科研之友
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摘要
Aim: The mechanisms underlying the fatigue that occurs in human muscle following sustained activity are thought to reside in one or more of the excitation-contraction coupling (E-C coupling) processes. This study investigated the association between the changes in select E-C coupling properties and the impairment in force generation that occurs with prolonged cycling. Methods: Ten volunteers with a peak aerobic power ((V) over dotO(2peak)) of 2.95 +/- 0.27 L min(-1) (mean +/- SE), exercised for 2 h at 62 +/- 1.3% ((V) over dotO(2peak). Quadriceps function was assessed and tissue properties (vastus lateralis) were measured prior to (E1-pre) and following (E1-post) exercise and on three consecutive days of recovery (R1, R2 and R3). Results: While exercise failed to depress the maximal activity (V-max) of the Na+,K+-ATPase (P = 0.10), reductions (P < 0.05) were found at E1-post in V-max of sarcoplasmic reticulum Ca2+-ATPase (-22%), Ca2+-uptake (-26%) and phase 1(-33%) and 2 (-38%) Ca2+-release. Both V-max and Ca2+-release (phase 2) recovered by R1, whereas Ca2+-uptake and Ca2+-release (phase 1) remained depressed (P < 0.05) at R1 and at R1 and R2 and possibly R3 (P < 0.06) respectively. Compared with E1-pre, fatigue was observed (P < 0.05) at 10 Hz electrical stimulation at E1-post (-56%), which persisted throughout recovery. The exercise increased (P < 0.05) overall content of the Na+,K+-ATPase (R1, R2 and R3) and the isoforms beta 2 (R1, R2 and R3) and beta 3 (R3), but not beta 1 or the alpha-isoforms (alpha 1, alpha 2 and alpha 3). Conclusion: These results suggest a possible direct role for Ca2+-release in fatigue and demonstrate a single exercise session can induce overlapping perturbations and adaptations (particularly to the Na+,K+-ATPase).
- 出版日期2011-12
