Moderate Intensity Endurance Exercise Training Increases Muscle Glycogen Content but Does Not Alter Substrate Oxidation in C57BL6 Mice

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.

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Progressive increase in human skeletal muscle AMPKα2 activity and ACC phosphorylation during exercise

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00101.2001 ◽

2002 ◽

Vol 282 (3) ◽

pp. E688-E694 ◽

Cited By ~ 95

Author(s):

T. J. Stephens ◽

Z.-P. Chen ◽

B. J. Canny ◽

B. J. Michell ◽

B. E. Kemp ◽

...

Keyword(s):

Skeletal Muscle ◽

Muscle Glycogen ◽

Human Skeletal Muscle ◽

Glycogen Content ◽

Vastus Lateralis ◽

Moderate Intensity ◽

Moderate Intensity Exercise ◽

Western Blots ◽

Muscle Glycogen Content ◽

Muscle Creatine

The effect of prolonged moderate-intensity exercise on human skeletal muscle AMP-activated protein kinase (AMPK)α1 and -α2 activity and acetyl-CoA carboxylase (ACCβ) and neuronal nitric oxide synthase (nNOSμ) phosphorylation was investigated. Seven active healthy individuals cycled for 30 min at a workload requiring 62.8 ± 1.3% of peak O2consumption (V˙o 2 peak) with muscle biopsies obtained from the vastus lateralis at rest and at 5 and 30 min of exercise. AMPKα1 activity was not altered by exercise; however, AMPKα2 activity was significantly ( P < 0.05) elevated after 5 min (∼2-fold), and further elevated ( P < 0.05) after 30 min (∼3-fold) of exercise. ACCβ phosphorylation was increased ( P < 0.05) after 5 min (∼18-fold compared with rest) and increased ( P< 0.05) further after 30 min of exercise (∼36-fold compared with rest). Increases in AMPKα2 activity were significantly correlated with both increases in ACCβ phosphorylation and reductions in muscle glycogen content. Fat oxidation tended ( P = 0.058) to increase progressively during exercise. Muscle creatine phosphate was lower ( P < 0.05), and muscle creatine, calculated free AMP, and free AMP-to-ATP ratio were higher ( P < 0.05) at both 5 and 30 min of exercise compared with those at rest. At 30 min of exercise, the values of these metabolites were not significantly different from those at 5 min of exercise. Phosphorylation of nNOSμ was variable, and despite the mean doubling with exercise, statistically significance was not achieved ( P = 0.304). Western blots indicated that AMPKα2 was associated with both nNOSμ and ACCβ consistent with them both being substrates of AMPKα2 in vivo. In conclusion, AMPKα2 activity and ACCβ phosphorylation increase progressively during moderate exercise at ∼60% of V˙o 2 peak in humans, with these responses more closely coupled to muscle glycogen content than muscle AMP/ATP ratio.

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Effects of endurance exercise-training on single-fiber contractile properties of insulin-treated streptozotocin-induced diabetic rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.01233.2004 ◽

2005 ◽

Vol 99 (2) ◽

pp. 472-478 ◽

Cited By ~ 14

Author(s):

Otto A. Sanchez ◽

LeAnn M. Snow ◽

Dawn A. Lowe ◽

Robert C. Serfass ◽

LaDora V. Thompson

Keyword(s):

