Chronic beta2-adrenergic stimulation induces oxidative-to-glycolytic and slow-to-fast twitch transition of skeletal muscle and attenuates training-induced increases in rate of Ca2+ uptake of the sarcoplasmic reticulum following 11 weeks of resistance training in active young men

The Biomedical Basis of Elite Performance 2016 (Nottingham, UK) (2016) Proc Physiol Soc 35, PC57

Poster Communications: Chronic beta2-adrenergic stimulation induces oxidative-to-glycolytic and slow-to-fast twitch transition of skeletal muscle and attenuates training-induced increases in rate of Ca2+ uptake of the sarcoplasmic reticulum following 11 weeks of resistance training in active young men

S. Jessen1, A. Kalsen1, M. Kreiberg1, J. Onslev1, N. Ørtenblad2, V. Backer1, J. Bangsbo3, M. Hostrup1

1. Department of Respiratory Research, Bispebjerg University Hospital, Copenhagen, Denmark. 2. Department of Sports Science and Biomechanics, University of Southern Denmark, Odense, Denmark. 3. Department of Nutrition, Exercise and Sports, Section of Integrated Physiology, University of Copenhagen, Copenhagen, Denmark.

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Chronic stimulation of β2-adrenoceptors increases Ca2+-handling, and induces shifts myosin heavy chain(MHC) I to MHCII isoform and from an oxidative to a glycolytic phenotype in animals. However, no study has investigated the additive effect of β2-adrenoceptor stimulation and resistance training in humans. In the present study we investigated the effect of 11 weeks of resistance training alone or in combination with β2-adrenergic stimulation on sarcoplasmic reticulum (SR) Ca2+ handling and MHC isoform distribution, as well as on oxidative and glycolytic enzymatic activity of skeletal muscle in young men. Twenty-six trained men were randomized to either placebo (PLA) or oral salbutamol (4×4 mg×d-1, SAL). Subjects completed a supervised 11-week resistance training intervention three times pr. week. Before and after the intervention, MHC isoform distribution, SR Ca2+ handling, and maximal activity of CS, HAD, PFK, LDH, and CK were measured in biopsies collected from the vastus lateralis muscle. In SAL, MHCIIa isoforms increased (P≤0.05) by 6±5% (mean±95%CI) with the intervention, whereas MHCI isoforms decreased (P≤0.05) by 6±6%. MHC isoform distribution did not change with the intervention in PLA. Rate of Ca2+ release increased (P≤0.05) in both groups with the intervention (SAL: 2.6±0.5 to 2.8±0.5 Ca2+×min−1(g×protein−1); PLA: 2.5±0.5 to 2.8±0.5 Ca2+×min−1(g×protein−1)). In SAL, time constant of Ca2+ uptake was unchanged with the intervention (-6%), whereas it was 14% lower (P≤0.01) after the intervention in PLA compared with before. In SAL, maximal activity of CS decreased (P≤0.01) with the intervention (32±3 to 29±3 µmol×g dw-1×min-1), whereas no change was observed in PLA (29±3 to 30±3 µmol×g dw-1×min-1). Likewise, maximal activity of HAD decreased (P≤0.001) with the intervention in SAL (24±2 to 20±2 µmol×g dw-1×min-1), while no change was observed in PLA (22±2 to 22±2 µmol×g dw-1×min-1). Maximal activity of LDH increased (P ≤ 0.001) with the intervention in SAL (463±83 to 524±83 µmol×g dw-1×min-1), whereas no change was observed in PLA (515±83 to 535±83 µmol×g dw-1×min-1). Maximal activity of PFK and CK did not change with intervention in either group. In conclusion, β2-adrenergic stimulation induces muscle fiber type transition towards a fast twitch glycolytic phenotype following resistance training. Furthermore, β2-adrenergic stimulation attenuates resistance training-induced increases in Ca2+ uptake function.



Where applicable, experiments conform with Society ethical requirements.

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