Muscle glycogen repletion from endogenous carbon sources during recovery from high intensity exercise in the fasted rat

1996 ◽  
Vol 157 (4) ◽  
pp. 427-434 ◽  
Author(s):  
S. NIKOLOVSKI ◽  
D. L. FAULKNER ◽  
T. N. PALMER ◽  
P. A. FOURNIER
1987 ◽  
Vol 253 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
E. M. Peters Futre ◽  
T. D. Noakes ◽  
R. I. Raine ◽  
S. E. Terblanche

High-intensity intermittent bicycle exercise was used to deplete muscle glycogen levels by 70% and elevate blood lactate levels to greater than 13.0 mmol/l. Thereafter subjects either cycled with one leg for 45 min followed by 45 min of passive recovery (partially active recovery) or rested for 90 min (passive recovery). During the first 45 min of partially active recovery 1) blood lactate (P less than 0.05) and pH levels (P less than 0.05) returned more rapidly to preexercise values than during passive recovery, 2) the rate of net glycogen resynthesis (0.28 mumol . g-1 . min-1) was the same in both legs, and 3) muscle lactate levels were significantly lower (P less than 0.05) in the passive than in the active leg. Thereafter the rate of net muscle glycogen resynthesis was unchanged (0.26 mumol . g-1 . min-1) and lactate removal could theoretically account for only 18% of the glycogen resynthesized. Overall, the rate of muscle glycogen resynthesis and muscle lactate removal was not different from that measured during passive recovery. After high-intensity exercise 1) glycogen repletion is not impeded by light exercise, and 2) blood glucose is an important substrate for glycogen resynthesis.


2001 ◽  
Vol 280 (1) ◽  
pp. E83-E91 ◽  
Author(s):  
Luis D. M. C.-B. Ferreira ◽  
Lambert Bräu ◽  
Sasha Nikolovski ◽  
Ghazala Raja ◽  
T. Norman Palmer ◽  
...  

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.


1997 ◽  
Vol 322 (1) ◽  
pp. 303-308 ◽  
Author(s):  
Lambert BRÄU ◽  
Luis D. M. C. B. FERREIRA ◽  
Sasha NIKOLOVSKI ◽  
Ghazala RAJA ◽  
T. Norman PALMER ◽  
...  

The aim of this study was to determine the role of the phosphorylation state of glycogen synthase and glycogen phosphorylase in the regulation of muscle glycogen repletion in fasted animals recovering from high-intensity exercise. Groups of rats were swum to exhaustion and allowed to recover for up to 120 min without access to food. Swimming to exhaustion caused substantial glycogen breakdown and lactate accumulation in the red, white and mixed gastrocnemius muscles, whereas the glycogen content in the soleus muscle remained stable. During the first 40 min of recovery, significant repletion of glycogen occurred in all muscles examined except the soleus muscle. At the onset of recovery, the activity ratios and fractional velocities of glycogen synthase in the red, white and mixed gastrocnemius muscles were higher than basal, but returned to pre-exercise levels within 20 min after exercise. In contrast, after exercise the activity ratios of glycogen phosphorylase in the same muscles were lower than basal, and increased to pre-exercise levels within 20 min. This pattern of changes in glycogen synthase and phosphorylase activities, never reported before, suggests that the integrated regulation of the phosphorylation state of both glycogen synthase and phosphorylase might be involved in the control of glycogen deposition after high-intensity exercise.


2021 ◽  
Author(s):  
Jeppe F. Vigh-Larsen ◽  
Niels Ørtenblad ◽  
Lawrence L. Spriet ◽  
Kristian Overgaard ◽  
Magni Mohr

1999 ◽  
Vol 165 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Balsom ◽  
Gaitanos ◽  
Söderlund ◽  
Ekblom

2019 ◽  
Vol 120 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Hamid Mohebbi ◽  
Iain T. Campbell ◽  
Marie A. Keegan ◽  
James J. Malone ◽  
Andrew T. Hulton ◽  
...  

Abstract Purpose The effect of hyperglycaemia with and without additional insulin was explored at a low and high intensity of exercise (40% vs 70% VO2peak) on glucose utilization (GUR), carbohydrate oxidation, non-oxidative glucose disposal (NOGD), and muscle glycogen. Methods Eight healthy trained males were exercised for 120 min in four trials, twice at 40% VO2peak and twice at 70% VO2peak, while glucose was infused intravenously (40%G; 70%G) at rates to “clamp” blood glucose at 10 mM. On one occasion at each exercise intensity, insulin was also infused at 40 mU/m2/per min (i.e. 40%GI and 70%GI). The glucose and insulin infusion began 30 min prior to exercise and throughout exercise. A muscle biopsy was taken at the end of exercise for glycogen analysis. Results Hyperglycaemia significantly elevated plasma insulin concentration (p < 0.001), although no difference was observed between the exercise intensities. Insulin infusion during both mild and severe exercise resulted in increased insulin concentrations (p < 0.01) and GUR (p < 0.01) compared with glucose (40%GI by 25.2%; 70%GI by 26.2%), but failed to significantly affect carbohydrate, fat and protein oxidation. NOGD was significantly higher for GI trials at both intensities (p < 0.05) with storage occurring during both lower intensities (62.7 ± 19.6 g 40%GI; 127 ± 20.7 g 40%GI) and 70%GI (29.0 ± 20.0 g). Muscle glycogen concentrations were significantly depleted from rest (p < 0.01) after all four trials. Conclusion Hyperinsulinaemia in the presence of hyperglycaemia during both low- and high-intensity exercise promotes GUR and NOGD, but does not significantly affect substrate oxidation.


2000 ◽  
Vol 88 (1) ◽  
pp. 219-225 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Ricardo Mora-Rodriguez ◽  
Lauri O. Byerley ◽  
Edward F. Coyle

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; ∼25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O2 uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (Rd glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 ± 4.6 vs. 38.8 ± 4.0 μmol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 ± 18 vs. 329 ± 15 μmol ⋅ kg− 1 ⋅ min− 1). The coingestion of MCT+CHO did increase ( P < 0.05) Rd glucose at rest compared with CHO (26.9 ± 1.5 vs. 20.7 ± 0.7 μmol ⋅kg− 1 ⋅ min− 1), yet during exercise Rd glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.


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