During high-intensity exercise, hard-working muscles quickly fatigue as they anaerobically break down glycogen, forming lactate, which causes the familiar `burning' feeling. This creates acidic conditions, which probably compromises calcium transport in the muscles, in turn reducing force development. Until recently, this scenario would have been the standard textbook answer, however recent compelling evidence shows that lactate might actually be beneficial, rather than detrimental, to force development in working heart and skeletal muscle. During strenuous exercise, working muscles lose potassium (K+), raising the extracellular K+concentration, which makes muscle cells less excitable and decreases force production. As muscles lose K+, lactate and circulating catecholamines – stress hormones such as adrenaline – also accumulate in the bloodstream. These compounds can counteract the negative effects of increased extracellular K+ concentration on muscles. In a recent paper, Frank de Paoli and co-workers from the University of Aarhus,Denmark, set out to investigate the combined effect of catecholamines and lactate on isolated rat skeletal muscle exposed to high concentrations of extracellular K+.
The team incubated rat soleus muscle in a temperature-controlled bath at 30°C, where they also controlled K+, lactate, adrenaline and carbon dioxide levels. To determine the effect of extracellular K+concentration on muscle contraction, they stimulated the muscle and measured its force generation as they raised K+ concentration in the bath from 4 to 15 mmol l–1. They found that this reduced force generation by 85%.
By adding lactate to the bath, the team found that force production recovered slightly in a dose-dependent manner, with 20 mmol l–1 lactate having maximal positive effect. Adding physiological levels of adrenalin (10–5 mol l–1) improved force production further under high K+ conditions, and when added together with 20 mmol l–1 lactate, the additive effect of the two compounds led to an almost full recovery of force production.
De Paoli and co-workers found that the adrenaline-induced force recovery was caused through improved excitability as a consequence of an increased Na+–K+ pump activity in the muscle cell membrane. This pump actively moves K+ back into the cell, and Na+out, increasing the chemical K+ gradient, which helps to re-polarise the muscle membrane and makes contraction more likely. By contrast, lactate had no effect on Na+–K+ pump activity, instead helping force recovery by decreasing intracellular pH. In short, a decreased intracellular pH enhances force production through a decrease in chloride channel activity, which in turn affects the balance of all the ions on either side of the membrane, again leading to a re-polarised membrane potential. Adrenaline did not change intracellular pH; hence, the protective effects of lactate and adrenaline on muscle excitability and force generation occur through two distinct mechanisms that have an additive effect.
These results suggest that circulating catecholamines and development of acidic conditions during exhaustive exercise may improve muscles' tolerance to elevated K+ levels. This implies that during high-intensity activity with high extracellular K+ and adrenaline, lactate actually serves as a performance-enhancing chemical, rather than being the cause of muscle fatigue. These exciting results were, however, all obtained using isolated muscles in a dish at a relatively low temperature. Only future experiments will determine whether the mechanisms outlined in this paper contribute significantly in live animals with intact contracting muscles.
