1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367–74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise.
2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 × 6 g of glucose/day, n = 6) or creatine (4 × 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment
3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 (P <0.05), throughout the whole of exercise bouts 2 (P <0.01), 3 (P <0.05) and 4 (P = 0.057) and during contractions 11–20 of the final exercise bout (P <0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels.
4. There is evidence to suggest that the decrease in the degree of muscle torque loss after dietary creatine supplementation may be a consequence of a creatine-induced acceleration of skeletal muscle phosphocreatine resynthesis. It is postulated that an increased availability of phosphocreatine would maintain better the required rate of ATP demand during contraction. This is supported by the observed lower accumulation of plasma ammonia during exercise after creatine ingestion.
