Low cell pH depresses peak power in rat skeletal muscle fibres at both 30°C and 15°C: implications for muscle fatigue

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Abstract
Historically, an increase in intracellular H+ (decrease in cell pH) was thought to contribute to muscle fatigue by direct inhibition of the cross‐bridge leading to a reduction in velocity and force. More recently, due to the observation that the effects were less at temperatures closer to those observed in vivo, the importance of H+ as a fatigue agent has been questioned. The purpose of this work was to re‐evaluate the role of H+ in muscle fatigue by studying the effect of low pH (6.2) on force, velocity and peak power in rat fast‐ and slow‐twitch muscle fibres at 15°C and 30°C. Skinned fast type IIa and slow type I fibres were prepared from the gastrocnemius and soleus, respectively, mounted between a force transducer and position motor, and studied at 15°C and 30°C and pH 7.0 and 6.2, and fibre force (P0), unloaded shortening velocity (V0), force–velocity, and force–power relationships determined. Consistent with previous observations, low pH depressed the P0 of both fast and slow fibres, less at 30°C (4–12%) than at 15°C (30%). However, the low pH‐induced depressions in slow type I fibre V0 and peak power were both significantly greater at 30°C (25%versus 9% for V0 and 34%versus 17% for peak power). For the fast type IIa fibre type, the inhibitory effect of low pH on V0 was unaltered by temperature, while for peak power the inhibition was reduced at 30°C (37%versus 18%). The curvature of the force–velocity relationship was temperature sensitive, and showed a higher a/P0 ratio (less curvature) at 30°C. Importantly, at 30°C low pH significantly depressed the ratio of the slow type I fibre, leading to less force and velocity at peak power. These data demonstrate that the direct effect of low pH on peak power in both slow‐ and fast‐twitch fibres at near‐in vivo temperatures (30°C) is greater than would be predicted based on changes in P0, and that the fatigue‐inducing effects of low pH on cross‐bridge function are still substantial and important at temperatures approaching those observed in vivo.

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