Abstract

OBJECTIVE or our study was to identify effects of acute fatigue on myofibrillar components and their function that persist beyond modifications to intracellular metabolic perturbations. Our HYPOTHESIS was that acute fatigue would induce differential phosphorylation in regulatory proteins in the sarcomere that would reduce tension and increase velocity and power. We used the following METHODS to test that hypothesis. Seven healthy, competitive athletes were recruited to participate (3 male, 4 female), entailing one session of unilateral fatiguing knee extension exercise to the point of task failure. Immediately after, bilateral percutaneous needle muscle biopsy was performed on the vastus lateralis muscle, providing a “fatigued” and “not fatigued” sample. Tissue was separated for phosphoproteomic analysis (western blot and isoelectric separation) and single fiber contractile mechanics (isotonic load clamps; isometric tension, velocity and power). Following mechanical assessment, myosin heavy chain (MHC) isoform was determined for each fiber via SDS-PAGE. Our RESULTS found no effect of fatigue on isometric tension across all fiber types. However, maximum shortening velocity was increased along with contractile power, consistent with our hypotheses. Surprisingly, our results varied by sex and fiber type, such that velocity was increased primarily in MHC IIA/X fibers in males, whereas females demonstrated a blunted response to fatigue. While baseline variation in regulatory protein phosphorylation (Myosin Binding Protein C; MyBP-C) were significantly correlated with power output in contractile power in fast isoforms (MHC IIA, MHC IIA/X) we did not detect significant alterations in phosphorylation of this protein with fatigue. We CONCLUDE that fatigue causes paradoxical increased in velocity and power that are particularly evident in males. While our measurement of MyBP-C phosphorylation did not detect effects of fatigue, other potential sarcomeric proteins may explain this paradoxical response to acute fatigue. Wu Tsai Human Performance Alliance This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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