Training-induced changes in hormonal and metabolic responses to submaximal

exercise

WILLIAM W. WINDER, ROBERT C. HICKSON, JAMES M. HAGBERG, AL1 A. EHSANI, AND JERRY A. McLANE Department of Preventive Medicine, Washington University School of Medicine, St. Louis, Missouri 63110

WINDER, WILLIAM W., ROBERT C. HICKSON, JAMES M. HAGBERG, ALI A. EHSANI, AND JERRY A. MCLANE. Traininginduced changes in hormonal and metabolic responses to submaximal exercise. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 46(4): 766-771, 1979.-Plasma glucagon and catecholamines increase during prolonged submaximal exercise, but the magnitude of the increase is less in endurance-trained individuals than in untrained subjects. We have studied the rapidity at which this adaptation occurs. Six initially untrained healthy subjects exercised vigorously (on bicycle ergometers and by running) 30-50 min/day, 6 days/wk, for 9 wk. Prior to the beginning of training and at 3-wk intervals thereafter, participants were subjected to 90-min bicycle ergometer test work loads that elicited 58 t 2% of the subjects’ initial maximal oxygen consumption. The major proportion of the traininginduced decrement in plasma glucagon and catecholamine responses to exercise was seen after 3 wk of training. We conclude that the hormonal component of the training adaptation occurs very early in the course of a vigorous endurance training program* human subjects; insulin; glucagon; catecholamines; ketosis; FFA mobilization during exercise

ENDURANCE

EXERCISE

TRAINING

postexercise

is a Complex

process

involving not only adaptations in skeletal muscle, but other organs and systems as well. Intramuscular and cardiovascular adaptations to training have been studied. in great detail (20,28). Major changes also occur in some endocrine responsesto exercise. Prior to training, plasma catecholamines increase markedly during prolonged exercise of moderate intensity (14, 18). After training, plasma catecholamines are much lower during work of the same absolute intensity (18). In untrained subjects, plasma glucagon increases gradually, reaching relatively high levels toward the end of a prolonged bout of exercise (1,5,6, 10, 14, 17). Endurance exercise training markedly diminishes this increase in plasma glucagon during exercise (5, 15, 17). Even though some of the training-induced hormonal changes have been studied rather extensively, little information is available on the time course of these adaptations and on their physiological consequences. The purpose of this study was to determine how soon after the initiation of a vigorous exercise training program these hormonal adaptations occur and to correlate changes in hormonal responses with training-induced metabolic changes. 766

METHODS

Training program. Six healthy male subjects participated in a 9-wk long endurance training program. Subjects worked on the bicycle ergometer and ran on alternate days. The bicycle ergometer work consisted of six 5 min bouts of pedaling at work loads that initially elicited the subjects’ maximal oxygen consumption (VOW,,,) by the end of each bout. The work intervals were separated by 2-min rest periods. On alternate days, subjects ran at a pace they could maintain for 40 min (3-5 miles). Two of the six subjects worked on the bicycle 6 days/wk instead of running on alternate days; all participants exercised 6 days/wk. Daily work loads were kept constant for the fast 4 wk of the study. At the end of the 4 wk, the subjects’ work capacity was increased. The bicycle work loads were then increased to levels that again elicited . vo zmax.Subjects were instructed to run at a more rapid pace on their running days; they then worked at these levels for the remaining 5 wk of the study. Determination of maximal oxygen consumption. Maximal oxygen consumption was determined on each subject prior to training and at the end of 9 wk of training as a measurement of the effectiveness of the training program. VO2 max has long been used as an indicator of the physical fitness of an individual (cf. Ref. 24). Subjects worked on bicycle ergometers (Quinton Instruments, Seattle, WA) at increasing work loads until oxygen consumption plateaued as a function of work load. Expired air was collected in meteorological balloons and analyzed with a Perkin-Elmer mass spectrometer (Pomona, CA). Volumes were measured with an American gas meter (Warren Collins, Braintree, MA). Exercise test. Prior to beginning the training program and at 3-wk intervals during the training, participants were subjected to a 90-min bicycle ergometer test at 58 t 2% Of initial VO2 max. At the end of the 9-wk training, subjects were tested twice: once at the same absolute work load and once at approximately the same relative work load at which they were tested prior to training (i.e., 62% of the new VOWmax). Thirty minutes prior to these tests, a catheter was inserted into an antecubital vein of the arm. Blood samples (8 ml) were collected via the venous catheter immediately prior to and after 30,60, and 90 min of exercise and again at 10,30, and 60 min postexercise. The catheter was flushed with 0.9% saline between samples. Ambient temperature was 70°C during the exercise; electric fans

