Muscle fatigue and excitation-contraction coupling responses following a session of prolonged cycling

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 () of 2.95 ± 0.27 L min^?1 (mean ± SE), exercised for 2 h at 62 ± 1.3%. 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 β2 (R1, R2 and R3) and β3 (R3), but not β1 or the α‐isoforms (α1, α2 and α3). 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).