eHm mac mo. NNH.H ¢Hm ch NNN HmN mm H m moH No.oH HH.vH mm.¢m Ho.om NH com Hm.N o.m.~.mm N.oH N.oH H.H¢m mac 0N.m aHN.H omm omN NNN ooN No H e moH Ho.¢H om.NH ov.m¢ mm.H¢ NH on mo.m m.m o.No m.NH N.NH o.mHN ems No.H mHm.o Non NmH mmN moH mm H H moH mm.oH NN.mH on.ac vw.m¢ HH ewe mH.m m.N N.No m.NH m.mH o.oHN was we. Hom.o New HeH mmN HmH vs N H NcH HN.mH oH.NH Ho.ov Na.mm oH om¢.mm.m m.H m.om H.aH N.NH m.o~m mom NN.¢ mNN.H can omN NNN NoN an m N HoH . mzom home Nu cN: co m: w> rag HocH .NN oHnmh 109 oe.NH Ho.nH oo.Nn oe.Ne NH ooo oo. n o.N o.no o.eH o.o o. HNn oHe oo. o nNN.H eHo nnN ooH eeN No H e eoH eo.oH nN.nH mo.oN No.eo NH oNo nn.N o.N N.oN o.N o.N N. ooN Hee oN. o ooo.H mNe HoN ooH oHN no N e noH Ho.oH oN.nH no.oe on.me NH oNo oo.N o.H o.nN N.NH N.oH o. oon oNe oN. e eoN.H ooe ooN ooH oHN oo H N NoH eo.nH oN.oH en.on Ho.oe HH ooe NH.n o.N o.oN N.NH N.NH o.Nnn NNe eN. e NHn.H oeo oeN HoH HoN oo H n oNH oH.nH oo.oH no.Ne No.oe NH ooo No.n o.n o.no m.oH N.oH o.eoN eee oo.N ooo.H one ooH NoH moH eN N H oNH oo.oH oN.nH oN.on oe.oe NH oNo no.N o.N N.oN o.o H.o H.NHn oee oo. o NHH.H HHm HnN noH NeN eo N n NNH Ne.NH no.eH oo.nn oo.oo nH ooo oo.N o.N H.No N.oH N.oH e.ooe ooe nn. o ooe.H moo noN eoH oHn oN.n e oNH Ho.eH No.NH no.Nn oe.oe HH oNe nN.N o.n N.eo o.N o.N N.eon oee ee. N oee.H Noo onN ooH ooN on N e eNH Ho.oH NN.NH Ho.Ne oN.me NH oNo oN.N o.N o.no o.n o.N H.oon Noe om.o ooN.H oNo onN ooH mnN NN n n nNH Ho.eH oN.oH Nn.oN oo.om oH one oo.o m.H o.NNH o.N o.N o.oHe Noe Hn.o oon.H ooo oHn ooH mnn oN n e NNH no.nH oo.HH oo.ne No.ne NH on oN.N o.n o.oo N.oH o.n o.Nen oNe oo.o eoN.H Hem meN NoH.ooN on H n oNH oN.nH oe.NH HH.He no.ee NH oeo on.n o.N n.NN N.oH N.oH o.ooN ome oN.e eoN.H oNe NNH ooH ooH em N N ooH ne.oH no.NH oo.ee on.ne oH oee on.n o.N n.NN o.eH N.oH e.oHn eoe He.m ooH.H HHm HoN ooH ooN oo n N NoH Ne.oH oo.HH oN.oe ee.Ne NH oom Ne.n o.N n.Ho o.NH N.NH o.nNn one NN.e ooN.H oNo onN ooH NeN oo H N ooH HN.nH eH.NH oo.ee Nn.ne NH oHo Ho.n o.H N.No N.oH N.NH o.Nen Hoe no. o oNn.H emo oHN ooH oHN em N N ooH oo.nH oo.HH oo.ne No.ee NH oem No.n o.N n.oN n.oN o.NH o.noN ooe No. o NHo.H oNe NoH ooN HoH No n H eoH on.nH oo.nH oN.oe Nm.oe HH ooe oo.N o.N o. NoH o.o o.N o.nee ooe No. o eoe.H Hoo oHn ooN oNn NN n n noH No.eH eN.eH oo.on oo.Ne HH ooe oN.n o.n N. no N.NH N.oH o.mon nme oN. o