Twenty-three healthy male subjects 20–36 yr of age (mean 23.37 ± 4.01) participated in the study. Written informed consent was obtained from each subject in compliance with the Institute Review Board of the University of Florida. Subjects were physically active but not specifically trained for the isokinetic dynamometer. Exclusion criteria included diagnosis for any orthopedic, neurological, or systemic problem, and a history of creatine and anabolic steroid use.
Subjects participated in two exercise test sessions (PRE and POST supplementation). Subjects were randomly assigned to either creatine supplementation (CRE) or a placebo (PLA). CRE and PLA treatments were administered in a double-blind fashion after the initial test session (T1). Subjects were initially familiarized with the exercise protocol to establish reproducible torque measures. Maximal voluntary contractions (MVC) were performed consisting of both knee flexion and extension movements at an angular velocity of 180°·s−1 on a Cybex II isokinetic dynamometer (Lumex Inc., Ronkokoma, NY). Calibration of the dynamometer with known weights was performed at each test session. All settings of the Cybex equipment were recorded individually for each subject and used consistently for both familiarity, PRE, and POST test sessions. Each subject’s body weight was recorded before each session.
Subjects returned 4–5 d after the familiarity session to perform the PRE test (TL), and then a second time for the POST test (T2) after a 5-d regimen of either the CRE or the PLA. All subjects were tested using their right extremity. Subjects were asked not to alter their diet or activity levels between tests and to avoid any intensive lower extremity exercise for at least 2 d (48 h) before their testing sessions.
Each test consisted of five sets of 30 maximal voluntary contractions with a 1-min rest between sets. Before each test subjects performed a warm-up of 13 repetitions (REPS), 3 REPS at approximately 50% MVC, and 10 REPS at 100% MVC, and then rested 5 min before testing. Soderlund and Hultman (26) reported that resynthesis of depleted levels of CrP were complete after 5 min of rest.
During testing, each subject was secured in a sitting position with a strap to restrain the thigh of the test leg and the upper trunk. Subjects were instructed to fully extend and flex the knee and to work maximally during each set of exercises. Strong verbal encouragement was given throughout the test session. After each set, subjects were required to take 1 min of rest before the onset of the next set. The knee strap was released during each rest period to ensure unrestricted blood flow to the quadriceps. Occlusion of circulation has been shown to decrease force output effecting the rate of glycogenolysis and ATP turnover rate (11).
After T1, subjects were instructed to take either the CRE (5 g creatine + 1 g glucose) or PLA (6 g glucose) 4 times daily over 5 consecutive days. Subjects were instructed to dissolve their supplement in warm water, grape juice, or sports drink and to avoid consumption of the supplement with caffeinated beverages. It has been demonstrated that caffeine eliminates creatine’s ergogenic effects (31). On the day after the final supplemental dose, subjects returned for T2.
The data is shown as the mean ± SD. A three-way mixed ANOVA was performed with one between factor for the main effects, group (placebo vs creatine), and two within factors, time (pre- and post-test supplementation), and sets (1–5). A priori comparisons of T1 and T2 of the fourth and fifth sets for CRE and PLA were performed. Body weight at T1 and T2 for the CRE and PLA groups were analyzed using a paired t-test with a Bonferroni’s correction.
There was a significant difference (P < 0.005) in PRE and POST body weights of the CRE group expressed in kg (PRE: 79.54 ± 14.31) and (POST: 80.41 ± 14.04) with a mean increase of 0.86 kg. The PRE and POST body weight changes of the PLA group were nonsignificant (P > 0.05) (PRE: 82.0 ± 13.10) and (POST: 82.14 ± 13.45).
