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LIBRARY

Michigan State
University

 

This is to certify that the

thesis entitled

THE EFFECTS OF DIET WITH SODIUM BICARBONATE

SUPPLEMENT UIDON MAXIMUM OXYGEN UPTAKE, THE

CHANGE IN BOLLD pH AND WORK CAPACITY IN
TRAINED ENDURANCE RUNNERS

presented by

Dwight D. Gaal

has been accepted towards fulfillment
of the requirements for

MOA. degree in Phys. Ed.

flaw/g2“
BM

Major professor
0-7639

, r_“'——\N~\_‘q

OVERDUE FINES:

   
   

    
   

I '54- .. 25¢ per day per item
, , . In ' < I
, a. m. t RETURNING LIBRARY MATERIALS: !
\‘<Lf§ii’-~,,'"',’ ":4 Place in book return to remove i
‘x ".” r,

\i-4 charge from circulation records

  

THE EFFECTS OF DIET WITH SODIUM BICARBONATE
SUPPLEMENT UPON MAXIMUM OXYGEN UPTAKE, THE
CHANGE IN BLOOD pH AND WORK CAPACITY

IN TRAINED ENDURANCE RUNNERS

BY

Dwight D. Gaal

A THESIS

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

MASTER OF ARTS

Department of Health, Physical Education and Recreation

1980

 

4/ ’I 11,] I ‘ \. ._
. 'IJ.‘ '

ABSTRACT
THE EFFECTS OF DIET WITH SODIUM BICARBONATE
SUPPLEMENT UPON MAXIMUM OXYGEN UPTAKE, THE CHANGE IN

BLOOD pH AND WORK CAPACITY IN
TRAINED ENDURANCE RUNNERS

By
Dwight D. Gaal

The purpose of this study was to determine the
effects of sodium bicarbonate (NaHCOB) ingestion
(.O65gm/kg.) under either high carbohydrate or high
fat-protein dietary conditions upon maximum oxygen
uptake (FOZmax), the change in pH of arterial blood
serum lactate levels and maximum treadmill performance
time (TMT) in marathon runners.

Eight male distance runners, 20-40 years of age,
served as subjects. They were assigned to each of four
treatment conditions; supplement/carbohydrate, supple-
ment/fat-protein, placebo/carbohydrate and placebo/fat-
protein.

A graded treadmill test was performed under each
of the four conditions. Arterialized blood samples
were analyzed for determination of blood lactic acid and
pH (Enzymatic method). Values for F02 were obtained via
the Douglas bag method. Length of run time to exhaus-
tion was recorded to measure performance capacity.

The results of this experiment indicated that the

change in lactic acid and pH observed under supplement

 

Dwight D. Gaal

conditions were statistically significant. The pH was
significantly higher under the supplement conditions.
Upon reaching the point of Fozmax there was a substan-
tial decrease in arterial blood pH as exercising mus-
cles began working anaerobically. Performance times
were not affected by either diet or supplement condi-

tions.

DEDICATION

I have dedicated this thesis to my loving grand-
father, Alfred B. Sprowl, from whom I have learned of
the importance of hard physical work in living a long,
healthy and rewarding life.

Also, to my dear parents, Wildred and Frank, for
their constant encouragement, support and understanding;
and to my brother, Craig, for instilling in me the
strength, persistence and assertiveness to overcome all
obstacles which may stand between me and my goals.

And finally, to a special person in my life who
has helped to make it all seem worth while, Jan Marie

Ryan.

ii

ACKNOWLEDGMENTS

I would like to express my most sincere thanks to
Dr. Wayne D. Van Huss for his aid and guidance during
this study and throughout my graduate studies.

My thanks also go out to Dr. William Heusner, my
academic advisor, for counseling and guidance during
my graduate studies.

Special thanks are due to Dr. Asghar Khaledan
for permitting me to be a part of his research team,
and to fellow researchers Shokr Fallah Bosjin, Ali
Motaghi and Peter Rodin for their tireless assistance
during the data collection.

I also wish to express my deepest gratitude to my
closest and dearest friends whose continued support made
the going considerably less rough. I need not mention
any names, for they know who they are.

Finally, I would especially like to thank one
friend in particular, Jack Washka, for his concern,
advice, foresight and his teaching excellence, during

my early college years.

iii

LIST OF TABLESOOOOOOOOOOOO0.0.........OOOOOOOOOOO
LIST OF FIGURESOOOOOOOOO...OOOOOOOOOOOOOOOOOOOOOO

LIST OF APPEFJDICESQOOOOOOO. ..... 0000...... ...... 0

Chapter

TABLE OF CONTENTS

I. INTRODUCTION TO THE PROBLEM
Statement of the Problem.................
Purpose of the Study........ ..... ..........

Research Hypotheses........ ..... .........

Research Plan............................
Limitations of the Study.... ..... .........
Definition Of Terr-[1800.00.00coo-0000000000

Acid—base Balance

Acidosis

Alactacid 0 Debt

Alkalosis

Anaerobic Glycolysis
Arterio-venous 02 Difference (A-V 0
Blood pH

Lactacid 0 Debt

Maximum Oxygen Uptake (V0 2max)
Oxygen Debt
Phosphofructokinase (PFK)

II. REVIEW OF THE LITERATURE

a)

b)
C)
d)
e)
f)

9)

The Involvement of Fat, Carbohydrate
and Protein in Energy Metabolism......

Page

.....vi

....vii

...viii

9

diff)

Oxygen Uptake during Aerobic Work... .....

Oxygen Uptake during Anaerobic Work...
Recovery from Work....................
Factors Which Limit Performance.......
The Effects of Diet upon pH and

Performance... ..........................

The Effects of Alkalizers on pH and

Performance. ........................

iv

. I

UIU'lrbt-D-UJH

ll
14
15
17

21

23

Chapter Page

III. RESEARCH METHODS
Experimental Design.......................... 27
Subjects..................................... 30
Exercise Test................................ 30
Measurement Procedure........................ 32
Respiratory Frequency..................... 32
Heart Rate................................ 32
Blood Sampling............................ 33
Lactate Analysis.......................... 34
Acid-base Parameters...................... 34
Energy Metabolism Measures................ 35
Dietary Measures.......................... 36
Test Protocol................................ 37
Statistical Analysis......... ...... .......... 40

IV. RESULTS AND DISCUSSION
a) Lactic Acid............................... 41
b) pH........................................ 46
0) Oxygen Uptake (V0 )....................... 51
d) Maximum Oxygen Up ake (V0 2max)............ 51
e) Performance............................... 56
Discussion................................... 56

V. SUMMARY, CONCLUSIONS AND RECOMMENDATIONS
Summary...................................... 62
Conclusions.................................. 64
Recommendations.............................. 64

APPENDICES

BIBLIOGRAPHY

LI ST OF TABLES

Table Page

2.1 Previous Studies: Effects of Alkalizer
upon Performance and Related Physiolog-
ical ParameterSOOOOOOOO0.0.0....OOOOOOOOOOOOOOOO 24

3.1 Supplement and Diet Conditions.................. 28
3.2 Treatment Conditions ............... . ....... ..... 28
3.3 Test Sequence in Latin Square Design............ 29
3.4 Subjects, Age, Height and Weight................ 29
3.5 Grade, Speed, Work and Rest Intervals in

the Multi—stage Treadmill Test.................. 31
4.1 Statistical Results, Lactate (mMol/L).... ..... .. 42
4.2 Changes in Lactate (mMOl/L) and

Statistical Results............................. 44
4.3 Statistical Results, pH....... ..... .... ..... .... 47
4.4 Changes in pH and Statistical Results........... 49
4.5 Statistical Results, Oxygen Uptake

(Liters/min.)............................ ..... .. 52
4.6 Statistical Results TMT and Vozmax)............. 54
4.7 Performance Time................................ 57
A.l High Carbohydrate Diet. ........ ................. 65
A.2 High Fat/Protein Diet. ..... ..................... 66
A.3 Summary of Food Intake of an Individual

SUbjectOOOCOI...OOOOOOOOOOOOO...0....0.0.0.9.... 6‘7

B.l Basic Data, Lactate (mMol/L) ...... .............. 68
C01 BaSj-C Data, pHOOOOOOOOO...OOOOOOOOOOOOOOQOOOOOOO 69
D.1 Basic Data, Oxygen Uptake (V02) (L/min.)........ 70

vi

Figure

2.1

LIST OF FIGURES

Page
Glycolytic Pathway........................... 8

Citric Acid Cycles and Electron Transport
PathwaySIIOQVIQIO'00l...CIOIQDO‘OOOI.00...... 9

Diet and Supplement Effect on Lactate........ 43
Lactate Changes under Different Conditions... 45
Diet and Supplement Effect on pH............. 48
pH Changes under Different Conditions. ..... .. 50

Diet and Supplement Effect on Oxygen
Uptake........... ........ . ................ 53

Results: (a) TMT, (b) Vozmax................ 55

Siggard—Andersen Alignment Nomogram.......... 72

Appendix
A.
B.

C.

LIST OF APPENDICES

Diets..................................
Basic Data, Lactate (mMol/L)...........
Basic Data, pH.........................
Basic Data, Oxygen Uptake (V02) (L/min)

Siggard-Andersen Alignment Nomogram....

viii

0.0..

Page
65
68
69
7O

72

__-

CHAPTER I

INTRODUCTION TO THE PROBLEM

The cause of fatigue during prolonged heavy exer-
cise has long been a subject of interest. As early as 1907
researchers have suspected a link between intercellular
lactic acid concentration and muscle fatigue (6,8,9,23,29,
45,57,74,75,79,80,100,112,125,146,147). In 1936, Dill,
Edwards and Margaria (52) concluded that the maximal in-
crease in lactic acid production in the muscle tissue is
proportional to the intensity and duration of the work in
which the muscles are involved. Additional studies have
supported this View (23,27,29,46,47,74,l37). During light
to moderate exercise there is little accumulation of lactic
acid in the blood (52). When work load exceeds that corres-
ponding to maximum oxygen uptake (VOZmax) there is a marked
increase in the lactacid oxygen debt (02 debt). At this
point the respiratory quotient (RQ) is at unity (1.0) or
above. The contraction of an 02 debt is indicative of a
shift to anaerobic metabolism, resulting in increased quan-
tities of lactic acid in the working muscles (27,102,163).
The lactic acid rapidly dissociates into H+ and lactate- ions
and the blood pH drops. The increased H+ ion concentration
is believed to interfere with muscle contraction as follows:

1. H+ ions compete with Ca++ ions for binding sites

along the muscle fiber membrane, thus preventing

muscle contractions (56,60,106,112,115).

 

2. excess acidity appears to interfere with trans-
mission of the nerve stimulus across the neuro-
muscular junction, interfering with contraction
(72).

3. the decrease in pH inhibits activity of phospho-
fructokinase (PFK), the rate limiting enzyme in
anaerobic glycolysis, resulting in feedback in—
hibition of glycolysis during intense muscular
work cauSing a decrease in ATP supply and thus,
fatigue (1,6,36,55,75,108,109,141).

Although the notion that lactic acid may be a causal
agent of muscular fatigue has at least a theoretically sound
basis, many researchers choose to believe that depletion of
glycogen stores in working muscles is more directly related
to muscular fatigue during heavy exercise (lasting 40—180
min.) (68,74,86,94,115).

It is now a well accepted fact that a high carbohy-
drate diet can increase the muscle glycogen content to more
than 49/1009 wet muscle (16,130). Such an elevated endo-
genous glycogen content is associated with increased endur-
ance work capacity (5,l4,23,66,67,71,73,74,88,115,159). A
great relative carbohydrate intake not only serves to in-
crease the intramuscular glycogen stores, but also seems to
have a synergistic effect on maintaining the acid-base balance
of the body. It has been shown that the arterial blood of

subjects on a high carbohydrate diet (greater than 60% CHO)

was more alkaline and in subjects on a high fat-protein
diet (about 50% fat and 30% protein), more acid (92).

The alkalinity of the blood may also be increased
by the oral ingestion or intravenous injection of sbdium
bicarbonate (NaHC03) (24,51,53,87). The findings of
Dennig (49) revealed that both the abilities to incur an
02 debt and to perform strenous work of greater than 20
minutes duration are increased significantly in the alkalotic
state, whereas both work capacity and 02 debt capacity are
decreased during acidosis. In a more recent investigation,
Jones‘g£;§l., (97) found that exercise performed in the
alkalotic state resulted in longer performance times at both
70% and 90% of Vozmax. Also, blood lactate at 70% Vozmax
and at exhaustion was consistantly highest in alkalosis and
lowest in acidosis. Although there are many studies support-
ing these findings (49,78,97,128), there are also conflicting
studies (96,124). Obviously there is a need for further re-
search into the area of bicarbonate supplementation and per-
formance in order to clear up the controversies which current-
1y exist. The present study is intended to offer new infor-

mation in this area.

'The Purpose of the Study
To determine the effects of diet (either high
carbohydrate or high fat-protein) with orally ingested
sodium bicarbonate (0.06Sg/kg body weight), upon Vozmax,
the change in pH of arterialized blood, and performance

during a multi-stage treadmill run to exhaustion.

Research Hypotheses

 

The present investigation was designed to test the
following research hypotheses:

1. Upon reaching the point of V02max there is a
substantial decrease in arterial blood pH as working muscles
begin to rely more heavily on anaerobic glycolysis for
energy production.

2. A high carbohydrate, as opposed to a high fat-
protein, diet will enhance endurance work capacity.

3. A high carbohydrate diet will increase the
akalinity of the blood.

4. Sodium bicarbonate, orally ingested (.06ng/kg.
body weight), will increase the alkalinity of the blood.

5. Sodium bicarbOnate ingestion, two hours prior to

exercise, will increase maximum performance time.

Research Plan

 

A Latin-square design with replication, in a single
blind protocol was used for the study. Eight subjects were
studied under four different treatment conditions with repli-
cation. All eight subjects were competitive marathon runners
residing in the mid-Michigan area. The scheduled treatments
were as follows:

1. High carbohydrate diet with NaHCO

3

2. High fat-protein diet with NaHCO3
3. High carbohydrate diet with placebo
4. High fat-protein diet with placebo.

Performance time, V02, VOZmax and energy metabolism

 

 

5
were measured during an exhaustive multi-stage treadmill run
under all four treatment conditions. For determination of
blood pH and lactate analysis, arterialized blood samples were
taken at rest, prior to exercise, and after each level of
exercise. Data analysis was accomplished using the two-way,
repeated measures analysis of variance (63) and the non-para-

metric sign test (152).

