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Effect of oral creatine supplementation on isokinetic torque production


Medicine & Science in Sports & Exercise: May 2000 - Volume 32 - Issue 5 - p 993-996
Applied Sciences: Biodynamics

GILLIAM, J. D., C. HOHZORN, D. MARTIN, and M. H. TRIMBLE. Effect of oral creatine supplementation on isokinetic torque production. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 993–996, 2000.

Purpose This study was conducted to examine the effect of oral creatine supplementation on the decline in peak isokinetic torque of the quadriceps muscle group during an endurance test.

Methods Twenty-three active, but untrained, male subjects performed isokinetic strength tests on a Cybex II dynamometer at 180°·s−1. The protocol consisted of pre- and post-tests with five sets of 30 maximum volitional contractions with a 1-min rest period between sets. Subjects returned to perform the posttest after 5 d of placebo (4 × 6g glucose·d−1, N = 12) or creatine (4 × 5g creatine + 1 g glucose·d−1, N = 11) supplementation. Supplements and testing were administered in a double blind fashion. Peak torque was measured during each contraction and the 30 contractions were averaged for each set.

Results A three-way mixed ANOVA with one between factor (placebo vs creatine) and two within factors (pre/post supplementation and sets 1–5) revealed no significant interactions, P > 0.05. The placebo vs creatine main effect was also nonsignificant, whereas the pre/post and set effects were significant (P < 0.05). Peak torque increased (∼ 3%) from pre- to post-testing, (P = 0.04), but the absolute magnitude of the differences is unlikely to be of any practical significance. Peak torque decreased from sets 1 to 4, whereas sets 4 and 5 were not different. A priori contrasts comparing the creatine group’s performance pre vs post test for the fourth and fifth sets were nonsignificant (P > 0.05).

Conclusions Based on within and between group comparisons, we were unable to detect an ergogenic effect of oral creatine supplementation on the decline in peak torque during isokinetic exercise at 180°·s−1.

Department of Physical Therapy, University of Florida, Gainesville, FL 32610

Submitted for publication March 1999.

Accepted for publication August 1999.

Address for correspondence: Jeffery D. Gilliam, University of Florida University of Florida, Department of Physical Therapy Department of Physical Therapy, P.O. Box 100154, Gainesville, FL 32610. E-mail:

1 There has been much controversy and many claims concerning the effects of supplementation with creatine monohydrate on exercise performance (5,7,12,15,19,21–24). Because of the many contradictory findings (6,7,22–24) confirmation of any proposed performance benefits through improved bioenergetics has been questionable.

Creatine is found predominately in skeletal muscle in which approximately two-thirds of the creatine content is in the form of creatine phosphate (13). Creatine phosphate is used as a source of energy to replenish adenosine triphosphate (ATP) during brief high intensity activities (2,16). The rate at which ATP is hydrolyzed is dictated by the level of force production of the muscle (16). It has been demonstrated that the whole muscle ATP content seldom falls more than 25–30% when at the point of exhaustion during high-intensity exercises (19,20). The rephosphorylation of adenosine diphosphate (ADP) to provide energy for continued muscle contraction is mandatory for continued function of power output. Creatine phosphate (CrP) is used for the process of rephosphorylation; however, stores of CrP can fall to a level of zero with continued high-intensity exercise and have been demonstrated to be finite. Consequently, CrP may have a limiting effect upon rephosphorylation of ADP to ATP (4,20).

A decline in CrP concentration in the muscle has been correlated with a reduced contractile capacity of the muscle (4). This decreased capacity of the muscle to contract characterizes muscle fatigue. Skeletal muscle fatigue has been described as a decline in force production over time (32). Fatigue of a muscle may also be described as the inability to recover from a bout of intense exercise activity that causes a decline in torque output (25).

Increases in intramuscular creatine levels of approximately 20–50% have been demonstrated after supplementation, with approximately 20% of this increase accounted for by CrP (14). Uptake of creatine into the muscle has been shown to be the greatest in the first 2 d of supplementation (14). In these subjects, renal excretion was 40, 61, and 68% of the creatine dose over the first 3 d indicating that the upper limit was being approached. Hultman et al. (17) demonstrated that although total creatine levels could be increased, the increases were predominately from free creatine levels and not phosphocreatine. It has also been suggested that resynthesis of phosphocreatine is augmented after creatine supplementation is challenged by intense isometric contractions via electric stimulation (9). This supposition suggests that an increased resynthesis rate from mitochondrial ATP is due to the increase in muscle creatine content causing an accelerated rate of flux through the creatine kinase reaction at the mitochondrial membrane. Therefore, it is suggested that after creatine supplementation there is both an increase in the creatine pool and also an increase in the rate of resynthesis (9). Both of these factors may limit the rate of force decline with repeated sets of explosive work.

The goals of this study were to examine the premise that quadricep fatigue is attenuated and recovery of quadriceps function enhanced by creatine supplementation. Fatigue was assessed by the decline in torque across 5 sets of 30 maximal voluntary contractions on an isokinetic dynamometer.

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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.

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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°·s1 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.

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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.

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Data analysis.

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.

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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).

Figure 1

Figure 1

Table 1

Table 1

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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·kg1 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·d1 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.

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