The effects of group, time, and set PRE to POST supplementation were nonsignificant (P > 0.05) (Fig. 1). Although, there was an increase in peak torque of approximately 3% between PRE and POST measurements for CRE and PLA (F (1,21) = 4.56, P = 0.04), with no difference between groups (Table 1). There was a significant set effect (F (4,21) = 236.52, P < 0.05), with each set declining similarly in both groups over the course of five sets to approximately 50% of the maximum torque recorded in set one (Fig. 1). The a priori contrasts comparing performance for the fourth and fifth sets of the CRE and PLA, pre- to post-supplementation were also nonsignificant (F (1,21) = 0.357, P > 0.05;F (1,21) = 1.93, P > 0.05).
Assurance of creatine loading is difficult without muscle biopsies. Increases in body weight have, however, implicated water retention during initial creatine loading. Harris et al. (14) demonstrated phosphocreatine loading in the CRE group, reporting a 6.4 mmol·kg−1 increase in mean PCr content with creatine uptake greatest during the first 2 d of supplementation. Significant increases in body weight averaging 1 kg during 6 d of creatine supplementation have been demonstrated (1). Hultman et al. (17) demonstrated weight gain was from water retention due to a marked decline in urine output during creatine supplementation. In our study, the magnitude of the body weight increase was significant for the creatine group which was similar to other studies (8,10,17).
Our data indicate that 5 d of creatine supplementation had no effect on maintaining peak isokinetic torque. The modest increase in torque (∼3%) from PRE to POST supplementation can possibly be attributed to a learning effect, because no difference was demonstrated between the CRE and PLA groups.
Our finding that creatine did not reduce the loss of torque across sets when comparing CRE and PLA are in contrast to those of Greenhaff et al. (12). Greenhaff et al. (12) found that creatine significantly reduced the torque loss at the second (P < 0.01) and third (P < 0.05) sets of exercise, but not the first, fourth, or fifth sets. They also indicated that portions of sets 1, 4, and 5 were significantly different by separating each set of 30 repetitions into sections corresponding to contractions 1–10, 11–20, and 21–30. Greenhaff et al. (12) analyzed each section by performing multiple Student’s t-tests on the data. The use of multiple t-tests inflates the overall rate of type I errors. Interestingly, investigations that have demonstrated differences have used multiple t-tests to analyze their data (5,15), whereas studies supporting the null hypothesis used an ANOVA to analyze their data (6,22–24).
The use of five sets of 30 repetitions with one 60-s rest period between sets was similar to the Greenhaff et al. (12) study. However, subjects in our study were instructed to maximally extend and flex their knee with no pause between contractions to more closely duplicate functional athletic performance. Greenhaff et al. had subjects passively flex to 90° after each knee extension. An increase in time used to passively flex the extremity over the course of five sets may have allowed for subjects to replenish CrP and ATP, which may be less typical of athletic endeavors.
Previous studies have indicated that creatine phosphate (CrP) stores are 98% depleted in 20 s of intense muscle contraction (18,27,28,30). Consequently, studies that examine the effect of creatine on single explosive bouts of exercise of 1–10 s in length may not be of sufficient duration to deplete normal levels of CrP (21). Studies in which subjects exercise for greater than 45 s may be too long in duration and, consequently, dilute any affect that may be present (24). An increase in phosphocreatine resynthesis has been demonstrated with supplementation (9,22) and has been implicated in the delay of fatigue after multiple sets of exercise (12,15); however, this was not found in our study.
Several studies on creatine supplementation with exercise durations of sufficient length, have contradicted one another. In swimming, Burke et al. (6) found no resistance to fatigue from creatine supplementation for sprint swimming of 25, 50, and 100 m (approximately 13- to 60-s duration). Balsom et al. (1) found creatine supplementation enhanced fatigue resistance during five repeated bouts of cycling lasting 6 s, and a 10-s bout of cycling. Yet in a similar study, Barnett et al. (3) found that creatine supplementation did not reduce the loss in power output during seven bouts of 10-s sprint cycling. In separate studies, Odland et al. (22) and Cooke et al. (7) found no benefit from creatine for 30 s, and 15 s × 2 sprint cycling, respectively. Birch et al. (5) found a positive effect from Cr ingestion during the initial two bouts of 3 × 30 s isokinetic sprint cycling tests. A study on running by Harris et al. (15) demonstrated an enhancement of running times with Cr supplementation during the final set of a 4 × 300 m and a 4 × 1000-m run. Terrillion et al. (29) did not find that Cr supplementation improved running times for 2 × 700-m runs in competitive male runners. Although variations in the methodology of these studies may account for the divergent findings, no clear pattern can be identified.