Limitations of the Study

 

l. The amount of daily exercise and sleep of the
subjects were beyond the control of the investigators and
may have affected their performances during the testing.

2. As in any repeated measures study involving ex-
haustive work, physiological and psychological fatigue are two
variables which may affect performance during testing, despite
efforts to take all standard precautionary measures.

3. The findings of this investigation are applicable
only to those athletes whose training programs are similar to

those of the subjects tested.

Definition of Terms

 

Acid-base Balance - the normal equilibrium between

 

acid and base in the blood plasma, expressed in the hydrogen
ion concentration, pH.

Acidosis - a state characterized by actual or relative
decrease in alkali in body fluids in proportion to the content
of acid.

debt

 

Alactacid On Debt - that portion of the gross 02

which is not involved in the removal of lactic acid from the

 

blood; the portion of recovery 02 used to resynthesize and
restore phosphagen (ATP and CP) in muscle following exercise.

Alkalosis - abnormally high alkali reserve of the

 

blood and other body fluids, with a tendency for an increase
in pH of the blood.

Anaerobic Glycolysis - the metabolic breakdown of

 

glucose to lactic acid; the only pathway within which high
energy phosphate bonds can be generated without the immediate

utilization of oxygen.

 

Arteriovenous Oxygen Difference (a-VOQ diff.) - the
difference in oxygen content between the blood entering and
leaving the pulmonary capillaries.

Blood pH — a measure of the acidity or alkalinity of

 

the blood; log of the reciprocal of the H ion concentration.

Lactacid 02 Debt - that portion of the gross 02 debt

 

which is involved in removal of lactic acid from the blood
and tissues during recovery from exercise.

Maximum Oxygen Uptake (VOQmax) — the maximum amount

 

of oxygen that the tissues can remove from the blood during

work per unit of time (usually expressed as L/min or ml/kg/min).

 

Oxygen Debt (09 Debt) - the elevated oxygen utili-
zation which occurs during recovery from exercise; represents
repayment of the deficit incurred during work.

Phosphofructokinase (PFK) — rate limiting enzyme in

 

anaerobic glycolysis; catalyzes reaction between fructose
6-phosphate and fructose l, 6 diphosphate in the glycolytic

pathway.

CHAPTER II

REVIEW OF THE LITERATURE

The literature which is related to this study has
been subdivided into the following six sections: a) the
involvement of fat, carbohydrate and protein in energy metabo-
lism, b) oxygen uptake during aerobic work, c) oxygen uptake
during anaerobic work, d) recovery from work, e) factors
which limit performance, and f) effects of alkalizers on pH

and performance.

a) The Involvement of Fat, Carbohydrate

and Protein in Energy Metabolism

 

The extent of the involvement of fat, carboydrate
and protein in energy metabolism is dependent upon the
following:

a) the individual's rate of energy metabolism,

b) substrate availability,

c) the physical condition of the individual, and

d) the intensity of the work.

Though all three foodstuffs may provide energy for muscle
contraction by way of the different metabolic pathways
(Figures 2.1,2.2), this study will focus mainly on fat and
carbohydrate metabolism. With few exceptions, protein is
called upon as a fuel source only during periods of star-

vation.

Glycogen
Phosphorylase l

Glucose
Hexok inose ATP
ADP

Glucose 6-phosphate

Fructose 6-ph05phate

ATP
Phosphofructo-
kinase ADP

Fructose l,6-diphosphate

F W

 

 

 

Dihydroxyacetone 1 ~ Glyceraldehyde
phosphate 3-phosphate
Glyceraldehyde i NAD‘ + P.
3-phosphate '
dehydrogenase NADH ., H‘

I, 3- Diphosphoglycerate
( C ADP
ATP
B-Phosphoglycerate
Al

2- Phosphoglycerate

ll\

 

Phosphoenalpyruvate

Pyruvote AD
kinase ATP

A t l .
Egg *— Pyruvate

Lagtate < NADHZ
De ydroqenase N AD

Lactate

Figure 2.1. Glycolytic Pathway.

* From Lehninger (117).

 

 

 

 

 

   
  
 
  
 
 

 

 

 

 

 

Amino Fatty
acids Glucose acids
Mobilization of Pyrulvate
acetyI-CoA
2H C02
Acetyl-COA
L
Citrate
Oxaloacetote
(cis - Aconitate)
The tricarboxylic Malate . -
acid cycle lsocitrate
Fumorate —C—O-—
a-Ketoglutarate l 2|
Succinate
SuccinyI-COA N 502
L.
NAD‘
Flavoprotein ADP + P
Coenzyme Q C— “1“:
Electron transport and
oxidative phosohorylation Cytochrome b ADP + pi
Cytochrome c C— “no
ADP + P,-
Cytochrome 03 <—
L 1l_A—P

 

2HI+ 302 A H20

 

 

 

Figure 2.2. Citric Acid Cycles and Electron Transport Pathways.

* From Lehninger (117).

10

During high intensity work of short duration energy
is derived from the endogenous phosphagens, ATP and CP, and
muscle glycogen (129). It was Chaveau (32) who, in 1896,
discovered a steady increase in the respiratory quotient
(RQ) with vigorous exercise. Most were in agreement with
Chaveau (32) that carbohydrate metabolism served as the
primary energy source for muscle contractions.

However, on the other hand, there were numerous
investigators who later claimed that fat, rather than car-
bohydrate, was being metabolized as their studies revealed
little difference between exercising and resting RQ's (13),
110). It was then concluded that both fat and carbohydrate
are the major substrates involved in muscle contraction (112).

Now it is well accepted that during heavy work of
short duration (80-90% VOZmax) anaerobic glycolysis is re—
sponsible for energy output (34,40,41,73,101,104,ll4,165).
Most researchers would agree that the concentrations of lactic
acid in the blood and working muscles, which accompanies
anaerobic work, might inhibit the mobilization of free fatty
acids (FFA). Therefore, fat metabolism is prevented from
participating in the energy output. As the intensity of the
work decreases and the duration increases, fats play an in—
creasingly important role in energy metabolism.

During prolonged submaximal work fats become the major
fuel for muscle contraction (34,58,73,103,l65). The relative
contributions of fats and carbohydrates during such exercise
is dependent, primarily, upon the intensity of exercise and

the aerobic capacity of the individual (16). The greater the

 

ll

aerobic capacity, the greater is one's ability to metabolize
fat (l6,34,73,83,84).

b) Oxygen Uptake During Aerobic Work

In the endurance trained individual a smaller pro-
portion of the cardiac output goes to the working muscles
because the decrease in blood flow to the kidneys, the liver
and other organs during exercise is less than in the untrain—
ed state (83,86). In order to compensate for the lower blood
flow to the working muscles in the trained state a series of
physiological adaptations occur within the skeletal muscles

themselves which allow for the extraction of more oxygen from

 

the blood (83.85.86). Among these adaptations are:
a) an increase in the size and number of skeletal
muscle mitochondria (26,54,83,84,85,86),
b) an approximately 100% increase in mitochondrial
enzymes (l9,54,84,85,86), and
c) an approximately 80% increase in myoglobin
concentration (84,85,86).
This increased V02 is further evidenced by an accompanying

increase in arterio-venous oxygen difference (A-V 0 diff)

2
when exercising at submaximal demands (15,85,86). In studies
conducted by Pernow §£.§l;_ (137), the increase in A-V 02
diff was linear in relation to both heart rate and V02.

Other differences in the metabolic response to the
same absolute work rate which appear after endurance train-
ing include a lower RQ during exercise (l9,54,56,86), a

slower depletion of muscle and liver glycogen stores

12
(54,56,85,86), and a smaller rise in the lactate concentrat-
ions of muscle and blood (85,86,146). All of these adaptive
responses to endurance training indicate a greater dependency
on the oxidation of fats for energy production (54,56,85,86).
Thus, in contrast to the muscle fiber hypertrophy which
occurs in strength training, the major reponse in endurance
training is an increase in the maximum capacity of the in-
dividual cells to consume 02 (26,54,85,86,112). This in-
crease in ability to metabolize substrate enables an individ—
ual to work at higher rates in the trained, as compared to
the untrained state (112,146). In general, endurance is a
function of the relative work rate. That is, the greater
the percentage of the V02 max that is required of an in-
dividual to perform a specific activity, the shorter is the
duration for which it may be endured (47,74,83). The greater

the rate of stimulation of the muscle, the higher the V0 and

2
therefore, in general, the more rapidly it fatigues.
Pollock (139) found the following significant differ—
ences between elite marathon runners and elite middle—long
distance runners:
a) elite middle-long distance runners generally have
a greater V02 max than elite marathon runners
(mean difference 4.7ml/kg/min; Steve Prefontaine-
84.4ml/kg/min; Derek Clayton-69.7ml/kg/min) (139),
b) the maximum treadmill time of the middle-long
distance group was greater than that of the mara-
thon group (i=255ec.) (139),

c) the elite marathon runners appeared to be more

efficient when working at a standard speed than

13

did other distance runners (139).

Pollock (139) determined that the difference in VOzmax
between the two groups was due, in part, to differences
in quantity and quality of training, with marathon runners
logging about 25nmi/wk. more than middle-long distance run-
ners. Also, the middle-long distance group did more high
intensity interval training which appears to enhance maxi-
mal treadmill time. He then concluded that although a
high VOZmax (greater than 70ml/kg/min) appears necessary
for successful distance running, it alone cannot be used
as a valid predictor of success among top runners.

In a follow up study, Fink, Costill and Pollock
(55) confirmed earlier observations which indicated that
the working muscles of elite distance runners (gastrocne-
mius and vastus lateralis) are composed predominantly of
slow-twitch fibers which have a very high oxidative capa-
city (102,148). Furthermore, there was significantly in-
creased activity of the Krebs cycle enzyme succinate de-
hydrogenase (SDH) in these muscle cells, which was in agree-
ment with earlier findings of Holloszy (85). Holloszy at-
tributed this increase in aerobic capacity to increases in
the levels of Krebs cycle enzymes, enzymes involved in the
oxidation of FFA, and components of the respiratory chain.
Fink SENSE} (55) concluded that although such endurance
training enhances the oxidative capacity of skeletal muscle,
it seems to have little influence on the enzymes of glyco-

genolysis.

14

The better marathon runners are able to maintain a
racing pace of 11—12 mph (86) while working at 70-85% VOZmax
(12,54,86). At the onset of prolonged work, such as a mara-

thon run, VO increases rather sharply for the first few min-

2
utes as the oxygen transport system gradually adjusts to the
work load. Eventually a steady state is attained as V02
levels off to meet the demands of the working muscles. The
attainment of this steady state coincides roughly with the
adaptations of cardiac output, heart rate and pulmonary
ventilation to the work load (137,166). Toward the end of
the race the athletes expend themselves to the point that
the V02 can no longer increase to keep pace with the coin-

ciding work load (35). The athlete is now working at greater

than 100% VOzmax and the anaerobic threshold is crossed.

c) Oxygen Uptake During

 

Anaerobic Work

 

The most readily available energy source for muscle
contraction is produced by the splitting of high energy phos-
phate bonds when adenosine triphosphate (ATP) is broken down
to form adenosine diphosphate (ADP) and inorganic phosphate
(Pi)” Concurrently ATP is immediately resynthesized by the
splitting of high energy creatine phosphate (CP). If not for
the fact that ATP is continuously resynthesized at approxi-
mately the same:2flx2as which it is utilized the muscular
stores of ATP and CP (average concentrations in man are about
4 and 16 moles/kg"l wet muscle respectively) would be spend
within a matter of seconds. Most researchers seem to agree

that there is a direct linear relationship between the

15

intensity of work and the decrease in concentration of
intramuscular phosphagens (100). Due to the limited supply
of CP within the muscle cells, this also is quickly exhausted
and an alternative energy source must come into play. Anae-
robic glycolysis provides the energy for continued ATP re-
synthesis, with the formation of lactic acid as a waste pro-
duct. This seems to occur when working at greater than about
80—85% VOZmaX for over a few seconds duration. The rate of
depletion of glycogen stores in working muscles, as well
as the rate of accumulation of lactic acid, dependent upon
the duration and intensity of exercise (66,67).

When the intensity of exercise increases beyond
100% Vozmax, the rate of glycogen depletion increases sharply
up until the point of exhaustion (35). Due to the high in—
tensity of such heavy exercise cessation of work occurs with—
in minutes, although the intramuscular glycogen stores aren't
entirely depleted (147). This is evidenced by the fact that
lactate formation still occurs. Without glycogen to metab-
olize lactate formation would not be possible. Therefore,
it would be reasonable to assume that some factor or factors
other than the availability of muscle glycogen must limit
work capacity under such conditions (67).

d) Recovery from Work

 

In 1933 Margaria et 31. (121) proposed dividing the
02 debt into the alactacid and lactacid portions. This
theory was later supported by Dill et a1. (52) in 1936. After

cessation of anaerobic exercise the V02 is still elevated for

16

some period of time, the length of which is dependent upon
the intensity and duration of work (52,74), as well as the
physical condition of the individual. There are several
factors which are responsible for the delayed return of V02
to normal resting values. Since the 02 stores of the body
are greatly reduced during strenuous exercise a portion of
the V02 of recovery is utilized:

a) to refill the myoglobin stores of muscles (3,74),

b) for the return of oxyhemoglobin to resting value

(3,74),
c) to replenish tissue fluids with dissolved 02
(74),
d) to restore intramuscular supplies of ATP and CP
which are depleted (about 60% and 100% respec-
tively) during exercise (3,74,102).
None of these oxygen dependent processes are involved in the
removal of accumulated lactic acid and, therefore, are col—
lectively termed the alactacid portion of 02 debt (3,35,52,
74,102,121,122). This portion of the 02 debt may be as
great as 3 1. and is believed to be paid within the first
5 minutes of recovery (52).

The lactacid 02 debt is contracted due to the forma—
tion of lactic acid during anaerobic metabolism (3,35,52,74,
102,122). Therefore, the repayment of this portion of the
02 debt will follow the same rate as lactic acid removal.
Cerretelli has reported the maximal 02 debt capacities of
the adolescent male and female to be 200-250 cal/kg of body

weight, respectively (31), but that values decrease with

17

changes in environment and with age.