~161-7567/79/oooO-~$~1.~~

Copyright

0 1979 the American

Physiological

Society

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TIME

COURSE

OF

HORMONAL

ADAPTATION

TO

PHYSICAL

were used to keep subjects cool. Subjects were tested late in the morning, 4-5 h after breakfast. Each subject ate the same breakfast before all tests during training as he did before the pretraining test. Subjects did not smoke cigarettes or drink caffeine-containing beverages 4-5 h prior to the test. Processing of blood. For glucagon and insulin assays, 3.0 ml blood was added to a chilled tube containing 3.6 mg EDTA and 1,500 U of aprotinin (Trasylol, FBA Pharmaceuticals, New York). For the catecholamine assays, 2.0 ml blood was added to a chilled tube containing 3 mg reduced glutathione, 0.1 mg pargyline, and 50 U heparin sodium. For glucose, 3-hydroxybutyrate, lactate, and glycerol assays, 1.0 ml blood was added to 2.0 ml 10% perchloric acid. The remaining blood was heparinized and used for the plasma free fatty acid (FFA) assay. All blood samples were kept ice cold and were centrifuged within 15-20 min of the time of collection. Plasma and perchloric acid extracts were stored frozen at -20°C until time of analysis. Assays. Samples for insulin, glucagon, and catecholamines were stored frozen until the end of the study so that all samples for each subject could be run in the same assay. Glucagon was measured by the method described by Faloona and Unger (9) using 30 K antiserum from Dr. R. Unger’s laboratory (University of Texas Medical School, Dallas, TX). Porcine glucagon (Eli Lilly, Indianapolis, IN) was used as a standard. Radioiodinated glucagon was obtained from Nuclear Medical Laboratories (Dallas, TX). Insulin was measured by a modification (7) of a radioimmunoassay method described by Herbert (19). Anti-insulin serum was obtained from Biotek Laboratories (St. Louis, MO). Radioiodinated insulin was obtained from New England Nuclear (Boston, MA). The human insulin standard was a gift from the Eli Lilly Company. Plasma epinephrine and norepinephrine were determined by the radiometric assay described by Cryer et al. (8). Catechol 0-methyltransferase was isolated from rat liver by the method of Axelrod and Tomchick (2). S[methyl-“Hladenosyl-L-methionine was obtained from New England Nuclear. The perchloric acid extracts were neutralized and analyzed for glucose (4), lactate (16), 3-hydroxybutyrate (30), and glycerol (21). Plasma free fatty acids were determined by the method of Novak (25). Statistical methods. Results are expressed as means t SE. The paired t test was used to evaluate the significance of differences. RESULTS

Assessment of the magnitude of the training adaptation. The average To zrnaxof the six subjects increased 22% as a result of this training program (Table 1). As can be seen in Fig. 1, heart rate was considerably lower after training compared to before at the same absolute work rate (850 t 74 kpm/min). Heart rate tended to be lower even when subjects were tested at approximately the same percentage of VOzmax (1,150 t 75 kpm/min) (Table 2). Blood lactate, also an indicator of the level of trhhg, was much lower at the same absolute work load at the

767

TRAINING

1. Effect of 9-wk training on body weight and VOWmax __--_~-------. -- .~..-~~--~ - -.----~---.----- -..TABLE

Weight, Subj

Age,

kg

VO

-.. - .~_~~_ Work

2 nrax, Win

Load for 90-min Test*

yr

Begin

End

65 98 74 80 94 74

64 97 72 77 91 73

2.86 3.87 3.51 2.85 4.16 3.51

3.30 4.97 4.23 3.65 4.67 4.58

750 1,050 750 600 1,050 900

1,050 1,400 1,050 900 1,300 1,200

3.46 kO.21

4.23 to.26

850 274

1,150 t75

A B c D E F

34 31 28 29 30 26

Means tSE

30

81

79

tl

t5

t5

* kpm/min.

