Carbohydrate feeding speeds reversal of enhanced glucose uptake in muscle after exercise

Young, John C.; Garthwaite, Susan M.; Bryan, J.; Cartier, Louis-Jacques; Holloszy, John O.

doi:10.1152/ajpregu.1983.245.5.r684

Cited by 32 publications

(37 citation statements)

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“…Studies in perfused rat hindlimbs (Young et al 1983) and in incubated epitrochlearis muscles (Cartee et al 1989) have demonstrated that the rate at which this increase is reversed in vivo is to a large extent determined by the diet ingested during the post-exercise period. Thus, carbohydrate deprivation slows, whereas carbohydrate feeding speeds reversal of the increase.…”

Section: Discussionmentioning

confidence: 99%

Glucose uptake and transport in contracting, perfused rat muscle with different pre‐contraction glycogen concentrations.

Hespel

Richter

1990

The Journal of Physiology

101

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SUMMARY1. Glucose uptake and transport, muscle glycogen, free glucose and glucose-6-phosphate concentrations were studied in perfused resting and contracting rat skeletal muscle with different pre-contraction glycogen concentrations. Rats were pre-conditioned by a combination of swimming exercise and diet, resulting in either low (glycogen-depleted rats), normal (control rats) or high (supercompensated rats) muscle glycogen concentrations at the time their hindlimbs were perfused.2. Compared with control rats, pre-contraction muscle glycogen concentration was approximately 40% lower in glycogen-depleted rats, whereas it was 40% higher in supercompensated rats. Muscle glycogen break-down correlated positively (r = 0-76; P < 0-001) with pre-contraction muscle glycogen concentration.3. Glucose uptake during contractions was approximately 50% higher in glycogen-depleted hindquarters than in control hindquarters; in supercompensated hindquarters it was 30 % lower. When rats with similar muscle glycogen concentrations were compared, glucose uptake in hindquarters from rats that had exercised on the preceding day was approximately 20 % higher than in hindquarters from rats that had not exercised on the preceding day.4. Muscle membrane glucose transport, as measured by the rate of accumulation of 14C-3-O-methylglucose in the contracting muscles, was 25 % lower in supercompensated than in glycogen-depleted muscles at the onset as well as at the end of the 15 min contraction period. 5. Intracellular concentrations of free glucose and glucose-6-phosphate were higher at rest and during the entire 15-min stimulation period in supercompensated muscles than in glycogen-depleted muscles, and glucose uptake during contractions correlated negatively with free glucose (r = -0'52; P < 0-01) as well as with glucose-6-phosphate (r = -0-49; P < 0-01) concentrations.6. It is concluded that: (a) The rate of glucose uptake in contracting skeletal muscle is dependent on the pre-contraction muscle glycogen concentration. Regulating mechanisms include limitations of membrane glucose transport as well as of glucose metabolism. (b) Contractions on the preceding day have a stimulating effect on glucose uptake during contractions of the same muscles on the next day.

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Section: Discussionmentioning

confidence: 99%

Glucose uptake and transport in contracting, perfused rat muscle with different pre‐contraction glycogen concentrations.

Hespel

Richter

1990

The Journal of Physiology

101

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“…Glucose uptake was markedly increased 60 min after exercise. Eighteen hours later, only ϳ50% of the increase in glucose uptake had worn off in rats fed a carbohydrate-free diet, whereas the increase in uptake had completely reversed in rats fed carbohydrate to raise muscle glycogen (68). Because there was no insulin in the perfusion medium, we erroneously attributed the persistent increase in glucose uptake 18 h after exercise to a slowing of reversal of the exercise-induced, insulin-independent increase in glucose uptake as a result of prevention of glycogen repletion.…”

Section: Persistent Effect Of Exercise On Muscle Glucose Transportmentioning

confidence: 99%

“…It was not clear whether this persistent effect of exercise was due to a persistent increase in insulin action or to a persistence of the exercise-induced, insulin independent increase in glucose transport that was additive to the effect of insulin. A follow-up experiment was, therefore, performed (68). Rats were exercised to deplete glycogen, and glucose uptake by perfused muscles was measured 60 min and 18 h after exercise in the absence of insulin.…”

