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

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.

Ten volunteers with a peak aerobic power (VO(2peak)) 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).

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 Ca(2+) -ATPase (-22%), Ca(2+) -uptake (-26%) and phase 1(-33%) and 2 (-38%) Ca(2+) -release. Both V(max) and Ca(2+) -release (phase 2) recovered by R1, whereas Ca(2+) -uptake and Ca(2+) -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).

These results suggest a possible direct role for Ca(2+)-release in fatigue and demonstrate a single exercise session can induce overlapping perturbations and adaptations (particularly to the Na(+), K(+)-ATPase).