Exacerbated potassium-induced paralysis of mouse soleus muscle at 37°C vis-à-vis 25°C: implications for fatigue. K+ -induced paralysis at 37°C.

The main aim was to investigate the effects of raised [K+]o on contraction of isolated non-fatigued skeletal muscle at 37°C and 25°C to assess the physiological significance of K+ in fatigue. Mouse soleus muscles equilibrated at 25°C had good mechanical stability when temperature was elevated to 37°C. The main findings at 37°C vis-a-vis 25°C were as follows. When [K+]o was raised from 4 to 7 mM, there was greater twitch potentiation, but no significant difference in peak tetanic force. At 10 mM [K+]o there was (1) a faster time course for the decline of peak tetanic force, (2) a greater steady-state depression of twitches and tetani, (3) an increase of peak force over 50–200 Hz (whereas it decreased at 25°C), (4) significant tetanus restoration when stimulus pulse duration increased from 0.1 to 0.25 ms and (5) greater depolarisation of layer-2 fibres, with no repolarisation of surface fibres. These combined data strengthen the proposal that a large run-down of the K+ gradient contributes to severe fatigue at physiological temperatures via depolarisation and impaired sarcolemmal excitability. Moreover, terbutaline, a β2-adrenergic agonist, induced a slightly greater and more rapid, but transient, restoration of peak tetanic force at 10 mM [K+]o at 37°C vis-a-vis 25°C. A right shift of the twitch force–stimulation strength relationship at 10 mM [K+]o was partially reversed with terbutaline to confer the protective effect. Thus, catecholamines are likely to stimulate the Na+–K+ pump more powerfully at 37°C to restore excitability and attenuate, but not prevent, the detrimental effects of K+.