ooH. H noo NoN HoN Hon eo N n NoH no.nH oo.HH oe.oe No.me HH oNe oH.n o.N o.No N.oH N.oH o.HNn noe oN. e neN. H Nno oHN HoN NNN em N N HoH No.oH Nn.eH oH.nn NH.Ho NH ooo No.N o.n e.oo N.oH N.oH o.oen nne oo. N ooN. H eom NNN NoN ooN No H e ooH ee.oH NN.eH no.nn oo.oe NH oHo oN.N o.N o.oo N.oH o.o o.oNn ene me. o Non.H Hem oNN noN HnN om H n ooH no.oH oo.oH oo.on oo.oe NH ooo HH.n o.N n.oo e.HH o.N H.eHe one we. N NNo.H ooo noN eoN eoN eo N n ooH oH.oH oN.NH Nn.ne mn.ne nH ooo mo.n o.n N.eN N.NH N.oH o.non HNe No. o oeo.H oNo noN ooN non NN n n NoH No.oH NN.oH Ho.Ne oo.Ne NH oHo nH.n o.N o.eo N.NH o.o H.oeN one me. H mno.H Hoe noH ooN NNH oo H H HoH on.NH No.mH Ho.on oo.oe NH oom mo.N o.N o.NN o.N o.N H.onn ooe oo. o ooH.H neo eeN ooN ooN eo N n .oeH no.nH nn.eH eN.on oN.oe oH oNe eo.N o.n o.oo o.o o.o e.ooN ome ne. H meo.o Hon eNH NoN HnH eN N H oeH nH.oH oo.eH Ho.on no.oe NH ooe Nm.N o.N o.Ho o.N H.m N.een one eo.o Nen.H Nom oeN ooN ooN on H n NeH Nzom homo NN oN: co m: o> :ox pocH .nN oHomh 112 oH.oH eN.eH HN.nn No.oe NH onn oo.N o.n H.No o.o o.o o.NoN oHe oH.n ooo.H nee ooN ooH HoN oN H n oNH NN.eH Ho.eH HH.Nn oN.oe HH ooe nH.n o.n N.No N.nH o.eH N.oNN oHe eN.H NNo.H nNn NeH NNH HnH Nn H H nNH oN.nH No.nH nN.en oe.on NH oon Hn.N o.N e.NN e.o o.n e.an oHe oo.o HoN.H HHn NNN NNH nHN oo H N NNH NH.HN No.nH oo.on nN.Ne HH nne no.N n.N n.nn o.n o.N e.ooH nee on.o Hno.o NNn oNH nNH HHH oN N H HNH NH.eH en.NH no.on no.oe oH one nn.n n.n H.oN e.HH o.n o.nen NNe nn.o oNn.H eon eNN nNH onN oN H n oNH NN.nH no.nH oo.oe nN.on nH ooo Nn.n n.N n.Ho N.NH N.NH H.onN one on.N NoH.H nee onH oNH HnH oo n H ooH oN.eH no.eH oH.on oN.nn oH one nH.N n.N o.eo o.n n.N o.Nnn NNe oN.o eoN.H oon HoN ooH oNN eN H e NoH oN.NH oN.nH oo.Nn HN.oe NH oon no.N o.n e.oo o.eH e.HH o.oNN NNe Nn.H oHo.H onn onH ooH oNH Nn H H ooH on.oH ee.nH nN.en Ho.oe NH onn Nn.H n.N o.ooH e.o H.n o.oNn nne nN.o nNN.H won oNN noH noN oo N e noH NH.oH NH.nH No.Nn No.Hn HH nne oo.H n.N N.oo e.o H.n N.nNn Noe on.o NeH.H Nnn oeN noH eNN eo n n eoH NN.NH oownH nN.Nn oH.Hn HH ooe Nn.N n.N N.no e.o H.n e.oen nne oH.n onH.H Hon oNN noH NoN oo N e noH oo.oH oo.nH oo.oe on.oe NH oNn oH.n n.N o.oo N.NH N.oH N.oen ooe oo.n oeo.H Hnn eoN NoH ooN eo n n HoH Nn.NH eo.nH oe.oN nN.en HH ooe oN.H n.H o.No H.n H.n N.oon ene Ne.o noN.H HNn ooN NoH eNN eN H e ooH