Effects of training on potassium, calcium and hydrogen ion regulation in skeletal muscle and blood during exercise

Abstract

Ionic regulation is critical to muscle excitation, contraction and metabolism, and thus for muscle function during exercise. This review focuses on the effects of training upon K+, Ca2+ and H+ ion regulation in muscle and K+ regulation in blood during exercise. Training enhances K+ regulation in muscle and blood and reduces muscular fatiguability. Endurance, sprint and strength training in humans induce an increased muscle Na+, K+ pump concentration, usually associated with a reduced rise in plasma [K+] during exercise. Although impaired muscle Ca2+ regulation plays a vital role in fatigue, little is known about possible training effects. In rat fast-twitch muscle, overload-induced hypertrophy and endurance training were associated with reduced sarcoplasmic reticulum Ca2+ uptake, consistent with fast-to-slow fibre transition. In human muscle, endurance and strength training had no effect on muscle Ca2+ ATPase concentration. Whilst muscle Ca2+ uptake, release and Ca2+ ATPase activity were depressed by fatigue, no differences were found between strength athletes and untrained individuals. Muscle H+ accumulation may contribute to fatigue during intense exercise and is also modified by sprint training. Sprint training may increase muscle Lac- and work output with exhaustive exercise, but the rise in muscle [H+] is unchanged or attenuated, indicating a reduced rise in muscle [H+] relative to work performed. Muscle buffering capacity can be dissociated from this improved H+ regulatory capacity after training. Thus, training enhances muscle and blood K+ and muscle H+ regulation during exercise, consistent with improved muscular performance and reduced fatiguability; however, little is known about training effects on muscle Ca2+ regulation during contraction.

Reflex inhibition during muscle fatigue in endurance-trained and sedentary individuals

“…In addition, the trained muscle fibre has greater density and sensitivity of acetylcholine receptors at the motor endplate (Desaulniers et al 1998), thus augmenting the generation of a post-synaptic potential. Similarly, a greater density of Na + /K + pumps in the muscle fibre membrane of endurance-trained muscle (McKenna et al 1996) may allow action potentials to propagate along the muscle fibre membrane with less distance-related decay in amplitude. It is possible that such peripheral adaptations could necessitate a reduction in the central drive to prevent endurance-trained subjects from overshooting the required force.…”

“…In addition, circulating potassium levels are lower in trained than in untrained individuals following fatiguing work at a similar workload (McCoy and Hargreaves 1992). This could be related to the greater Na + /K + pump activity in the fibre membrane of endurancetrained individuals (McKenna et al 1996). Furthermore, the improved capillarization of muscle following endurance training could result in improved metabolite clearance (Brodal et al 1977).…”

Does oxidative capacity affect energy cost? An in vivo MR investigation of skeletal muscle energetics

“…In this line, it has been shown in vitro that lactate-H ? exchange via monocarboxylate transporter (Burgomaster et al 2007;McKenna et al 1996) and Na ? -H ?…”

Specific training improves skeletal muscle mitochondrial calcium homeostasis after eccentric exercise

“…An expected adaptation pathway is through improved calcium homeostasis. In skeletal muscle, there is evidence that prior same-day exercise as well as aerobic training improves sarcoplasmic reticulum calcium regulation (Holloway et al 2005;McKenna et al 1996). This is likely to lead to subsequent improvement in mitochondrial calcium content and limit dysfunction, but the effects of prior training on skeletal muscle mitochondria has not been well described.…”