P. D. Balsom

Creatine in Humans with Special Reference to Creatine Supplementation

SummarySince the discovery of creatine in 1832, it has fascinated scientists with its central role in skeletal muscle metabolism. In humans, over 95% of the total creatine (Crtot) content is located in skeletal muscle, of which approximately a third is in its free (Crf) form. The remainder is present in a phosphorylated (Crphos) form. Crf and Crphos levels in skeletal muscle are subject to individual variations and are influenced by factors such as muscle fibre type, age and disease, but not apparently by training or gender. Daily turnover of creatine to creatinine for a 70kg male has been estimated to be around 2g. Part of this turnover can be replaced through exogenous sources of creatine in foods, especially meat and fish. The remainder is derived via endogenous synthesis from the precursors arginine, glycine and methionine. A century ago, studies with creatine feeding concluded that some of the ingested creatine was retained in the body. Subsequent studies have shown that both Crf and Crphos levels in skeletal muscle can be increased, and performance of high intensity intermittent exercise enhanced, following a period of creatine supplementation. However, neither endurance exercise performance nor maximal oxygen uptake appears to be enhanced. No adverse effects have been identified with short term creatine feeding. Creatine supplementation has been used in the treatment of diseases where creatine synthesis is inhibited.

Creatine supplementation and dynamic high-intensity intermittent exercise

Two intermittent high‐intensity exercise protocols were performed before and after the administration of either creatine or a placebo, and performance characteristics and selected physiological responses were studied. Each exercise protocol consisted of 10 6‐s bouts of high‐intensity cycling at 2 exercise intensities (130 rev/min [EX130]: ∼820 W and 140 rev/min [EX140)]: ∼ 880 W) so that in EX130 the same amount of exercise was performed before and after the administration period, whereas an exercise intensity in EX140 was chosen to induce fatigue over the 10 exercise bouts. Sixteen healthy male subjects were randomly assigned to the 2 experimental groups. A double‐blind design was used in this study. There were no significant changes in the placebo group for any of the measured parameters. Performance towards the end of each exercise bout in EX140 was enhanced following creatine supplementation, as shown by a smaller decline in work output from baseline along the 10 trials. Although more work was performed in EX140, after vs before the administration period, blood lactate accumulation decreased (mean and SEM), from 10.8 (0.5) to 9.1 (0.8) mmol·l−1 and plasma accumulation of hypoxanthine decreased from 21.1 (0.4) to 16.7 (0.8) μmol·l−1, but there was no change in oxygen uptake measured during 3 exercise and recovery periods [3.18 (0–1) vs 3.14 (0.1) l·min−1]. In EX130 blood lactate accumulation decreased, from 7.0 (0.5) to 5.1 (0.5) mmol·l−1, and oxygen uptake was also lower, decreasing from 2.84 (0.1) to 2.78 (0.1) l·min−1. A significant increase in body mass (11 kg: range 0.3 to 2.5 kg) was found in the creatine group. The mechanism responsible for the improved performance with creatine supplementation are postulated to be both a higher initial creatine phosphate content availability and an increased rate of creatine phosphate resynthesis during recovery periods. The lower blood lactate and hypoxanthine accumulation can also be explained by these mechanisms.

Physiological responses to maximal intensity intermittent exercise

SummaryPhysiological responses to repeated bouts of short duration maximal-intensity exercise were evaluated. Seven male subjects performed three exercise protocols, on separate days, with either 15 (S15), 30 (S30) or 40 (S40) m sprints repeated every 30 s. Plasma hypoxanthine (HX) and uric acid (UA), and blood lactate concentrations were evaluated pre- and postexercise. Oxygen uptake was measured immediately after the last sprint in each protocol. Sprint times were recorded to analyse changes in performance over the trials. Mean plasma concentrations of HX and UA increased during S30 and S40 (P<0.05), HX increasing from 2.9 (SEM 1.0) and 4.1 (SEM 0.9), to 25.4 (SEM 7.8) and 42.7 (SEM 7.5) µmol · l−1, and UA from 372.8 (SEM 19) and 382.8 (SEM 26), to 458.7 (SEM 40) and 534.6 (SEM 37) µmol · l−1, respectively. Postexercise blood lactate concentrations were higher than pretest values in all three protocols (P<0.05), increasing to 6.8 (SEM 1.5), 13.9 (SEM 1.7) and 16.8 (SEM 1.1) mmol · l−1 in S15, S30 and S40, respectively. There was no significant difference between oxygen uptake immediately after S30 [3.2 (SEM 0.1) l · min−1] and S40 [3.3 (SEM 0.4) l · min−1], but a lower value [2.6 (SEM 0.1) l · min−1] was found after S15 (P<0.05). The time of the last sprint [2.63 (SEM 0.04) s] in S15 was not significantly different from that of the first [2.62 (SEM 0.02) s]. However, in S30 and S40 sprint times increased from 4.46 (SEM 0.04) and 5.61 (SEM 0.07) s (first) to 4.66 (SEM 0.05) and 6.19 (SEM 0.09) s (last), respectively (P<0.05). These data showed that with a fixed 30-s intervening rest period, physiological and performance responses to repeated sprints were markedly influenced by sprint distance. While 15-m-sprints could be repeated every 30 s without decreases in performance, 40-m sprint times increased after the third sprint (P<0.05) and this exercise pattern was associated with a net loss to the adenine nucleotide pool.