CARDIAC HYPERTROPHY m POSTPUBERTAL
LABORATORY RATS AFTER CONTROLLED RUNNING
EXERCISE

Thesis for the Degree of M. A.
MICHIGAN STATE UNW‘ERS’HY
KWOK - WA! H0
1970

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ABSTRACT

CARDIAC HYPERTROPHY IN POSTPUBERTAL LABORATORY
RATS AFTER CONTROLLED RUNNING EXERCISE

BY

Kwok-Wai Ho

This study was designed to obtain in vitro anthro-
pometric measurements of the cardiac muscle in postpubertal
rats after different intensities of interval training.

Thirty-two male albino rats (Spartan Sprague-
Dawley strain) were divided randomly into four equal
groups, three exercise groups, each of which was subject
to a different interval training program, and one control
group. The animals were 71 days old at the start of the
experiment.

For two weeks prior to the initiation of the
study, the treatment animals were housed in spontaneous
activity cages for foot conditioning and acclimatization
to the laboratory. During the study, all the rats were
maintained in sedentary cages. The three treatment groups
were trained once daily, five days per week (Monday-
Friday), for eight weeks. Training was performed in

small animal controlled-running wheels.

Kwok-Wai Ho

At the end of the training period, the animals
were fasted for twenty-four hours. They then were
decapitated and their hearts were fixed in a 10 per cent
formaldehyde solution. Afterwards, the ventricular
length, the ventricular weight, the atrial weight, and
the total heart weight of each animal were determined.

A transverse slice of each heart was cut at a standard
location and stained with Hematoxylin and Eosin. The
slide was projected and the outline of the section was
traced. From the tracing, the cross-sectional area, the
ventricular chamber size, and the ventricular free wall
area of the heart were measured with a planimeter.

The exercised animals had significantly larger
heart measurements than the control group in regard to
the ventricular length, the total heart weight, the
ventricular weight, the atrial weight, and the left and
right ventricular chamber area (P = .10). Among the
exercised groups, the long interval training group had
the largest right ventricular chamber area (P = .10).
Measurements of the left ventricular chamber area showed
that the long and the short interval training groups had
larger chamber areas than the medium interval training _
group (P = .10). The short and the medium interval
training groups had greater total heart weight, ventri-
cular length, and ventricular weight in comparison to

the long interval training group (P = .10). No

Kwok-Wai Ho

significant differences in the above mentioned variables
were found between the short and the medium interval

training groups.

CARDIAC HYPERTROPHY IN POSTPUBERTAL LABORATORY

RATS AFTER CONTROLLED RUNNING EXERCISE

BY

Kwok-Wai Ho

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirement
for the degree of

Master of Arts

Department of Health, Physical Education
and Recreation

1970

ACKNOWLEDGMENTS

This study is dedicated to all of you, the peOple
I have met here, whose love and understanding is forever
appreciated.

I would especially like to thank Dr. William
Heusner, my major advisor and Dr. Wayne Van Huss whose
advice and assistance made this study possible. I would
also like to thank the staff of the Human Energy Research
Laboratory at Michigan State University for their assist-

ance in this study.

ii

Chaper
I.
II.
III.
IV.

V.

TABLE OF CONTENTS

INTRODUCTION . . . . . . . . . . .
REVIEW OF LITERATURE. . . . . . . . .
METHODS O O O I O I O O O O O I 0

RESULTS 0 O O O O I O I O O I O 0
SUMMARY, CONCLUSIONS, AND RECOMMENDATIONS. .
Summary . . . . . . . . . . . .

Conclusions. . . . . . . . . . .
Recommendations . . . . . . . . .

BIBLIOGRAPHY O O O O O I O O O I O O . .

APPENDICES

Appendix

A.

Standard Eight-Week, Short-Duration, High-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in Controlled-
Running Wheels. . . . . . . . . . .

Standard Eight-Week, Medium-Duration, Moderate-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in Controlled-
Running Wheels. . . . . . . . . . .

Standard Eight-Week, Long-Duration, Low-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in Controlled-
Running Wheels. . . . . . . . . . .
Basic Data--All Animals. . . . . . . .

Herxheimer's Heart Size Data on the 1928
Olympic Athletes . . . . . . . . . .

iii

Page

16
21
26
26
27
28

30

38

39

40

41

45

LIST OF TABLES

Table Page
1. Table of Mean Values for All Groups . . . . 22

A-l. Standard Eight-Week, Short-Duration, High-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in
Controlled-Running Wheels . . . . . . 38

8-1. Standard Eight-Week, Medium-Duration, Moderate-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in
Controlled-Running Wheels . . . . . . 39

C—1. Standard Eight-Week, Long-Duration, Low-
Intensity Endurance Training Program for
Postpubertal and Adult Male Rats in
Controlled-Running Wheels . . . . . . 40
D-l. Basic Data--All Animals . . . . . . . . 41

E-l. Herxheimer's Heart Size Data on the 1928
Olympic Athletes . . . . . . . . . 45

iv

LIST OF FIGURES

Figure Page

1. Sample of the Projected Cross Section . . . l9

CHAPTER I

INTRODUCTION

It is well known that vigorous physical exercise
over an effective period may produce cardiac hypertrophy
both in animal and human subjects. With hypertrophy, the
heart enlarges its dimensions and its weight increases.
The muscle fibers of the heart probably remain unchanged
in quantity, but increase in diameter and length by an
increase in the number of sarcomeres. The detailed bio—
chemical process of cardiac hypertrOphy is unknown. It
is believed that the hypertrophy develops as a result of
an increase in nucleic acids and protein synthesis, a
process stimulated by elevated ATP (adenosine triphos-
phate) metabolism.

If one considers the heart as a muscular pump, its
size and shape must affect the mechanics of its operation.
There is no doubt that the hypertrophied athlete's heart
is highly efficient. However, research in intact organ-
isms on the adaptation of the cardiovascular system to
muscular activity is limited by the techniques that can

be used without impairing the subject's (particularly in

man) health or performance. An additional problem arises
when the researcher attempts to control accurately differ-
ent intensities of exercise in animal training. The
interval training wheel for rats is designed to solve
this problem by carefully controlling different inten-
sities of running exercise for rats, as well as varying
rest periods during the animals' interval running.

This study was conducted as an attempt to measure,
in vitro, the anthropometric changes of the cardiac muscle
in postpubertal rats following different intensities of

interval training for eight weeks.

