Since 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.

Seven male subjects performed repeated bouts of high-intensity exercise, on a cycle ergometer, before and after 6 d of creatine supplementation (20 g Cr H2O day-1). The exercise protocol consisted of five 6-s exercise periods performed at a fixed exercise intensity, interspersed with 30-s recovery periods (Part I), followed (40 s later) by one 10 s exercise period (Part II) where the ability to maintain power output was evaluated. Muscle biopsies were taken from m. vastus lateralis at rest, and immediately after (i) the fifth 6 s exercise period in Part I and (ii) the 10 s exercise period in Part II. In addition, a series of counter movement (CMJ) and squat (SJ) jumps were performed before and after the administration period. As a result of the creatine supplementation, total muscle creatine [creatine (Cr) + phosphocreatine (PCr)] concentration at rest increased from (mean +/- SEM) 128.7 (4.3) to 151.5 (5.5) mmol kg-1 dry wt (P < 0.05). This was accompanied by a 1.1 (0.5) kg increase in body mass (P < 0.05). After the fifth exercise bout in Part I of the exercise protocol, PCr concentration was higher [69.7 (2.3) vs. 45.6 (7.5) mmol kg-1 dry wt, P < 0.05], and muscle lactate was lower [26.2 (5.5) vs. 44.3 (9.9) mmol kg-1 dry wt, P < 0.05] after vs. before supplementation. In Part II, after creatinine supplementation, subjects were better able to maintain power output during the 10-s exercise period (P < 0.05). There was no change in jump performance as a result of the creatine supplementation (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Seven male subjects performed 15 x 40m sprints, on three occasions, with rest periods of either 120 s (R120), 60 s (R60) or 30 s (R30) between each sprint. Sprint times were recorded with four photo cells placed at 0, 15, 30 and 40 m. The performance data indicated that whereas running speed over the last 10 m of each sprint decreased in all three protocols (after 11 sprints in R120, 7 sprints in R60 and 3 sprints in R30), performance during the initial acceleration period from 0-15 m was only affected with the shortest rest periods increasing from (mean +/- SEM) 2.58 +/- .03 (sprint 1) to 2.78 +/- .04 s (spring 15) (p < .05). Post-exercise blood lactate concentration was not significantly different in R120 (12.1 +/- 1.3 mmol.l-1) and R60 (13.9 +/- 1.2 mmol.l-1), but a higher concentration was found in R30 (17.2 +/- .7 mmol.l-1) (p < .05). After 6 sprints there was no significant difference in blood lactate concentration with the different recovery durations, however, there were significant differences in sprint times at this point, suggesting that blood lactate is a poor predictor of performance during this type of exercise. Although the work bouts could be classified primarily as anaerobic exercise, oxygen uptake measured during rest periods increased to 52, 57 and 66% of maximum oxygen uptake in R120, R60 and R30, respectively. Evidence of adenine nucleotide degradation was provided by plasma hypoxanthine and uric acid concentrations elevated post-exercise in all three protocols. Post-exercise uric acid concentration was not significantly affected by recovery duration.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiological 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 less than 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) mumol.l-1, and UA from 372.8 (SEM 19) and 382.8 (SEM 26), to 458.7 (SEM 40) and 534.6 (SEM 37) mumol.l-1, respectively. Postexercise blood lactate concentrations were higher than pretest values in all three protocols (P less than 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 less than 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 less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined the influence of reduced oxygen availability on the ability to perform repeated bouts of high intensity exercise on a cycle ergometer. Seven male physical education students performed 10 exercise bouts (of 6 s each), interspersed with 30-s recovery periods, under hypoxic and normoxic conditions. The hypoxic condition was carried out in a low pressure chamber at 526 mmHg. Subjects were instructed to try to maintain a target pedalling speed of 140 rev min-1 during each exercise period. The mean power output of the first exercise bout was approximately 950 W. In both experimental conditions, all subjects were able to maintain the target speed for the first 3 s of each of the 10 exercise bouts. During the last 3-s interval of each exercise period the target speed was not maintained in both conditions over the 10 sprints. However, the reduction was greater in the hypoxic condition (P < 0.05). Post-exercise blood lactate accumulation was higher with hypoxia [10.3 (0.7) vs. 8.5 (0.8) mmol l-1, P < 0.05]. Oxygen uptake, measured during the exercise and recovery periods of sprints 6-9, was lower in the hypoxic condition [3.03 (0.2) vs. 3.19 (0.2) 1 min-1, P < 0.05]. These results indicate that a reduction in oxygen availability during high intensity intermittent exercise results in a higher accumulation of blood lactate and a lower oxygen uptake. The ability to maintain a high power output is impaired.