The purpose of this work was to determine the effect of resistance exercise (RE)-induced hormonal changes on the satellite cell (SC) myogenic state in response to muscle damage. Untrained men ( n = 10, 22 ± 3 yr) and women ( n = 9, 21 ± 4 yr) completed 2 sessions of 80 unilateral maximal eccentric knee extensions followed by either an upper body RE protocol (EX) or a 20-min rest (CON). Muscle samples were collected and analyzed for protein content of Pax7, MyoD, myogenin, cyclin D1, and p21 before (PRE), 12 h, and 24 h after the session was completed. Serum testosterone, growth hormone, cortisol, and myoglobin concentrations were analyzed at PRE, post-damage, immediately after (IP), and 15, 30, and 60 min after the session was completed. Testosterone was significantly ( P < 0.05) higher immediately after the session in EX vs. CON for men. A significant time × sex × condition interaction was found for MyoD with an increase in EX (men) and CON (women) at 12 h. A significant time × condition interaction was found for Pax7, with a decrease in EX and increase in CON at 24 h. A significant time effect was found for myogenin, p21, and cyclin D1. Myogenin and p21 were increased at 12 and 24 h, and cyclin D1 was increased at 12 h. These results suggest that the acute RE-induced hormonal response can be important for men to promote SC proliferation after muscle damage but had no effect in women. Markers of SC differentiation appeared unaffected by the hormonal response but increased in response to muscle damage.
This project was designed to assess the effects of time of day and training status on the benefits of caffeine supplementation for cycling performance. Twenty male subjects (Age, 25 years; Peak oxygen consumption, 57 mL·kg−1·min−1) were divided into tertiles based on training levels, with top and bottom tertiles designated as ‘trained’ (n = 7) and ‘untrained’ (n = 7). Subjects completed two familiarization trials and four experimental trials consisting of a computer-simulated 3-km cycling time trial (TT). The trials were performed in randomized order for each combination of time of day (morning and evening) and treatment (6mg/kg of caffeine or placebo). Magnitude-based inferences were used to evaluate all treatment effects. For all subjects, caffeine enhanced TT performance in the morning (2.3% ± 1.7%, ‘very likely’) and evening (1.4% ± 1.1%, ‘likely’). Both untrained and trained subjects improved performance with caffeine supplementation in the morning (5.5% ± 4.3%, ‘likely’; 1.0% ± 1.7%, ‘likely’, respectively), but only untrained subjects rode faster in the evening (2.9% ± 2.6%, ‘likely’). Altogether, our observations indicate that trained athletes are more likely to derive ergogenic effects from caffeine in the morning than the evening. Further, untrained individuals appear to receive larger gains from caffeine in the evening than their trained counterparts.
Prior studies from our laboratory suggest that the-163 C > A polymorphism of the Cytochrome P450 (CYP1A2) gene influences the ergogenic effect of caffeine. Although this polymorphism has been known to influence the inducibility of hepatic CYP1A2 and the rate of caffeine metabolism, levels of caffeine and/or metabolites have never been reported in these aforementioned studies (1, 12, 16). Thus, a mechanistic link between the polymorphism and the ergogenic effect of caffeine is lacking. The purpose of this study was to determine if the CYP1A2 polymorphism affected caffeine metabolism between the genotypes (AA homozygotes and C allele carriers). Twenty male subjects were recruited for this study. Subjects participated in two 3km cycling time trials with placebo (all-purpose flour) and caffeine (6mg/kg body weight anhydrous caffeine) supplementation. "Slow metabolizers" were characterized as possessing a "C" allele on the first intron of that gene (grouped AC heterozygotes, and CC homozygotes), and "fast metabolizers" were those who were homozygous for the A allele. C allele carriers had significantly higher serum caffeine after one hour (C allele carriers = 14.2 ± 1.8 ppm, AA homozygotes = 11.7 ± 1.7 ppm). While there was a main effect for caffeine ingestion on time trial performance, there was no caffeine x genotype interaction (C allele carriers: Placebo = 297 ± 20.8 sec, Caffeine = 292 ± 20 sec; AA homozygotes: Placebo = 318.3 ± 34.5 sec; Caffeine = 307.9 ± 21.9 sec). Results from this study suggest that C allele carriers have higher serum caffeine after one hour than AA homozygotes, consistent with the assertion that C allele carriers metabolize caffeine slower. These findings do not support a genetic influence on the ergogenic effect of caffeine in a 3km cycling trial.
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