One factor that appears to separate contradictory findings of previous studies examining the affects of creatine supplementation were the data analyses. Several studies that have used appropriate statistical analyses were negative, and those with more liberal analyses demonstrated positive results. This study followed a preplanned statistical analysis. The results of this study indicated that 5 d at 20 g·d−1 of creatine did not attenuate quadricep muscle fatigue during five sets of 30 repetitions. Because of the numerous contradictory studies on creatine’s role on increasing exercise/athletic performance, further research is needed to confirm any potentially positive effects. Although this study did not confirm that acute creatine loading enhances athletic performance, studies examining chronic creatine loading during training may prove otherwise.
1. Balsom, P. D., B. Ekblom, K. Soderlund, et al. Creatine supplementation and dynamic high-intensity intermittent exercise. Scand J. Med. Sci. Sports 3:143–149, 1993.
2. Balsom, P. D., K. Soderlund, and B. Ekblom. Creatine in humans with special reference to creatine supplementation. Sports Med. 18:268–280, 1994.
3. Barnett, C., M. Hinds, and D. G. Jenkins. Effects of oral creatine supplementation on multiple sprint cycle performance. Aust. J. Sci. Med. Sport. 28:35–39, 1996.
4. Bergstom, J. Local changes of ATP and phosphocreatine in human muscle tissue in connection with exercise. Circ. Res. 20:91–96, 1967.
5. Birch, R., D. Noble, and P. L. Greenhaff. The influence of dietary creatine supplementation on performance during repeated bouts of maximal isokinetic cycling in man. Eur. J. Appl. Physiol. 69:268–270, 1994.
6. Burke, L. M., D. B. Pyne, and R. D. Telford. Effect of oral creatine supplementation on single-effort sprint performance in elite swimmers. Int. J. Sport Nutr. 6:222–223, 1996.
7. Cooke, W. H., P. W. Grandjeann, and W. S. Barnes. Effects of oral creatine supplementation on power output and fatigue during bicycle ergometry. J. Appl. Physiol. 78:670–673, 1995.
8. Earnest, C. P., P. G. Snell, R. Rodriguez, A. L. Almada, and T. L. Mitchell. The effect of creatine monohydrate ingestion on anaerobic power indices, muscular strength and body composition. Acta Physiol. Scand. 153:207–209, 1995.
9. Greenhaff, P. L., K. Bodin, R. C. Harris, et al. The influence of oral creatine supplementation on muscle phosphocreatine resynthesis following intense contraction in man. J. Physiol. 467:75P, 1993.
10. Greenhaff, P. L., K. Bodin, K. Soderlund, and E. Hultman. Effect of oral creatine supplementation on skeletal muscle phosphocreatine resynthesis. Am. J. Physiol. 266:E725–E730, 1994.
11. Greenhaff, P. L., K. Soderlund, E. Hultman. Energy metabolism in single human muscle fibres during intermittent contraction with occluded circulation. J. Physiol. 460:443–453, 1993.
12. Greenhaff, P. L., A. Casey, A. H. Short, et al. Influence of oral creatine supplementation of muscle torque during repeated bouts of maximal voluntary exercise in man. Clin. Sci. 84:564–571, 1993.
13. Harris, R. C., E. Hultman, and L-O. Nordersjo. Glycogen, glycolytic intermediates and high-energy phosphates determined in biopsy samples of muscles quadriceps femoris of man at rest: methods and variance of values. Scand. J. Clin. Lab. Invest. 33:109–120, 1974.
14. Harris, R. C., K. Soderlund, and E. Hultman. Elevation of creatine in resting and exercise muscle of normal subjects by creatine supplementation. Clin. Sci. 83:367–374, 1992.