The difference between the 0 requirements of the

2

working muscles and the V02 during a work period to exhaus—

tion (3,28,35) is termed the 0 deficit. This occurs at

2

the beginning of exercise.

e) Factors Which Limit Performance

 

For decades there has been much controversy among
exercise physiologists concerning the issue of development
of fatigue. As early as 1907, Fletcher and Hopkins (57)
reported high lactic acid concentrations in muscle fatigue
during heavy work. Since then, many researchers have con-
firmed their observations (6,ll,12,l4,16,20,21,23,27,30,46,
47,49,50,74,75,76,100,102,ll3,122,123,125,137). In 1931,
Orskov (133) demonstrated that muscle lactate climbed from
resting concentrations of 2 - 8 mM/kg wet weight to as much
as 30 mM/kg wet weight during strenuous exercise. An in-
crease in lactic acid reportedly interferes with muscle
contraction via the following mechanisms:

a) the abundance of dissociated H+ competes with

Ca++ for binding with troponin (56,64,112);
thus, actin-myosin cross bridging is inhibited,

b) the increased acidity seems to disturb the trans-

mission of the nerve stimulus across the neuro-
muscular junction (72),

c) the fall in pH has an inhibitory effect on the

activity of phosphofructokinase (PFK), one of the

most important rate limiting enzymes in anaerobic

18

glycolysis, resulting in inhibition of glycol—
isis during intense muscular work (1,2,6,54,56,
90,108,109,115,l35,14T).

Bang (20) found that when work continued for greater
than 10 minutes blood lactate concentrations tended to de—
crease. Astrand gg gl. (12) added further support to the
hypothesis that lactate production is a function of work in—
tensity. Their data showed lower blood lactate concentra-
tions ambng subjects given standardized submaximal and
maximal work loads after racing over distances of 10-85 km
(l—8hr.), than among a control group which performed the
same tests after prolonged rest. They found that the greater
the duration (the lower the intensity) and the lower the
lactate concentration of the blood. After 10 km. (35—36 min.),
average lactate was 12.5 mEq/l; after 30 km. (1 hr. 50 min.-
1 hr. 56 min.), average lactate was 6.1 mEq/l; and after 50 km.
(3 hr. 6 min. — 3 hr. 18min.) average lactate was 3.5 mEq/l.
Also, the duration of work with a maximal load was reduced
among the experimental group after prolonged exercise. While
Astrand (12) suggested that the endurance exercise had re—
sulted in an impaired ability to obtain energy from anaerobic
sources, Bang (20) proposed that prolonged work induced an
increase in the utilization of exogenous lactate.

Although in agreement that lactic acid accumulation
is involved in the development of fatigue Hermansen (74)
points out that the rate of ATP resynthesis might be the most

important limiting factor in maximal exercise of short

l9

duration. However, he conceded that intracellular pH could
conceivable be a limiting factor. In treadmill studies con-
sisting of 5 maximal work periods to exhaustion (35-50 sec.),
Hermansen (74) found dramatic increases in blood lactate
concentrations, accompanied by an equally dramatic decrease
in blood pH. The blood pH, however, continued to fall after
each work bout, from pH 7.21 after the first period, to

pH 6.98 after the fifth period. These findings are in direct
disagreement with the hypothesis of Asmussen (8,9), which
suggests that exhaustion occurs when the subject exceeds a
certain set concentration level for lactate within the work-
ing muscle groups during anaerobic work. Saltin was, at
least, in partial agreement with Hermansen in stating that
lactate, per se, might not cause fatigue. The simultaneous
drop in the pH and rise in blood lactate might well decel-
erate many biochemical reactions in the cell which would,
therefore, limit the availability of ATP (147).

Due to the fact that a direct causal relationship
between lactate accumulation and fatigue has not been estab—
lished, some believe it is sufficient to indicate that there
seems to exist an imbalance between the rate of glycolysis
and the oxidative capacity of the muscle (3,6,39,42,99,107).
Jorfeldt (99) attributes the limitation of the oxidative
capacity to pyruvate oxidation and/or electron transport
through the mitochondrial membrane; a process which neces-
sitates the intramitochondrial oxidation of extramitochon—

drial NADH.

20

Hultman EE.2AL (89) suggested that the limiting factor
during anaerobic exercise is the availability of intramuscular
phosphagens. Considering Hultman's findings, as well as their
own, Hermansen and Osnes (75) reported that a lack of metabolic
substrate, rather than blood pH, limited work capacity in maxi-
mal intermittent work.

When considering heavy exercise of 40-180 minutes
duration, muscle biopsy samples have revelaed muscle glycogen
depletion along the order of 60-90% in man (115). Also,
studies of diet and performance have indicated enhanced per-
formances when glycogen stores were increased (l3,34,37,68,
74,86,94,ll4}. Therefore, many researchers (68,74,86,94,115)
feel that the depletion of intramuscular glycogen stores is,
most likely, the limiting factor in exercise lasting 40-180
minutes. During short-term continuous exercise, exhaustion
cannot be related to depletion of glycogen or phosphagen
stores as pH drops rapidly to the point of cessation of ex-
ercise while glycogen depletion reportedly takes at least
50—60 minutes (6,147).

Those who oppose the lactic acid theory argue that
although the rate of lactate accumulation is nicely correlated
with the onset of fatigue, total lactate accumulation is not
necessarily greatest at the time of fatigue (146). However,
if the rate of accumulation is the key here, then total ac-
cumulation would not be relevant.

There are other types of physical activity in which
fatigue occurs in the absence of high levels of lactic acid.

Such is the case with prolonged heavy work or maximal exercise.

 

21

Supporters of the lactic acid theory would then counter that
if an increase in lactate utilization actually occurs during
endurance exercise (12,20,43,53,76,94,ll9), then lactate pro-
duction would be masked by its simultaneous uptake by working
muscles.

Saltin (146) also observed that lactate accumulation
started at a higher percentage of V02max among trained ath—
letes during prolonged exercise. He concluded that at least
a year of continuous training is necessary in order to obtain
submaximal V02 and at the same relative workload. Therefore,
the capacity to perform prolonged work increases with training.

f) The Effects of Diet upon

 

pH and Performance

 

In an attempt to solve the multitude of questions
concerning the relationship between diet and performance Krogh
and Lindhard (114) studied the effects of diet upon energy
metabolism. _Their findings showed that the ability to per-
form prolonged work was enhanced by consuming a carbohydrate-
rich diet. Numerous other studies have reinforced these
observations (4,19,34,37).

With the development of Bergstrdm's muscle biopsy
technique, Bergstrgm gg El; (21) discovered that the con-
sumption of high carbohydrate diet would increase the levels
of intramuscular glycogen beyond those normally found.
Similar results were obtained through studies conducted by

Hermansen g; a1. (73), Hultman g: al. (88) and Saltin and

Astrand (144). Although these investigators all observed an

22
improvement in endurance work capacity among the subjects
studied, a causal relationship was not exactly clear.
However, performance time to exhaustion was believed to be
increased due to a rise in intracellular water content,
the elevated supply of muscle glycogen, or the increased
alkalinity of the blood under such high carbohydrate dietary
conditions (25,92,130).

Although fat is the major fuel for prolonged heavy
exercise, a high fat diet may negatively affect one's en—
durance work capacity. Central nervous system interference,
the increased energy requirements of fat oxidation and the
resultant acidosis caused by the intermediates of fat meta-
bolism (acetoacetic acid and betahydroxybutyric acid) are
the mechanisms through which a fatty diet hinders endurance
performance, according to Asmussen (10).

Manipulation of the diet is reported to bring about
changes in the acid—base status of the blood (117,140,164).
During anaerobic work the rate of lactate accumulation is
dependent upon pH. Studies have shown that lactate production
is greater following high carbohydrate diet than a high fat-
protein diet when subjects exercised at a standard work load

of 70-75% of vo max (21,73,88). Astrand (13) and Bergstrom

2
gg al. (21) have suggested that increased anaerobic activity
and a greater dependency of working muscles on larger intra-
muscular glycogen stores are most likely responsible for

this increase. As anaerobic metabolism increases, fat

metabolism is decreased (51,58).

23

Following a high carbohydrate diet exercise induces
an elevation of blood glucose which appears to be related
to enhanced glucose production in the liver (143): or de-
pressed glucose uptake by active muscles (161). However,
the rise in glucose consumption which occurs during anaerobic
work results in a shift from fat to carbohydrate metabolism
(68) as lactic acid accumulates in the muscle cells (93).
Some investigators have found that diets which are high in
meat intake tend to increase the acidity of the urine (25,
130), while fruit and vegetable rich diets produce an alka-
line urine (25). It is speculated that those foods which
contain organic phosphorus, when metabolized, are responsible
for the production of this acid (117). Recently, Hunter (92)
discovered a rise in blood pH following a high carbohydrate
diet (greater than 60%) and a fall in blood pH following a
high fat-protein diet (about 50% fat; 30% protein). While
some studies have shown that the pH of the blood rises after
a meal (95), others seem to find that no consistent changes
whatsoever occur after eating (43,151).

g) The Effects of Alkalizers on

 

pH and Performance

 

Studies show that during mild exercise the pH of the
blood remains relatively constant (116). In exercise of
moderate intensity the pH falls slightly with blood lactate
concentrations stabilizing during steady state. However,
during severe exercise there is a sharp drop in blood pH

which corresponds to a steep rise in both lactic and pyruvic

 

 

24

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25

acids (16,46). Therefore, it is obvious that pH is de-
pendent upon the intensity and duration of exercise, as
well as the condition of the subject and the environmental
conditions (47). Although the normal arterial pH at rest
is about 7.4 (69), values as low as 6.8 have been recorded
following severe exercise (118). In order to maintain
homeostasis under such circumstances, the bicarbonate—
carbon dioxide buffer system acts to neutralize almost all
of the lactate that enters the blood via the following
reaction:

H+ + Boo;—

 

H +HO

—-—¥
CO3...__CO2 2

2

with H CO being converted to CO and H O (7), a very slight

2 3 2 2
amount of dissociated H+ and HCO3 remain in the form of

H2C03, a weak acid. The resultant CO is expelled from the

2
lungs causing the reaction to shift to the right. This
rise in CO2 output is detectable as an increased RQ (126).
When lactic acid rises to higher values, other buffer systems
(protein, kidneys and lungs) begin to play increasingly im-
portant roles (134,160).

It appears that the buffering capacity of the blood
may be improved through oral ingestion or intravenous in—
jection of sodium bicarbonate (NaHCO3) (l7,18,48,49,97,94,
156). In light of this information much research has been
carried out regarding the effect of alkalizers on perform-
ance (Table 2.1).

In studies conducted by Johnson and Black (96) and
Margaria gg gig (123), trained distance runners showed no signs

of enhanced performance due to ingestion of alkalizers

 

26

prior to work. However, Atterbom (17,18), Jones gg gig
(97,98), Simmons and Hardt (156) and Dennig gg 2A; (48,49)
found work time to exhaustion to be increased when the un-
trained subjects started from an alkalotic state. Thus,
the untrained subjects showed a greater alkalizer effect
than did the trained runners in both long duration, low
intensity and short duration, high intensity exercise.

It has also been demonstrated that both blood
lactic acid concentrations (48,49,70,97,98,158) and
maximum 02 debt capacity can be increased under alkaline
conditions (48,51), though other research (122) showed
non-significant increases in lactic acid under like cir-

cumstances.

CHAPTER I I I

Research Methods

 

The present study was undertaken to investigate the
effects of orally ingested sodium bicarbonate (.06Sg/kg
NaHC03) upon a) the changes in pH of the blood, b) perform-
ance time, c) lactic acid concentrations and d) maximum ox-
ygen uptake, under two dietary conditions: a) high carbo-
hydrate, b) high fat-protein. The supplement was admini-

stered prior to a multi—stage run to exhaustion.

Experimental Design

 

Eight fit male subjects (long distance runners),
20 to 40 years of age, were studied under four treatment
conditions (Tables 3.1 and 3.2) arranged in a Latin Square
design (Table 3.3). The treatments consisted of high carbo-
hydrate or high fat-protein diet conditions supplemented
with sodium bicarbonate (NaHC03) or placebo (dextrose,
C6H1206) taken orally in capsule form. The supplement was
taken two hours prior to exercise in single blind fashion.

The treadmill run schedules were arranged by div-
iding the eight subjects into two equal groups of four sub-
jects each. The first group A, dieted on Mondays, Tuesdays
and Wednesdays and were tested on Thursdays. The second

group B, dieted on Tuesdays, Wednesdays and Thursdays and

were tested on Fridays.

27

Table 3.1.

Treatment
Conditions

 

l

2

Table 3.2.

High fat-protein

Supplement and Diet Conditions

Supplement

gm/kg. of
Body Weight

 

 

Sodium bicarbonate
Sodium bicarbonate
Placebo (dextrose)

Placebo-(dextrose)

Treatment Conditions

 

0.065
0.065
0.05

0.05

 

fl

mat.
Carbohydrate
Fat-protein
Carbohydrate

Fat-protein

High carbohydrate

 

 

 

 

0 Condition Condition
.o
w
o 4 3
o
H
O.)
4.)
a
a
E
o
H
a.
0.: (D
a '3 Condition Condition
c
o
L firm 2 1
5:4
mam
T30
O-r-l
mm

 

 

29

Table 3.3 Test SequenceixiLatin Square Design

 

 

 

 

 

 

 

 

Subject Test Sequence
SF 3 4 l 2
BR 2 . 3 4 1
DA 1 2 3 4
DS 4 l 2 3
cc ’1 4 3 2
BM 4 3 2 l
BK 3 2 l 4
GS 2 l 4 3

 

 

 

 

 

 

Table 3.4 Subjects, Age, Height and Weight

Age Height Weight
Subject (yr.) (in.) (1b.)

SF 20 71 152
BR 26 70 146
DA 27 72 157
DS 28 66 120
CC 29 65 121
BM 31 67 162
BK 37 71 148

GS 40 67 163

30

Subjects

Eight fit, male long distance runners, ranging in
age from 20-40 years, volunteered as subjects for the study
(Table 3.4). All subjects were currently engaged in train—
ing programs and all were experienced marathon runners.
Prior to treadmill running a medical history and informed
consent form were procured from each subject. A modified
Bruce Protocol (Table 3.5) was used to stress test each sub-
ject prior to participation in the study, with treadmill
speed and grade increasing after every three minute work
interval. Measures of heart rate and blood pressure (BP)
were taken after each work interval. The electrocardio-

graph (ECG) was monitored continuously throughout the tests.

