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|153||Contraction-induced changes in skeletal muscle Na(+), K(+) pump mRNA expression - importance of exercise intensity and Ca(2+)-mediated signalling.|
Nordsborg NB; Kusuhara K; Hellsten Y; Lyngby S; Lundby C; Madsen K; Pilegaard H
Acta Physiol (Oxf) 2010; 198(4): 487-98
PubMed ID: 19895607
AIM: To investigate if exercise intensity and Ca(2+) signalling regulate Na(+),K(+) pump mRNA expression in skeletal muscle. METHODS: The importance of exercise intensity was evaluated by having trained and untrained humans perform intense intermittent and prolonged exercise. The importance of Ca(2+) signalling was investigated by electrical stimulation of rat soleus and extensor digitorum longus (EDL) muscles in combination with studies of cell cultures. RESULTS: Intermittent cycling exercise at approximately 85% of VO(2peak) increased (P < 0.05) alpha1 and beta1 mRNA expression approximately 2-fold in untrained and trained subjects. In trained subjects, intermittent exercise at approximately 70% of VO(2peak) resulted in a less (P < 0.05) pronounced increase ( approximately 1.4-fold; P < 0.05) for alpha1 and no change in beta1 mRNA. Prolonged low intensity exercise increased (P < 0.05) mRNA expression of alpha1 approximately 3.0-fold and alpha2 approximately 1.8-fold in untrained but not in trained subjects. Electrical stimulation of rat soleus, but not EDL, muscle increased (P < 0.05) alpha1 mRNA expression, but not when combined with KN62 and cyclosporin A incubation. Ionomycin incubation of cultured primary rat skeletal muscle cells increased (P < 0.05) alpha1 and reduced (P < 0.001) alpha2 mRNA expression and these responses were abolished (P < 0.05) by co-incubation with cyclosporin A or KN62. CONCLUSION: (1) Exercise-induced increases in Na(+),K(+) pump alpha1 and beta1 mRNA expression in trained subjects are more pronounced after high- than after moderate- and low-intensity exercise. (2) Both prolonged low and short-duration high-intensity exercise increase alpha1 mRNA expression in untrained subjects. (3) Ca(2+)(i) regulates alpha1 mRNA expression in oxidative muscles via Ca(2+)/calmodulin-dependent protein kinase (CaMK) and calcineurin signalling pathways. Nordsborg, N B