15. Harris, R. C., M. Viru, P. L. Greenhaff, and E. Hultman. The effect of oral creatine supplementation on running performance during maximal short-term exercise in man. J. Physiol. 467:74, 1993.
16. Hultman, E., J. Bergstrom, and N. M. Anderson. Breakdown and resynthesis of phosphorylcreatine and adenosine triphosphate in connection with muscular work in man. Scand. J. Clin. Lab. Invest. 19(Suppl. 94):56–66, 1967.
17. Hultman, E., K. Soderlund, J. A. Timmons, G. Cederbland, and P. L. Greenhaff. Muscle creatine loading in men. J. Appl. Physiol. 81:232–237, 1996.
18. Hultman, E, P. L. Greenhaff, J-M. Ren, and K Soderlund. Energy metabolism and fatigue during intense muscle contraction. Biochem. Soc. Trans. 19:347–353, 1991.
19. Jansson, E., G. A. Dudley, B. Norman, and P. A. Tesch. ATP and IMP in single human muscle fibers after high intensity exercise. Clin. Physiol. 7:337–345, 1987.
20. Karlsson, J., and B. Saltin. ATP and CP in working muscles during exhaustive exercise in man. J. Appl. Physiol. 29:598–602, 1970.
21. Maughan, R. J. Creatine supplementation and exercise performance. J. Sports Nutr. 5:94–101, 1995.
22. Odland, L. M., J. D. Macdougall, M. A. Tarnopolsky, A. Elorriaga, and A. Borgmann. Effect of oral creatine supplementation on muscle Pcr and short-term maximum power output. Med. Sci. Sports Exerc. 29:216–219, 1997.
23. Redondo, D., E. Dowling, B. Graham, S. Jones, A. Almada, and W. Williams. The effect of oral creatine monohydrate supplementation on running velocity. Int. J. Sports Nutr. 6:213–221, 1996.
24. Rossiter, H. B., E. R. Cannell, and P. M. Jakeman. The effect of oral creatine supplementation on the 1000-m performance of competitive rowers. J. Sports Sci. 14:175–179, 1996.
25. Sinacore, D. R., B. I. Bander, and A. Delitto. Recovery from a 1-minute bout of fatiguing exercise: characteristics, reliability, and responsiveness. Phys. Ther. 74:234–244, 1994.
26. Soderlund, K., and E. Hultman. ATP and phosphopcreatine changes in single human muscle fibers after intense electrical stimulation. Am. J. Physiol. 261:E737–E741, 1991.
27. Soderlund, K., P. Greenhaff, and E. Hultman. Energy metabolism in Type I and Type II human muscle fibers during short-term electrical stimulation at different frequencies. Acta Physiol. Scand. 144:15–22, 1992.
28. Spriet, L. L., K. Soderlund, M. Bergstrom, et al. Anaerobic energy release in skeletal muscle during electrical stimulation in men. J. Appl. Physiol. 62:611–615, 1987.
29. Terrillion, K. A., F. W. Kolkhorst, F. A. Dolgener, and S. J. Joslyn. The effect of creatine supplementation on two 700-m maximal running bouts. Int. J. Sport Nutr. 7:138–143, 1997.
30. Thorsson, P. A. A., and N. Fugaitsuka. Creatine phosphate in fiber types of skeletal muscle before and after exhaustive exercise. J. Appl. Physiol. 66:1756–1759, 1989.
31. Vandenberghe, K., N. Gillis, M. Van Leemputte, P. Van Hecke, F. Vanstapel, and P. Hespel. Caffeine counteracts the ergogenic action of muscle creatine loading. J. Appl. Physiol. 80:452–457, 1996.
32. Westerblad, H., D. G. Allen, J. D. Bruton, F. H. Andrade, and J. Lannergren. Mechanisms underlying the reduction of isometric force in skeletal muscle fatigue. Acta Physiol. Scand. 162:253–260, 1998.