CHAPTER II

REVIEW OF LITERATURE

The most important phenomenon in cardiovascular
adjustment during muscular activity is the increased blood
flow to the exercising muscles. The increased flow is
needed for several reasons: to supply more nutrients to
the muscles as sources of energy for contraction, to re-
move waste products which otherwise would accumulate
rapidly and impair the function of the muscle, and to
permit a greater dissipation of heat produced by muscular
activity. If circulation to the muscles does not in-
crease, muscular contraction cannot be sustained for any
significant length of time, and consequently exercise
must stop. This increased cardiac output is achieved by
an increase both in the number of heart beats per minute
and in the volume of blood pumped with each beat (stroke
volume). Therefore, repeated muscular activities increase
work-loads both in ventricles and atria, and vigorous
muscular activities over an effective period are believed
to constitute the stimuli for the so-called physiological
hypertrophy of the cardiac muscle in healthy individuals

or animals.

As early as 1628, Harvery stated "the stronger,
more muscular, and more substantial the build of men,
thicker, heavier, more powerful and fibrous the heart,
and the auricles and arteries are proportionally increased
in thickness, strength, and all other respects" (37, p.
132).

Early observations of Bergmann (1884), Parrot
(1893), Grober (1908), and Hesse (1921) showed that the
size of the heart of an animal would reflect its degree
of activity. Wild animals possess relatively larger
hearts than domesticated animals, and birds which fly
great distances or which fly clumsily with more wing
actions have unusually large hearts (25, 77).

Dietlen and Schieffer reported that hard military
work would cause the heart to increase in size (22, 25).

In 1896 before the use of X-ray, Henschen carried
out his measurements by percussion and found an enlarge-
ment in the heart of ski runners (22, 25). Among the
early researchers, Schott (1897) was the first to employ
X-ray and found an unusual enlargement in athletes' hearts
following a wrestling bout; however, inaccuracies were
shown in his work (22, 25). The introduction of Moritz'
(1908) orthodiagraph enabled Schieffer (1916) and Diethen
(1919) to improve the accuracy of the observations. They
reported that the area of the heart in habitual cyclists
was greater than that in occasional cyclists or non-

cyclists of the same body size and age (22, 25, 77).

Since, a lot of researches have been conducted to relate
muscular activities with heart size. However, there is

no agreement between the experimental results. The obser-
vations of Lee (1917) on Harvard oarsmen, of Cohn (1920)
on returned soldiers, of Farrell (1929) on American trans-
continental runners, of Eyster (1930) on athletes with
prolonged athletic history, and Keys (1938) on college
athletes showed that athletes and heavy workers have the
same heart size as normal individuals of the same size

and age (21, 27, 30, 53, 58). But many other researchers
have found that vigorous athletic activities and hard
physical labor produce cardiac muscle hypertrophy in men
and animals (8, 22, 23, 24, 25, 38, 39, 41, 47, 48, 49,
59, 60, 77, 78, 82, 84, 85, 93).

Herrmann (1926) weighed the hearts of dogs and
found that the average heart-weight ratio (per kilogram
of body weight) was 7.98 gm/kg for normal mongrels, 13.4
for ten racing greyhounds, and 17.3 for the best racing
greyhounds. He therefore concluded that heart hyper-
trophy, produced by exercise, is related to the degree
of the exercise (39). X-ray studies of athletes' hearts
usually have involved measuring the transverse diameter
of the heart shadow. After examining several thousand
athletes in various sports, Deutsch and Kauf reported
that the athletes who participated in rowing, ski-running,

and cycling had the largest hearts. They concluded that

the psychic strain and the excitement of certain sports
could cause an enlargement of the heart (25). Hodges
and Eyster reported that the transverse diameter of the
heart had a higher correlation (.5738) with body weight
than with age (.2371) or heart (.2140) (40). 1

Assuming that the heart was a sphere with radius
equal to one-half of the transverse diameter of the
heart shadow, Herxheimer calculated the heart volume to
weight ratio of hundreds of top athletes (Appendix E)
and concluded that exercises of strength, speed, or maxi-
mal effort will induce hypertrophy of skeletal muscle,
but will only increase the heart mass to a small extent.
However, exercises of vigorous endurance will lead to
heart hypertrophy but will leave the body muscles un-
changed in size (22, 25). Herxheimer's theory was empha-
sized by Steinhaus and was confirmed recently by Nocher
and Reindell (64).

In general, cardiac enlargement (hypertrophy and
dilation) appears first in the left heart and then in the
right heart (59). In 1923 Herxheimer claimed that the
heart would enlarge symmetrically on both sides of its
vertical bisector and 1:2.2 was the ratio given of the
transverse diameter of the right to the left segment of
the heart after the enlargement (22). In 1919 under
experimental conditions, Hiramatsu was the first to find

hypertrophy in the right side of the heart (25).

Cureton published an extensive study of athletes'
hearts in 1951 (22). He reported that track men who com-
peted in long sprints (200, 400, and 800m) and swimmers
who competed in the 200m and the 800m relay usually had
a larger proportionate enlargement in the right trans-
verse diameter. This is believed to be the result of the
larger effort exerted by the right ventricle in ejecting
blood into the lungs at times when the chest was con-
stricted. Long distance runners generally had enlarge-
ment on the left side and would breath more easily and
fully than the sprinters (22).

Other studies showed that hypertrophy developed
in animals when they were subjected to induced anoxemia
in a decompression chamber (80, 81, 83, 84, 86), and in
men living at high altitudes (51, 70). The hypertrophy
involved mainly the right ventricle and was produced pre-
sumably by the increased work load imposed by the pul-
monary hypertension associated with hypoxia (81, 84). It
was also shown that comparable anoxemia might result in
long sprints, especially in swimming 200m or running 400m
(22, 23). Thus, it is obvious that enlargement of the
heart depends on the intensity of training, the type of
training, and the duration of training. The sports which
make the greatest demands on the circulatory system pro-
duce the greatest cardiac hypertrophy.

When hypertrophy develops, the number of fibers

(nuclei) remains unchanged, but their diameter increases,

and the fibers lengthen by an increase in number of
sarcomers (60). This is believed to be the result of an
increase in nucleic acids and protein synthesis, a process
stimulated by stronger ATP (adenosine triphosphate) metabo-
lism. However, the obvious factor stimulating the develop-
ment of myocardium hypertrophy is anaerobic ATP resynthesis
occurring when the oxidiZing phosphorylation of ATP
directly corresponds to the needs of the functioning
heart (59). In this so-called "physiologic" hypertrophy,
which occurs in athletes or hard laborers, the weight of
the heart rarely exceeds 500 gm, which has been designated
as the critical heart weight by Linzbach (60).