Exercise Test

 

The protocol for the multi-stage intermittent tread-
mill runs involved alternation of three-minute work inter-
vals with three-minute rest intervals. A maximum of six
work levels was attainable. During each rest interval the
speed and grade of the treadmill were increased for the
following work interval in accordance with Table 3.5. In
each test the subject was run to exhaustion. A light-weight
nylon safety harness was worn routinely to prevent falling
on the treadmill. The harness is a necessary safety pre-
caution when running to exhaustion as it gives the subject
the confidence and security to perform all out without fear
of falling. The final work interval was followed by a stand-

ard recovery period of 15 minutes.

 

31

A testing schedule was devised which allowed for the
testing of each subject at the same time of day and on the
same day of the week throughout the study. The subjects were
tested between the hours of l p.m. and 6 p.m. every Thursday
and Friday. The schedule was adhered to as strictly as
possible. Each of the eight subjects was tested under all

four treatment conditions.

Table 3.5 Grade, Speed, Work and Rest Intervals in the

Multi-stage Treadmill Test.

 

 

 

 

 

 

 

 

EXERCISE LEVEL Time Speed Grade
rest level (min) (mph) (%)
A 3 6 5
a 3
B 3 7 6
b 3
C 3 8 7
c 3
D 3 9 8
d 3
E 3 19 9
e 3
F 3 10 12
f 3
Recovery 15

 

 

 

 

 

 

 

32

Measurement Procedures

 

Regpiratory Frequency
Measurement of the respiratory frequency was made
using a Sanborn pressure transducer (Model 268 A), coupled
with an Otis-McKerrow respiratory valvel by a flexible
plastic tube. A Sanborn Twin-Visa Recorder2 was utilized
to record the output cycle from the intravalve pressure
transducer in the following manner:
a) During each minute of the work interval for
10 seconds.
b) During each minute of the rest interval for
10 seconds.
The pressure differences for respiration which were

recorded were then counted and converted to minute values.

Heart Rate

 

The heart rate was monitored on a Cambridge 3030 ECG
unit3 using disposable 3M Red Dot Electrodes4 arranged in
a single bipolar V5 electrocardiographic lead. The heart
rate was recorded as follows:

a) During the first 3 work intervals, HR was re—

corded every minute.

 

lOtis-McKerrow, Warren Collins Company, Braintree, Mass.

2Sanborn Company, Twin Viso Recorder, Cambridge, Mass.
3Cambridge Instrument Company, Inc., 73 Spring St.,Ossining,N.Y.

43M Red Dot Electrodes, Minn. Mining & Mfg. Co.,St.Paul,Minn.

 

33

b) During each rest interval, HR was recorded at
the end of the first and third minutes.

0) During the remaining work intervals, HR was
recorded every 30 seconds.

d) During recovery HR was recorded after each
minute for the first three minutes;-every two
minutes from minute four to minute nine; every

three minutes from minute ten to minute fifteen.

Blood Sampling

 

Two hundred twenty microliters (ul) of anaerobic
arterialized capillary blood were collected in two capil-
lary tubes (120 pl, herparinized; 100 pl, unherparinized).
The samples were drawn from the subjects' prewarmed, clean,
dry finger tip (151,152,153). In order to prewarm the
finger tip the hand was enclosed in a rubber bag of warm
(no less than 450C) water. The blood samples were taken:

a) Prior to exercise.

b) Immediately after the completion of each work
level.

c) Immediately following the termination of the
exhaustion work level, and at 5, 10, and 15
minutes during the standard recovery period.

The two blood samples were taken for determination of

blood lactate concentration and acid-base parameters.

 

34

Lactate Analysis

 

The unheparinized blood sample (100 ul) was combined
with 200 ul of cold 8% perchloric acid and was then centri-
fuged at approximately 32 gs. The plasma—perchloric acid
mixture was lifted with disposable syringesl, labeled and
'stored at 0-3OC for 3-6 days before being analyzed. The
enzymaticmicromethod of Mohme—Lundholme (127) was used to
determine lactate concentration. A Sigma lactic acid
chemical kit2 was used for the enzymatic reaction and the
Gilford Stasar II Spectrophotometer3 was employed for the

analysis of NADH at 340nm.

Acid—Base Parameters

 

The heparinized (120‘p1) blood samples were collect-

ed for direct determination of P0 Pco2 and pH by utilizing

2'
the Radiometer blood micro system4. BE and HCO3_ were deter-
mined indirectly using the Siggard-Andersen Nomogram (Appenu

dix E). Blood samples were stored at 2—3OC for 2 hours prior

to analysis (58).

 

lPlastic, Beckton-Dickinson Co., Rutherford, N.M.

2Sigma Chemical Co., Box 14508, St. Louis, MO.
3Gilford Instruments, Oberlin, OH.
4Radiometer PHM75, MK2 and BM53, 73 EMDRVPVEJ, Copehagen

N.V., Denmark.

 

35

Energy Metabolism Measures

 

 

The collection of respiratory gas was achieved using
the Douglas bag tmethod. Samples were collected in labeled
neoprene weather balloons. Bags were changed by using a
5-way automated switching valvel adjoined, via an 18 inch
corrugated plastic hose, to the Otis-McKerrow respiratory
valve. Resistance within the circuit was less than 20mm H20
at 227 L/min. flow. Expired gas was collected continuously
throughout the duration of the tests from the beginning of
the first work interval through the entire fifteen minute
recovery period. Bags were collected in the following order:

a) During the first three levels of work with bags

changed every minute (one minute per bag).

b) During the rest intervals with bag changes made

after the first and third minute (two minutes
per bag)._

c) During the last three work levels with bag chan-

ges every thirty seconds (thirty seconds per bag).

d) During the recovery period, bags were changed

after each minute for the first three minutes
(one minute per bag), every two minutes from min-
ute four through nine (two minutes per bag), and
every three minutes from minute ten to minute

fifteen (three minutes per bag).

 

lVan Huss-Wells automated switching valve.

36

Upon filling, a bag would immediately be trans-
ported to the adjoining room and analyzed for volume and
content of the expired gases in less than 5 minutes. Deter-
minations of percent C02 and 02 was accomplished simultan-
eously by using the Beckman LB-2 and OM—ll analyzers, re-
spectivelyl. All gas was pumped from the bags and through
a dry DTM-ll gas meter2 at a rate of 50 L/min. Measures of
energy metabolism were calculated according to Consolazio,
Johnson, and Pecora (36). The gas analyzers were adjusted
to the zero points by the use of compressed helium. Using
a Haldane chemical analyzer3 oxygen and carbondioxide con-
centrations (17.78% 2; 4.31% C02) of a standard gas sample
were determined.‘ The known standard gas sample and room air
were used to calibrate the analyzers. The energy metabolism
variables consisted of the following: respiratory quotient,
oxygen uptake, maximum oxygen uptake, oxygen debt and venti-
lation. Environmental conditions were kept relatively con-
stant with temperatures ranging from 72-780F and humidity

between 45 and 52 percent.

“Dietary Measures

 

The dietary demands of this study required that the

subjects be on either of two different diets: either high

 

lBeckman Industries, Inc., 3900 River Rd., Shiller Park, IL.
2American Meter Co., (Singer), Model DTM-ll, 13500 Philmont
Ave., Philadelphia, PA.

3Arthur H. Thomas Co., Philadelphia, PA.

 

37

fat-protein (HF) or high carbohydrate (HC) diets, for three
days before test runs. Subjects were instructed as to which
diet to follow and they also received lists of standard
American foods, HF or HC (Appendix A), depending upon the
treatment to which they were assigned for that particular
week. It was requested that they maintain a relatively
constant total caloric intake and also to keep their physical
activity at a relatively constant level.

On the day of testing, prior to the run, the subject

was required to fill out the dietary recall form (Appendix A).
This allowed for accurate calculation of the percent of fat,
protein and carbohydrate consumed over the preceeding three
day period. From these calculations it was then determined

if the subjects had met the qualifications for their assigned
dietary conditions. In order to qualify the subjects had to
comply with the following conditions:

a) high fat-protein diet: greater than 42% fat,
greater than 21% protein, less than 34% carbo-
hydrate.

b) high carbohydrate diet: less than 34% fat, less

than 15% protein, greater than 53% carbohydrate.

Test Protocol

 

While the speed and grade of the treadmill were ad-
justed with the subject straddling the treadmill the ECG
was monitored to ensure proper attachment of electrodes.

The nylon harness; suspended from the ceiling, was fitted

38
and secured. The rubber bag was filled about half full with
warm (450C) water and fastened over the subject's hand which
had not been involved in the pre-exercise blood sample. The
head gear holding the regulator in place was adjusted and
the nose clip and mouth-piece were put into place. For these
few moments prior to work the expired gas was channeled back
into the room through the 5-way valve. When all were ready,
the treadmill was started at the first work level (6 MPH,
5% grade). At this same instant the switch starting the
automated gas bags was thrown to initiate collection of the
respiratory gas and also, to start the first timer.

During the work intervals the gas bags were changed
every minute or every thirty seconds, depending on the work
level. The bags were then immediately transferred from the
treadmill room to the room adjacent for analysis. The sub-
ject was kept informed of the time remaining until the end
of the work level and throughout each work level he was en-
couraged to keep working hard until the end of the interval.
At about 15 seconds prior to the end of the work interval
the subject was informed that the treadmill would soon stop
and the final 10 seconds would be counted down aloud. To
prevent falling the subject would hold onto the hand rail
for about the final 5 seconds of work and would then hop
back off of the treadmill and into the straddle position.

At this moment a second timer would automatically start to
time the rest interval. As the treadmill slowed to a com-

plete stop it was adjusted for the next work level.

39

During the rest interval a bench was situated over
the treadmill and the subject was seated and kept warm and
dry with towels. Expired gas was collected throughout the
entire three minute rest interval at one and two minute
intervals. The water bag was removed from the hand and the
finger was dried, sterilized with alcohol and blood was
drawn for analysis by piercing the finger tip with a lancet.
The blood samples were then immediately prepared for analy-
sis and storage and the finger was wiped with alcohol and
taped. Again the rubber bag filled with the warm water
(45°C) was secured to the opposite hand. Respiratory rate
and heart rate were also recorded during the entire rest
interval. The bench was removed from the treadmill with
about 30 seconds remaining in the rest interval and, again,
the subject assumed the straddle position over the tread-
mill. The first timer was reset and at the beginning of
the next work level the procedures were repeated.

These procedures were followed through each level up
to the point of exhaustion. At this time the treadmill was
stopped, and the subject was seated. For the entire 15 min—
ute recovery period heart rate and respiratory rate were
continuously monitored and collection of expired gas also
continued. At 5, 10 and 15 minutes of recovery blood samples
were immediately taken following the procedures described
previously. After the recovery period all of the equipment
was removed, the fingers were carefully cleaned and bandaged,

and the subject was oriented for the following week's test.

 

40

StatiStical Analysis

 

Using subjects, diet and supplement as independent
variables a repeated measures analysis of variance was con—
ducted with a separate analysis run for each of the inde-
pendent variables. This program was run under the Statist-
ical Package for the Social Sciences (SPSS) and was analyzed
on a 6500 Control Data computer.

The significance level was set at P< .10. In cases
of continuous, curvilinear data, as in exercise responses
across time, the Sign Test was used (152). The Sign Test
permits the utilization of all test points without the

necessity of curve fitting.

 

CHAPTER IV

RESULTS AND DISCUSSION

The purpose of this investigation was to study the
effects of orally ingested sodium bicarbonate (.065 gm/kg)
under high fat-protein and high carbohydrate dietary condi-
tions upon pH, V02max and performance time to exhaustion
during a multi-stage treadmill run. The data are presented
in the following order:

a) Lactic acid before the run, lactic acid after
each level of the run, lactic acid during recovery and the
changes in lactic acid from before to after the run;

b) pH before the run, pH after each level of the
run, pH during recovery and the changes in pH from before
to after the run;

c) V02 before the run, V02 after each level of
the run, V02 during recovery and the changes in V02 from
before to after the run;

d) V02max when it occurs during the run;

e) Performance time.

a) Lactic Acid

The results for lactic acid are presented in

Tables 4.1 and 4.2, Figures 4.1 and 4.2 and Appendix B.

The only statistically significant differences in lactic

acid production occurred after the fifth level of exercise

and at the third level of recovery (LS-R3). The greatest

of these differences were obtained with NaHCO3 supplementation.

41

 

 

 

 

 

 

 

Table 4.1. Statistical Results, Lactate (mMol/L).
Conditions ANOVA
NaHCO3 NaHCO3 Placebo Placebo
+ + + +
CHO Fat-Pro CHO Fat—Pro S D I
Variables (5C) (5F?) (PC) (PFP) P P P
8 PH
7 1.07 1.04 1.04 1.24 0.74 0.76 0.69
SD 0.9 0.7 0.7 0 5
(b) L1
7' 2.23 1.41 1.57 1.61 0.65 0.44 0.40
SD 2.4 0 4 0.6 0.8
(c) L2
7’ 1.88 1.71 2.33 1.80 0.45 0.32 0.60
SD 1.3 0 4 0.7 0.9
(d) L3
7 3.08 3.36 4.76 3.12 0.37 0.40 0.23
SD 2.3 1.3 2 4 1.8
(e) L4
7 6.45 6.62 6.20 5.50 0.56 0.82 0.71
SD 4.5 2 7 1 6 3.0
(f) L5
7’ 10.19 10.37 7.00 8.52 0.34 0.76 0.80
SD 4.7 7.4 4.6 5.5
(9) R1
Y' 10.84 11.41 10.02 8.48 0.26 0.77 0.53
SD 4.1 4.4 2.7 5.3
h R2
7' 9.92 9.42 7.66 9.25 0.37 0.69 0.44
SD 2.5 4.0 2 0 4.6
1 R3
7' 7.92 7.66 6.53 7.28 0.48 0.80 0.67
SD 2.6 1.7 2.8 2.3
PW = Pre-work; L1 - L5 = Leve1 15 of work.
R1 - R3 = Five. ten and fifteen minutes of recovery
S = Supplement; 0 = Diet; I = Interaction

 

Ole? Effect By Supplement

 

 
    

 

 

 

 

 

 

   

 

 

 

 

     

 

 

 

 

IS 0 ..
l I
12 5 - l I
I ' I
3 IO 0 - I
g P GRADE SPEED
- 7 5 _ , . (%) (MPH)
E 9 10
*- 5 0 v- 0 9
3 O—0 SC o——o PC 7 a
J 2 5 » o-—--o SFP os-uo PFP 6 7
- - __ 5 6
O 0 ‘ 1 1 1 '—"1'_f—‘l 1—1 H H 1L 11 1 1 1 O O
5 IO I5 PW O 3 6 9 12 15 5 IO IS
L. Lg L, L. L.
RECOVERY WORK RECOVERY
TIME (mm) TIME (mm)
(o) SODIUM BICARBONATE (D) PLACEBO
'5 0 Supplement Effect By Duet
.. 12 5 »
.E GRADE SPEED
w 7 5 " “~\ (%) Imam
:- ‘O 9 '0
3 so I- a 9
3 0—0 SC 0—4 SH: 7 3
2 5 r- o----o PC own-o pro 6 7
----=°" ' -"f’" 5 6
O 0 ‘ —T_T_'l l'_‘l l—‘l 1""-l F 1 1 1 1— 1 1 41 1 1 1 O 0
WI 0 3 6 9 12 I5 5 IO 15 9w 0 3 5 IO 15
LI L2 L! LG L! L,
WORK RECOVERY RECOVERY
TIME (mm) TIME (mm)
(C) CARBOHYDRATE (d) FAT-PROTEIN
Pooled Reswts
I5 0 r ——
- I2.5 b
5 .
i 10.0 1-
g GRADE SPEED
('l) (MPH)
E 7 5 1- °
F 9 IO
8 5 O b 8 9
J H S 0—0 C 7 4. 9
2.5 . o——--o P 0.--.0 FR 6 7
1 5 6
0 0 ' —'r—'—1-—1 H H 1—-1 rt 1' 1 r r w 1 1 0 0
Pw o 3 6 9 12 15 5 10 15 5 IO 15
L. L1 L3 L. L;
WORK RECOVERY RECOVERY
TlME (mm) TIME (mm)
(c) SUPPLEMENT (1) DIET

Figure 4.1. Diet and Supplement Fffect on Lactate.

