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LETTER TO THE EDITOR |
Texas A&M University, Health and Kinesiology College Station, TX
Address correspondence to Steven E. Riechman, PhD, MPH, Texas A&M University, Health and Kinesiology, 149 Read Bldg., Mailstop 4243, College Station, TX 77843. E-mail: sriechman{at}hlkn.tamu.edu
Dr. Lambert has pointed out an important possibility to explain our results, which we have considered. However, we have some reservations on the mechanism of cholesterol impacting training responses through testosterone, which limits our enthusiasm. It is an attractive hypothesis since cholesterol is a precursor of testosterone, certain low fat diets reduce androgens, and there are indisputable effects of supraphysiological doses of testosterone and testosterone depletion (1) on skeletal muscle. In our study, lean mass and saturated fat intake were significantly correlated, but after adjusting for dietary cholesterol, the association was greatly reduced. This may support what Dr. Lambert alludes to, that the data on fat intake and androgens could be an artifact of the strong association between dietary saturated fat and dietary cholesterol. Although the rate-limiting step in steroid biogenesis is cholesterol transport into the mitochondria, it is not clear whether this process can be influenced by changes in dietary or blood cholesterol levels or whether this will change testosterone levels specifically. Our main reservation, however, is the minimal amount of evidence that normal variability in blood testosterone is associated with the normal variability in muscle gain with resistance training. For example, women only have 5%–10% of the resting testosterone and no acute testosterone response to resistance training as compared to males (2), yet their short-term percent gains in muscle strength and mass are the same (3–4). To confound the issue further, testosterone responses to resistance training reported in the literature are inconsistent and seem to be context specific, some contexts that are inconsistent with skeletal muscle hypertrophy. For example, nutritional supplementation protocols known to enhance hypertrophy also have been shown to reduce or block testosterone responses to resistance training (2). In balance, some studies, but not all, have shown only "hypertrophy" training protocols increase testosterone, although bodybuilders tend not to have a response (2). In the two studies that we identified reporting a specific association of normal variability in testosterone to skeletal muscle adaptations (5,6), there were mixed effects on strength and mass and whether the association was with basal or exercise response of testosterone. If blood testosterone in the physiological range plays more than a permissive role in muscle responses, it may be due to specific increases in tissue sensitivity through increased receptor number or binding affinity shown to increase with exercise (7) or local conversion of precursors [e.g., androstenedione (2)]. Unilateral leg training designs support a concept that muscle hypertrophy is tissue specific and systemic effects such as those expected by testosterone may not play a role (8). Therefore, we believe it is unlikely that we would find a significant association between dietary and blood cholesterol and muscle adaptations that was explained by changes in blood testosterone in our study population.
Nonetheless, we are conducting studies specifically designed to advance or disprove the hypothesis that elevated dietary cholesterol consumption increases blood testosterone acutely and chronically in older adults, and this increase is directly related to variability in muscle gain with resistance training.
References
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