However, when the heart is stimulated to do
heavier work for a long time period by some pathological
mechanism such as hypertension or aortic valvular disease,
it's weight will exceed this physiologic limit and may
reach 1,000 gm or more. If the hypertrophy is associated
with a normal ventricular chamber and residual blood
volume, it is described as concentric and occurs in the
early stages of chronic pressure load; e.g., vavular
stenosis or arterial hypertension. If the hypertrOphy
is associated with a ventricular chamber and residual
blood volume larger than normal as in valvular regurgi—
tation or myocardial disease, it is described as eccen-
tric. Both concentric and eccentric hypertrophy are
generally referred to as pathologic hypertrophy. In

concentric hypertrophy, contrary to the classical concept,

there is an absolute increase in the number of fibers
(more nuclei), which are only moderately thickened.
Apparently, the increase in the number of muscle fibers
is due to the longitudinal cleavage between points of
anastomosis of the myocardial syncytium. In eccentric
hypertrophy, the cardiac chamber is dilated with
destruction and fibrosis of some muscle fibers. The
surviving fibers undergo splitting and rearrangement, as
in the concentric type, but attain a diameter greater
than that of the concentric type when hearts of equal
weight are compared (6, 60).

Experimental studies of the behavior and basic
properties of hypertrophied hearts are few (34, 50).
Experimental heart hypertrophy is usually produced by
increasing the resistance to the ventricular ejection;
e.g., increasing the resistance in the aorta or pulmonary
artery. The response is characterized by a marked in-
crease in the contractile function of the myocardium
(estimated from the tension developed) with respect to
the increase in the resistance (62).

Dieckhoff (1936) used the heart-lung preparation
to study hypertrophied cat hearts and found a higher
arterial pressure and cardiac output in them than in
normal cat hearts (6, 50). Beznak also reported a
higher cardiac output (by the direct Pick-method) in

hypertrophied rat hearts when the rats were at rest.

10

However, he found no difference in the infusion rate
between hypertrophied and normal rat hearts (9).

Geha, Kerr, Whitehorn and their co-workers claimed
that hypertrophied heart muscle was capable of better
performance than nonhypertrOphied heart muscle (33, 50,
92). For given diastolic lengths, they found that a
greater tension developed in the columnac carnae of the
left ventricle of rat hearts which had been hypertrophied
from repeated swimming to exhaustion (92). The maximal
tension (per unit weight of papillary muscle) was also
found to be significantly greater in the hypertrophied
left ventricle of rats (50). In dogs, it was found that
the hypertrophied right ventricle performed more work
(per unit gross mass of the myocardium) than the normal
right ventricle (33).

However, Grimm and his associates found no differ-
ences between hypertrophied and normal rat papillary
muscle in tension production (per unit weight), water
content, total protein concentration, or actomyosin con-
centration (35). Sandler and Dodge, who calculated the
tension and stress of the inner wall of the left ventricle
during a cardiac cycle by measuring the pressure, the
dimensions, and the wall thickness of the ventricle from
biplane angiocardiograms, also noted that the force per
unit area of the ventricular wall in subjects with left
cardiac hypertrophy was not different from those with

normal left ventricles (73).

11

Another study reported that the oxygen consumption
per minute per unit mass of the hypertrophied left vent-
ricle was within the range of normal values, but the data
did not permit the calculation of myocardial oxygen uptake
per stroke because heart rates were not recorded (11).
However, in dogs, the data of West indicated no difference
in oxygen consumption per stroke per unit mass of tissue
between normal and hypertensive animals (91). From these
data, one might eXpect that the hypertrophied fibers of
the heart would develop greater contractile force because
of the increase in mass of the contractile tissues but
not because of the increased functional capacity of the
cellular elements. This was believed by Badeer (6) and
may fall in the "second stage" of the "complex and wear"
hypothesis, which states that the process of cardiac
hypertrophy occurs in three stages. This hypothesis was
proposed by Meerson in 1965 (62).

Cardiac performance is usually investigated by
considering the size and shape of the heart which is
regarded either as a pump made of muscle or as a muscle
acting as a pump. Woods applied Laplace's law to evalu-
ate the heart-wall tension in 1892 (94). Burch assumed
a spherical shape for the left ventricle and assigned
different volumes to demonstrate changes in the ventricular-
wall tension (15, l6, 17). Burton and others also investi-

gated the problem in the same manner (7, 18, 73).

12

In general, Laplace's law applies to a strained
"membrane" separating two spaces of any shape. It states
that if a slit is cut in the membrane, the two edges of
the slit will be pulled apart with a force proportional
to the length of the slit. The wall of the ventricle is
a strained "membrane" when the heart contracts; so, a
slit in the ventricular wall could be pulled apart.

There is also a pressure gradient existing between the

inner and outer ventricular wall. The equation is:

P = T(-—'+ E—) (A)

Where P is the ventricular systolic blood pres-
sure; T is the ventricular tension; and R1 and R2 are the
"principal radii of curvature" at any point on the
ventricular wall.

For the special case of a spherical ventricular
wall, where the radii of curvature are equal (R1 = R2),

the general equation becomes:
P = —- (B)

Woods assumed that the thickness of the ventri-
cular wall (t) at any point was proportional to the

tension developed in the wall during systole; i.e.,

t = KT (C)

13

where K is a constant and is equal to the tension in a
unit thickness of the wall. Substituting (C) into (B),

one obtains:

P = -——- (18, 94) (D)

According to Badeer, the force of contraction of
the ventricular wall is defined as the integral of the
force developed in the myocardium by a unit length of the
circumference and the entire thickness of the wall of a
given chamber over the whole period of systole. The

mural force during systole is:

WI
ml

Mural force = TS = (#)

where:

HI

is the mean force per unit cross-sectional
area of the wall,

(D

is the mean thickness of the wall,

rdl

is the mean transmural pressure, and

ml

is the mean radius, during systole.

When hypertrophy develops, the thickness of the
chamber wall increases. If the tension in the heart
muscle remains unchanged, any increase in the mural force
will be due to an increase in the thickness (S) rather
than to an increase in the mean force per unit cross-

sectional area of the wall (6).

14

Whether or not the hypertrophied heart will pro-
duce a greater tension per unit mass of its muscle than
the normal heart is still unknown. However, there is no
doubt that the hypertrophied athlete's heart is highly
efficient. Trained athletes with heart beats over 200
per minute, systolic pressures up to 240 mm Hg without
any disorders in the coronary blood circulation, stroke
volumes as large as 200 m1 and minute output as much as
35 liters have been recorded. Astrand has reported a

3 in a well-trained

maximum oxygen absorption of 5,800 cm
athlete working under a 400-Watt load. The heart rate of
a well-trained athlete can reach its maximum value within
5 to 8 seconds after the beginning of work, while in un-
trained subjects maximum rate occurs only after 30 to 40
seconds. Towards the end of the first second of work the
trained athlete's heart rate reaches 75 per cent of its
eventual maximum rate (59).