Begin

End

Absolute

Relativet

t End of training.

160 I

w 120 Ia OL + 100 [r a W I 80

EXERCISE

AT. 58+ 2’?le OF INITIAL , V02mox ,

30

60

90 TI ME

FIG.

1. Effect

submaximal

1

I

10

30

60

1

POST

POST

POST

(Mid

of 9-wk training on heart rate response exercise at same absolute work load.

to prolonged

end of the 9-wk training period (Fig. 2). Glucagon and insulin. Prior to training, plasma glucagon increased progressively during prolonged exercise and remained elevated long after exercise had ended (Fig. 3). After 9-wk training, plasma glucagon during exercise of the same intensity and duration was not significantly different from resting values (Fig. 3). The entire traininginduced decrement in the plasma glucagon response to exercise had occurred within 3 wk of the beginning of training (Fig. 4). Plasma insulin decreased during exercise and the magnitude of the decrease after training was similar to pretraining responses (Fig. 3). CatechoZamines. Prior to training, plasma epinephrine increased from resting values of 0.08 t 0.02 rig/ml to 0.64 t 0.04 at the end of the 90-min exercise bout. Plasma norepinephrine increased from 0.26 t 0.05 rig/nil to 1.81 t 0.40 during this long-term bout of exercise. As can be seen in Fig. 5; the catecholamine response was much lower after training. As with glucagon, this adaptation occurred very early in the course of this vigorous training program (Fig. 5).

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768

WINDER

TABLE 2. Effect of 9-wk training on hormonal and metabolic responses to 90-min exercise at same absolute and same relative work load Pretraining 850 k 74 kpm/ min

Heart rate, beats/min Blood lactate, mM Blood glucose, mM Blood glycerol, mM Plasma FFA, mM Blood 3-hydroxybutyrate, mM, 60-min postexercise Plasma insulin, j,JJ/ml Plasma glucagon, pg/ ml Plasma norepinephrine, w/d Plasma epinephrine, ng/mJ

166 3.10 4.50 0.37 1.06 0.41

rfr t t t, t t

3 0.40 0.12 0.03 0.08 0.09

After 850 f 74 kpm/ min

126 1.37 4.78 0.24 0.80 0.17

t 2* sf: 0.31* t 0.15 k 0.02* t 0.02* t 0.03*

-

INSULIN

AL.

0 Pre -Traming A 9 Wks Training

9-wk Raining 1,150 + 75 kpm/ min

156 2.57 4.16 0.28 0.72 0.28

t k t t t t

6 0.35 0.21 0.04 0.07* 0.10

3.6 t 1.0 173 t 11

5.6 t, l.l* 121 t 18*

3.9 t 1.1 141 t, 15*

1.81 t 0.40

0.81 k 0.24*

1.55 t 0.50

0.64 -+ 0.04

0.29 t 0.03*

0.42 t 0.07*

With the exception of 3-hydroxybutyrate, rate were taken after 90 min of exercise. from the pretraining responses, P < 0.05.

**f

ET

blood samples * Significantly

and heart different

d- EXERCISE

AT 5822% I VO2 mox

30

I

1

60 TIME

3. Effect of 9-wk training prolonged submaximal exercise FIG.

Training

,

OF INITIAL

1

1 I

90 10

30

60

POST

POST

POST

(Mid

on plasma glucagon and insulin at same absolute work load.

during

19Or 18

0

EXERCISE

OF INITIAL ATQ;8fmzt 1 2

30

I

60 TI ME

90

1

I

I

10

30

60

POST

POST

POST

(Mid

FIG. 2. Effect of 9-wk training on blood lactate submaximal exercise at same absolute work load.

