Creatine Phosphokinase and Muscle Damage: RESPONSE


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Dear Editor-in-Chief:Our manuscript (4) was one of the first peer-reviewed papers to explore the effects of carbohydrate and protein (CHO+P) beverages on endurance performance and muscle damage. As such, we agree that future investigators should examine similar research questions using a variety of methodologies, including “direct” measures of muscle damage. However, we disagree with Dr. Koller’s position that “CPK is not a relevant measure of muscle damage.” Dr. Koller cited studies (1,2,3) that showed no linear correlations between muscle histology data and CPK. However, in each of these studies CPK was elevated in conditions where direct measures of muscle damage were present. There are numerous methodological and statistical justifications for the absence of linear correlations between these variables that do not preclude CPK’s relevance as an indirect measure of muscle damage.CPK data are obtained from venous blood and thus represent an indirect measure of “overall” muscle damage from the working musculature, while biopsies produce localized data. Due to individual variation in recruitment patterns during large muscle exercise, it is not surprising that these variables are often not directly correlated. Statistically, there are numerous limitations to using correlations to compare methodologies. Beaton et al. (1) concluded that poor correlations between CPK and histology measures were “most likely due to the extreme interindividual variations in serum C[P]K activity.” We also observed large interindividual differences in CPK responses (4), but unlike others (1,2,3) our analysis involved a within-group comparison, reducing the statistical impact of interindividual variation.Dr. Koller discussed a number of potential mechanisms for the release of CPK. It is clear that the nuances of CPK release in response to muscle exertion are not well understood. While it is possible that elevated CPK levels may be due to leaking from monocyte cell membranes, in response to an adaptive response to “damage sensors,” or other mechanisms, these factors may themselves be related to direct or indirect consequences of muscle damage.It should also be noted that our conclusion of reduced muscle damage was not entirely based on reduced CPK levels in the CHO+P trial. Decrement in muscle function is expected to accompany muscle damage, as demonstrated by decreased peak torque values (1). If performance differences between beverage trials are viewed as a baseline (i.e., 29% longer in the CHO+P trial), the larger performance difference between beverage trials during the subsequent ride (40% longer in the CHO+P trial) supports the notion that muscle function was less impaired following the CHO+P trial. While numerous factors could contribute to these differences, this indirectly supported our conclusion of reduced muscle damage in the CHO+P trial.We appreciate Dr. Koller’s concerns and agree that other measures of muscle damage should be utilized to support or refute these findings. However, his statement that “it cannot be concluded that [CHO+P] produces reductions in muscle damage in endurance athletes” is too strong. We maintain that our conclusions were the most logical and appropriate interpretation of the data.Michael J.

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