It is believed that the increased residual volume
of the left ventricle is secondary to physiologic hyper-
trophy, in that it provides for an immediate increase in
circulating blood when the athlete is put under stress.
Therefore, the increase in the residual volume is not a
Sign of cardiac weakness (59, 60). Nocker, Reindell
and Kenl showed that about one-third of the heart's
energy is derived by oxidizing lactic acid when the

subject is at rest. This fraction, however, can run up

to 40, 61, and 56 per cent when the subject is subjected

15

to moderate work, strenuous work, and recovery respectively.
Since the amount of lactate consumption depends on the mass
of the heart muscle, the larger heart of the distance
runner, by its increase in bulk, further contributes

relief to the metabolic machinery by burning off the acid

metabolites produced by the muscles (64).

CHAPTER III

METHODS

Thirty-two male albino rats (Spartan Sprague-
Dawley strain) were randomly divided into four equal
groups at 71 days of age:

1. Group S--Short-duration (high-intensity

endurance) training group.

2. Group M--Medium-duration (moderate-intensity

endurance) training group.

3. Group L—-Long-duration (low-intensity

endurance) training group.

4. Group C--Control (sedentary) group.

For two weeks prior to the initiation of the
study, the treatment animals were housed in spontaneous
activity cages for foot conditioning and acclimatization
to the laboratory. During the study, all of the animals
were maintained in sedentary cages which offered no oppor-
tunity for exercise. Water and Wayne Lab Blocks were
available ad_libitum. The cage quarters and training
facilities were kept at a constant temperature of 72°F;

however, no attempt was made to control the humidity.

16

17

The treatment animals were trained in small animal
controlled-running wheels once daily, five days per

week (Monday-Friday), for eight weeks. The animals
learned to run by avoidance-response-operant-conditioning.
The controlled-running wheels and interval training pro-
grams were developed by the Human Energy Research Labo-
ratory at Michigan State University.

Groups S, M, and L were trained with different
training programs. A detailed breakdown of the training
data is shown in Appendices A, B, and C. The performance
data of each animal were recorded daily. Several animals
were destroyed due to leg injury during training. The
lighting in the training room was maintained at a dim
level so that the light in each wheel (the conditioning
stimulus) would have a more dramatic effect. All unneces-
sary noise was avoided during the daily training bouts.

When the eight-week training period was completed,
the animals in all groups were fasted for twenty-four
hours. After the twenty-four-hour fast, the animals were
weighed and then decapitated. The heart with a small stem
of the aorta still attached was quickly removed. The
other great vessels were roughly trimmed away. The blood
was expelled from the chambers, and the heart was washed
free of blood with distilled water. Each heart then was
suspended by a thread from the aortic stem and fixed in
a 10 per cent formaldehyde solution. After the fixation

period of four days, the great vessels of each heart were

18

carefully trimmed. The surface of the heart was flushed,
and the atria were removed as cleanly as possible by
careful dissection along the atrioventricular groove.

The length of the ventricle from the apex to the entrance
of the pulmonary artery was measured by calipers. The
heart was transversely dissected along a line which was

55 per cent of the ventricular length from the apex. All
measurements and dissections were performed on the ventral
aspect of the heart.

The heart sections were blotted dry, and the total
heart weight was determined. Then, the atriums were re-
moved from the balance and total ventricular weight was
determined. The total atrial weight was obtained by
subtraction.

The sections containing the apex of the heart
were then dehydrated in graded concentrations of alcohol.
Following dehydration, they were embedded in paraffin and
sectioned on a microtome at eight microns per slice start-
ing from the end opposite to the apex. The first ten
slices of each heart were discarded while the eleventh
slice was stained with Hematoxylin and Eosin.

After staining, the slides were projected and
magnified approximately 10.76 times on a solid background,
46 inches away, by a Sawyer 500R slide projector. The
outline of each cross section was traced and the respec-
tive areas were measured by planimeter. Figure 1 shows

how the various ventricular areas were arbitrarily

of

RV
RC

LC
LV

19

RV

 

LV

Figure l.--Sample of the Projected Cross Section
Animal No. S-l.

Right Ventricular Free Wall Area
Right Ventricular Chamber Area
Septum Area

Left Ventricular Chamber Area
Left Ventricular Free Wall Area

20

separated for measurement purposes by an extended straight
line drawn through the two extremities of the right ventri-
cular chamber. Although in this way the left ventricular
free wall and the septum would seem to be separated, they
were considered and measured as one area (the left
ventricle-septum area) as there is no anatomical evidence
for such a line of demarcation (32, 52). Fulton and his
associates have emphasized the usefulness of the ratio of
the left ventricular free wall plus septum divided by
right ventricular free wall (LV + S/RV), for the septum
increases in prOportion to the increase in the weight of
the free wall of either ventricle (32, 52).

The method of separation used in this study pro-
vides technical simplification and creates no ambiguities
when different ratios are compared, for the technique
yields quite uniform results (32, 52).

Mean values of the data for each treatment group
were calculated. Analysis of variance was used to analyze
the data. Student-Newmen-Keuls statistical technique was
used to compare the differences between individual groups
due to training. The probability of making a type I
error was held to the .10 level for this investigation;
however, due to the small sample size the same obser-
vation was made whenever P g .25. All raw data are given

in Appendix D.

CHAPTER IV

RESULTS

The measurement of ventricular_volume has long

been a technical problem. Many efforts have been made

since the discovery of the X-ray, but none have been

 

satisfactory to all investigators (75). Such a technique
is extremely important, for without it one cannot deter—
mine the overall power and performance of the heart muscle.
Indeed, Starling concluded that when the heart was free
from its hormonal and nervous influences, its energy dur-
ing systole was directly proportional to the diastolic
volume (76).

The data of the present study agree with the
general opinion that vigorous physical exercise over an
effective period produces cardiac hypertrOphy. The data
in Table 1 show that in general hypertrophied hearts in-
crease in weight, length, total cross-sectional area, and
both left and right ventricular chamber areas.

The total heart weight of all exercised animals,
both on an absolute and a relative basis, was 22 per cent

greater than that of the controls. Such a difference,

21

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24

however, is far less than those which have been found in
some pathologically enlarged human hearts. If a general
comparison can be made between rats and men, this differ-
ence would fall below the "critical heart weight" of
Linzbach (60).

The cross-sectional areas of the hearts of the
exercised animals also show that enlargements of the left
and right ventricular chamber areas are associated with
increased total heart weight or ventricle weight. These
cross-sectional differences do not occur in concentric or
eccentric types of pathological hypertrophy.

Among the exercised groups, the long-duration
running group had significantly smaller absolute ventri-
cular length, total heart weight, and ventricular weight
than either the medium- or_the short-duration running
groups (P g .10) (Table 1). This group also had a sig-
nificantly larger mean right ventricular chamber area
(P g .10) and a somewhat lower ratio of left ventricular
free wall plus septum area divided by right ventricular
free wall (P g .25). Thus, it may be hypothesized from
the data of this study that there may have been a tendency
toward right ventricle domination in the long-duration
running group.