during

prolonged

Glucose, glycerol, FFA, and 3-hydroxybutyrate. Prior to training, blood glucose decreased an average of 18 mg/ 100 ml by the end of exercise (Fig. 6). After training, blood glucose did not change significantly during or after the 90-min bout. Plasma FFA and blood glycerol concentrations at the end of the 90.min exercise bout were lower after training compared to pretraining. A large training-induced decrement in the concentration of these compounds in blood was seen in the postexercise period (Fig. 6). In the test prior to training, blood 3-hydroxybutyrate increased rapidly in the postexercise period. The magnitude of this postexercise ketosis was much less after training (Fig. 6). This reduction in degree of postexercise ketosis was seen after 3 wk of training (Fig. 7). The time

3 WEEKS

6 OF TRAINING

4. Time course of effect of training on plasma of 90-min exercise at 58 & 2% of initial vOzmax. FIG.

9 glucagon

at end

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TIME

COURSE

OF

HORMONAL

ADAPTATION

TO

PHYSICAL

n

1.8 n

NE

I

01

3 WEEKS

5. Time at end of 90-min FIG.

1 6 OF TRAINING

course of effect of training on plasma exercise at 58 st 2% of initial BOB,,,.

I

9

769

TRAINING

We were particularly interested in the new finding that the entire training-induced decrement in plasma glucagon response to prolonged exercise takes place within 3 wk of the beginning of the vigorous training program (Fig. 4). In agreement with the idea that the lower catecholamine levels are responsible for lower plasma glucagon after training is the fact that the time course of the reduction in catecholamine response (Fig. 5) is very similar to the time course of the reduction in glucagon response (Fig. 4). Evidence has recently been presented by Galbo et al. (14) indicating that in man catecholamines are probably less important in controlling glucagon release during prolonged exercise than are other factors. They found that a)- or P-adrenergic blockage with phentolamine or propranolol did not prevent the increase in plasma glucagon during prolonged exercise. Interpretation of these results was complicated by the observation that plasma catecholamines were higher during prolonged exercise after P-adrenergic blockade than during a control exercise bout (cf. Ref. 14). Maintenance of plasma glucose concentrations by glucose infusion reduces both epinephrine and glucagon responses to long-term exercise (cf. Ref. 14). Blood glucose appears to be maintained at

catecholamines

course of this adaptation appeared to correlate more closely with glucagon responses than with postexercise FFA and glycerol levels (Fig. 7). Hormonal and metabolic responses at the same relative work load after training. At the end of the 9-wk training program when subjects worked for 90 min at 62 t 2% of their new Vozmax, responses in general were similar to the pretraining responses when subjects were working at a considerably lower work load (Table 2). Plasma FFA, plasma glucagon, and plasma epinephrine were lower at the end of the 90-min bout even at the higher work load at the end of training when subjects worked at approximately the same percentage of maximal oxygen uptake as they did prior to training.

BLOOD

GLUCOSE

BLOOD

GLYCEROL

c

mM u

1

1

PLASMA

I

I

1

1

1

I

I

1

FFA

mM

I

L DISCUSSION

Studies in animals and in human subjects have previously indicated that plasma glucagon and catecholamines increase during prolonged exercise (1, 5,6, 10, 14, 17, 18). The increase in glucagon has been said to be caused by effects of high levels of catecholamines on the a-cells of the pancreatic islets (14, 23). The fact that plasma glucagon does not increase significantly during exercise after training (Figs. 2 and 4) is likely due to the fact that the plasma catecholamine levels during exercise are much lower after training than before (Fig. 5 and Table 2). Additional support for this concept is found in the fact that when subjects worked at higher work loads at the end of 9-wk training so that the catecholamine response approached the pretraining response, plasma glucagon was significantly elevated after 90 min of exercise (Table 2) .

0 Pre -Training n 9 Wks Training

Oa4

r

BLOOD

34iYDROXYBUTYRATE

EXERCISE

AT 58 2 2% VO2 mox

30

OF INITIAL/ I

60

1

1

90 10

30

60

POST

POST

POST

TIME

1

(MINI

FIG. 6. Effect of 9-wk training on levels of metabolites in blood during and following prolonged submaximal exercise at same absolute work load.

