It can be speculated that these changes in blood flow may lead to an increased substrate pool for skeletal muscle by virtue of increased glucose and O2 uptake . Specifically, extracellular ATP directly promotes the increased synthesis and release of nitric oxide (NO) and prostacyclin (PGl2) within skeletal muscle and therefore directly affects tissue vasodilation and blood flow . Specifically, increasing skeletal muscle Ca2+ influx and intracellular concentrations have been shown to significantly increase both the total number of thin filaments binding and the speed at which the filaments slide .
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Our results indicated greater increases in LBM and muscle thickness in response to oral ATP versus placebo. However, we have to point out that the mechanisms that ATP mediates changes in skeletal muscle performance are still under investigation and need to be fully elucidated. Prior to our research, there was limited data evaluating the effects of supplemental ATP on physiological responses that would improve long-term muscular performance. The mixed model in SAS® was used with the main effects of treatment, week and treatment by week, with the value for week 0 used as a covariate. The mixed model ANOVA in SAS® was used with the main effects of treatment, time and treatment by time, with the value for week 0 used as a covariate.
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