The exercised animals showed significantly differ-
ent values from those of the control group in regard to
the ventricular length, the total heart weight, the

ventricular weight, the atrial weight, and the left and

25

right ventricular chamber area (P = .10). Among the
exercised groups, the long interval-training group had

a larger mean right ventricular chamber than either the
short or the medium group (P = .10). Measurements of the
left ventricular chamber showed that the long and short
groups had larger chambers than the medium interval-
training group (P = .10). Both the short and the medium
interval-training groups had greater total heart weight,
ventricle length, and ventricle weight than the long

training group (P = .10).

CHAPTER V

SUMMARY, CONCLUSIONS, AND RECOMMENDATIONS

Summary

This study was designed to obtain in vitro
anthropometric measurements of the cardiac muscle in
postpubertal rats after different intensities of interval
training.

Thirty-two male albino rats (Spartan Sprague-
Dawley strain) were divided randomly into four equal
groups--three exercise groups, each of which was subject
to a different interval training program, and one control
group. The animals were 71 days old at the start of the
experiment.

For two weeks prior to the initiation of the study,
the treatment animals were housed in spontaneous activity
cages for foot conditioning and acclimatization to the
laboratory. During the study, all the rats were main—
tained in sedentary cages. The three treatment groups
were trained once daily, five days per week (Monday-
Friday), for eight weeks. Training was performed in

small animal controlled running wheels.

26

27

At the end of the training period, the animals
were fasted for twenty-four hours. They then were
decapitated and their hearts were fixed in a 10 per cent
formaldehyde solution. Afterwards, the ventricular
length, the ventricular weight, the atrial weight, and
the total heart weight of each animal were determined.

A transverse slice of each heart was cut at a standard
location and stained with hematoxylin and eosin. The
slide was projected and the outline of the section was
traced. From the tracing, the cross-sectional area, the
ventricular chamber size, and the ventricular free wall
area of the heart were measured with a planimeter.

Mean values of the data for each treatment group
were calculated. Analysis of variance was used to
analyze the data. Student-Newman-Keuls statistical tech—
nique was used to compare the differences between indi-
vidual groups due to training. The probability of making
a type I error was held to the .10 level for this in-
vestigation; however, due to the small sample size

the same observation was made whenever P g .25.

Conclusions

 

l. The results of this study indicate that
vigorous physical exercise over an eight-
week period produces cardiac hypertrophy in

postpubertal laboratory rats.

28

The hypertrophied hearts increase in weight,
length, total cross-sectional area, and both
left and right ventricular chamber areas.
Among the exercised groups, the long-duration
running group had significantly smaller
absolute ventricular length, total heart
weight, and ventricular weight than either
the medium- or the short-duration running
group. This group also had a significantly
larger mean right ventricular chamber area
and a somewhat lower ratio of the left ventri-
cular free wall plus septum area divided by

right ventricular free wall.

Recommendations

 

The physiological and mechanical details per—
taining to running in rats are unknown. It
will be necessary, therefore, to use a variety
of different training programs in order to
better define aerobic and anaerobic types of
exercise for rats. Such definition is needed
in order to compare the effects of different
exercise programs on cardiac hypertrophy.
Experience has shown that the ability of rats
to learn to run in a forced-exercise program

and their performance while running on a

29

particular program may be strain specific.
Learning and training programs developed for
a particular strain may not be suitable for
another strain of rats. The researcher should
bear this in mind if replication is attempted.
The method used to dissect the ventricles
transversely was not ideal due to errors in
sectioning. Thus, measurement on the total
cross-sectional area may not have been abso-
lutely accurate. A better method must be
sought.

In addition, only twenty slides were satis-
factory and complete enough to illustrate the
total cross-sectional area from the total of
twenty-seven hearts which were sectioned and
stained. Therefore, modification of the

histology technique is needed.

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APPENDICES

APPENDIX A

STANDARD EIGHT-WEEK, SHORT-DURATION, HIGH-
INTENSITY ENDURANCE TRAINING PROGRAM FOR
POSTPUBERTAL AND ADULT MALE RATS IN
CONTROLLED-RUNNING WHEELS

38

TABLE A-1.--Standard eight-week, short-duration, high-intensity endurance
training program for postpubertal and adult male rats in controlled-running

 

 

 

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2=T 2 1.0 00.10 10 40 3 5.0 1.2 2.0 39:45 600
3=W 3 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600
4=T 4 1.0 00:10 10 40 3 5.0 1.2 2.5 39:45 750
5=F 5 1.0 00:10 10 40 3 5.0 1.2 2.5 39:45 750
2 1=M 6 1.0 00:10 10 40 3 5.0 1.2 2.5 39:45 750
2=T 7 1.0 00:10 10 40 3 5.0 1.2 3.0 49:30 900
3=W 8 1.0 00:10 10 40 3 5.0 1.2 3.0 49:30 900
4=T 9 1.0 00:10 10 40 3 5.0 1.2 3.0 49:30 900
5=F 10 1.0 00:10 10 40 3 5.0 1.2 3.0 49:30 900
3 1=M 11 1.0 00:10 10 4O 3 5.0 1.2 3.0 49:30 900
2=T 12 1.5 00:10 15 40 3 5.0 1.0 3.5 59:15 1050
3=W 13 1.5 00:10 15 40 3 5.0 1.0 3.5 59:15 1050
4=T 14 1.5 00:10 15 40 3 5.0 1.0 3.5 59:15 1050
5=F 15 1.5 00:10 15 40 3 5.0 1.0 3.5 59:15 1050
4 1=M 16 1.5 00:10 15 40 3 5.0 1.0 3.5 59:15 1050
2=T 17 1.5 00:10 20 34 3 5.0 1.0 4.0 60:00 1020
3=W 18 1.5 00:10 20 34 3 5.0 1.0 4.0 60:00 1020
4=T 19 1.5 00:10 20 34 3 5.0 1.0 4.0 60:00 1020
5=F 20 1.5 00:10 20 34 3 5.0 1.0 4.0 60:00 1020
5 1=M 21 1.5 00:10 20 34 3 5.0 1.0 4.0 60:00 1020
2=T 22 1.5 00:10 25 22 4 2.5 1.0 4.5 57:10 990
3=W 23 1.5 00:10 25 22 4 2.5 1.0 4.5 57:10 990
4=T 24 1.5 00:10 25 22 4 2.5 1.0 4.5 57:10 990
5=F 25 1.5 00:10 25 22 4 2.5 1.0 4.5 57:10 990
6 1=M 26 1.5 00:10 25 22 4 2.5 1.0 4.5 57:10 990
2=T 27 1.5 00:10 30 14 5 2.5 0.8 5.0 54:10 875
3=W 28 1.5 00:10 30 14 5 2.5 0.8 5.0 54:10 875
4=T 29 1.5 00:10 30 14 5 2.5 0.8 5.0 54:10 875
5=F 30 1.5 00:10 30 14 5 2.5 0.8 5.0 54:10 875
7 1=M 31 1.5 00:10 30 14 5 2.5 0.8 5.0 54:10 875
2=T 32 2.0 00:10 35 10 6 2.5 0.8 5.5 54:00 825
3=W 33 2.0 00:10 35 10 6 2.5 0.8 5.5 54:00 825
4=T 34 2.0 00:10 35 10 6 2.5 0.8 5.5 54:00 825
5=F 35 2.0 00:10 35 10 6 2.5 0.8 5.5 54:00 825
8 1=M 36 2.0 00:10 35 10 6 2.5 0.8 5.5 54:00 825
2=T 37 2.0 00:10 40 7 7 2.5 0.8 6.0 51:10 735
3=W 38 2.0 00:10 40 7 7 2.5 0.8 6.0 51:10 735
4=T 39 2.0 00:10 40 7 7 2.5 0.8 6.0 51:10 735
58F 40 2.0 00:10 40 7 7 2.5 0.8 6.0 51:10 735

