L-glutamine and L-alanine Improve Energy Status and Skeletal Muscle Cytoprotection in Rats Submitted to Heavy Resistance Exercise: 3322 Board #191 June 2 9 30 AM - 11 00 AM

Strenuous exercise results in muscle damage and low cellular energy levels, which activates the AMP-activated protein kinase (AMPK), a sensor of energy status, as well as induces the expression of forkhead box O1 (FOXO1), linked to delayed skeletal muscle regeneration. Glutamine and alanine are the most important gluconeogenic and cytoprotection-related amino acids, and have been demonstrated to attenuate exercise-induced muscle damage and inflammation. However, whether these amino acids have a role in regulating energy status and muscle damage during heavy resistance exercise (HRE) remain largely unknown. PURPOSE: To evaluate the effects of chronic oral supplementation with L-glutamine and L-alanine in their free form (GLN+ALA, ALA) or as the dipeptide L-alanyl-L-glutamine (DIP) on energy status, muscle damage and cytoprotection markers in skeletal muscle of rats submitted to heavy resistance exercise (HRE). METHODS: Forty adult male Wistar rats (n 8/ group) were submitted to 8-week HRE, which consisted of climbing a ladder with progressive loads (25 to 100% of body weight), and to supplementation delivered in a 4% solution in drinking water, in the last 21 days of HRE. Phosphorylation of AMPK and FOXO1, as well as the expression of apoptosis-inducing factor (AIF) and the 27 kDa heat shock protein (HSP27) were assayed in tibialis anterior muscle by western blotting. RESULTS: HRE promoted skeletal muscle damage by increasing AIF and HSP27 contents in muscle of CTRL (by 85%) and ALA (by 158%) groups (p<0.05 vs sedentary). Conversely, GLN+ALA and DIP attenuated these effects. Additionally, supplements containing L-glutamine decreased the exercise-induced phosphorylation of AMPK by 24% (p<0.05 vs. CTRL and ALA groups) and of FOXO1 by 53% in muscle of rats treated with GLN+ALA and DIP (p<0.05 vs. SED, CTRL and ALA groups). CONCLUSION: Chronic oral supplementation with L-glutamine (given along with free L-alanine or as dipeptide) improved muscle energy status by decreasing AMPK phosphorylation and promoted muscle protection by decreasing FOXO1 phosphorylation and HSP27 and AIF contents in response to HRE. Supported by FAPESP Grant 2012/21087-4.