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770

WINDER

140 Pcl /ml 120

mM

mM

0.5 0.4

Tr

BLOOD-34iYDROXYBUTYRATE

lf

0.3 mM

t\

0.1 I WEEKS

T

3 OF

6 TRAINING

9

F ‘IG. 7. Time course of effect of training on glucagon, glycerol, FFA, -and 3-hydroxybutyrate in blood taken from subjects 60 min following end of 90-min exercise bout at 58 & 2% of pretraining vo 2 max.

slightly higher levels during and following exercise after training (Fig. 6). Thus, blood glucose may be the most important factor determining glucagon and catecholamine levels during prolonged exercise. Fitts et al. (11) and Baldwin et al. (3) previously showed that trained rats use less liver glycogen during exercise than do nontrained rats working at the same intensity. Although measurement of liver glycogen was not possible in this study, we suspect that because of the lower glucagon and catecholamine levels, the subjects mobilized lessliver glycogen during exercise after training than before. The fact that at the end of prolonged exercise, plasma catecholamines, plasma FFA, and blood glycerol are lower after training (Fig. 6) leads us to suspect that the rate of mobilization of FFA from lipid depots remote to the working muscle is decreased with training. Plasma fatty acid concentration is also lower in endurancetrained rats than in nontrained rats during prolonged moderate exercise (32). In addition to the fact that the catecholamine response is not as great after training, two recent reports present evidence for a decrease in sensitivity of adipose tissue to catecholamine-stimulated lipolysis (22, 29). All of these observations seem paradoxical to

ET

AL.

the well established fact that during long-term exercise, a greater proportion of the energy requirement is derived from fat oxidation in trained individuals compared to nontrained. The respiratory quotient is lower in trained than in nontrained subjects during exercise (26), thus indicating a shift toward fat as a source of energy. The source of this fat has not been clearly defined, however. Froberg et al. (13) reported that in man, intramuscular triglycerides can serve as a major source of energy during exercise. He estimated from respiratory quotients and triglyceride analysis of muscle biopsies that 75% of the fatty acids oxidized during prolonged exhausting exercise were derived from muscle triglycerides (13). To our knowledge, no information is available concerning the effect of training on the rate of intramuscular lipid utilization during exercise, but we predict on the basis of the apparently lower rates of lipid mobilization after training, that the trained individual obtains a greater proportion of his energy requirement during long-term submaximal exercise from intramuscular lipid stores. Obviously, plasma concentrations of substrates are not absolute indicators of turnover rates. It is possible that the lower fatty acid and glycerol concentrations during exercise after a period of training are a result of increased capacity to utilize these substrates rather than a reduction in the rate of mobilization (20). The results of this study confnm previous observations (cf. Ref. 32) indicating that the magnitude of postexercise ketosis is less after training. The capacity of skeletal muscle of endurance-trained rats to oxidize 3-hydroxybutyrate and acetoacetate is greater than in muscle of untrained rats (31). Thus, the capacity of trained individuals to maintain low levels of blood ketone bodies may be due in part to a greater rate of ketone oxidation. The results of the present study however, imply that the rate of postexercise ketogenesis is less in the trained individual. Prior to training, plasma fatty acids and glucagon remained elevated long after cessation of exercise. After training, plasma glucagon and FFA are much lower in the postexercise period. Both FFA and glucagon concentrations have been implicated as being important in regulation of the rate of hepatic ketogenesis (12, 27). During the course of the 9 wk of training, as subjects were tested periodically, the reduction in degree of postexercise ketosis seemed to follow more closely the decline in postexercise glucagon concentration than the decline in plasma FFA concentration (Fig. 7). This finding suggests that the postexercise plasma glucagon concentration may be an important determinant of the degree of postexercise ketosis. In summary, we have demonstrated that the traininginduced reduction in catecholamine and glucagon responses to prolonged submaximal exercise occurs relatively early in the course of a vigorous endurance training program. The maximal adaptation in these responses occurs within 3 wk of the beginning of training. We thank the subjects who were splendidly cooperative during the course of this time-consuming study. We are indebted to Dr. John 0. Holloszy for his constructive suggestions, to Ms. Sandy Zigler and Mrs. Janet Yawitz for typing the manuscript, and to Mrs. May Chen and Mrs. Mary Van Auken for skillful technical assistance.

