Age Does Not Influence Mitochondrial-Related Transcript Expression Following A Resistance-Training Bout

Abstract

Mitochondrial dysfunction has been theorized to contribute to age-associated muscle atrophy. Deficits in muscle mass are thought to be due to a degree of anabolic resistance to growth-promoting stimuli; however, it is not known whether mitochondrial dysfunction contributes to an impaired synthetic response following resistance exercise. While long-term resistance training has been shown to influence mitochondrial transcripts, the acute response has not been well characterized. PURPOSE: To determine the ability of a single resistance-training bout to alter mitochondrial-related transcript abundance and whether such a response is influenced by age. METHODS: 19 younger (YNG; n=10, 21±3 y) and older (OLD; n=9, 70±4 y) sedentary males completed a single unilateral resistance-training bout for the knee extensors (four sets of 10 repetitions at 75%1RM for leg extension and leg press exercises). Muscle biopsies were taken from the unexercised leg to establish baseline measures and from the exercised leg at three, 24 and 48 hours post exercise along with blood from the antecubital vein. RESULTS: Both groups had similar lean body mass (66.0±10.8 kg YNG; 62.9±6.4 kg OLD); however OLD had reduced strength (leg press: 228±94 lbs YNG; 161±50 lbs OLD; leg extension: 117±47 lbs YNG; 82±23 lbs OLD; p<0.05). Serum creatine kinase was elevated over baseline to a similar extent for both groups at 24 and 48 h post-exercise (289±153% at 24h, 267±161% 48 h; p<0.001). PGC-1α mRNA increased three h post-exercise (441±274%, p<0.01), while Tfam mRNA was elevated at 24 h (123±29.5%, p<0.05). In contrast, ND1 and ND4 mRNA were repressed 48 h after exercise (82±60% and 63±26% of baseline, p<0.05). No effects of age were noted except for ND4 mRNA, where expression in YNG was elevated relative to OLD 24 h post-exercise (154±57%, p<0.05), before dropping to a repressed level similar to the older group at 48 h. CONCLUSION: Age does not appear to influence the dynamics of the PGC-1α, Tfam and ND1 mRNA response to a single resistance-training bout. Further work is required to clarify the significance of the signaling pathways responsible for the induction of PGC-1α, and whether this results in the co-activation of proteins responsible for the induction of mitochondrial adaptations to exercise.