05)b-Main effect for Genotype (p < 0.05) Discussion The major finding of the present study is that caffeine affects 40-kilometer time trial performance in cyclists homozygous

for the A variant to a greater degree than those who possess the C variant. Specifically, caffeine decreased 40-km time by an average Selleckchem CFTRinh-172 of 3.8 minutes in the AA homozygotes as compared to 1.3 minutes in the C allele carriers. To our knowledge, this is the first study to implicate a specific polymorphism as a potential cause of the variation in the ergogenic effect of caffeine supplementation. Sachse et al. [10] observed slower caffeine metabolism in C allele carriers who smoke, suggesting that this CYP1A2 polymorphism may affect the inducibility of the Cytochrome P450 enzyme. Caffeine has also been shown to increase risk of heart disease in

C allele carriers but not AA homozygotes [11, 12], ostensibly because caffeine is metabolized at a higher rate in the AA homozygotes. Given these prior findings, it could be hypothesized that a slower Idasanutlin molecular weight metabolism would be advantageous for maximizing the ergogenic benefit of caffeine. Alternatively, Hallstrom et al. [13] found that coffee consumption was associated with decreased bone mineral density in AA homozygotes, but not C allele carriers. The authors speculated that the rapid accumulation of caffeine metabolites may have been responsible for this finding [13]. In support of this contention, paraxanthine and theophylline (downstream metabolites of caffeine metabolism) have higher binding affinities with adenosine receptors than caffeine [16]. Thus, it is possible that a faster caffeine metabolism in AA homozygotes created a more rapid production of paraxanthine and/or theophylline and therefore enhanced the ergogenic effect. This possibility is speculative as no markers of caffeine metabolism were available. Future studies should https://www.selleckchem.com/products/riociguat-bay-63-2521.html determine caffeine metabolism Dichloromethane dehalogenase during exercise

across these genotypes to better determine the mechanism of the observed effect. Despite the fact that there was a significant Genotype × Treatment interaction for 40-km time, it should also be noted that the AA homozygotes had a slower placebo 40-km time and the caffeine supplementation served to decrease 40-km time for AA homozygotes to a level comparable to C allele carriers (Figure 1). This raises the concern that the results were driven by a difference in cycling performance capabilities between the two groups, rather than the genetic polymorphism. Collomp et al. [17] observed that caffeine improved swimming velocity in trained, but not untrained swimmers. O’Rourke et al. [18] observed a similar 5-km performance improvement from caffeine in both well-trained and recreational runners. Thus, one would expect performance capabilities to have no effect on caffeine response, or to affect it in the opposite direction of what was observed in the present study.