NN.oH Ho.NH on.oe no.oe nH ooo oo.N n.N n.Ho N.oH o.N N.nen oNe oo.o eHH.H oNn noN ooH oNN on n e onH no.eH oN.nH oo.He nN.ne nH ooo no.n n.N N.eN n.oH N.nH n.NNn one Nn.e non.H HNn noN ooH HoH en N N NnH oo.NH oH.nH oN.on oN.oe NH oon Nn.n o.N N.eN N.nH N.NH N.onn one on. onN.H eon oeN ooH oNN en N N onH nN.eH No.eH oo.He Nn.ee NH oen Ho.n n.N n.nN o.eH e.HH N.NNN one Ne.N eoN.H nne HoH ooH oeH oN N H nnH on.oH oN.nH Ho.en en.on NH oNn Hn.N n.H o.oo e.o e.o N.eon ooe ee.N oon.H ooo NoN ooH noN on N n enH No.NH nH.NH eo.ee oo.ne NH oon oN.n n.N H.No N.oH o.n e.oon nNe Ne.e eoo.o ooe NeN HoH oNN No n N nnH oe.eH oo.nH nN.He nN.ne HH ooe eo.N o.n n.oo N.NH N.oH e.nNN nNe NN.o oHo.o oNn NeH HoH onH oo n H NnH oN.eH eo.NH oe.Ne oo.ne HH ooe eH.n o.n o.HN o.eH N.oH n.HoN eNe oo.o nnH.H Nee NnH NoH neH oo n H onH ne.oH nH.eH No.Nn No.Ne nH oHo Nn.N n.N H.oo o.o o.n n.Noe noe oN.n oon.H Neo NHn noH ooN oo N e oeH Ho.oH oN.nH nn.nn oN.on NH oon Ne.N o.N o.oo e.o H.n N.nen eoe NN.o nNN.H eon enN eoH eeN on N n oeH oo.oH oo.eH oN.en oH.on NH oon no.H o.n o.ooH H.n n.N o.Hon oNe No.o NoH.H noo ooN eoH NoN on n e oeH oo.nH NH.eH nN.nn No.oe HH ooe nH.n o.N o.HN o.o o.o o.Nen Hee oe.o ooe.H oNn ooN eoH NeN oN H n oeH NN.oH oN.NH nN.en No.on HH ooe NN.N n.H n.oo o.N e.o N.oon Nee eo.o nNo.o Noe NoN noH onN oN H n eeH oH.eH oo.NH nn.ee oo.Ne nH ooo nN.n n.N o.HN N.nH N.oH H.ooN ooe oo.N onH.H oee oNH ooH HoH oN N H neH Nzoo bozo no oN: oo n: o> zaz (mm on 3o: No< no oo< h: h: No< 3: za on on oz nHN oHN oHN mHz oo< on an own cum Ll. m .H.e.o=eoo AN o.eee 113 No.nH oN.oH no.oN oN.oH no.NH NH.nH oH.oH oo.oH No.oH oH.eH Nn.oH no.oH eo.oH no.eH He.nH Nn.eH oo.eH HN.oH No.NH eo.NH Ne.oH oo.oH Nn.oH Hn.NH oN.eH eN.nH nN.nH No.eH Ho.NH oo.eH eH.nH oe.eH nn.nH Ho.nH eH.oH eo.eH oo.HH NH.nH on.eH nH.HH No.eH NH.nH ee.nH oo.nH no.eH Nn.nH No.on oe.nn Ne.Nn ee.Nn oo.oN eo.en NH.on on.Ne ne.on on.oe oo.en ne.on eo.Nn en.Nn oH.en nN.on oo.en NN.on Ho.on eo.oe no.oe no.oe eH.Nn oH.nn eo.Nn oo.Hn nH.ee no.Ne No.nn on.oe Ho.en oN.on Ne.oe no.oe oN.on oo.oe oN.Nn oN.oe oN.en No.on oo.en oo.on oN.Nn oH.Nn ne.Nn oN.oe oNe ooe Nn.N eN.N no.n HH.N on.N NN.N oN.N ooe on.N nne oo.N V'fiOthDNtDHQM‘DOlmor-OD LON GONNNQQQNGNNNNNQNQ O Q OM 0Q NV‘DO‘OQONOVMW‘DHONMHQ’HmOm Q Q h m \DO‘DO’OI—‘DOGDQDV'NNVOHNWNIRNV N.onn ooe N.HoN e.ooN