Exercise Training ◽

Endurance Exercise ◽

Extensor Digitorum Longus ◽

Diabetic Rats ◽

Contractile Properties ◽

Extensor Digitorum ◽

Single Fiber ◽

Moderate Intensity ◽

Specific Tension ◽

Endurance Exercise Training

The purpose of this study was to characterize the contractile properties of individual skinned muscle fibers from insulin-treated streptozotocin-induced diabetic rats after an endurance exercise training program. We hypothesized that single-fiber contractile function would decrease in the diabetic sedentary rats and that endurance exercise would preserve the function. In the study, 28 rats were assigned to either a nondiabetic sedentary, a nondiabetic exercise, a diabetic sedentary, or a diabetic exercise group. Rats in the diabetic groups received subcutaneous intermediate-lasting insulin daily. The exercise-trained rats ran on a treadmill at a moderate intensity for 60 min, five times per week. After 12 wk, the extensor digitorum longus and soleus muscles were dissected. Single-fiber diameter, Ca2+-activated peak force, specific tension, activation threshold, and pCa50 as well as the myosin heavy chain isoform expression (MHC) were determined. We found that in MHC type II fibers from extensor digitorum longus muscle, diameters were significantly smaller from diabetic sedentary rats compared with nondiabetic sedentary rats ( P < 0.001). Among the nondiabetic rats, fiber diameters were smaller with exercise ( P = 0.038). The absolute force-generating capacity of single fibers was lower in muscles from diabetic rats. There was greater specific tension (force normalized to cross-sectional area) by fibers from the rats that followed an endurance exercise program compared with sedentary. From the results, we conclude that alterations in the properties of contractile proteins are not implicated in the decrease in strength associated with diabetes and that endurance-exercise training does not prevent or increase muscle weakness in diabetic rats.

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Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

Journal of Applied Physiology ◽

10.1152/jappl.1984.56.4.831 ◽

1984 ◽

Vol 56 (4) ◽

pp. 831-838 ◽

Cited By ~ 1018

Author(s):

J. O. Holloszy ◽

E. F. Coyle

Keyword(s):

Skeletal Muscle ◽

Blood Glucose ◽

Exercise Training ◽

Endurance Exercise ◽

Muscle Glycogen ◽

Lactate Production ◽

Strenuous Exercise ◽

Mitochondrial Content ◽

Respiratory Capacity ◽

Endurance Exercise Training

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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Skeletal Muscle Glycogen Content at Rest and During Endurance Exercise in Humans: A Meta-Analysis

Sports Medicine ◽

10.1007/s40279-018-0941-1 ◽

2018 ◽

Vol 48 (9) ◽

pp. 2091-2102 ◽

Cited By ~ 23

Author(s):

José L. Areta ◽

Will G. Hopkins

Keyword(s):

Skeletal Muscle ◽

Endurance Exercise ◽

Muscle Glycogen ◽

Glycogen Content ◽

Meta Analysis ◽

Muscle Glycogen Content ◽

Skeletal Muscle Glycogen ◽

Exercise In Humans

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The effect of exercise training on leptin levels in obese males

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.274.2.e280 ◽

1998 ◽

Vol 274 (2) ◽

pp. E280-E286 ◽

Cited By ~ 31

Author(s):

W. J. Pasman ◽

M. S. Westerterp-Plantenga ◽

W. H. M. Saris

Keyword(s):

Exercise Training ◽

Body Fat ◽

Endurance Exercise ◽

Exercise Program ◽

Moderate Intensity ◽

Body Fat Percentage ◽

Fat Percentage ◽

Insulin Levels ◽

Endurance Exercise Training ◽

Plasma Leptin

The effect of endurance training on plasma leptin levels was investigated in 15 obese male subjects (age 37.3 ± 5.2 yr, body weight 96.5 ± 13.6 kg, and body mass index 29.8 ± 3.0 kg/m2) in a weight loss and exercise program. After 4 mo of treatment consisting of a very low energy diet (VLED) and endurance exercise training (3–4 times weekly, 1 h sessions, moderate intensity), two groups were formed. One group continued the exercise sessions (trained subjects, n = 7) and the other group stopped with the exercise program (control, n= 8). Measurements of anthropometry, aerobic power, and fasted blood samples were executed at fixed time points (0, 2, 4, 10, and 16 mo). With partial regression analysis, keeping the changes in insulin and body fat percentage constant, it was shown that the number of hours of exercise training was significantly correlated with changes in leptin levels, during the 16-mo period ( r = 0.56, P < 0.05). Changes in insulin levels were significantly related to the changes in leptin levels ( r = 0.47, P < 0.05), which were less for changes in body fat percentage ( r = 0.42, P = 0.07). During the VLED, the change in insulin concentration affected leptin levels significantly ( r = 0.79) but changes in body fat percentage were not noted. It is concluded that endurance exercise training decreased plasma leptin levels independently of changes in plasma insulin levels and body fat percentage.

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