The measurement of K e + concentration changes in human muscles during volitional contractions

Abstract

Changes of extracellular potassium concentration [( K+]e) were measured in human muscles during volitional isometric contractions using liquid ion-exchanger electrodes. In principle, an intramuscular injection needle containing a microelectrode with a side-pore was inserted into the brachioradialis muscle. After insertion of the needle, the glass ion-selective microelectrode (ISM) could be moved out of the protective trocar shield into the muscle tissue. The average values of [K+]e in human muscles during maximal effort rose from 4.5 mmol/l K+ to 9.5 mmol/l K+. These values correspond closely to those previously found in muscles of experimental animals.

Measurement of Na+,K+-ATPase Activity in Human Skeletal Muscle

“…Second, the optimal K ϩ activation for human skeletal muscle was achieved with 10 mM KCl, in agreement with other substrate assays for Na ϩ ,K ϩ -ATPase (23,24). Interestingly, the optimal K ϩ -stimulating concentration is equivalent to the peak muscle interstitial [K ϩ ] reported during maximal muscular contractions in humans (25).…”

Conduction Velocity of Quiescent Muscle Fibers Decreases During Sustained Contraction

“…Blood flow has indeed a main role in the maintenance of the force level during muscle contraction, as shown by the comparison of sustained and intermittent maximal exercises (Pitcher and Miles 1997). Accordingly, larger K ϩ extracellular concentrations were observed after high-force isometric contractions with respect to intermittent contractions (Vyskocil et al 1983). In the ischemic conditions studied, the accumulation of K ϩ thus progressed at a faster rate than with normal blood circulation.…”

Spreading of fatigue-related effects from active to inactive parts in the medial gastrocnemius muscle of the cat

“…Long-lasting activation of a muscle leads to a noticeable increase in extracellular K + concentration (Juel 1988;Juel et al 1990;Bangsbo et al 1993;Hallen 1996). This should in turn decrease the resting membrane potential as well as the amplitude and the propagation of action potentials (Vyskocil et al 1983;West et al 1996). Reduced action potentials would decrease the release of Ca 2+ from the sarcoplasmic reticulum, thus diminishing the force output (Westerblad et al 1993;Fitts 1994;Cairns and Dulhunty 1995).…”