TY - JOUR
T1 - Inactivity and exercise training differentially regulate the abundance of Na+, K+-ATPase in human skeletal muscle
AU - Wyckelsma, Victoria L
AU - Perry, Ben D
AU - Bangsbo, Jens
AU - McKenna, Michael John
N1 - CURIS 2019 NEXS 331
PY - 2019
Y1 - 2019
N2 - Physical inactivity is a global health risk that can be addressed through application of exercise training suitable for an individual's health and age. People's willingness to participate in physical activity is often limited by an initially poor physical capability and early onset of fatigue. One factor associated with muscle fatigue during intense contractions is an inexcitability of skeletal muscle cells, reflecting impaired transmembrane Na+/K+ exchange and membrane depolarisation, which are regulated via the transmembranous protein, Na+,K+-ATPase (NKA). This short review focuses on the plasticity of NKA in skeletal muscle in humans following periods of altered usage, exploring NKA upregulation with exercise training and downregulation with physical inactivity. In human skeletal muscle, the NKA content quantified by the [3H]ouabain binding site content shows robust, yet tightly constrained upregulation of 8-22% with physical training, across a broad range of exercise training types. Muscle NKA content in humans undergoes extensive downregulation with injury that involves substantial muscular inactivity. Surprisingly, however, no reduction in NKA content was found in the single study which investigated short-term disuse. Despite clear findings that exercise training and injury modulate NKA content, the adaptability of the individual NKA isoforms in muscle (α1-3 and β1-3) and of the accessory and regulatory protein FXYD1, are surprisingly inconsistent across studies, for exercise training, as well as for injury/disuse. Potential reasons for this are explored. Finally, we provide suggestions for future studies to provide greater understanding of NKA regulation during exercise training and inactivity in humans.
AB - Physical inactivity is a global health risk that can be addressed through application of exercise training suitable for an individual's health and age. People's willingness to participate in physical activity is often limited by an initially poor physical capability and early onset of fatigue. One factor associated with muscle fatigue during intense contractions is an inexcitability of skeletal muscle cells, reflecting impaired transmembrane Na+/K+ exchange and membrane depolarisation, which are regulated via the transmembranous protein, Na+,K+-ATPase (NKA). This short review focuses on the plasticity of NKA in skeletal muscle in humans following periods of altered usage, exploring NKA upregulation with exercise training and downregulation with physical inactivity. In human skeletal muscle, the NKA content quantified by the [3H]ouabain binding site content shows robust, yet tightly constrained upregulation of 8-22% with physical training, across a broad range of exercise training types. Muscle NKA content in humans undergoes extensive downregulation with injury that involves substantial muscular inactivity. Surprisingly, however, no reduction in NKA content was found in the single study which investigated short-term disuse. Despite clear findings that exercise training and injury modulate NKA content, the adaptability of the individual NKA isoforms in muscle (α1-3 and β1-3) and of the accessory and regulatory protein FXYD1, are surprisingly inconsistent across studies, for exercise training, as well as for injury/disuse. Potential reasons for this are explored. Finally, we provide suggestions for future studies to provide greater understanding of NKA regulation during exercise training and inactivity in humans.
KW - Faculty of Science
KW - Na+,K+ pump
KW - Physical activity
KW - Disuse
U2 - 10.1152/japplphysiol.01076.2018
DO - 10.1152/japplphysiol.01076.2018
M3 - Review
C2 - 31369327
VL - 127
SP - 905
EP - 920
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 4
ER -