TY - JOUR

T1 - Muscle ionic shifts during exercise: Implications for fatigue and exercise performance

AU - Hostrup, Morten

AU - Cairns, Simeon Peter

AU - Bangsbo, Jens

N1 - Copyright © 2021 American Physiological Society. All rights reserved.

PY - 2021

Y1 - 2021

N2 - Exercise causes major shifts in multiple ions (e.g., K+, Na+, H+, lactate-, Ca2+, and Cl-) during muscle activity that contributes to development of muscle fatigue. Sarcolemmal processes can be impaired by the trans-sarcolemmal rundown of ion gradients for K+, Na+, and Ca2+ during fatiguing exercise, while changes in gradients for Cl- and Cl- conductance may exert either protective or detrimental effects on fatigue. Myocellular H+ accumulation may also contribute to fatigue development by lowering glycolytic rate and has been shown to act synergistically with inorganic phosphate (Pi) to compromise cross-bridge function. In addition, sarcoplasmic reticulum Ca2+ release function is severely affected by fatiguing exercise. Skeletal muscle has a multitude of ion transport systems that counter exercise-related ionic shifts of which the Na+/K+-ATPase is of major importance. Metabolic perturbations occurring during exercise can exacerbate trans-sarcolemmal ionic shifts, in particular for K+ and Cl-, respectively via metabolic regulation of the ATP-sensitive K+ channel (KATP) and the chloride channel isoform 1 (ClC-1). Ion transport systems are highly adaptable to exercise training resulting in an enhanced ability to counter ionic disturbances to delay fatigue and improve exercise performance. In this article, we discuss (i) the ionic shifts occurring during exercise, (ii) the role of ion transport systems in skeletal muscle for ionic regulation, (iii) how ionic disturbances affect sarcolemmal processes and muscle fatigue, (iv) how metabolic perturbations exacerbate ionic shifts during exercise, and (v) how pharmacological manipulation and exercise training regulate ion transport systems to influence exercise performance in humans.

AB - Exercise causes major shifts in multiple ions (e.g., K+, Na+, H+, lactate-, Ca2+, and Cl-) during muscle activity that contributes to development of muscle fatigue. Sarcolemmal processes can be impaired by the trans-sarcolemmal rundown of ion gradients for K+, Na+, and Ca2+ during fatiguing exercise, while changes in gradients for Cl- and Cl- conductance may exert either protective or detrimental effects on fatigue. Myocellular H+ accumulation may also contribute to fatigue development by lowering glycolytic rate and has been shown to act synergistically with inorganic phosphate (Pi) to compromise cross-bridge function. In addition, sarcoplasmic reticulum Ca2+ release function is severely affected by fatiguing exercise. Skeletal muscle has a multitude of ion transport systems that counter exercise-related ionic shifts of which the Na+/K+-ATPase is of major importance. Metabolic perturbations occurring during exercise can exacerbate trans-sarcolemmal ionic shifts, in particular for K+ and Cl-, respectively via metabolic regulation of the ATP-sensitive K+ channel (KATP) and the chloride channel isoform 1 (ClC-1). Ion transport systems are highly adaptable to exercise training resulting in an enhanced ability to counter ionic disturbances to delay fatigue and improve exercise performance. In this article, we discuss (i) the ionic shifts occurring during exercise, (ii) the role of ion transport systems in skeletal muscle for ionic regulation, (iii) how ionic disturbances affect sarcolemmal processes and muscle fatigue, (iv) how metabolic perturbations exacerbate ionic shifts during exercise, and (v) how pharmacological manipulation and exercise training regulate ion transport systems to influence exercise performance in humans.

U2 - 10.1002/cphy.c190024

DO - 10.1002/cphy.c190024

M3 - Journal article

C2 - 34190344

VL - 11

SP - 1895

EP - 1959

JO - Comprehensive Physiology

JF - Comprehensive Physiology

SN - 2040-4603

IS - 3

ER -