Effects of endurance exercise training on muscle glycogen accumulation in humans

1999 ◽  
Vol 87 (1) ◽  
pp. 222-226 ◽  
Author(s):  
Jeffrey S. Greiwe ◽  
Robert C. Hickner ◽  
Polly A. Hansen ◽  
Susan B. Racette ◽  
May M. Chen ◽  
...  

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 ± 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher ( P < 0.05) in the trained than in the untrained state: 10.5 ± 0.2 and 4.5 ± 1.3 mmol ⋅ kg wet wt−1 ⋅ h−1, respectively. Muscle glycogen concentration was higher ( P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher ( P < 0.05) in the trained than in the untrained state (10.7 ± 1.2 and 4.7 ± 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise ( r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.

1997 ◽  
Vol 82 (2) ◽  
pp. 711-715 ◽  
Author(s):  
Akira Nakatani ◽  
Dong-Ho Han ◽  
Polly A. Hansen ◽  
Lorraine A. Nolte ◽  
Helen H. Host ◽  
...  

Nakatani, Akira, Dong-Ho Han, Polly A. Hansen, Lorraine A. Nolte, Helen H. Host, Robert C. Hickner, and John O. Holloszy.Effect of endurance exercise training on muscle glycogen supercompensation in rats. J. Appl. Physiol. 82(2): 711–715, 1997.—The purpose of this study was to test the hypothesis that the rate and extent of glycogen supercompensation in skeletal muscle are increased by endurance exercise training. Rats were trained by using a 5-wk-long swimming program in which the duration of swimming was gradually increased to 6 h/day over 3 wk and then maintained at 6 h/day for an additional 2 wk. Glycogen repletion was measured in trained and untrained rats after a glycogen-depleting bout of exercise. The rats were given a rodent chow diet plus 5% sucrose in their drinking water ad libitum during the recovery period. There were remarkable differences in both the rates of glycogen accumulation and the glycogen concentrations attained in the two groups. The concentration of glycogen in epitrochlearis muscle averaged 13.1 ± 0.9 mg/g wet wt in the untrained group and 31.7 ± 2.7 mg/g in the trained group ( P < 0.001) 24 h after the exercise. This difference could not be explained by a training effect on glycogen synthase. The training induced ∼50% increases in muscle GLUT-4 glucose transporter protein and in hexokinase activity in epitrochlearis muscles. We conclude that endurance exercise training results in increases in both the rate and magnitude of muscle glycogen supercompensation in rats.


1997 ◽  
Vol 83 (3) ◽  
pp. 897-903 ◽  
Author(s):  
R. C. Hickner ◽  
J. S. Fisher ◽  
P. A. Hansen ◽  
S. B. Racette ◽  
C. M. Mier ◽  
...  

Hickner, R. C., J. S. Fisher, P. A. Hansen, S. B. Racette, C. M. Mier, M. J. Turner, and J. O. Holloszy. Muscle glycogen accumulation after endurance exercise in trained and untrained individuals. J. Appl. Physiol. 83(3): 897–903, 1997.—Muscle glycogen accumulation was determined in six trained cyclists (Trn) and six untrained subjects (UT) at 6 and either 48 or 72 h after 2 h of cycling exercise at ∼75% peak O2 uptake (V˙o 2 peak), which terminated with five 1-min sprints. Subjects ate 10 g carbohydrate ⋅ kg−1 ⋅ day−1for 48–72 h postexercise. Muscle glycogen accumulation averaged 71 ± 9 (SE) mmol/kg (Trn) and 31 ± 9 mmol/kg (UT) during the first 6 h postexercise ( P < 0.01) and 79 ± 22 mmol/kg (Trn) and 60 ± 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogen concentration was 164 ± 21 mmol/kg (Trn) and 99 ± 16 mmol/kg (UT) 48–72 h postexercise ( P < 0.05). Muscle GLUT-4 content immediately postexercise was threefold higher in Trn than in UT ( P < 0.05) and correlated with glycogen accumulation rates ( r = 0.66, P < 0.05). Glycogen synthase in the active I form was 2.5 ± 0.5, 3.3 ± 0.5, and 1.0 ± 0.3 μmol ⋅ g−1 ⋅ min−1in Trn at 0, 6, and 48 or 72 h postexercise, respectively; corresponding values were 1.2 ± 0.3, 2.7 ± 0.5, and 1.6 ± 0.3 μmol ⋅ g−1 ⋅ min−1in UT ( P < 0.05 at 0 h). Plasma insulin and plasma C-peptide area under the curve were lower in Trn than in UT over the first 6 h postexercise ( P < 0.05). Plasma creatine kinase concentrations were 125 ± 25 IU/l (Trn) and 91 ± 9 IU/l (UT) preexercise and 112 ± 14 IU/l (Trn) and 144 ± 22 IU/l (UT; P < 0.05 vs. preexercise) at 48–72 h postexercise (normal: 30–200 IU/l). We conclude that endurance exercise training results in an increased ability to accumulate muscle glycogen after exercise.


