ELEVATED MUSCLE GLYCOGEN AND ANAEROBIC ENERGY-PRODUCTION DURING EXHAUSTIVE EXERCISE IN MAN

1. The effect of elevated muscle glycogen on anaerobic energy production, and glycogenolytic and glycolytic rates was examined in man by using the one-legged knee extension model, which enables evaluation of metabolism in a well-defined muscle group. 2. Six subjects performed very intense exercise to exhaustion (EX1) with one leg with normal glycogen (control) and one with a very high concentration (HG). With each leg, the exhaustive exercise was repeated after 1 h of recovery (EX2). Prior to and immediately after each exercise bout, a muscle biopsy was taken from m. vastus lateralis of the active leg for determination of glycogen, lactate, creatine phosphate (CP) and nucleotide concentrations. Measurements of leg blood flow and femoral arterial-venous differences for oxygen content, lactate, glucose, free fatty acids and potassium were performed before and regularly during the exhaustive exercises. 3. Muscle glycogen concentration prior to EX1 was 87.0 and 176.8 mmol (kg wet wt)-1 for the control and HG leg, respectively, and the decreases during exercise were 26.3 (control) and 25.6 (HG) mmol (kg wet wt)-1. The net glycogen utilization rate was not related to pre-exercise muscle glycogen concentration. Muscle lactate concentration at the end of EXI was 18.8 (control) and 16.1 (HG) mmol (kg wet wt)-1, and the net lactate production (including lactate release) was 26.5 (control) and 23.6 (HG) mmol (kg wet wt)-1. Rate of lactate production was unrelated to initial muscle glycogen level. Time to exhaustion for EX1 was the same for the control leg (2.82 min) and HG leg (2.92 min). 4. Muscle glycogen concentration before EX2 was 14 mmol (kg wet wt)-1 lower than prior to EXI. During EX2 the muscle glycogen decline of 19.6 mmol (kg wet wt)-1 for the control leg was less than for the HG leg (26.2 mmol (kg wet wt)-1). The muscle lactate concentrations at the end of EX2 were about 7-8 mmol (kg wet wt)-l lower compared to EX1, and the net lactate production was reduced by 40 %. The exercise time during EX2 was 0.35 min shorter for the control leg, while no difference was observed for the HG leg. 5. Total reduction in ATP and CP was similar during the four exercise bouts, while a higher accumulation of inosine monophosphate (IMP) occurred during EX2 for the control leg (0.72 mmol (kg wet wt)-1) compared to the HG leg (0.20 mmol (kg wet wt)-1). There was no difference in leg oxygen uptake or leg oxygen deficit between the exercise bouts. 6. It is concluded that: (a) elevated muscle glycogen does not influence glycogenolytic or glycolytic rates and fatigue; (b) previous intense exercise reduces lactate production and time to exhaustion in spite of recovery being long enough for lactate (pH) and K+ to return to pre-exercise levels. These findings suggest that muscle and blood lactate concentrations are not the only crucial factors for inhibiting anaerobic carbohydrate usage during intense skeletal muscle contractions and the development of fatigue.