Abstract

Muscle glycogen content has been associated with the onset of fatigue following prolonged exercise. However, the mechanisms that result in fatigue following glycogen depletion are unclear. PURPOSE In this study, we investigated the hypothesis that muscle glycogen content may influence sarcoplasmic reticulum (SR) Ca2+-handling properties in skeletal muscle during prolonged exercise. METHODS Two groups of untrained volunteers (peak aerobic power; VO2peak; 3.8 and 3.4 L/min, respectively) cycled at 55% of their VO2peak following either a 4-day dietary normal (NCHO; 2354 kcal; 53% CHO; 31% Fat; 16% Protein) diet or a LCHO (1676 kcal; 21% CHO; 57% Fat; 22% Protein) diet. Sarcoplasmic reticulum function was assessed in homogenates prepared from tissue extracted from vastus lateralis at rest and after 30 and 60 min of exercise and at fatigue. RESULTS Pre-exercise muscle glycogen content was reduced (p < 0.01) by 25% in the LCHO group compared to the NCHO group. Muscle glycogen content was also lower (p < 0.01) after 30 and 60 min of exercise in LCHO compared to the matching time points in NCHO, but was not different at fatigue. Exercise reduced (p < 0.05) maximal Ca2+-ATPase activity, Ca2+-uptake and Ca2+-release in both the NCHO and the LCHO groups. However, neither the sensitivity (pCa50) nor the cooperativity (Hill coefficient) of the Ca2+-ATPase enzyme were affected by exercise or by diet. When the different experiments were compared, larger reductions (p < 0.05) in SR Ca2+-uptake rates were found after 30 min of exercise in the LCHO group (−18%) compared to the NCHO group (−8%). Additionally, an 18% greater reduction in Phase 2 Ca2+-release, but not Phase 1 Ca2+-release, was observed after 30 min of exercise in LCHO compared to NCHO. CONCLUSIONS These results indicate that LCHO reduces the time course of exercise-induced reductions in SR Ca2+-handling properties in human skeletal muscle during exercise compared to NCHO. (Supported by Gatorade Sports Science Institute).

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