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TIME

COURSE

OF

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ADAPTATION

TO

PHYSICAL

R. C. Hickson and J. A. McLane were postdoctoral research trainees supported by National Institutes of Health Training Grant AM-05341. J. M. Hagberg was a postdoctoral research trainee supported by National Institutes of Health Training Grant 5-T32-HL-07081. This study was supported in part by a National Institutes of Health

771

TRAINING Biomedical School. Received

Research

31 July

Support

1978; accepted

Grant

to Washington

in final

form

University

13 November

Medical

1978.

REFERENCES 1. AHLBORG, G., P. FELIG, L. HAGENFELDT, R. HENDLER, AND J. WAHREN. Substrate turnover during prolonged exercise in man. J. Clin. Inuest. 53: 1080-1090, 1974. 2. AXELROD, J., AND R. TOMCHICK. Enzymatic 0-methylation of epinephrine and other catechols. J. BioZ. Chem. 233: 702-705,1958. 3. BALDWIN, K. M., R. H. FITTS, F. W. BOOTH, W. W. WINDER, AND J. 0. HOLLOSZY. Depletion of muscle and liver glycogen during exercise-protective effect of training. Pfluegers Arch. 354: 203212, 1975. 4. BERGEMEYER, H. U., E. BERNT, F. SCHMIDT, AND H. STORK. DGlucose. Determination with hexokinase and glucose-6-phosphate dehydrogenase. In: Methods of Enzymatic Analysis, edited by H. U. Bergemeyer. New York: Academic, 1974, p. 1196-1201. 5. BLOOM, S. R., R. H. JOHNSON, D. M. PARK, M. J. RENNIE, AND W. R. SULAIMAN. Differences in the metabolic and hormonal response to exercise between racing cyclists and untrained individuals. J. Physiol. London 258: 1-18, 1976. 6. BOTTGER, I., E. SCHLEIN, G. R. FALOONA, J. P. KNOCHEL, AND R. H. UNGER. The effect of exercise on glucagon secretion. J. Clin. EndocrinoZ. Metab. 35: 117-125, 1972. 7. CONLEE, R. K., M. J. RENNIE, AND W. W. WINDER. Skeletal muscle glycogen content: diurnal variation and effects of fasting. Am. J. PhysioZ. 231: 614-618, 1976. 8. CRYER, P. E., J. V. SANTIAGO, AND S. SHAH. Measurement of norepinephrine and epinephrine in small volumes of human plasma by a single isotope derivative method: response to the upright posture. J. CZin. EndocrinoZ. Metab. 39: 1025-1029, 1974. 9. FALOONA, G. R., AND R. H. UNGER. Glucagon. In: Methods of Hormone Radioimmunoassay, edited by B. M. Jaffe and H. R. Behrman. New York: Academic, 1974, p. 317-330. 10. FELIG, P., J. WAHREN, R. HENDLER, AND G. ALBORG. Plasma glucagon levels in exercising man. N. EngZ. J. Med. 287: 184-185, 1972. 11. FITTS, R. H., F. W. BOOTH, W. W. WINDER, AND J. 0. HOLLOSZY. Skeletal muscle respiratory capacity, endurance, and glycogen utilization. Am. J. Physiol. 228: 1029-1033, 1975. 12. FRITZ, I. B., AND L. P. K. LEE. Fat mobilization and ketogenesis. In: Handbook of Physiology. EndocrinoZogy. Washington, DC: Am. Physiol. Sot. 1972, sect. 7, vol. I, chapt. 37, p. 579-596. 13. FROBERG, S. O., L. A. CARLSSON, AND L.-G. EKELAND. Local lipid stores and exercise. In: Muscle MetaboZism during Exercise, edited by B. Pernow and B. Saltin. New York: Plenum, 1971, p. 307-313. 14. GALBO, H., E. A. RICHTER, J. HILSTED, J. J. HOLST, N. J. CHRISTENSEN, AND J. HENRICKSSON. Hormonal regulation during prolonged exercise. Ann. NY Acad. Sci. 301: 72-80, 1977. 15. GALBO, H., E. A. RICHTER, J. J. HOLST, AND N. J. CHRISTENSEN. Diminished hormonal responses to exercise in trained rats. J. AppZ. PhysioZ.: Respirat. Environ. Exercise Physiol. 43: 953-958, 1977. 16. GUTMANN, I., AND A. W. WAHLEFELD. L-(+) Lactate. Determination with lactate dehydrogenase and NAD. In: Methods of Enzymatic Analysis, edited by H. U. Bergemeyer. New York: Academic,