n.eHn o.NNn o.ooN o.eNn n.non o.Non o.eon H.nNn n.Nnn o.HNn H.onn N.HoN e.eon o.oNn o.nNn n.Nen H.NHn H.oNn o.Nnn NH.N nN.n oo.n nN.o HN.n no.n nH.o no.n oN.n He.n nN.o ooe oN.N on.o HN.o oHe no.n NN.o No.n Nn.n oo.o ne.n eo.o Ne.N N.onn one oN.e NHN.H onN.H oNo.H HnN.H ooe.H oHN.H NHn.H oNo.H nen.H HoH.H Hnn.H eNN.H oNe.H NNn.H nNe.H noN.H Nnn.H oon.H ooo.o Noe.H oeH.H oon.H NNn.H O 0 F; G' N NHNMMMMHHNFNHMHMNMHNNMM nzoo oHN homo oHN no oNz oo n: o> 1oz No=H .nN oHnON 119 on. eN Non.N Ho.oe oeN NonN noH Nooo.o oe Nn.o n He.n no.e oNn on H N NNH o9 no oHo.N no.oN HnN onoH oon Neoo.o on oo. e N eo.N nn.n oen oN N H HNH o. NoH NNH.n No.oe ooo HNoH oo Neoo.o on Ne. H N nH.n Nn.n nNn oN H n oNH HN.oo onn.N oo.oH HnN eeeH o HNoo.o oo NN.e H Ho.N oo.N oon oo n H ooH no. no oNN.H oo.oN HnoH NnnH o HNoo.o on eH.n H NN.N oo.N oNn eN H e NoH n. ooH ooo.n ne.en NHNH HenN oon Neoo.o oo oo.o N HN.e eo.e oNn Nn H H ooH n. NoH oNe.N No.NH Noo ooeH o o o o o nH.n nH.n Hon oo N e noH eH.oN NNo.H en.nH HNo ooNH noH Nooo.o oo no.n n oo.N no.n oon eo n n eoH n.nHH oHo.N Hn.oH ono oNeH o o o o o oo.N No.N Hon oo N e noH NN. em oNo.N no.oH onn noNH o HNoo.o oo nn. e H HN.N No.N Hon eo n n HoH o. eoH nNo.N Ne.NN oNo eooN o HNoo.o onH o. nH H nH.N oN.e nnn eN H e ooH o9 oN eoH.N on.Hn NnN eoHH oeN Neoo.o on nN.H N NN.N Ne.N Non on n e onH o.ooH ooo.N nN.en NNo NnoH o HNoo.o on no.H H no.N nH.N eon en N N NnH en. mo oHn.N No.oN Noo NoeH o HNoo.o oo oo.N H oe.N oo.N oon en N N onH 9 nHH onn.N on.nn nHNH NnNH onH Nooo.o on on. n n on.N Nn. n non oN N H nnH oo.oN non.N NN.oH oHo noeH ooH Nooo.o on on. n n ne.N oN. n oon on N n enH oN.no nHN.N Ho.nn eHn oonH noH Nooo.o on oo.N n oN.N nH.n non No n N nnH H.oNH oHo.N on.oN oNo onnH oon Neoo.o oo on.o N on.N NN.n non oo n H NnH n.nNH non.N en.ee oeoH HNNH oon Neoo.o nN on.a N oe.N oo.n oon oo n H onH no.oo NNo.N on.HN new oNnH oo Nooo.o on n9 n n on.N oN.n oon oo N e oeH H. noH eHo.n nn.nH HHo HonH oon Neoo.o on oN. N N o9 N nH. n oNn on N n oeH n. NNH Non.N HN.nN eoo NeoH oo Neoo.o oo HN.o N no. n No. n won on n e oeH o.NHH ooo.N oN.en non HonH onn Neoo.o oo oH.e N nN.N No.N Nen oN H n neH oo.oo nen.N oo.nH ono HeeH o HNoo.o oo on.n H oe.N oo.N nen oN H n eeH N.NNH oNn.N on.on NooH noeH oo Neoo.o ne Hn.n N on.N oo.n NNn oN N H neH N.HnH Nnn.n en.on Hoo ooNH oo Neoo.o ne