Six weeks of high-load resistance and low-load blood flow restricted training increase Na/K-ATPase sub-units α2 and β1 equally, but does not alter ClC-1 abundance in untrained human skeletal muscle

Abstract

Contractile function of skeletal muscle relies on the ability of muscle bers to trigger and propagate action potentials (APs). These electrical signals are created by transmembrane ion transport through ion channels and membrane transporter systems. In this regard, the Cl-ion channel 1 (ClC-1) and the Na+/K--ATPase (NKA) are central for maintaining ion homeostasis across the sarcolemma during repetitive AP ring inherent of intense contractile activity. Therefore, this randomized controlled trial (RCT) aimed to investigate the changes in ClC-1 and speci c NKA subunit isoform expression in response to 6 weeks ( 18training sessions) of heavy-load resistance exercise (HLRE) and low-load blood ow restricted resistance exercise (BFRRE), respectively. Also, the potential associations between protein expression and contractile performance were investigated. We show that muscle ClC-1 abundance was not affected by either exercise modality, whereas NKA subunit isoforms 𝛼 2 and 𝛽 1 increased appx. 80-90% with BFRRE (p<0.05) and 70-80% with HLRE (p<0.05). No differential impact between exercise modalities was observed. At baseline, ClC-1 protein expression correlated inversely with dynamic knee extensor strength (r=-0.365, p=0.04). No correlation was observed between NKA subunit content and contractile performance at baseline. However, training-induced changes in NKA 𝛼 2 subunit (r=0.603, p<0.01) and 𝛽 1 subunit (r=0.453, p<0.05) correlated with changes in maximal voluntary contraction. These results suggest that the initial adaptation to resistance exercise does not involve changes in ClC-1 abundance in untrained skeletal muscle.

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

“…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 ).…”