Abstract
Increased mitochondrial content is a hallmark of exercise‐induced skeletal muscle remodeling. For this process, considerable evidence underscores the involvement of transcriptional coactivators in mediating mitochondrial biogenesis. However, our knowledge regarding the role of transcriptional corepressors is lacking. In this study, we assessed the association of the transcriptional corepressor Rb family proteins, Rb and p107, with endurance exercise‐induced mitochondrial adaptation in human skeletal muscle. We showed that p107, but not Rb, protein levels decrease by 3 weeks of high‐intensity interval training. This is associated with significant inverse association between p107 and exercise‐induced improved mitochondrial oxidative phosphorylation. Indeed, p107 showed significant reciprocal correlations with the protein contents of representative markers of mitochondrial electron transport chain complexes. These findings in human skeletal muscle suggest that attenuated transcriptional repression through p107 may be a novel mechanism by which exercise stimulates mitochondrial biogenesis following exercise.
Highlights
Skeletal muscle is a highly plastic tissue having the ability to undergo functional adaptations in response to external stimuli including exercise, which is known to improve metabolic health and enhance physical performance (Fluck and Hoppeler 2003; Coffey and Hawley 2007; Gundersen 2011)
We assessed the influence of exercise-induced skeletal muscle adaptation on retinoblastoma susceptibility (Rb) and p107 in human participants from a previous study reporting that markers of mitochondrial content and function increased during training (Ydfors et al 2016)
The level of p107 decreased significantly (P < 0.05) further by T9 in the pre-exercise samples by as much as 61%. These results suggest that 3 weeks of high-intensity interval training (HIIT) reduced protein expression level of p107, but not Rb in human skeletal muscle
Summary
Skeletal muscle is a highly plastic tissue having the ability to undergo functional adaptations in response to external stimuli including exercise, which is known to improve metabolic health and enhance physical performance (Fluck and Hoppeler 2003; Coffey and Hawley 2007; Gundersen 2011). Exercise-induced skeletal muscle adaptations are manifested by changes in metabolic function (Green et al 1992) that include increases in the content and oxidative capacity of mitochondria (Holloszy 1967; Holloszy and Coyle 1984). Leading models propose that the greater mitochondrial oxidative capacity following chronic exercise result from continual and coordinated stimulation of transcriptional pathways. This process results in a steady state accumulation of mitochondrial proteins manifesting as greater a 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society
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