 

 

APPENDIX B

STANDARD EIGHT-WEEK, MEDIUM-DURATION, MODERATE-
INTENSITY ENDURANCE TRAINING PROGRAM FOR
POSTPUBERTAL AND ADULT MALE RATS IN
CONTROLLED-RUNNING WHEELS

39

TABLE B-1.--Standard eight-week, medium-duration, moderate-intensity endurance
training program for postpubertal and adult male rats in controlled-running

 

 

wheels.

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E4 ma) EU E A :1: us E 4.) AF; xA O
HID +40 «H u w~v ~' m 8" an» 364

w ‘H wv E-om [-c «4 U4 :1) Q. :5

O O A .. u 0 m x U) A. AA AA
00 XE: u mu 04-, U A 100‘ «10 MU
' >‘ >1 OE Hw-I m 0.5 ~ E21 0 (:0 HO u> 4J4)
x (U 41 U-H 0E OJ (DO 0 ~40 £2 :10) OH 00) 0!!)
3 o a 4:8 3‘” m mcn z EAm m m m B‘L BIZ B~v
1=M l 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600 1200
2=T 2 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600 1200
3=W 3 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600 1200
4=T 4 1.0 00:10 10 28 4 5.0 1.2 2.5 51:40 700 1120
5=F 5 1.0 00:10 10 28 4 5.0 1.2 2.5 51:40 700 1120
2 1=M 6 1.0 00:10 10 28 4 5.0 1.2 2.5 51:40 700 1120
2=T 7 1.0 00:10 10 27 4 5.0 1.2 3.0 50:20 810 1080
3=W 8 1.0 00:10 10 27 4 5.0 1.2 3.0 50:20 810 1080
4=T 9 1.0 00:10 10 27 4 5.0 1.2 3.0 50:20 810 1080
5=F 10 1.0 00:10 10 27 4 5.0 1.2 3.0 50:20 810 1080
3 1=M 11 1.0 00:10 10 27 4 5.0 1.2 3.0 50:20 810 1080
2=T 12 1.5 00:10 10 26 4 5.0 1.0 3.5 49:00 910 1040
3=W 13 1.5 00:10 10 26 4 5.0 1.0 3.5 49:00 910 1040
4=T 14 1.5 00:10 10 26 4 5.0 1.0 3.5 49:00 910 1040
5=F 15 1.5 00:10 10 26 4 5.0 1.0 3.5 49:00 910 1040
4 1=M 16 1.5 00:10 10 26 4 5.0 1.0 3.5 49:00 910 1040
2=T 17 1.5 00:15 15 19 4 5 0 1.0 3.5 52:00 997 1140
3=W 18 1.5 00:15 15 19 4 5.0 1.0 3.5 52:00 997 1140
4=T 19 1.5 00:15 15 19 4 5.0 1.0 3.5 52:00 997 1140
5=F 20 1.5 00:15 15 19 4 5.0 1.0 3.5 52:00 997 1140
5 1=M 21 1.5 00:15 15 19 4 5.0 1.0 3.5 52:00 997 1140
2=T 22 1.5 00:15 15 14 5 5.0 1.0 4.0 53:45 1050 1050
3=W 23 1.5 00:15 15 14 5 5.0 1.0 4.0 53:45 1050 1050
4=T 24 1.5 00:15 15 14 5 5.0 1.0 4.0 53:45 1050 1050
5=F 25 1.5 00:15 15 14 5 5.0 1.0 4.0 53:45 1050 1050
6 1=M 26 1.5 00:15 15 14 5 5.0 1.0 4.0 53:45 1050 1050
2=T 27 1.5 00:20 20 11 5 5.0 0.8 4.0 55:00 1100 1100
3=W 28 1.5 00:20 20 11 5 5.0 0.8 4.0 55:00 1100 1100
4=T 29 1.5 00:20 20 11 5 5.0 0.8 4.0 55:00 1100 1100
5=F 30 1.5 00:20 20 11 5 5.0 0.8 4.0 55:00 1100 1100
7 1=M 31 1.5 00:20 20 11 5 5.0 0.8 4.0 55:00 1100 1100
2=T 32 1.5 00:25 25 9 5 5.0 0.8 4.0 55:25 1125 1125
3=W 33 1.5 00:25 25 9 5 5.0 0.8 4.0 55:25 1125 1125
4=T 34 1.5 00:25 25 9 5 5.0 0.8 4.0 55:25 1125 1125
5=F 35 1.5 00:25 25 9 5 5.0 0.8 4.0 55:25 1125 1125
8 1=M 36 1.5 00:25 25 9 5 5.0 0.8 4.0 55:25 1125 1125
2=T 37 1.5 00:30 30 8 5 5.0 0.8 4.0 57:30 1200 1200
3=W 38 1.5 00:30 30 8 5 5.0 0.8 4.0 57:30 1200 1200
4=T 39 1.5 00:30 30 8 5 5.0 0.8 4.0 57:30 1200 1200
5=F 40 1.5 00:30 30 8 5 5.0 0.8 4.0 57:30 1200 1200

 

 

APPENDIX C

STANDARD EIGHT-WEEK, LONG-DURATION, LOW-INTENSITY
ENDURANCE TRAINING PROGRAM FOR POSTPUBERTAL
AND ADULT MALE RATS IN CONTROLLED-
RUNNING WHEELS

 

40

TABLC C-l.--Standard eight-week, long-duration, low—intensity endurance training
program for postpubertal and adult male rats in controlled-running wheels.