 

 

 

 

Table 4.2. Changes in Lactate (mfiol/L) and Statistical
Results.
(fixtfitidms ANOWA
Namxa Nam113 lexfix> P1ax£x>
+ + + + S D I
CHO Fat-Pro CHO Fat-Pro P P P
AP-L5
LactateP 1.07 1.04 1.04 1.24
LactateL5 10.19 10.97 7.00 8.52
ALactatePL5 9.12 9.33 5.96 7.28 0.32 0.74 0.83
AP-Rl
LactateP 1.07 1.04 1.04 1.24
LactateRl 10.84 11.41 10.02 8.48
ALactatePR1 9.77 10.37 8.98 7.24 0.16 0.93 0.64
AP-R3
LactateP 1.07 1.04 1.04 1.24
LactateR3 7.92 7.66 6.53 7.28
ALactatePR3 6.85 6.62 5.49 6.04 0.66 0.97 0.99
AL5-R1
LactateL5 10.19 10.37 7.00 8.52
LactateRl 10.84 11.41 10.02 8.48
ALactateLSRl .65 1.04 3.02 .04 0.80 0.76 0.12
AL5-R3
LactateL5 10.19 10.37 7.00 8.52
Lactate R3 7.92 7.66 6.53 7.28
AIactateLSRB 2.27 2.71 .47 1.24 <0.09* 0.55 0.46
PW = Pre-work; Ll-LS = Level 1-5 of work.
R1 - R3 = Five, ten and fifteen minutes of recovery
S = Supplement; D = Diet; I = Interaction

 

 

 

 

DWFERENCESIN LACTATE

A PRE WORK TO LEVEL 5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A PRE WORK TO RECOVERY I

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1——1
b-fi
1-——.
SC 569 pc PFP c FF 5 p
CONDITIONS DIET SUPPLEMENT

A LEVEL 5 TO RECOVERY I

mm

sc see pc 969 c FP s 9
00111011101115 0151 SUPPLEMENT

A LEVEL 5 TO RECOVERY 3

 

 

 

0 FR 7 s p

10.0 -
r—1 ”—1
A 7_5 b- 1——-'
\
2 r— h
.5
11.1 5 0 -
y.
c
..—
o
a
-J 2.5 >-
a
O O -
sc srp PC prp c FF 5 p
CONDITIONS DIET SUPPLEMENT
A PRE WORK TO RECOVERY 3
I00 .—
S 151+
5 r—‘_—— —-—
5 r—-1 F_
E at)»
y.
o
q
.1
<1 2 5 b
0.0 -
sc SFP PC PFP 0 PP s P
CONDITIONS DIET SUPPLEMENT
IO 0 1-
:' 7.5+-
\
T:
2
E.
Lu 5 O '-
p—
a
p.
U
<1
4 2 5 h m
.. r‘“ I I’m
0.0L ,
sc srp PC PFP
CONDITIONS

Figure 4.2.

DIET SUPPLEMENT

Lactate Changes under Different Conditions.

46

None of the other comparisons yielded any significant
differences.

Using the Sign Test, no significant differences
were observed when all points were considered (Figure 4.1
a-f). No observable differences were evident in Figure
4.1 a, b and f in which dietary conditions were compared.
There were, however, substantial differences observed when
NaHCO3 and placebo supplementation were compared (Figure
4.1 c, d and e). The most visible lactate change point
occured at level 2 under placebo conditions. Under the
NaHCO3 supplementation there were distinct change points
at levels 2 and 3, the lactate values were higher both at
levels 4 and 5, and during recovery as well. The statisti—
cal analyses used were inadequate for testing the differen-
ces between the lactate curves for the supplement data
(Figure 4.1 c, d and e). However, it is evident that the
curves appear to be quite different. No decision regarding
statistical significance may be made based upon these graphs.
Yet, when considering the ALB-R3 ANOVA difference, one can
conclude that NaHCO3 supplementation yields high lactate
levels, and that this lactate is rapidly reduced (Figure
4.1 e).

21.28

Results of blood pH appear in Tables 4.3 and 4.4,
Figure 4.3 a-f, Figure 4.4 and Appendix C. In the ANOVA
analysis significant NaHCO3 effects were detected in the

pre-run measure (P=.O9) (Table 4.3) and in the difference

47

Table 4.5. Statistical Results, pH,

 

 

 

 

 

Conditions ANOVA
NaHCO3 NaHCD3 Placebo Placebo
+ + + +
CHO Fat-Pro CHO Fat-Pro S D Ii
Variables (SC) (SFP) (PC) (PFP) P P P
(a) PM
7' 7.43 7.44 7.42 7.41 0.09* 0.90 0.19
50 0.02 0.03 0.03 0.02
(6) L1
7’ 7.41 7.42 7.40 7.38 0.12 0.71 0.57
50 0.04 0.03 0.03 0.06
c L2
7' 7.42 7.41 7.40 7.39 0.15 0.55 0.93
so 0.04 0.04 0.04 0.06
(d) L3
7' 7.39 7.38 7.35 7.36 0.17 0.88 0.73
50 0.04 0.07 0.06 0.06
(e) L4
7' 7.30 7.31 7.28 7.26 0.25 0.73 0.63
50 0.07 0.09 0.08 0.09
(f) L5
7' 7.23 7.24 7.23 7.18 0.28 0.48 0.30
50 0.07 0.07 0.05 0.07
(91 R1
7' 7.19 7.21 7.18 7.20 0.71 0.38 0.84
50 0.06 0.05 0.09 0.09
(h) R2
7' 7.26 7.25 7.26 7.23 0.60 0.33 0.72
50 0.05 0.06 0.07 0.08
(1) R3
7' 7.31 7.29 7.29 7.26 0.37 0.39 0.75
so 0.05 0.07 0.07 0.11

 

PW = Pre-work; L1 - L5 = Level 1-5 of work.
R1 - R3 = Five, ten and fifteen minutes of recovery.
* = Statistical Significance

S = Supplement; 0 = Diet; I = Interaction

 

48

0191 Effect 8y Stoplemem

SPEE D
("H1

   

 

 

 

Q 10
O 9
7 O
6 7
5 6
1 1 fl 1 1 f O J- O
5 IO IS 5 IO '5
L1 L. L. L. L. L. L. L. L. L.
WORK RECOVERY WORK RECOVERY
TIME (mm) TIME (IN-.1
(0) 599151111 EIQARBQNATE (b) emcee:-

mplemem Effec? By DIeI

 

   

 

 

 

     

 

 

 

74‘ l,
7 40 1- "“ H 5::
I
; 0’--c PFP
7’ 35 -
7 3C 7-
3 I GRADE seats
7 25 L (’0) (MPH:
g 9 1O
7 20 “v- -— O 9
! —— 7 e
7 ~: '. _ 5 7
l -— 5 6
1 i
—-«-——-—-I “—I t—I I——I ? fl 1 1 1 0 0
PW O 3 6 9 I2 IS IO 15
L. L. L' L. .
WORK RECOVERY WORK RECOVER»
TIME (mm) TIME (mm)
(c) CARBOHYDRATE (a) FAT-PRC'E‘N
P9018: PCSUI’S
O—-—-0 5 O——O C
l o—--o P o---o FP
I
L
L ‘ canoe SPEED
I (90) “PHI
9 IO
' 9 9
1— ' 1 ’ °
7 '5 I—- 1 6 7
I r-—-— ' 5 6
P O SHGHOHZr 75 g 1 1— 1 1 1 O O
W I I I0
L. L. L. L. L. IS 5 IO IS
WORK RECOVERY RECOVERY
TIME (mm) TIME (mm)
(0) SUPPLEMENT II) DIET

Figure 4.5. Diet and Supplement Effect on pH.

49

Table 4.4. Changes in pH and Statistical Results.

 

 

 

 

Ckmdithm IRKNA
NaHCO3 NaHCO3 Placebo Placebo
+ + + + s D I
CHO Fat-Pro CHO Fat-Pro P P P

AP-—L5

pHP 7.43 7.44 7.42 7.41

pRLS 7.23 7.24 7.23 7.18

ApHPLS 0.20 . 0.20 0.19 0.23 0.44 0.55 0.39
AP-Rl

pHP 7.43 7.44 7.42 7.41

pHRl 7.19 7.22 7.18 7.20

ApHPRl _ 0.24 0.22 0.24 0.21 0.91 0.30 0.87
AP-R3

pHP 7.43 7.44 7.42 7.41

pHR3 7.31 7.30 7.30 7.26

ApHPRB ' 0.12 0.14 0.12 0.15 0.58 0.29 0.94
~AL5--R1

pHLS 7.23 7.24 7.23 7.18

pHRl 7.19 7.22 7.18 7.20

APHLSRl 0.04 0.02 0.05 0.02 <0.03* 0.31 0.96
AL5-R3

p85 7.23 7.24 7.23 7.18

pHR3 7.31 7.30 7.30 7.26

APHLSRB 7.08 0.06 0.07 0.08 0.77 0.81 0.95
PW = Pre-work; Ll-LS = Level 1-5 of work.
R1 - R3 = Five, ten and fifteen minutes of recovery.

* = Statistical Significance

S =

_Supp1ement; D = Diet; I = Interaction

 

 

 

 

5O

DIFFERENCES IN pH

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A PRE WORK TO LEVEL 5 A PRE WORK TO RECOVERY I
QSOP
0.25 I- I—1
~—
0201- ___ r-0 F—_
3 on-
a
DIO-
005-
0.005
so SFP Pc PFP 0 PP s P sc SFP Pc PFP c FP s P
CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT
A PRE‘WORK T0 RECOVERY 3 A LEVEL 5 TO RECOVERYI
0.30 —
0.25 -
020 1-
% 0 l5 -
O.IO '-
m
o... . I—t—I , ED 13:1
sc SFP Pc PFP c FF 5 P so SFP PC PFP c FP s P
CONDITIONS DIET SUPPLEMENT CONDITIONS DIET SUPPLEMENT

A LEVEL 5 TO RECOVERY 3
0.30 r'

0.25 -

O.20 1-

 

005-

 

 

 

 

0.00 *-

 

 

 

sc SFP PCPFP 'c'PP’ s P
0011101110115 0151 SUPPLEMENT

Figure 4.4. pH changes under Different Conditions.

 

51
between measures taken at the end of exercise and at 5
minutes of recovery (ALB-R1; P=.03) (Table 4.4). No other
statistically significant differences were observed among
the ANOVA results. Even so, it is worth mentioning at
this time that all of the pH values were higher under the
bicarbonate supplementation than under the effect of the
placebo (Figure 4.3 c, d and e). From the Sign Test for
comparisons it was evident that a signifiCant effect of
bicarbonate (P=.Ol) upon pH occurs under both dietary con-
ditions. The pH values were higher at all collection points
when NaHCD3 was ingested. The ANOVA results and Figure 4.3
a, b and f show that the diet did not significantly affect
the pH values in these subjects.

0) Oxygen Uptake‘(V00)

 

No statistically significant differences were ob-
served in the 902 results presented in Figure 4.5, Table 4.5
and Appendix D. The typical linear increase in 002 with in-
creasing work load was observed until peaking, during level

4 in most instances. Thereafter, V0 tapered off (level 5)

2
(Figure 4.5).

d) Maximum Oxygen Uptake (Fogmax)

 

Measures of VOZmax under the various conditions
appear in Figure_4.6 and Table 4.6. Although the highest
values were observed under high carbohydrate/sodium bi-
carbonate conditions, these differences were not statis-
tically significant. The point of VOZmax was consistent-

ly preceded by a rise in lactic acid and followed by a

 

52.

Table 4.5. Statistical Results, Oxygen Uptake (L/min).

