Effects of high‐intensity intermittent training on potassium kinetics and performance in human skeletal muscle

Abstract

A rise in extracellular potassium concentration in human skeletal muscle may play an important role in development of fatigue during intense exercise. The aim of the present study was to examine the effect of intense intermittent training on muscle interstitial potassium kinetics and its relationship to the density of Na + ,K + -ATPase subunits and K ATP channels, as well as exercise performance, in human skeletal muscle. Six male subjects performed intense one-legged knee-extensor training for 7 weeks. On separate days the trained leg (TL) and the control leg (CL) performed a 30 min exercise period of 30 W and an incremental test to exhaustion. At frequent intervals during the exercise periods interstitial potassium ([K + ] I ) was determined by microdialysis, femoral arterial and venous blood samples were drawn and thigh blood flow was measured. Time to fatigue for TL was 28% longer (P < 0.05) than for CL (10.6 ± 0.7 (mean ± S.E.M.) versus 8.2 ± 0.7 min). The amounts of Na + ,K + -ATPase α 1 and α 2 subunits were, respectively, 29.0 ± 8.4 and 15.1 ± 2.7% higher (P < 0.05) in TL than in CL, while the amounts of β 1 subunits and ATP-dependent K + (K ATP ) channels were the same. In CL [K + ] I increased more rapidly and was higher (P < 0.05) throughout the 30 W exercise bout, as well at 60 and 70 W, compared to TL, whereas [K + ] I was similar at the point of fatigue (9.9 ± 0.7 and 9.1 ± 0.5 mmol l −1 , respectively). During the 30 W exercise bouts and at 70 W during the incremental exercise femoral venous potassium concentration ([K + ] v ) was higher (P < 0.05) in CL than in TL, but identical at exhaustion (6.2 ± 0.2 mmol l −1 ). Release of potassium to the blood was not different in the two legs. The present data demonstrated that intense intermittent training reduce accumulation of potassium in human skeletal muscle interstitium during exercise, probably through a larger re-uptake of potassium due to greater activity of the muscle Na + ,K + -ATPase pumps. The lower accumulation of potassium in muscle interstitium in the trained leg was associated with delayed fatigue during intense exercise, supporting the hypothesis that interstitial potassium accumulation is involved in the development of fatigue.

Human muscle net K+ release during exercise is unaffected by elevated anaerobic metabolism, but reduced after prolonged acclimatization to 4,100 m

“…Together, these studies support the suggestion of a link between anaerobic energy production and muscular K ϩ release via the degree of intramuscular acidosis. However, an attempt to block the K ATP channels during exercise failed to affect interstitial K ϩ accumulation (26). This finding may be because K ATP channels are not carrying a significant K ϩ current during exercise or because the pharmacological intervention was not effective.…”

“…For example, the higher blood lactate concentration causes plasma osmolality to increase, which results in a fluid shift from the interstitium to the blood. Because a high diffusional barrier may exist for K ϩ across endothelial cells (26,29), interstitial K ϩ may simply have been elevated by a reduced dilution space, and K ϩ release may have been higher because the concentration gradient between the interstitial space and the blood has been increased. Another approach to studying the potential coupling of intramuscular acidosis to K ϩ release has been by manipulation of systemic or local acid/base homeostasis by ingestion or infusion of buffers.…”

Post-Match Changes in Muscle Damage Markers among U-21 Soccer Players

“…Th is statement was supported by the observation of muscle interstitial potassium concentrations higher than 11 mmol/l during exhaustive exercise Note: K-potassium; Na-sodium: *p < 0.05 from the corresponding pre-match value. (Nielsen et al, 2004). Th e aforementioned values are high enough to depolarize the muscle membrane potential and reduce force development markedly (Cairns & Dulhunty, 1995).…”

Skeletal muscle fatigue – regulation of excitation–contraction coupling to avoid metabolic catastrophe

“…varies between 3.5 and 4.0 mM. However, this increases to 10-14 mM during muscle activity (Juel et al, 2000;Mohr et al, 2004;Nielsen et al, 2004;Street et al, 2005). In vitro at 37˚C, maximal tetanic force is not affected until the [K + ] e reaches 10 mM; at or above that concentration, tetanic force decreases (Cairns et al, 2011).…”