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1 Department of Physiology, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: Akh{at}fi.au.dk.
Intensive exercise is associated with a pronounced increase in extracellular K+ ([K+]o). Due to the ensuing depolarisation and loss of excitability this contributes to muscle fatigue. Intensive exercise also increases the level of circulating catecholamines and lactic acid, which both have been shown to alleviate the depressing effect of hyperkalemia in slow-twitch muscles. Due to their larger exercise-induced loss of K+, fast-twitch muscles are more prone to fatigue caused by increased [K+]o than slow-twitch muscles. Fast-twitch muscles also produce more lactic acid. We therefore compare the effects of catecholamines and lactic acid on the maintenance of contractility in rat fast-twitch (EDL) and slow-twitch (soleus) muscles. Intact muscles were mounted on force transducers and stimulated electrically to evoke short isometric tetani. Elevated [K+]o (11 and 13 mM) was used to reduce force to around 20 % of control force at 4 mM K+. In EDL the 
2-agonist salbutamol (10-5 M) restored tetanic force to 83 ± 2 % of control force, whereas in soleus salbutamol restored tetanic force to 93 ± 1 %. In both muscles, salbutamol induced hyperpolarization (5-8 mV), reduced intracellular Na+ content and increased Na+-K+ pump activity, leading to an increased K+ tolerance. Lactic acid (24 mM) restored force from 22 ± 4 % to 58 ± 2 % of control force in EDL, an effect that was significantly lower than in soleus. These results amplify and generalize the concept that the exercise-induced acidification and increase in plasma catecholamines counterbalance fatigue arising from rundown of Na+ and K+-gradients.
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