 

 

 

 

 

 

 

Conditions ANOVA
uauco uanco Placebo Placebo
0 3 + 3 4 6
_ CHO FotoPro CHO Fat-Pro S 1110 1
Variables "In x SD (SC) (SFP) (PC) (PFP) P P P
Level 1 1 i z 2.26 3 0.26 2.35 : 0.46 2.29 : 0.31 2.31 = 0.22 0.41 0.89 0.92
. 2 i = 3.18 : 0.44 3.11 : 0.74 3.41 3 0.51 3.42 = 0.42
3 I : 3.40 z 0.45 3.39 : 0.50 3.42 = 0.48 3.48 = 0.41
1 i : 1.72 : 0.28 1.68 2 0.36 1.62 : 0.36 1.63 = 0.41 0.56 0.81 0.92
°‘ 2.3 II = 0.77 = 0.08 0.76 = 0.11 0.77 : 0.15 0.74 : 0.15
Level 2 1 i = 2.73 : 0.40 2.76 z 0.27 2.78 : 0.30 2.82 : 0.36 0.62 1.00 0.57
:- 2 i : 4.02 : 0.55- 3.85 : 0.48 3.95 = 0.49 4.03 = 0.46
3 i = 4.09 : 0.44 3.97 = 0.56 4.08 = 0.67 4.23 z 0.58
_ 1 i z 2.06 : 0.33 2.03 : 0.36 2.04 : 0.48 2.03 = 0.41 0.82 0.90 0.97
8
2-3 x : 0.83 = 0.11 0.83 = 0.14 0.80 : 0.20 0.80 : 0.14
Level 3 1 i : 3.20 = 0.37 3.22 = 0.37 3.19 = 0.42 3.25 = 0.37 0.69 0.43 0.42
:- 2 'i = 4.86 z 0.81 4.53 : 0.54 4.23 = 0.83 4.65 .-. 0.53
3 '11 : 4.46 = 0.83 4.76 : 0.52 4.44 : 0.80 4.79 = 0.71
1 i = 2.54 = 0.58 2.64 = 0.48 2.62 : 0.52 2.70 = 0.51 0.35 0.90 0.61
" 2-3 x = 1.00 : 0.22 1.00 : 0.23 1.33 = 0.89 1.07 = 0.21
Level 4 1 i : 3.58 : 0.58 3.81 : 0.61 3.80 = 0.50 3.75 2 0.48 0.76 0.77 0.80
‘a 2 11 : 4.54 z 0.54 4.88 : 0.65 4.62 z 0.65 4.73 : 0.84
3 i :. 5.23 = 0.37 4.66 : 0.75 4.78 = 1.17 4.78 z 1.07
_ 1 i : 2.94 = 0.60 3.04 = 0.47 2.71 = 1.00 3.03 = 0.44 0.83 0.93 0.41
' 2.3 I : 1.32 = 0.25 1.26 = 0.20 1.70 : 1.00 1.46 z 0.31
Leve1 s a 1 'i : 4.08 = 0.31 4.09 = 0.48 4.29 : 0.51 3.77 : 0.86 0.77 0.31 0.27
[00011ng 1 i = 3.16 = 0.75 3.40 z 0.84 3.25 = 0.69 '3.00 : 0.91 0.71 0.92 0.48
2 II : 1.71 : 0.48 1.49 : 0.36 1.50 z 0.29 1.50 = 0.48 .
3 ‘x’ = 1.25 = 0.36 1.24 = 0.22 1.15 z 0.22 ‘ 1.08 = 0.41
4-5 I .-. 0.95 = 0.13 0.92 = 0.11 0.93 = 0.21 0.95 = 0.29 0.59 0.79 0.93

6-7 ‘x’ = 0.77 .-. 0.13 0.81 : 0.05 0.85 = 0.27 0.81 : 0.15
8-9 11 z 0.75 0.11 0.72 2 0.07 0.70 0.11 0.76 = 0.28
10.12 I = 0.63 = 0.07 0.66 = 0.07 0.65 0.10 0.61 = 0.15 0.35 0.91 0.60
13-15 11 = 0.63 : 0.06 0.61 : 0.07 0.64 = 0.18 0.62 = 0.11

00

 

u - Hort; II - lost Interval; S - 5000100001; 0 - DIet; I - IntornctIon

SO

SO

40

V0, (1 1mm 1

30

20

SO

50

4C

(1 lmm)

1

30

V0

20

OO

60

V0! II/min)

Figure 4.

 

 

 

U'l
\N

 

 

 

 

 

 

 

 

 

 

 

 

 

             

 

 

 

| 0181 E11861 By Supplemem I
I HSC I HPC
I o---o SFP I o-«PFP
I l
| ;‘ I 00405 SPEED
' (”.1 (MPH)
r—I ——I 9 10
| 9 9
I 7 o
1 . I . I I 6 7
I— i I 5 J I l - I I I I 5 6
fi111fi11fi1111rfi1 fi1tf 1 11111100
0 3 6 9 12 IS 18 21 24 27 3 6 9 12 15 O 3 6 9 12 I IS 2124 27 3 6 9 12 IS
WRIWRIWRIWRIW WRIWRIWRIWRIW
L. L, L. L. L. RECOVERY L. L. L. L. L. RECOVERY
11741: (171111) TIME (mm)
ID) SODIUM BICARBONPTE ID) PLACEBO
. Supplement E1180? By D181
I
' o—oSC HSPD
I pug PC ' «“0pr
I
I GRADE SPEED
(’01 (MPH)
.—.I 9 I 10
. ‘ O 9
I .——l 7 8
I *m 7 1 I 5 ’
-—-. . ' S +- 6
'. I - 1 , . . I 1
1 fl 1 J1 if 1 1 t m 1 1 1 1 T r n 1 1 1 T 41 1 1 7‘1 1 . 1 1 7 O 'L O
O 3 6 9 l2 15 I8 2' 24 27 3 6 9 l2 15 O 3 6 9 12 15 IS 2' 24 27 3 6 9 12 15
WRIWRIWRIWRIW wmwmwmwn.w
L. L. L) L. L. RECOVERY L. L. L; L. L. RECOVERY
TIME (mm) TIME Imml
(C) CARBOHYDRL'E Id) FAT-PROTEIN
I Pooled Resws I
I HS HE
I o-«P oo-o FP
|
l
I GRADE SPEED
(90) IMPN‘
,__.. 9 IO
. I B 9
\ 1 .
I ‘ 6 7
m I I S S
Jfi T I I I Y—T j T 1 o o
27 3 6 9 12 IS 3 S 9 12 15
WRIWRIWRIWRI W
L. L. L: L. L. RECOVERY L. L. L. L. L. RECOVERY
TIME (mm) TIME (mm)
ID) SUPPLEMENT (I) DIET

5. Diet and Supplement Effect on Oxygen Uptake.

:ofluomumucH n H upmfla n D “ucmamammsm n m

 

54

vm.h mm.HH ma.m mo.m Om
mm.o mm.o Pb.o mm.on Hh.Hh mm.Hh mm.mh x

 

A.mx\asv xmsmoa lav

o.mm 0.0HH o.mHH o.¢oa Om
Hm.o om.o mm.o mh.omh mm.mmh om.hmh mm.HHm M

A.omwv mafia wocmEu0mu0m Amy

 

 

m a a Lasso Aomv “mama Rome mmanmnum>
H a m 00m1umm omo cumuomm omo
+ + m + m +
onwomam onwomam oommz oommz

 

¢>Oz<, . mucwsumwua

 

meNo> com mesa oucmEMOMAmm .muasmmm Hmofiumflumum m.v mqmde

PEI-{1'_C‘.II<I¢'IA.T.11;I- “MC (' CC)

 

77.5

75.0

72.5

70.0

67.5

65.0

55

(a) PE RFCPA‘AANCE TIME

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 4.6.

 

 

'11—'-
"’ ‘1" T 1 T
..L ...L ' ‘17
c-Jh-

_L .I- d a ..._ .. u- ‘I' “I“ 1L I. .—
‘I.’ T I T L T T T J; 1 T
8: SFP PC PFP 0 PP s P
COI‘IDITICNS D1ET SUPPLEMENT

(b) MAXIMJM OW GEN UPTAKE

1~ T '1

 

1' I T
.1 _L
_L i

 

 

 

 

 

 

 

 

II

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1 .1 -1 .1 1 1 -1 -1 .1 .1 .I -1

T T '1' T T T I_ T T J;

so 81? Pc PFP c FF 8 P
CONDITIONS DIET SUPPLEMENT

Results: (a) TMT, (b) TOZmaX.

56
rather dramatic drop in pH of arterial blood.

e) Performance

 

In order to determine the effects of the dietary
and supplementary treatments upon performance time to ex-
haustion a two-way analysis of variance was used. Though
seven of the eight subjects studied reached the point of ex-
haustion consistently by level 5, subject SF lasted well
into level 6 under all treatment conditions (Table 4.7).
His shortest run lasted 67 sec. into level 6 (PFP treatment).
The shortest mean performance time was obtained under the
SC treatment (Table 4.7, Figure 4.5).

The pooled data indicated thatthe greatest mean per-
formance time oCcurred when the supplement was given, but
that no significant differences in performance time existed
between supplementary and dietary conditions.

Discussion

 

It was the intention to study the effects of orally

ingested NaHCO under both high carbohydrate and high fat-

3
protein dietary conditions upon changes in the pH of ar-
terial blood, Vozmax and performance time to exhaustion
during an intermittent multi-stage treadmill run. All
subjects were tested under all four conditions following
the modified Bruce protocol.

At this time it is important to review the research
hypotheses:

1. Upon reaching the point of Fozmax there is a sub-

V

stantial decrease in arterial blood pH as working muscles

57

TABLE 4.7. Performance Time (secs)

 

 

 

 

 

 

 

 

Treatments
NaHCO NaHCO Placebo PlaCebo
+ + + +
CHO Fat—Pro CHO Fat-Pro
Subjects (SC) (SFP) (PC) (PFP)
(a) Performance Time
SF 0990 1023 0997 0967
BM 0616 0640 0639 0627
DS 0856 0858 0825 0767
BR 0814 0816 0792 0810
DA 0840 0799 0810 0805
GC 0780 0800 0787 0769
BK 0830 0788 0780 0831
GS 0764 0656 0660 0750
3? 811.25 797.50 786.25 790.75
SD 104.0 119.0 110.0 95.0

 

58
begin to rely more heavily on anaerobic glycolysis for
energy production.

The VD data and arterial blood pH data appear to

2
support this hypothesis. As 902 approaches its maximum,
lactic acid accumulation is accelerated. Once V02max is
reached an even sharper rise is observed (Figure 4.1, Ap-
pendix B and Appendix D). The largest drop in pH occurs
consistently within 3 min. after the attainment of VDzmax
(Appendices C and D). Margaria (120 has Shown that a per-
iod of a few minutes must be allowed to account for diffus-
ion of lactic acid from muscle cells to the blood when
considering such pH changes. In regards to this relation-
ship Clarke (35) has stated,
"Once again we return to the biochemical scheme that
suggests a direct relationship between the production
of metabolites and intake of oxygen; some point will
be reached whereby oxygen uptake will fail to increase
appreciably with an increase in work load. Quite clear-
lqrit will.involve the functional support of the respir—
atory and circulatory systems, as well as the metabolic
pathways, and when the full contribution of each is
realized the oxygen uptake stabilizes at its maximum
value. Continuted work is at the expense of anaerobic
mechanisms responsible for lactate build-up in attain-
ment of maximum work performance."
No significant differences in the point at which
Fozmax was reached occurred as a result of dietary mani—
pulation or supplement ingestion (Table 4.6 b, Fibure 4.6 a
and Appendix D). However, performance time to exhaustion
was consistently longer under the SC condition (Table 4.6
and Figure 4.6).
2. A high carbohydrate diet, as opposed to a high

fat-protein diet, will enhance endurance work capacity.

 

59

This hypothesis cannot be accepted on the basis of
the data obtained in the present investigation. Although
the data show that the subjects did run a very slight amount
longer when on a high carbohydrate diet, these differences
were not of statistical significance.

The findings of Saltin and Hermansen (34) and
Hultman (90) all show very significant increases in perform-
ance time under high carbohydrate conditions. The facts
that the diets in the aforementioned studies were more severe
and the subjects in the present study were highly trained
marathon runners, as opposed to being untrained, could account,
in part, for the gross differences in statistical results.

3. A high carbohydrate diet will increase the alka-
linity of the blood.

The data do not totally support this hypothysis.
Under the high carbohydrate treatment the pH was slightly
elevated (Figures 4.3e and 4.4) (P=.O9) when the placebo
was given or when the diet data were pooled. However, if
the supplement was given, no diet effect was noticable
(Figure 4.3a). Under such circumstances both diets showed
similar results. Therefore, it is the conclusion of this
researcher that a high carbohydrate diet increases the alka-
linity of the blood of marathon runners in the absence of
NaHCO3 supplementation.

4. Sodium bicarbonate, orally ingested (0.065 gm/kg.

body weight), will increase the alkalinity of the blood.

60

The data collected in the present study support this
hypothesis. The pH values obtained were consistently higher
with NaHCO3 supplementation (Figure 4.3 c, d and e) at all
points of collection. There was no observable increase in
PCO2 levels due to alkalization in this investigation, as
had been reported by Dennig (48,49) and Jones gg El; (97,
98). It can, however, be concluded that NaHC03, orally
ingested prior to exercise, increases the alkalinity of
the blood of marathon runners.

5. Sodium bicarbonate ingestion, two hours prior
to exercise, will increase maximum performance time.

Due to the data obtained from the present investi-
gation this hypothesis can be neither accepted nor rejected
(Figure 4.6a and Table 4.6a). The present data are in dis—
agreement with the results of Simmons and Hardt (156),
Dennig (48,49) and Jones et 21; (97,98), all of whom found
alkalizing agents to significantly improve performance time
to exhaustion. The results of the present study are in the
same direction, however, the differences were not statisti—
cally significant.

The present results are, nevertheless, in agreement
with those of Karpovich and Sinning(105), Johnson and Black
(96) and Margaria e; El; (124). These researchers were un-
able to detect any significant increases in maximum perform-
ance time in endurance athletes following alkalizer supple-

mentation.

61

Holloszy (83,84,85,86) and Baldwin and Winder (19)
suggest that a glycogen sparing mechanism accounts for the
seemingly greater stability of the acid-base balance of the
blood in highly trained endurance athletes. This mechanism
is believed to result from the increased ability of the
working muscles to oxidize pyruvate, free fatty acids and
ketones in the trained state. In addition, endurance
trained athletes have demonstrated an enhanced tolerance to
acid metabolites, which is believed to be due to an accentu—
ated buffering capacity of the blood. Therefore, alkalizing
agents might serve to increase the alkaline reserve of the
blood in untrained subjects, whereas highly trained subjects
may have already improved the buffering capacity of their
blood through their training. The present investigation, as

well as the related literature, support this stand.

 

CHAPTER V
SUMMARY, CONCLUSION AND RECOMMENDATIONS
Summary
The purpose of this study was to determine the

effects of high carbohydrate and high fat-protein diets
supplemented with orally ingested sodium bicarbonate
(0.065 gm/kg. body weight) upon maximum oxygen uptake, the
change in pH of arterial blood IKNHHD lactate levels, and
maximum treadmill performance time in marathon runners.