Nn.e N Nn.n oo.n een eN H e HeH eh nN nzH H-ooH o=< NzH omzm zo oz< oz 24 :o No< zo on on oz gm xa zza xo xo no on o .A.o.acoov nN oHomN 120 ee.oo nNo.N NH.oN nHo oHNH onn Neoo.o oo Ho. n N oo.H Ho.N oHn on H N nooo No.No n.N no.oN Hoo oooH o HNoo.o oo on. N H o9 H oo. N enn No n N HoN e.noH nHN.N oo.oN oHo NnnN one Neoo.o oo e.nH N no. n n9 n nnn on n e ooN on.oN nno.H No.nn Noo oHNH onn Neoo.o ne Nn.e N no.N oe.N oNn en N N ooH oN.NN noo.N nN.oe nNo oeo o HNoo.o on HH.e H oN.H oo.N NNn en N N NoH eo.No HHn.N no.NN ooo oooN ooH Nooo.o on oo. n n eo. n on.e eon on H N ooH oo.oo eNo.N oo.oH ooo noNH o HNoo.o oo en. o H no. N No. N Hon No n N noH eN.no eNN.n oN.HH noN NooH o HNoo.o oo N.oH H Ho.N N9 n nnn on N n eoH HH.Ho onN.N nN.Ne nNN noHH oeN Neoo.o on HH.n N NH.N o9 N Non No n N noH Nn.oo noN.N on.nN HNn NNHH o HNoo.o on NN.N H nH.N HN.N oon oN H n NoH Ne.oo HeH.N Nn.nN noo eoeH o HNoo.o on No. e H oN. N No. n non eo n n HoH N.HNH ooo.N en.on noo eHNN oeN Neoo.o ne e9 n N nN. n oe. e Non eN H e ooH Hn.No ooN.N oe.NN oHN NNnH oo Neoo.o ne o9 n N Nn.N NH.n oon oo H N ooH oN.no oNN.N nH.Ne nno enoH o o o o o NH.N eH.N onn en N N ooH NN.No oNn.N Nn.ne ono nooH onn Neoo.o oo 9 oH N oo.H oN.n HHn on H N NoH on.No non.N No.Ne eHoH NooH o HNoo.o on oN. n H ne. n eN. n NHn oo H N ooH o.noH ooo.N on.oN oNn oNoH o o o o o HH. N nH. N oon eo n n noH Nn.oN Noe.N eo.ne Heo ooo o HNoo.o oNH NH.n H Nn.H eo.H oon No n N eoH oH.oN ooH.N no.oe eHn nHoH o HNoo.o oo oe.H H oo.N oH.N oon on n e NoH oN.No ooe.N NH.on oeo NoNH oon Neoo.o oo nn.n N on.H NN.N oon No n N HoH on.No ooo.H HN.oN nNo NooH o HNoo.o oNH oo.n H No.N oo.n nen on N n oNH n.ooH ooN.N Hn.nN noHH nHoH oo Neoo.o oo on.o N No.N oN.n oHn eN H e oNH NN.eo NHn.N oo.en NNo onoH oo Neoo.o oo HN. o N oH.H oH.N nen en N N NNH oH.oo eoo.N nH.Hn Hno HNnH oo Neoo.o on oo. e N nn.N oo.N NHn oN H n oNH en.oo eHN.N oN.Nn NNo oNnH oo Neoo.o ne No. N N ne.N oN.N oNn Nn H H nNH eh np nzH H-ooH oo< NzH com; 24 oz< oz 24 :o No< zo on no oz xo xo .NN xo xo no No In .N.o.ucoov nN oHomN 121 Table 26. NetaboliSm room performance and intakes of Lake City steers born in 1989 HR HR HR MR N0 86 SG PN HT ADFI ADG IADG 101 2 3 60 521 8.4 0.92 1.36 102 l 2 74 303 4.5 0.08 0.97 103 l l 66 303 6.8 1.05 1.05 105 4 l 62 460 8.3 0.79 1.47 106 3 l 56 453 8.0 0.52 1.50 107 2 l 68 