Resistance training upregulates skeletal muscle Na+, K+-ATPase content, with elevations in both α1 and α2, but not β isoforms

Abstract

The Na + ,K + -ATPase (NKA) is important in regulating trans-membrane ion gradients, cellular excitability and muscle function. We investigated the effects of resistance training in healthy young adults on the adaptability of NKA content and of the specific α and β isoforms in human skeletal muscle. MethodsTwenty-one healthy young males (22.9 ±4.6 y; 1.80 ±0.70 m, 85.1 ±17.8 kg, mean±SD) underwent 7 weeks of resistance training, training three time per week (RT, n=16) or control (CON, n=5). The training program was effective with a 39% gain in leg press muscle strength (p=0.001). A resting vastus lateralis muscle biopsy was taken before and following RT or CON and assayed for NKA content ([ 3 H]ouabain binding site content) and NKA isoform (α1, α2, β1, β2) abundances. ResultsAfter RT, each of NKA content (12%, 311 ±76 vs 349 ±76 pmol.g wet weight -1 , p=0.01), NKA α1 (32%, p=0.01) and α2 (10%, p<0.01) isoforms were increased, whereas β1 (p=0.18) and β2 (p=0.22) isoforms were unchanged. NKA content and isoform abundances were unchanged during CON. ConclusionsResistance training increased muscle NKA content through upregulation of both α1 and α2 isoforms, which were independent of β isoform changes. In animal models, modulations in α1 and α2 isoform abundances in skeletal muscle may affect fatigue resistance during exercise, muscle hypertrophy and strength. Whether similar in-vivo functional benefits of these NKA isoform adaptations occurs in human muscle with resistance training remains to be determined.

A century of exercise physiology: effects of muscle contraction and exercise on skeletal muscle Na+,K+-ATPase, Na+ and K+ ions, and on plasma K+ concentration—historical developments

“…In healthy humans, 12 studies from 1990 to 2017 investigated the effects of training on NKA c in m. vastus lateralis , with consistent findings that endurance, high intensity and resistance training induced an 8–25% upregulation of NKA c , which was unrelated to mean training intensity, cumulative training time or training duration (Wyckelsma et al 2019 ) and a similar upregulation in NKA c after resistance training was recently confirmed (Altarawneh et al 2020 ). In chronic heart failure patients, there was no effect of training on m. vastus lateralis NKA c (Green et al 2001 ), whilst in contrast, in young patients with Type I diabetes, NKA c was increased by 8% after sprint training (Harmer et al 2006 ).…”

“…More recent training studies also show considerable differences in adaptability of NKA isoforms. Resistance training increased both α 1 (32%), α 2 (32%), with β 1 and β 2 unchanged (Altarawneh et al 2020 ), whilst, in another study, induced large increases in α 2 (70%) and β 1 (78%), with these also similarly increased after low-load resistance training with restricted blood flow (Wang et al 2023 ). High-intensity interval training for 6 weeks increased α 1 (41%) and β 1 (10%), but not α 2 (Lemminger et al 2022 ), did not change α 2 or β 1 , but increased glycosylated β 1 and lowered FXYD5 in Type IIa muscle fibres (Hostrup et al 2023 ).…”

Phase angle, muscle tissue, and resistance training

“…2B, evidence suggests that RT increases the content of pumps in both diseased [84] and healthy populations [82,85] by 15%. Also, considering the long-term upregulation effect of RT on the NA + , K + , and ATPase in muscle cells [82,86], the combined effect of the increase on these cell membrane structures is expected to enhance cell depolarization and repolarization processes, thus increasing the muscle contractile performance, preserving muscle function, and inhibiting the accumulation of fatigue at the cellular level of the muscle tissue. Although the increased electrolytic fluidity arising from the increase in sodium-potassium pumps could also represent a decrease in extra-to intracellular R and favorably increase PhA, particularly when applying stimulation frequencies within the β-dispersions range [87], no information to date exists linking these effects to changes in bioelectrical components.…”