Eight healthy, highly trained male marathon runners,
20-40 years of age, from the mid—Michigan area, served as
subjects. Each subject was randomly assigned to a treatment
condition and was then rotated through weekly testing under
all treatment conditions, i.e., supplement/carbohydrate,
supplement/fat—protein, placebo/carbohydrate and placebo/fat-
protein. The sodium bicarbonate supplement and dextrose
placebo were given in gelatin capsules in dosages of 0.065
and 0.050 grams per kilogram of body weight, respectively.
Each diet was followed for three days prior to testing. The
supplement was administered two hours prior to work.

Immediately prior to exercise testing each subject
completed a dietary recall (Appendix A). Plastic food models
were used in order to estimate serving sizes and to estimate
what percentage of the caloric intake was derived from carbo-

hydrate, fat and protein.

62

 

 

63

The treadmill test was comprised of six three-minute
work intervals of increasing difficulty, alternated with
three-minute rest intervals. Upon reaching the point of
exhaustion the subjects' recovery was monitored for fifteen
minutes. Measures of energy metabolism were executed through-
out all levels of exercise, all rest intervals and all during
the recovery period, using the Douglas bag method.

The enzymatic method was used for lactate analysis
of arterialized capillary blood. pH and PCO.2 analysis was
performed using the Astrup method. Blood samples were taken
before exercise, immediately after each level of exercise
and after five, ten and fifteen minutes of recovery.

The two-way, repeated measures analysis of variance
(ANOVA) and the non-parametric sign test were used for data
analysis.

There were no statistically significant differences
observed in oxygen uptake, maximum oxygen uptake or perform-
ance time under any of the treatment conditions.

Arterial blood pH data recorded prior to exercise
showed a significant alkalizer effect (P=.O9). Significant
supplement effects were also detected in the difference
between pH measures at the end of exercise and at the end
of the first five minutes of recovery (ALB-R1) (P=.03).

The sign test yielded consistently higher values for pH with
sodium bicarbonate supplementation under both dietary regimens
(P=.Ol). Also, the greatest changes in pH consistently oc-
curred within five minutes after maximum oxygen uptake was

reached.

 

 

64

The lactate data revealed that a significant effect
occurred between the fifth level of exercise and fifteen
minutes of recovery (ALB-R3) (P=.O9). Lactate differences
were found to be highest when sodium bicarbonate was admin-

istered.

Conclusions

 

1. Upon reaching the point of VOzmax there was a
substantial decrease in arterial blood pH as working muscles
began to rely more heavily on anaerobic glycolysis for
energy production.

2. A high carbohydrate diet, as opposed to a high
fat-protein diet, did not significantly increase maximal
treadmill performance time of trained marathon runners.

3. A high carbohydrate diet increased the alka-
linity of the blood in trained marathon runners.

4. Sodium bicarbonate, orally ingested in the
dosage of 0.065 gm/kg. body weight, increases the alkali—
nity of the blood in trained marathon runners.

5. Sodium bicarbonate ingestion, two hours prior
to exercise, did not significantly increase the maximal

treadmill performance time of trained marathon runners.

Recommendations

 

1. In further studies of this nature, physical
activity and dietary conditions should be more tightly

regulated.

APPENDICES.

APPENDIX A

DIETARY RECALL

 

 

 

65

Table A.1. High Carbohydrate Diet.

 

DIET: HIGH CARBOHYDRATE

 

Foods that can be consumed
in agy amounts:

 

Fruit (except cranberries, plums, prunes)
Vegetables (except corn and lentils)
Bread

Cereal

Potatoes, Rice, Macaroni

Margarine

Sugar

Skim Milk (no more than 3 servings of whole milk)
Cottage Cheese

Lettuce

Pancakes

No more than one serving of any
combination of the following
can be consumed each day:

 

 

 

Meat

E99

Fish

Nuts (including peanut butter)
Corn, Lentils

Cranberries, Plums, Prunes
Cakes and Cookies, plain
Butter

AN EFFORT MUST BE MADE TO KEEP YOUR TOTAL CALORIC INTAKE RELATIVELY
CONSTANT. A BODY WEIGHT LOSS OR GAIN DURING THE CONTROLLED DIET
PERIOD COULD EFFECT THE EXPERIMENTAL RESULTS.

 

 

 

66

Table A.2. High Fat/Protein Diet.

 

DIET: HIGH FAT - PROTEIN

 

Foods that can be consumed
in any amounts:

 

Meat

Fish

Fowl

Eggs

Nuts

Peanut Butter
Bacon
Butter

Corn
Lentils
Cranberries
Lettuce
Margarine

AT LEAST 3 SERVINGS OF ANY COMBINATION OF HEAT, FISH, AND FONL MUST
BE CONSUMED EACH DAY.

No more than three servings of any
combination of the following can
be consumed each day:

 

Fruit

Vegetables

Bread

Cereal

Potatoes, Rice, Macaroni
Margarine

Sugar

Milk

Cakes and Cookies, plain
Pancakes

AN EFFORT MUST BE MADE TO KEEP YOUR TOTAL CALORIC INTAKE RELATIVELY
CONSTANT. A BODY WEIGHT LOSS OR GAIN DURING THE CONTROLLED DIET
PERIOD COULD EFFECT THE EXPERIMENTAL RESULTS.

 

67

.chtgca ace .mc—c::: .9c.» :_c.a ..ccccucE ..yuozxman nobs~ucuc

 

.(hCh

 

 

fil .l. .114; i- Jill Jalnllulll

 

 

"Ecsuo

«caseu«> vca ocuu_voz

 

coon

 

 

)ouw .maaow

 

 

oo-ou .QOH

 

 

wooco .mcqaaou
.eum_cU:£c .ocvc:o.cau>m .uom:m
.>__ua .Ema .avcuu .lnuuu up“

 

no; atom

 

.uuo .cuaczmaov
.noxuucaa .ovoou vuxan

 

av-oua vo:u«ucu
can .mnwuou eunun naps:

 

 

mo~am-w~> van nouns. nozuo

 

wagons .oagzu "coaumuoa

 

mo~pmuuwu> soadoa .coouu away;

 

¢u_:uu wauumu val accumach

 

wouu93ln:

 

.uuu .souu .uawz

 

~«o .500uan uacaon
..c.u:n .~:«Enwuul .mcnop vu«uo

 

mmmm

 

wovuzu

 

Ag“:

 

 

 

 

 

 

 

 

 

 

.. mmueszzé.
czo cmtwr. .eu .m>< _c.:h .fia Illlrl.1fi| : udwquam

 

.u>< —:.c# mur=;cu
zen to; muc_>uom .5 LoLE=z

 

 

 

 

 

 

 

 

 

A_~.o=.m sac coca

 

 

IIIIIII'I.IIIIIIII Ill . '|.I‘

 

.rpm_¢;m _<;c_>_;z_ 2,. :. mz<hz_ :COL AD >¢<It2m

 

>_:;v.

u “5.. 5.6

 

.pommgbm HmswfiflwsH cm %o 8%ch boom mo rmHoriaBm .mé manna

APPENDIX B.

BASIC DATA, LACTATE

 

(mMol/L)

 

 

 

68

 

 

 

o~.n oo.. .n.m ~m.m ac.“ -._ .o.° o~.o .m.o ~¢.~ .o.. .~.~ am.. on._ ...N m~.o am.c A..o an
.~.. m~.. a... ~m.o as.» ~_.m oo.. .0.. .w.. an.» as.“ ~°.o_ so.“ o~.o ok.. nn.~ sm.— .a.. u

-- -. -- .- -- -- -- -- -. mmqm mmqm mmdufi ..uu. mmnm mmqm “mam ”mum ..uu. no
.o... as... .~.._ mo.c_ .m.~ on.~ nm.. as._ .e.o m~.u a~.o mo.a -- no.“ o~.n on.~ n~.. -.o .-
.o.o c_.~. m~.. ~_.c. ~..e ”0.. mo.~ 08.. N... oo.. no... m~.a .o.. .u.~ .fi.. o~.~ ~n.. ...o no
o_.~ ou.n ca.n .o.a no.” mo.~ .e.o no.. on.. no.n ~..m o..e ca.m mo.. “a." he._ n~.. -._ ¢a
on.°_ ._.._ ~u.~. A“... As.» No.m ou.~ .o.~ nh._ -- -- -- .- -- .- .- -- -- c.

-- -. -. -- .- -. -- -- -- oe.a .o.m -.o. ox.” an.“ oo.. o~.~ . .n.~ .A.. an
...o o~... o..c. -- ao.o as.” .o.~ on.~ 0a.. to.. no.. ~o.o -- m¢.m N..m no.~ ...~ .~.. :-
~o.m so.” ”5.9 ~..o a..° a..o o~.o _~.o oo.° .- .5.“ so... m~.n_ em.” 0... o... Au.o .m.o cm

2.5 5:295 . 88.: “j

80.. mo.n ~... 9”.“ ~.~ on.. m..c ...o so.c co.~ mm.~ oo.. .K.. .m.. .n.~ -.. ~..~ .o.o a»
oo.~ ~..a ...__ an.o_ ~o.o on.” .s.. _.._ .¢._ ~a.x ~0.a .o.c_ ...o. m..o no." no._ n~.~ so.. .—
o..m .m.o no.5 -. ~o.~ .n.. mm._ oa.o “9.9 mmqm qumw mmqm~ “mama nmqmq flmqm mmdm Mmqm .mmam nu
om.a o¢.o .o.c. o..o_ o..o K..~ “9.. “A._ .m.c -- ...o. a.... .m.» n..n ~n.~ _~._ No.° mm.o a.
m~.a n..o .A... oo.. m..e no.. o_.~ a... n..o mn.c_ ae.o_ m_.o_ o~.n_ am.~. an.» .o.. n~.n nm.. nu

-- -- -- -- -- -- -- -- -- mm.. an.o _o.o on.» o~.. o..~ so.o on.o ~m.e ¢=
cs.“ .o.o. .o.o~ m_.- am.~ as." oo.. m=.o .o.o m..~ .o.o. an.n. a~.o as.” no.. on.. ma.» o~.~ cu
mm.m an.o_ n~.o_ ~a.c ~_.m _~.~ ac.. so.~ m°.~ -- -- -- -- -- -- -- -- -- an
aa.m so.» mo.s .. m_.a an.m -.~ am._ nu._ -- -- -- .- -- -- -- -- -. x-

-- so." me.o_ sm._ 0... o“.— a... as.. m~.° -- Na.“ .o.» no.“ co.~ m~.o No.9 no.9 an.o an

«3...... . as... 3.81%
hLU>MUUK ALOZWUOK SLO>WUO¢ —0m04 —0"0d puma .— —vm0 a —O”0 .— aumu ALO>MUOK ALO>W908 ALO>W8¢ pomfid p0”0d ~0M04 pomfld —0”0d 1““ no 8H3

'I'. ...‘ll-.££.

 

 

003......0»

.Ag\ao:av weapoag .mpam camam

k....DI>II.‘D.§.‘.-O:..IDI...O.”t ..’..

. Em canoe

APPENDIX C

BASIC DATA, pH

69

 

 

 

 

...o no.9 oc.o so.o ac.o oc.o oo.o oc.c ~o.o ho.o No.9 ao.c me.c mo.o oc.o wo.c no.o no.c on
c~.~ n~.~ o~.~ c_.~ o~.s on.~ on.“ on.“ .w.~ o~.~ o~.~ e_.~ n~.s cw.“ mm.“ oo.h o~.~ ~v.~ u
ad ad _aa aa amm mm am“ an as “mm mm. man in: an. m4. mu. mu. m4. 3
-.s A... -- ~_.~ ¢~.~ ~n.~ on.“ an.~ .v.~ ¢_.~ op.“ o_.~ o_.~ a_.~ ~n.~ cm.“ mn.n ov.u an
u~.~ n~.n c~.~ c_.~ m~.~ on.~ on.~ on.~ nv.~ mm.~ o~.~ _~.~ o~.~ m~.~ an.“ we.“ ce.~ ...u 90
he.“ o~.~ o~.~ o~.~ -.~ .n.~ on.~ on.~ _q.~ on.“ cm.~ on.“ c~.s on.s ~..~ oc.~ mc.s ~o.~ «a
n..~ -.~ 0..“ .~.~ an.“ mc.n ~..K n..~ ~v.. on.~ nn.~ KN.“ n~.~ a~.~ an.n oe.~ un.~ _'.s a.