410 7.9 1.66 1.57 108 4 3 70 544 7.5 1.18 1.35 110 4 2 58 485 5.7 0.16 1.30 111 l 3 52 417 7.0 1.93 1.36 113 3 2 64 532 9.2 0.55 1.39 114 3 3 72 537 9.5 0.76 1.49 117 2 2 54 408 7.1 0.78 1.36 118 3 3 72 449 5.1 -0.84 0.98 119 2 2 54 403 6.5 0.31 1.23 120 l 3 52 405 6.7 1.34 1.28 126 2 l 68 399 5.6 0.09 1.14 128 4 3 70 576 8.2 0.25 1.42 129 3 2 64 449 5.9 -0.16 1.23 130 2 3 60 464 6.3 1.18 1.09 133 2 l 68 378 7.0 0.96 1.29 134 4 l 62 458 7.4 0.52 1.30 135 2 3 60 548 8.0 1.43 1.61 136 4 2 58 557 7.5 0.47 1.50 137 4 3 70 551 7.5 0.50 1.45 140 3 2 64 478 7.8 0.00 1.32 141 3 3 72 571 9.1 0.67 1.54 143 4 l 62 449 7.4 0.87 1.40 144 2 2 54 401 5.4 0.63 1.26 145 3 l 56 410 7.7 0.96 1.50 146 2 3 60 578 7.2 1.43 1.49 147 3 l 56 442 8.4 1.13 1.40 148 l 2 74 276 4.1 0.31 0.90 149 3 2 64 496 6.5 0.23 1.50 151 1 l 66 299 5.8 0.26 0.98 152 3 3 72 501 7.4 1.43 1.07 156 3 2 64 551 9.0 0.78 1.59 159 3 l 56 426 7.0 0.79 1.44 160 4 l 62 471 8.5 0.00 1.40 161 2 2 54 426 6.8 0.39 1.23 162 3 2 64 517 8.0 0.31 1.34 163 3 3 72 635 10.7 1.34 1.62 164 l 3 52 371 6.1 1.01 l 12 165 2 ,2 54 464 7 6 0.70 1 2 l 9 l. l Table 26 (cont’d.). 122 MR MR N0 88 56 PM HT ADFI ADG 167 hNh-fithNw-FNNH-DDNH-hHHNH-hNH‘hNUHw‘hubWNN “NNHNHHwwwHwNwi-‘wa‘d“NHNwNHNHHNNwNwa-‘Nw 60 449 54 396 56 467 70 587 72 489 58 494 70 557 64 449 74 351 56 435 68 399 58 408 62 426 74 319 60 460 58 503 66 303 54 385 52 347 66 310 70 544 52 317 68 374 62 444 70 521 74 297 60 492 68 371 70 464 72 446 60 474 66 324 56 399 58 469 62 417 58 462 54 424 62 394 Nmai0‘05N01NV”mm-FNO'IO‘UIO‘UIUIOIO!NNAGU‘NNNQNO‘NQWNN OwadfiHNU‘O‘C‘OWNOQUIOOUIO'OU'H-fiOiNOiOUlhi-‘O-‘ONUIDHNHN CHOOOOOHOOHNOOOOHOOOOOOHOOOOOHOOOOOHOH D HHHHO—IO—It—Il-lt—IO-IO—lI—lt-lt—IHHOHHOHHHHHHHHHHHHHh‘I—IHHH O O O O O O O O O O O O O O O O O 123 Metabolism room performance and intakes of Lake City steers born in 1990 Table 27. MR MR MR MR N0 86 SG PN HT ADFI ADG IADG 26178312417618510351065710435914059991450656 44530027415124343145444.5401.41033431804334.2501 1.1111111111111111111111111111111110111111111 00257679255775606891735089947933740658674042 6186450633900.526146350680920396—5508796434420 1.1011011110111111...011111010110001110010110111 4203752134840.79075283042908435627245187208516 124 Table 27 (cont’d.). HR HR MR MR N0 86 56 PM HT ADFI ADG IADG 692720821860858156110111106839407 