Loss of K⁺ from active muscles, leading to increased extracellular K⁺ concentration ([K⁺]_o), has been proposed to contribute to muscle fatigue by reducing excitability. Since strenuous exercise increases muscle temperature, it is of interest to know how temperature elevation modifies the sensitivity of skeletal muscles to increased [K⁺]_o.

Intact soleus muscles from humanely killed 4-week-old Wistar rats were mounted isometrically on force transducers and stimulated 2 s every 10 min with pulses of 0.2 ms duration. Choice of stimulation frequency (30-90 Hz) was based on a force frequency analysis to make certain that full tetanic force was obtained at all temperatures. During the experiments muscles were exposed to controlled changes in [K⁺]_o and temperature while force production was recorded. Compound action potentials were measured and M-wave area was taken as an expression of excitability.

As shown in Fig. 1, increasing [K⁺]_o from 4 to 10 mM at 20 °C reduced tetanic force production to 14 ± 4 % and M-wave area to 10 ± 7 % of the control level. At 10 mM K⁺ temperature elevation from 20 to 30 °C restored force production and M-wave area to 67 ± 14 and 65 ± 12 %, respectively. Force and M-wave area were closely correlated (r ² = 0.955, P < 0.001). Other experiments showed that when temperature was elevated from 20 to 35 °C the level of [K⁺]_o required to reduce tetanic force by 50 % increased from 8.8 to10.7 mM (n = 6, Student’s two-tailed t test).

The protective effect of elevated temperature on force production disappeared when ouabain (10^-3 M) was added to muscles, indicating that a temperature-dependent increase in the Na⁺-K⁺ pump activity contributed to the protective effect. Measurements of ouabain-suppressible ⁸⁶Rb⁺ uptake showed that increasing the temperature from 20 to 30 °C augmented Na⁺-K⁺ pump activity by 93 % (n = 9).

It is concluded that the sensitivity of skeletal muscles to high [K⁺]_o is reduced by elevated muscle temperature. We suggest that this effect is due to a protection of the excitability in part mediated by increased Na⁺-K⁺ pump activity. In addition, a reduction in slow inactivation of voltage-gated sodium channels associated with high muscle temperatures, may contribute to the observed reduction in sensitivity to extracellular K⁺ (Ruff, 1999).

All procedures accord with current National and local guidelines.