Section: Persistent Effect Of Exercise On Muscle Glucose Transportmentioning

confidence: 99%

Exercise-induced increase in muscle insulin sensitivity

Holloszy¹

2005

Journal of Applied Physiology

375

278

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“…To try to distinguish between these possibilities, Jack Young and others in my lab exercised rats to deplete muscle glycogen and measured glucose uptake and 3-MG accumulation by their perfused muscles 1 h or 18 h later (133). Both glucose uptake and 3-MG accumulation were markedly increased 60 min after exercise.…”

Section: Reversal Of Enhanced Glucose Uptake After Exercisementioning

confidence: 99%

A forty-year memoir of research on the regulation of glucose transport into muscle

Holloszy

2003

American Journal of Physiology-Endocrinology and Metabolism

112

111

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Holloszy, John O.A forty-year memoir of research on the regulation of glucose transport into muscle. Am J Physiol Endocrinol Metab 284: E453-E467, 2003; 10.1152/ajpendo.00463.2002.-This historical review describes the research on the regulation of glucose transport in skeletal muscle conducted in my laboratory and in collaboration with a number of colleagues in other laboratories. This research includes studies of stimulation of glucose transport, GLUT4 translocation, and GLUT4 expression by exercise/muscle contractions, the role of Ca 2ϩ in these processes, and the interactions between the effects of exercise and insulin. Among the last are the additive effects of insulin and contractions on glucose transport and GLUT4 translocation and the increases in muscle insulin sensitivity and responsiveness induced by exercise.MY FRIEND, MIKE MUECKLER, in his role as Editor of the American Journal of Physiology-Endocrinology and Metabolism, asked me to write this review in the form of a memoir describing my research on glucose transport and metabolism in muscle. As this is a personal history rather than a general review, I hope that my colleagues working in this area will forgive me for focusing primarily on the work of my laboratory. There are a number of broad reviews of this area available (17,35,54,65,69,117,122,134). HOW IT BEGANDuring medical school and specialty training in internal medicine and endocrinology/metabolism, I became interested in the concept that the chronic metabolic diseases of advancing age, atherosclerosis, type 2 diabetes, and hypertension, are largely due to lifestyle and environmental factors and, therefore, to a considerable extent, preventable. In addition to the evidence regarding the role of diet, studies by Jeremy Morris and others comparing physically active and inactive people suggested that exercise deficiency might be playing a role. As a consequence of my interest in the role of exercise deficiency in the development of coronary atherosclerosis, I was recruited by the Heart Disease Control Program of the United States Public Health Service (USPHS) in 1961 and stationed at Dr. Tom Cureton's Physical Fitness Research Laboratory at the University of Illinois. Tom Cureton was a pioneer in the area of endurance exercise training, and he and his graduate students conducted a noon hour exercise program for middle-aged university faculty and Champaign-Urbana businessmen.My assignment was to organize and conduct studies on the effects of the exercise program on risk factors and heart function. These studies were conducted with the help of Jim Skinner, who was one of Cureton's graduate students, and other members of the Fitness Research Laboratory. We found that exercise lowered serum triglycerides and improved heart function (70,71,118). However, what really fascinated me was the remarkable and rapid improvement in exercise capacity and endurance that occurred in response to the exercise training. This phenomenon so intrigued me that I decided to investigate the underlying biological mechani...

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Carbohydrate feeding speeds reversal of enhanced glucose uptake in muscle after exercise

Cited by 32 publications

References 0 publications

Glucose uptake and transport in contracting, perfused rat muscle with different pre‐contraction glycogen concentrations.

Glucose uptake and transport in contracting, perfused rat muscle with different pre‐contraction glycogen concentrations.

Exercise-induced increase in muscle insulin sensitivity

A forty-year memoir of research on the regulation of glucose transport into muscle

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