2000 ◽  
Vol 278 (4) ◽  
pp. E588-E592 ◽  
Author(s):  
Jian-Ming Ren ◽  
Nicole Barucci ◽  
Bess A. Marshall ◽  
Polly Hansen ◽  
Mike M. Mueckler ◽  
...  

The purpose of the present study was to determine the rates of muscle glycogenolysis and glycogenesis during and after exercise in GLUT-1 transgenic mice and their age-matched littermates. Male transgenic mice (TG) expressing a high level of human GLUT-1 and their nontransgenic (NT) littermates underwent 3 h of swimming. Glycogen concentration was determined in gastrocnemius and extensor digitorum longus (EDL) muscles before exercise and at 0, 5, and 24 h postexercise, during which food (chow) and 10% glucose solution (as drinking water) were provided. Exercise resulted in ∼90% reduction in muscle glycogen in both NT (from 11.2 ± 1.4 to 2.1 ± 1.3 μmol/g) and TG (from 99.3 ± 4.7 to 11.8 ± 4.3 μmol/g) in gastrocnemius muscle. During recovery from exercise, the glycogen concentration increased to 38.2 ± 7.3 (5 h postexercise) and 40.5 ± 2.8 μmol/g (24 h postexercise) in NT mice. In TG mice, however, the increase in muscle glycogen concentration during recovery was greater (to 57.5 ± 7.4 and 152.1 ± 15.7 μmol/g at 5 and 24 h postexercise, respectively). Similar results were obtained from EDL muscle. The rate of 2-deoxyglucose uptake measured in isolated EDL muscles was 7- to 10-fold higher in TG mice at rest and at 0 and 5 h postexercise. There was no difference in muscle glycogen synthase activation measured in gastrocnemius muscles between NT and TG mice immediately after exercise. These results demonstrate that the rate of muscle glycogen accumulation postexercise exhibits two phases in TG: 1) an early phase (0–5 h), with rapid glycogen accumulation similar to that of NT mice, and 2) a progressive increase in muscle glycogen concentration, which differs from that of NT mice, during the second phase (5–24 h). Our data suggest that the high level of steady-state muscle glycogen in TG mice is due to the increase in muscle glucose transport activity.


1999 ◽  
Vol 31 (Supplement) ◽  
pp. S54 ◽  
Author(s):  
J. S. Greiwe ◽  
R. C. Hickner ◽  
P. A. Hansen ◽  
S. B. Racette ◽  
M. M. Chen ◽  
...  

1990 ◽  
Vol 258 (3) ◽  
pp. H842-H847 ◽  
Author(s):  
S. E. DiCarlo ◽  
V. S. Bishop

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)


2002 ◽  
Vol 92 (6) ◽  
pp. 2368-2374 ◽  
Author(s):  
Annette N. Senitko ◽  
Nisha Charkoudian ◽  
John R. Halliwill

In sedentary individuals, postexercise hypotension after a single bout of aerobic exercise is due to a peripheral vasodilation. Endurance exercise training has the potential to modify this response and perhaps reduce the degree of postexercise hypotension. We tested the hypothesis that endurance exercise-trained men and women would have blunted postexercise hypotension compared with sedentary subjects but that the mechanism of hypotension would be similar (i.e., vasodilation). We studied 16 endurance-trained and 16 sedentary men and women. Arterial pressure, cardiac output, and total peripheral resistance were determined before and after a single 60-min bout of exercise at 60% peak oxygen consumption. All groups exhibited a similar degree of postexercise hypotension (∼4–5 mmHg; P < 0.05 vs. preexercise). In sedentary men and women, hypotension was the result of vasodilation (Δresistance: −8.9 ± 2.2%). In endurance-trained women, hypotension was also the result of vasodilation (−8.1 ± 4.1%). However, in endurance-trained men, hypotension was the result of a reduced cardiac output (−5.2 ± 2.4%; P < 0.05 vs. all others) and vasodilation was absent (−0.7 ± 3.3%; P < 0.05 vs. all others). Thus we conclude the magnitude of postexercise hypotension is similar in sedentary and endurance-trained men and women but that endurance-trained men and women achieve this fall in pressure via different mechanisms.


1984 ◽  
Vol 56 (4) ◽  
pp. 831-838 ◽  
Author(s):  
J. O. Holloszy ◽  
E. F. Coyle

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.


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