POTASSIUM REGULATION DURING EXERCISE AND RECOVERY IN HUMANS - IMPLICATIONS FOR SKELETAL AND CARDIAC-MUSCLE

Authors
Citation
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
Citations number
84
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00222828
Volume
27
Issue
4
Year of publication
1995
Pages
1011 - 1022
Database
ISI
SICI code
0022-2828(1995)27:4<1011:PRDEAR>2.0.ZU;2-Z
Abstract
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.