Journal Title (Medline/Pubmed accepted abbreviation): Appl Physiol Nutr Metab
Page numbers: 507-511
doi (if applicable):
Summary of Background and Research Design
Hypothesis:A standard creatine-loading protocol would significantly impair joint range of movement (ROM).
Subjects:40 healthy, recreationally active males (no structured training, physical activity <2 times/wk) with mean age = 24 y, mean body weight = 83.6 kg and no prior exposure to creatine supplementation
Experimental design:Independent groups, randomized, double-blind
Treatments and protocol:Subjects were randomly assigned to either a control group (C, n = 20) or a creatine monohydrate supplementation (CS, n = 20) group. The C group drank a creatine-free, orange-flavored drink, whereas the CS group consumed 25 g/day of creatine monohydrate dissolved in an orange flavored drink for 5 days, followed by 5 g/day for an additional 3 days. At the beginning and the end of each supplementation period, the subjects were tested on 15 different measures of joint ROM, all done using the same goniometer. Subjects refrained from exercise for 48 h prior to the testing and excluded any flexibility training other than mild maintenance stretches as part of the subjects’ normal warm-up routines. Environmental conditions (temperature, relative humidity) were the same for each treatment and time of day was consistent for each subject. Body mass was also measured before and after the supplementation period.
Summary of Research Findings
There was no determination of muscle cell creatine levels in response to the creatine monohydrate supplementation, but there was a body mass gain of 1.6 kg in the CS group versus no change in the C group, a finding consistent with the existing literature on creatine supplementation. Of the 15 different joint measurements obtained, there were significant decreases in ROM for 3: shoulder extension (15.8%), shoulder abduction (1.7%), and dorsiflexion of the foot (14.8%). No other findings were statistically significant.
Interpretation of findings/Key practice applications:
Given the relatively large number of joint tests employed in this study, it is conceivable that at least one would be statistically significant due to chance. However, the authors suggested that one potential explanation for these findings is that, in each of the 3 measures that were significant, the agonist muscle (the one doing the contracting/stretching) was small relative to the mass of the antagonist muscle being stretched. Creatine has been shown to increase muscle strength and the authors proposed that perhaps the increased force production in the agonist muscle might have be insufficient to overcome the increased force production that also occurred in the larger antagonist muscles. The authors also delineated two potential mechanisms by which creatine might affect ROM: 1) stiffness caused by elevated intracellular water content; and/or 2) creatine-induced changes in muscle cell volume may affect neural outflow from muscle spindles.
It would have been interesting to see if the findings in this paper were also applicable to habitual creatine users and in those with heavier levels of physical activity than reported for the subjects in this study. It was also not clear from the paper if the same technician performed all the ROM measurements.