-- n~.~ c~.~ m..~ -.~ .n.~ on.~ o~.~ an.“ .n.~ km.“ -.K -.s n~.~ o~.~ on.“ an.“ -.~ no
on.~ ~n.~ o~.~ .. -.~ mn.~ co.“ no.5 ~v.~ mm.“ .n.~ wo.~ -- an.“ cm.“ ...s nc.~ mv.~ :-
on.~ pn.. c~.~ on.“ we.“ av.~ v..~ ...s cc.“ o~.~ o~.~ _~.~ o~.~ ...h m..n mo.~ ~v.~ mc.~ u»

.acao c..aoca-a.c . oaou._a ~lmmqummwlnlmmmmuflm
se.c oc.e no.o so.c ao.c ~o.o vo.o no.0 no.c mc.o mc.o oo.o so.o so.c vo.o eo.o cc.c No.9 on
o~.. m~.~ .~.~ c~.~ .n.~ an.~ .v.~ ~c.~ we.“ .n.~ o~.~ op.“ n~.~ on.“ on.~ ~w.~. _v.u no.“ n
ma “MN an Ad. mwM .Mq ma am. an .MA. m4. a4. mflfl.mflw m3. dq._mq.mflfl e
o~.~ o~.s o—.~ o~.~ e~.~ mn.~ An.“ ...A nv.~ o~.~ -.K ¢_.~ o~.~ -.~ an.“ an.n an.“ on.~ an
o~.~ an.“ 5..» o~.~ m~.~ mm.~ _ ov.~ an.~ -- a~.~ m~.~ o~.~ o~.~ a~.~ on.~ Ne.“ —q.~ -.~ 99
mn.~ ne.~ o~.~ -.n an.“ cm.“ on.~ cc.“ ~o.~ on.~ ~n.~ m_.~ m~.n Na.“ o..~ we.“ nq.~ o¢.~ «a
mm.“ .n.s - m~.~ -- we.“ nu.“ cv.~ cc.“ mv.~ ~n.~ an.“ m~.~ ow.“ en.~ no.“ ~m.s om.n s..s .-
-.~ _~.s u_.~ .~.~ ~m.~ .v.~ ...s ov.~ ~v.~ m~.~ 9..“ m—.~ o~.~ an.~ on.~ on.s ~v.s n..~ ma
q..~ o_.~ o~.~ -- m..~ on.~ cc.“ ac.“ ~v.~ on.~ .n.~ m~.~ -- on.“ an.“ —v.~ on.“ n..~ :-
.m.~ a~.~ c~.s on.“ we.“ x¢.~ co.~ oo.~ co.“ .n.~ o~.~ m~.~ ~n.~ cc.“ oc.n ov.~ nv.~ ~¢.~ an
Ammamaa:floagz mfldfidfimm.
Acopwuoc AgusMuox sco>wucx .omea .onod .omoa _omoa .ohud gun” Acc>wuoz sco>Muo¢ >Lo>wuo¢ —omoa _onod .umod —om~a —o»oa gnu” nouonasm

..E-

PIEDDP

 

.mm .mme oammm

.r.o canoe

APPENDIX

BASIC DATA, OXYGEN UPTAKE (L/min)

 

7O

...9 99.9 9~.9 m—.9 9“,: .9.9 99.9 .9.9 99.9 9v.9 99.9 .9.9 «9.9 99.. 99.9 99.9 .m.9 .9.9 .9.9 n9.9 99.9 v_.c 99.9 99.9 99.9 99.9 m—.9 .9.9 —v.9 ~v.9 m~.9 9m

99.: .9.9 99.9 .9.9 99.9 99.9 99.. 99.n n9.c 99.9 99.n 9v.— m9.n 99.v n9.v m9.n 99.— .K.m 99.: 99.. rm.n 99.9 n9.~ n9.v n9.v 99.9 v9.9 no.9 m..n ~9.n _n.~ x
99.9 ~v.9 —'.— 99.9 ~9.— m... an.— 99.n -- - cc.n 9¢.— 9n.n «9.. no.9 —c.p —Q._ sw.n 99.. 99.9 n..n 99.. “N.“ 99.. 99.. 99.9 99.9 99.9 ~9.o 99.9 ~0.~ mu
«9.: 99.9 n9.9 99.9 99.9 9~.— c¢.— mc.n - - ca.. 99.. ac.n 99.9 9—.m 9¢.n 99.9 .9.9 99.9 9... c..n 99.9 r:.— v—.v 99.n 99.9 .9.9 mm.— os.n sn.n 9~.~ 99
«9.9 99.9 99.9 99.9 99.9 99.9 99.9 n9.~ -- -- m..n 9—.— 99.~ s..v m—.v .99.n 99.9 '~.m 99.n 99.9 as.“ 99.9 99._ pv.n o..n at.“ ~9.9 —m.— m—.n _—.n .9.9 99
99.9 no.9 99.9 n~.9 99.9 99.9 9o.— cm.n - - 0.”. 99.9 v-.n 99.9 99.9 99.n 99.. mm.~ —-.m 99.. 9~.n 99.9 nn.~ 9a.. m... 99.~ 99.9 99.— —o.n ~9.n m..~ (9
99.9 99.9 .9.9 .9.9 ~..— 9o.— n-.~ an.~ -- .9.9 ¢~.v w... vv.n .9.9 99.. mm.n .9.9 at.“ .9.9 a... nc.~ 99.9 99.~ nc-n '9.n —..~ nc.9 99.— 9~.n -.n v~.~ c9
«v.9 99.9 99.9 99.9 99.9 9~.9 99.9 .9.9 - -- ~—.~ 9—.— n—.~ m~.~ 99.9 99.9 .9.— c~.m ~s.n 99.9 99.n 99.9 on.— oc.n mo.n —9.~ 99.9 99.. 99.~ -.~ ~9.~ 99
99.9 99.9 99.9 99.9 99.9 99.9 99.. 9~.n - -- u- - -- -u -o 9... 9n.- nv.n 99.9 mn.m 99.n po.9 o~.~ 99.9 99.. nn.n 99.9 9~.~ n... 99.9 99.~ :9
99.9 99.9 99.9 99.9 o... 9~.— 99.. 9~.n no.9 99.9 99.. v..— 9_.n ~—.o no.9 —n.v 99.9 ~v.~ 99.9 ~9.m 99.n 90.9 99.. 9n.c o~.w .9.9 99.9 99.. cv.n om.n 99.~ um

 

 

 

 

 

 

 

 

 

9..9 9..9 ...9 .9.9 .9.9 99.9 99.9 99.9 99.9 99.9 .9.9 99.. 99.. .... 99.9 99.9 99.9 99.9 99.9 99.9 9..9 99.9 9..9 .9.9 99.9 99.9 9..9 99.9 9..9 .9.9 .9.9 99
.9.9 99.9 99.9 99.9 99.9 9... 99.. 99.9 99.9 .9.9 99.. 9... ...9 9... 99.. 99.9 99.. 99.9 .... 99.. 99.9 99.9 .9.9 99.. 99.9 99.9 ...9 99.. 9..9 ...9 99.9 9
.9.9 .9.9 99.9 99.9 99.. 9... 99.. 99.9 -- .- -- - .. .- .9.9 9... 9... 99.9 99.9 99.9 99.9 .... .9.9 .9.. .9.. 9..9 99.. 99.9 99.9 99.9 ...9 99
99.9 99.9 99.9 99.9 .9.9 9... 9... 9... - - 99.. 9... 99.9 .9.. 9... .9.9 99.9 99.9 99.. 9... 99.9 99.9 .9.. 99.9 99.9 .9.9 99.9 9... 99.9 .9.9 99.9 99
.9.9 99.9 99.9 99.9 ...9 99.9 99.. 99.9 -- -- - 99.9 9... 99.9 99.. 99.9 9... 99.9 99.. 99.. ...9 99.9 9... 99.9 99.9 9..9 99.9 9... 99.9 99.9 99.. 99
9..9 .9.9 99.9 99.9 99.9 99.. 9... 9... -- 99.9 99.. .9.. 9..9 9..9 .9.. .9.9 .9.9 99.9 .9.. 99.. 99.9 99.9 99.. 99.. 99.. .9.9 99.9 9... 99.9 99.9 99.9 .9
99.9 9..9 99.9 99.9 .9.. .9.. 9... .9.9 -- -. 9..9 .9.. .9.9 9..9 99.. 99.9 .9.. 99.9 .9.. 99.. .9.9 .9.. 99.9 .9.. 9... 99.9 99.9 9... 99.9 99.9 99.9 .9
9..9 99.9 99.9 99.9 9..9 .9.9 .9.. 99.9 -- 99.. 99.9 99.9 .9.9 99.. 99.. .9.9 99.9 9... 99.9 .9.9 99.9 .9.9 99.. 99.9 99.9 99.9 99.9 9... 99.9 .9.9 99.. 99
99.9 99.9 .9.9 .9.9 99.9 99.. .... .9.9 -- - -- -- - -- .9.9 .9.. 99.. 99.9 .9.9 9..9 .9.9 .9.9 99.9 99.9 99.. 9..9 99.9 .9.9 99.. 99.. .9.9 :9
99.9 99.9 99.9 9... 99.. 99.. .9.9 99.. 99.9 9..9 .9.. .9.. 9... 99.9 99.9 .9.. 99.9 99.9 99.9 9... 9... 99.9 99.. 99.. 99.. 99.9 99.9 99.. .9.9 .9.9 99.9. 99

~muq.mmm.uumuuqunn

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9.-9. 9-9 .-9 9-. 9 9 . 9 9 . 9-9 . 9 9 . 9-9 . 9 9 . 9-9 . 9 9 . 9.9 . 9. 9 . .99.

5.... .... ll. 2. .99.... 3. I119. .... LL. 5
9 ...9. . .99.. 9 .9.9. 9 .9... . .9.99. 99.9....»

 

..9999999999 ...9 99999

 

71

 

 

 

 

 

 

 

 

 

 

 

 

.9.9 .9.9 .9.9 99.9 ...9 -.9 2.9 69.9 8.9 99.. 96.9 9~.9 66.9 2.9 99.9 .9.9 2.9 96.9 ~99 69.9 26.9 3.9 2.9 99.9 96.9 2.9 ...9 2.9 99.9 2.9 66.9 99
.9.9 99.9 2.9 .9.9 2.9 6~.. 66.. 96 96.9 2.6 696 9~.. 696 996 ~96 .96 8.. 696 2.6 69.6 -6 66.9 696 966 996 26 2.9 99.. 666 ...6 966 u
.9.9 -n 2.9 ~66 ..9 3.. 69.. .96 .u 3 -. a. o. -o 9.6 8.6 ~6.. 9.6 6.6 99.6 96.6 69.. 9.6 6.6 86 26 99.9 9.6 '6 '6 26 .9.9
69.9 99.9 2.9 ~9.9 2.9 8.. .6.. 966 - .- 9.9.6 96.. 2.6 8.9 ...9 66.6 8.9 996 2.6 966 9.6 2.9 66.. 8.6 9.6 26 2.9 2.. 666 ~66 6~6 2
69.9 69.9 96.9 2.9 66.9 2.. 69.. 996 .- - 2.6. 6... 996 9~6 69.6 9.6 .9.9 996 .66 8.6 86 .9.9 6... 69.6 . 696 666 99.9 96.. ~66 26 2.. 8
99.9 99.9 99.9 ~96 69.9 99.. 69.. 86 - -- ~66 96.. 966 666 6.6 966 96.9 696 8.6 2.6 9~6 69.9 696 .96 996 26 69.9 .96.. 666 99.. 966 8
.9.9 2.9 69.9 2.9 .9.. 66.. 8.. 2.6 o- 96.9 66.6 69.. 2.6 696 ...9 996 69.. 86 2.6 96.6 996 96.9 966 9~6 ~66 696 ~96 696 .96 696 6.9.. 2
96.9 99.9 69.9 69.9 2.9 2.9 69.9 .9.. -n 966 26 26.9 ~96 69.6 .96 9.6 62.9 69.. 96.6 2.6 26 .9.9 9.9... -6 .~.6 966 99.9 2.. 26 26 696 99
.9.9 99.9 2.9 ~9.9 69.9 66... 99.. 2.6 3 - u- -n - 3. 99.9 66.6 .96.. 26 99.9 66.... 26 .9.9 ~96 69.9 2.6 6.6 2.9 86 6.6 26 26 2
99.9 2.9 2.9 8.9 6.9.. 96.. 2.. .66 66.9 -.9 ~96 9... 996 99.... 66.9 86 ~96 .966 99.6 99.6 996 .9.9 2.. 69.6 ~96 9.6 2.9 99.. .66 96.6 966 99

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8.9 99.9 ...9 2.9 2.9 2.9 96.9 2.9 99.9 .9.9 .6.9 2.9 99.9 96.9 69.9 99.9 -.9 99.9 69.9 .9.9 26.9 ...9 66.9 66.9 99.9 96.9 8.9 2.9 96.9 66.9 9~.9 99
69.9 69.9 2.9 2.9 96.9 2.. 2.. 9.6 9.9 99.9 996 2.. 696 2.... 69.6 996 8.. 696 96.6 86 96.6 69.9 696 996 ~96 26 2.9 2.. 36 9.6 9~6 h
2.9 2.9 2.9 2.9 2.. 66.. 6... .96 - - 99.6 2.. 9.9.6 996 69.6 8.6 2.. 9.6 .9.9 696 66.6 99.9 666 ~96 2.6 .96 69.9 6.6 26 696 9.6 no
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3.9 99.9 69.9 8.9 '6 .... 26 -. -- 8.6 3.6 6... 8.. o- 96.6 9.6 2.9 696 9.6 R6 26 2.9 29.. 666 96.6 966 69.9 66.. 36 =6 69.. 99
99.9 69.9 .66 69.9 96.9 2.. 2.. 696 u. 3 o. 3 - u- -- .96 2.. 66.6 ~96 3.9 ~96 69.9 696 66.6 .9.9 966 26.9 .96 2.6 .96 696 2
99.9 69.9 2.9 2.9 .9.9 .9.9 ~... 9.9... 2.9 3.9 96.6 96.9 .96 ~66 99.7 996 3.9 69.. 696 96.9 996 2.9 2.. .96 696 996 2.9 ~6.. ..6 26 26 In

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9 .999. 9 .999. 9 .999. 9 .29. . .29. 99.99....»

 

.AQHS\HV Amo>v mxwpmb mmmhxo .mpmm 09mwm ...Q magma

APPENDIX E

SIGGARD-ANDERSEN ALIGNMENT NOMOGRAM

C ode 98‘ 20]

 

72

SlGGAARD-ANDERSEN ALIGNMENT MONOGRAM

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Total-CO, mMol I plum. 'co:
60 - 7.17 C mm Hg
1 HCOT mfg" plum; __ $0
so-i ,,
5 Inc Excess __
SO 3 "15¢! blood or pluma ,_
50-1 ..
.. "I ,
‘0—__ ‘0 " +
"—‘ _~ 0 o L— 15
2 -‘ .
.1 -E >—
35; '2' y
.1 _: y
—_ _“ p—
-—i .1 '-
30—? 30.; 7.. .—
—3 1 — 20
j '1 ..
—_j ‘1 7 7 :-
25—3‘ 75"? I.
' 71 7 5 L,
—‘ F
3 . '— 25
1 ‘1 :-
1 1 7.5 :_
“ 20—- :_
20% J :_
j a 7 ‘ POUCH! IGOHQI’ICCMOB .— Jo
_ q E.
. _
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“ Duo and how :—
4 _‘o
.4 A".".' u-
7 1 Clo-HM)
4 Venom
—4
4 7 o E-
50
‘ ILooo ACID-BASE VALUES
_ Actual pH
9—
6 3 Ion-on 60
.4 MW‘
Duo E-cou
0" 6 7 MEQ'I blood F
To!" CO: 70
nMoH plum. .
7“ e 6
.0
6—1
90
J
_ omen VALUES ‘00
Home loans
9'1“ 9m 1‘0
OI on
“12?.qu '1‘. 120
‘—
OI on ("won
Paloma H9 130
140
§ ‘50
CO'vaHT 9:2 ‘I" Iv MOIOIEYII A s IMMU’VIJ T3 Oil-t. co-umnau uv “mun

 

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N ‘ a .- 'l ‘
I

Figure 3.1. Siggard-Andersen Alignment Nomogram.

BIBLIOGRAPHY

10.

 

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