. ‘1'. Jam—glut ‘3-=ul=18—'-..:1 —

 

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I: U) 0‘) G M 00) E-*

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.2 L4 #0 (DA a) O O 3-H «I '0 E-r-I 0.0 MB
3 a m m E o E A m u E E m -H E x-a C);

Hm ~40) ~~l 41 UV v w [4" mu 3

u—a 44 UV Bu: 8 A 'H m o. :1

O O A .. u o m x m A- AA AA
4’0) x: U mu mu 0 A mm mo mo
' >: >1 0E H-H m 0.21 o E: 0 EU #0 4J> um
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3 D D «:8 3v :2: mm 2 £40: (I) aim E40. em («V
l 1=M 1 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600 1200
2=T 2 1.0 00:10 10 40 3 5.0 1.2 2.0 39:45 600 1200
3=W 3 1.0 00:10 10 4O 3 5.0 1.2 2.0 39:45 600 1200
4=T 4 1.0 00:20 10 30 2 5.0 1.2 2.0 34:40 600 1200
5=F 5 1.0 00:30 15 20 2 5.0 1.2 2.0 34:30 600 1200
2 1=M 6 1.0 00:40 20 15 2 5.0 1.2 2.0 34:20 600 1200
2=T 7 1.0 00:50 25 12 2 5.0 1.2 2.0 34:10 600 1200
3=W 8 1.0 01:00 30 10 2 5.0 1.2 2.0 34:00 600 1200
4=T 9 1.0 02:30 60 4 2 5.0 1.2 2.0 31:00 600 1200
5=F 10 1.0 02:30 60 4 2 5.0 1.2 2.0 31:00 600 1200
3 1=M 11 1.0 02:30 60 4 2 5.0 1.2 2.0 31:00 600 1200
2=T 12 1.0 05:00 0 1 5 2.5 1.0 2.0 35:00 750 1500
3=W 13 1.0 05:00 0 1 5 2.5 1.0 2.0 35:00 750 1500
4=T 14 1.0 05:00 0 1 S 2.5 1.0 2.0 35:00 750 1500
5=F 15 1.0 05:00 0 1 5 2.5 1.0 2.0 35:00 750 1500
4 1=M 16 1.0 05:00 0 1 5 2.5 1.0 2.0 35:00 750 1500
2=T 17 1.0 07:30 0 1 4 2.5 1.0 2.0 37:30 900 1800
3=W 18 1.0 07:30 0 1 4 2.5 1.0 2.0 37:30 900 1800
4=T 19 1.0 07:30 0 1 4 2.5 1.0 2.0 37:30 900 1800
5=F 20 1.0 07:30 0 l 4 2.5 1.0 2.0 37:30 900 1800
5 1=M 21 1.0 07:30 0 1 4 2.5 1.0 2.0 37:30 900 1800
2=T 22 1.0 07:30 0 l 5 2.5 1.0 2.0 47:30 1125 2250
3=W 23 1.0 07:30 0 l 5 2 5 1.0 2.0 47:30 1125 2250
4=T 24 1.0 07:30 0 1 5 2.5 1.0 2.0 47:30 1125 2250
5=F 25 1.0 07:30 0 l 5 2.5 1.0 2.0 47:30 1125 2250
6 1=M 26 1.0 07:30 0 1 5 2.5 1.0 2.0 47:30 1125 2250
2=T 27 1.0 10:00 0 l 4 2.5 0.8 2.0 47:30 1200 2400
3=W 28 1.0 10:00 0 1 4 2.5 0.8 2.0 47:30 1200 2400
4=T 29 1.0 10:00 0 1 4 2.5 0.8 2.0 47:30 1200 2400
5=F 30 1.0 10:00 0 l 4 2.5 0.8 2.0 47:30 1200 2400
7 1=M 31 1.0 10:00 0 l 4 2.5 0.8 2.0 47:30 1200 2400
2=T 32 1.0 10:00 O 1 5 2.5 0.8 2.0 60:00 1500 3000
3=W 33 1.0 10:00 0 1 5 2.5 0.8 2.0 60:00 1500 3000
4=T 34 1.0 10:00 0 1 S 2.5 0.8 2.0 60:00 1500 3000
5=F 35 1.0 10:00 0 1 5 2.5 0.8 2.0 60:00 1500 3000
8 1=M 36 1.0 10:00 0 1 5 2.5 0.8 2.0 60:00 1500 3000
2=T 37 1.0 12:30 O 1 4 2.5 0.8 2.0 57:30 1500 3000
3=W 38 1.0 12:30 0 1 4 2.5 0.8 2.0 57:30 1500 3000
4=T 39 1.0 12:30 0 1 4 2.5 0.8 2.0 57:30 1500 3000
5=F 40 1.0 12:30 0 1 4 2.5 0.8 2.0 57:30 1500 3000

 

APPENDIX D

BASIC DATA--ALL ANIMALS

41

 

 

 

oom.A nov.A mo>.A m.vm¢ mmIU
mvm.A mwm.A th.A m.mmv AmIU
mmN.A mov.A Amm.A o.¢mm omuU
mmm.A oww.A ooh.A m.MAv man
wmm.A omm.A oom.A m.vv¢ man
neN.A Amm.A mAm.A «.mAv nan
ovm.A «mm.A Amm.A m.Amv mmIU
hem.A mmv.A mmm.A mmm m.mmm vmuA
OAe.A th.A mom.A mwn «.mAq mmnA
mAe.A mmm.A mAm.A wmn 0.0mm ANIA
nvm.A Aom.A mAm.A wow m.mmm omlA
wAv.A mum.A vmm.A wmm o.mAv mAIA
hov.A mum.A mnm.A mmm v.Anm mAIA
mhv.A mom.A omm.A wvm o.mov EAIA
Amm.A mA>.A mAm.A wmm n.mAv mAlz
mmv.A mmo.A mam.A won w.nAv mAlz
nom.A mmw.A mom.A mAb m.nmv NAIE
hmv.A mmm.A mum.A wmm ¢.Amm AAIS
mam.A mmm.A hqm.A wvm A.mmm mu:
mvv.A mom.A mmm.A wvm m.mmm mam
mmm.A mmw.A voo.m was m.mwm hum
mme.A mmo.A vvm.A wow v.Amv mum
NAm.A 0mm.A omm.A wmm m.vAv mum
chm.A Amm.A mum.A won v.oov vnm
ovm.A mmv.A Amm.A wvm o.mwm mum
mAm.A mow.A mum.A wmm o.mov mum
.mEm mm4.n .mam mno.n .mEO mnm.a wmm .mam m.moe Hum
unmAmz psmAmB pnmmm numcmA UmumAmEOU Emnmonm pnmAmz .oz AmEAcd
onAnpam> Amuoe onAnucm> chsAmnB mo m hpom

 