120423920054140442354443315152165 11111101111111111111111111111111] 1788350906793109791.179437309883559 323209070859330304656268453223116 110110111011111111111110111111111 859224679804653406486963894055815 774867464677778796776687778677787 13477198179950 152349848 31 8154 4534.443 0 381 2 272 6 34 4 43 4 44 8 41 2 44 6 49 2 44 4 51 0 36 0 33 4 45 0 37 125 mHm. oNHN mmmNH nNN.H can mmNm mac.H oNN nNnH Hoo.o oHN omoH omm.o NnN NmmH on m c NHn.H ommH mvaH nno.H omH oemH on.o mmH NomH oom.H mmH oHNH mmm.o noN mcmH an N ¢ HnH.H ova NoHvH amo.o omN msNN oNH.H oHN mon msa.o NNN ooNH Nw H e omH.H onH mmmoH mon.o va omoN omm.o ooH eNNH ooo.c mmH mNmH mam.o noN mNmH NN m m «nN.H NHNH moomH mmm.o mmH mosH ¢mo.o ooH HmNH oeN.H me ommH ooN.o MON mmmH co N m mHm.H mmmH acomH cmo.o mVN NvoN Nen.H mmH mva NwH.H moN vme on H m mom.H ONHN oeoNH nnH.H omm amNm nNe.H ¢NN ocoH nNN.H oHN memH NNN.o NmN mNmH on m N ¢om.H mocN mNNmH NNo.H vNN moMN amm.H vNN man moH.H oHN HNoH cam.o NnN HooH em N N Hom.H oHuH moHNH mNm.o mvN NNON ¢o¢.H amH eNeH ¢NM.H MON mooH mm H N NNo.H mNmH ¢m- Nas.o oHN memH oom.o oeH mmm va.H mmH smm mom.o neH m¢m Nm m H ¢mm.o mmNH Nvmo cos.o oeH Hmm HoN.o O¢H mmm oNN.H mmH mas Hom.o moH o¢~ en N H mHo.H omHH ammo mmm.o mNH NooH on.H mmH mes mmm.o meH mHm no H H _MHH_ «Human m Hanna“ a bdmuwm N momma“ a umpsum Ho¢.H NON NnoH mm¢.H O¢N wmmH noN.H eNN mHmH moo.N eNN N¢aH vmm.H mHN oonH on m c moN.H NON msmH N¢N.H O¢N NNHN mnm.H cNN mHmH NmN.H eNN mmmH aom.H oHN oonH on N c om¢.o NON mNmH vm¢.H ocN mmmH mmH.H eNN mmmH m¢w.H ¢NN momH mmN.H nHN momH No H v enn.H NNH NmmH vmm.H oHN mmmH nno.H me cmoH onH.N eNN NNNN eNo.H oHN HomH NN m m osm.H NNH mmmH cmm.o oHN HNNH mmm.H omH HONH eHa.H ¢NN “NNN HNo.N oHN mHvH ¢o N m oom.o NmH NonH cHN.H oHN Na¢H oN¢.H mmH mmoH maw.H «NN NNNH mmN.H oHN m¢mH mm H m mam.H ch oan oNn.H ocN mHmH mON.H ¢NN mNNH ¢mm.H eNN mch NNo.H eHN nNNH on m N Ham.c NON wmmH noN.H oeN mmmH voH.H ¢NN NNoH ¢mm.H ¢NN NomH ¢N¢.H oHN mmoH em N N NNm.o NmH noNH ¢NN.H oHN «NmH oHc.H omH mmmH mom.H omH NonH cmN.H mmH onH mm H N NNw.o onH mam mmN.H omH emu ocm.o ovH emu nen.H 0¢H can oon.H mmH Nmo Nm m H oco.o onH mam Hnn.H omH mom Nno.H oeH won eoN.H oeH NmN Hnn.H mmH m¢m ¢N N H HHo.o omH NNN nnN.H omH on mHm.o ovH ¢HN oN¢.H ocH Hum oNn.H mmH oen on H H wa< oz< Hz: wo< oz< Hz: wo< oz< Hz: wo< oz< Hzo