1974, p. 1464-1468. 17. GYNTLEBERG, F., M. J. RENNIE, R. C. HICKSON, AND J. 0. HOLLOSZY. Effect of training on the response of plasma glucagon to exercise. J. AppZ. Physiol.: Respirat. Environ. Exercise Physiol. 43: 302-305, 1977. 18. HARTLEY, L. H., J. W. MASON, R. P. HOGAN, L. G. JONES, T. A. KOTCHEN, E. H. MONGEY, F. E. WHERRY, L. L. PENNINGTON, AND P. T. RICKETTS. Multiple hormonal responses to prolonged exercise in relation to physical training. J. AppZ. Physiol. 33: 607-610, 1972. 19. HERBERT, V., K-S. LAU, C. W. GOTTLIEB, AND S. J. BLEICHER. Coated charcoal immunoassay of insulin. J. CZin. EndocrinoZ. 25: 1375-1384, 1965. 20. HOLLOSZY, J. O., AND F. W. BOOTH. Biochemical adaptations to endurance exercise in muscle. Annu. Reu. Physiol. 38: 273-291, 1976. 21. KREUTZ, F. H. Enzymatische Glycerinbestimmung. KZin. Wochenschr. 40: 362-363, 1962. 22. LEBLANC, J., M. BOULAY, S. DULAC, M. JOBIN, A. LABRIE, AND S. ROUSSEAU-MIGNERON. Metabolic and cardiovascular responses to norepinephrine in trained and nontrained human subjects. J. AppZ. Physiol.: Respirat. Environ. Exercise Physiol. 42: 166-173, 1977. 23. LUYCKX, A. S., AND P. J. LEFEBVRE. Mechanisms involved in the exercise-induced increase in glucagon secretion in rats. Diabetes 23: 81-93, 1974. 24. NAGLE, F. J. Physiological assessment of maximal performance. Exercise Sports Sci. Rev. 1: 313-338, 1973. 25. NOVAK, M. Calorimetric ultramicromethod for the determination of free fatty acids. J. Lipid Res. 6: 431-433, 1965. 26. SALTIN, B., AND J. KARLSSON. Muscle glycogen utilization during work of different intensities. In: MuscZe MetaboZism during Exercise, edited by B. Pernow and B. Saltin. New York: Plenum, 1971, p. 289-299. 27. SCHADE, D. S., AND R. P. EATON. Glucagon regulation of plasma ketone body concentration in human diabetes. J. CZin. Invest. 56: 1340-1344, 1975. 28. SCHEUER, J., AND C. M. TIPTON. Cardiovascular adaptations to physical training. Annu. Rev. Physiol. 39: 221-251, 1977. 29. SHEPHERD, R. E., W. 0. SEMBROWICH, H. D. GREEN, AND P. D. GOLLNICK. Effect of physical training on control mechanisms of lipolysis in rat fat cell ghosts. J. AppZ. Physiol.: Respirat. Environ. Exercise Physiol. 42: 884-888, 1977. 30. WILLIAMSON, D. H., J. MELLANBY, AND H. A. KREBS. Enzymatic determination of D(-)-/?-hydroxybutyric acid and acetoacetic acid in blood. Biochem. J. 82: 90-96, 1962. 31. WINDER, W. W., K. M. BALDWIN, AND J. 0. HOLLOSZY. Enzymes involved in ketone utilization in different types of muscle: adaptation to exercise. Eur. J. Biochem. 47: 461-467, 1974. 32. WINDER, W. W., K. M. BALDWIN, AND J. 0. HOLLOSZY. Exerciseinduced increase in the capacity of rat skeletal muscle to oxidize ketones. Can. J. Physiol. PharmacoZ. 53: 86-91, 1975.

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Training-induced changes in hormonal and metabolic responses to submaximal exercise.

Training-induced changes in hormonal and metabolic responses to submaximal exercise WILLIAM W. WINDER, ROBERT C. HICKSON, JAMES M. HAGBERG, AL1 A. E...
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