.mAmEAEm AAmIImumU UAmmmII.AIQ MAAAB

42

 

 

 

 

 

 

 

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emo.v nvm.o mmm.~ mmm.m 84A.o Amuo
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mmm.4 mwm.o Am~.m mhm.m 44A.o mmso
mvo.¢ mm~.o mmm.m meo.m ooA.o mmuo
mmm.4 v>~.o mmm.m mom.m «An.o emuo
mam.m mum.o m¢e.~ Hmo.m «NA.o mmuo
44m.4 mov.o eqm.m mmo.¢ AmA.o «mun
4AA.4 mmm.o mmm.m meh.m NGA.° mmuq
men.4 mmm.o 4mm.m mAA.4 men.o Amun
mme.4 Noe.o mAm.m Amm.m va.o omuq
smv.e oem.o ~A4.m mme.m mmn.o mAuA
m«o.m ome.o mmh.m mvm.v Hun.o mAuq
Amm.v mev.o mmm.m AAA.¢ mmA.o AAuA
mmm.e Aoq.o mmh.m mmn.e ema.o mAaz
mem.4 «Av.o em¢.m mom.m meA.o mnuz
4mm.v Amm.o m¢¢.m mom.m mmA.o «an:
omA.m mve.o mqm.m nmm.e NGA.o AAuz
nmm.v mmq.o 4mm.m mmo.v mmA.o mus
mmm.4 mmm.o mmo.m mmo.v mmA.o mum
mmA.m ovv.o mmm.m mam.v OEA.o bum
mem.¢ mme.o «we.m nmm.m mEA.o mum
mme.4 om¢.o omm.m meo.v mEA.o m-m
mmm.4 nem.o -4.m mme.m Amn.o «um
Amm.4 mov.o mmm.m mam.m mmA.o mum
one.v mnm.o mAA.m mmo.v mmA.o mum
omm.¢ mnm.o Amm.m mmm.m .msm mmA.o Aum

A one .83 mmom I OAU .uz mmom I oAU.u3 amom A OAv.u3 mmom unmnmz .02

m: numcmq m. .u: mnnum m. .u: mno m: .u: unmmm mnnum Amsna¢

mnonnpcm> unnucm> Amuoe

 

.Am.ucoov Auo mAm<H

43

 

 

m.NAA v.v o.> m.vNA NmIU
o.>AA m.¢ m.m m.AmA mNIU
m.mAA N.m m.m «.mmA mNIU
A.hOA m.m N.m m.mAA hmIU
A.hAA N.m m.NA N.hMA wNIA
m.mOA v.5 m.VA o.NMA MNIA
m.mAA v.m m.m N.hMA omIA
o.MAA N.m m.nA h.mMA mAIA
m.ANA n.m w.mA A.mVA hAIA
o.AmA A.m A.MA N.NmA mAIZ
h.ANA o.m m.m m.MMA mAIE
m.omA o.h A.MA v.0vA NAIS
o.omA m.m N.AA b.mmA AAIE
m.v0A v.5 m.AA m.mmA ml:
m.MAA h.w m.AA m.AMA mlm
A.mmA m.m m.AA o.¢vA him
A.wNA m.h m.mA N.mVA mlm
m.NOA m.m N.5A m.mmA mlm
w.MAA v.0 A.vA m.vMA mlm
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Amenm neQEsz m w Ailmend menm mend mend .OZ AmEAEA

soAuoem Amuoav mend Amumem neQEmSU usmAm neAEmLU pmeA EoApoem AmAOB
mam merAnuce> m e A

 

.Am.ucoov Ana mqmee

44

 

 

OAmh.m m.mm n.mm mmIU
mmmv.m m.om N.em mNIU
enmm.m >.mm m.nm mNIU
mwmm.m m.vm «.mm hmIU
mmAm.m m.~m m.vm vmuA
mmwv.m A.mm b.v~ mmIA
mvum.m b.mm m.mm omlA
oomm.m o.mm o.mm mAnA
omoe.m «.mm ¢.mm hAIA
mmmm.m h.~OA m.mm mAIz
vaA.v m.hm m.m~ mAlz
«Ach.v m.mm A.Am NAIS
mmmm.m h.mm m.v~ AAuz
vvmh.m m.mm m.Am an:
mvmm.¢ m.Am m.AN mum
mmom.v m.AOA N.Am hum
heme.v m.MOA m.mm mum
Aomv.m m.mn m.m~ mum
mnom.m A.mm n.v~ mum
Avmh.m .mmEo h.Am .mmEo A.e~ Anm
mend erAnuce> unmAm Amend er mend .oz AmEAad

 

mend Enumem
mam mend eAeAnuce> umeA

IAnpse> m I mend Enumem
mam mend eAeAnuce>
m a no men< Enumem
mam mend erAnuce> umeA

eAOAnuce> unmAm

 

.xm.ucoov Ana wands

APPENDIX E

HERXHEIMER'S HEART SIZE DATA ON THE
1928 OLYMPIC ATHLETES

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Eonm meumASOAmo enenmm m on Amsqe eEdAo> chms oAumn unmAe3\eEsAo> es» ene£3«

 

45

 

 

 

m.mn h.w 9.4 m Amcnasnemv mnmuannmm
m.mn ~.m “.4 m.mm\n mm nee cannumoea
n.mA n.m A.e m.~e\n mm Anomnuc mnmucnnmm
m.mn m.m e.e m.om\n an mnmccsn mocmumnmnmaon
4.4n o.m m.v m.mm\n mm mnmuenn usmnmz
m.mn m.m e.q n.mm\n em mnchsn mocmumnmumnmmnz
m.mn ~.m 5.4 mm\n en mumnnonu ucnnmm
v.mn m.m m.4 e.~m\n wn mnmxom
e.vn 4.m m.m b.nm\n mm swamnmo
4.4A m.m ~.m >.mv\n en mumnnono eocmumnmumaoq

m.mn o.m m.4 n.me\n m4 mnmccsn
eocmumAm mam conumnmz
Amnnenmz mmmn
m.oe\n NA mumnnono mam xnm
m.me\n on mnmxom
~.ee\n en gee consumoeo
m.mm\n mn mnmfiEnem
m.me\n mm meuencum n>mmm
m.om\n an mnmccsn mocmumnmumnmmnz
m.>m\A NA mneacsn eocmumAmumEOA
m.om\A mA mneAxm mnucsoelmmonU
Amnnmumz mmmn

neueEon neueEon neueEon unmmez mmom

 

 

 

eEsAo> z coAumoAmAmmmAU
Amuoe emmne>d pmeA emmne>d usmAm emmne>d unmem emmne>d

 

.meueAnum UAQEon mmmA esp co mumm eNAm unmes m.neEAe£xnemll.Aum mAmdB

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