wo< oz< Hzo zm an em OH I e mOHme m waflgmm M ummgmm H vcwuum mama cw cson mgmmam huwu mxma kc Ucwgmq he mcwmm flea mmxmucp cm; .QN wPQMH 126 OOH.H HHOH NNOcH NO0.0 eNN OOOH OOH.H OON OHOH NON.O OOH OOOH OO0.0 OON NONH OO O c OON.H OOOH NNOOH HOO.H OOH NNO HOO.H OOH OOHH OOO.H OOH OOHH HOO.H OOH HONH OO N. v OHO.H OOOH NOONH NHH.H NOH OeeH NHN.O OOH ONOH eOH.H OON HOOH ¢N H c ONN.H OOON HOOOH OH0.0 OON OOON NOO.H NON OeOH ¢¢H.H ONN OHON OOO.H NON NOON OO O O HON.H OOOH OOOvH eO0.0 OeH NeHH NN0.0 OON OOOH NOO.H OOH «NOH OOO.H OON ¢ONH OO N O OON.H OONH OOOOH OHH.H OON NOOH OOO.H ONN OOOH OvO.H NON O¢NH ON H O ONO.H NNNH ONNNH ONO.H OHN OOOH OON.H OON OOOH NNH.H OOH NOOH ONN.H OON OOOH NO O N NOO.H OOOH OOOOH ONO.H ONH ONO OOO.H vNH OOOH ¢O0.0 OOH OOOH OOO.H ¢NH NeeH cm N N OO¢.H OONH HHOOH OOO.H OON NOOH NN0.0 eNN OOHN ONO.H NON NNHN OO H N OOH.H ONNH OOON OON.H OOH OOOH O¢0.0 OOH OHO eOH.H OeH NOO ON0.0 OOH HOO OO O H NO0.0 OHNH ONOO HO¢.O OOH ONO OON.O OOH NHO OHN.O OeH eNN OON.H OOH NNO ON N H OOO.H OOO ONHO NN0.0 eOH OOO OON.O NHH ONN HON.H OHH ONN NO H H HOHHH «HHHOM O OOHLOO O OOHLOO N OOHLOO O OoHLmO OOO.H OOH HOOH O¢0.0 OOH ONNH OOH.H OON ONOH NOO.H OOH NONH NO¢.H OON NOOH OO O c NOO.H HOH OHOH OOO.H OOH OOOH OON.H eNH NOOH OOO.H OOH OHNH OOO.H NOH OHOH OO N e OOO.H OOH OOvH OOO.H OOH OONH HOO.H OON HOOH OOO.H OHN ONOH ONN.H OON NNNH «N H e OON.H OHN OOOH NO0.0 ONN OHOH NHN.H NON OOOH ONH.H OHN ONOH NOO.H OON OOOH ¢O O O ONO.H OHN OHOH OOO.H eNN NvOH OON.O NON OOOH OOO.H OHN ONOH OOO.H OON HOOH Om N O NO0.0 OHN OOOH OO0.0 ONN OHOH ONO.H NON HONH HNO.H OHN NONH HOO.H OON NH¢H ON H O OON.H OOH OOOH OOO.H OOH NOOH OOO.H OON OONH OOO.H OOH OOOH OOO.H NOH HOHH NO O N ¢ON.H NOH HNHH OOO.H OOH OONH OOO.H ¢NH OOHH OOO.H NOH NONH HHO.H OOH OON ¢O N N O¢N.H OHN OONH OO¢.H eNN OOOH OO0.0 NON OOOH NHO.H OHN OOOH ¢v¢.H OON HOHH OO H N OON.H OOH NOO OO0.0 O¢H OON NOO.H OOH ONN OOO.H OOH NOO OON.H OOH NOO OO O H ¢O0.0 OOH ONN HON.H OcH NOO OOO.H OOH HNO NNO.H OOH HON ONH.H OOH HOO ON N H HNO.H OOH OOO OO0.0 NHH HHO OO0.0 OHH OOO OOO.H OOH OOO NNH.H OOH NOO NO H H OO< Oz< Hzo OO< O2< H2O OO< O2< H2O OO< Oz< H2O OO< Oz< H2O 2O Om OO w OOHOOM v OOHLOO O wowgmm N umpgwm H OOHNOO OGGH HZ. :LOD memum humu mxma $6 $0..st an mcwmm Ucm mmxmucw :wn— .mN mpg—Oh. HICHIGRN STRTE UN HI @I lullllllfllll“ 312 300,90