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.
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.