Mi. Lindinger, POTASSIUM REGULATION DURING EXERCISE AND RECOVERY IN HUMANS - IMPLICATIONS FOR SKELETAL AND CARDIAC-MUSCLE, Journal of Molecular and Cellular Cardiology, 27(4), 1995, pp. 1011-1022
This review summarizes the main cellular mechanisms involved in potass
ium regulation in plasma and skeletal muscle during exercise. The effe
cts of exercise-induced hyperkalemia and post-exercise hypokalemia on
the cardiac action potential are reviewed in light of recent research
on Na+ and K+ channel activity. Specific consideration is given to Krelease from contracting skeletal muscle, K+ uptake by contracting ske
letal muscle, K+ uptake by non-contracting tissues during the period o
f exercise, and K+ uptake by skeletal muscle recovering from contracti
le activity. The onset of exercise is associated with a net release of
K+ from contracting skeletal muscle that results in an increase in pl
asma [K+]. Resultant decreases in intracellular [K+] and increases in
interstitial [K+] in contracting skeletal muscle have been implicated
in the fatigue process. The rate and magnitude of increase in plasma [
K+] is dependent on exercise intensity, trained state of the individua
l, and on drugs such as beta-adrenoceptor blockers and caffeine. Durin
g exercise, the uptake of K+ from the blood by non-contracting tissues
may be important in preventing plasma [K+] from rising to excessive l
evels that will impair skeletal muscle and myocardial excitability and
contractility. Cessation of exercise results in a rapid decrease in p
lasma [K+], often to 3 mEq/l or less with intense exercise, that may b
e maintained for prolonged periods, The rapid increases and decreases
in plasma [K+] with onset and cessation of exercise, respectively, has
been implicated in altered myocardial function and sudden cardiac dea
th, Recent studies suggest that increases in catecholamines during exe
rcise are cardioprotective to the arrhythmogenic effects of hyperkalem
ia.