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Beta -adrenoceptor agonist salbutamol increases protein turnover rates and alters signalling in skeletal muscle after resistance exercise in young men

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Vis graf over relationer

The effect of beta2 -adrenoceptor stimulation on skeletal muscle protein turnover and intracellular signalling is insufficiently explored in humans, particularly in association with exercise. In a randomized placebo-controlled crossover study with 12 trained men, the effect of beta2 -agonist (6 × 4 mg oral salbutamol) on protein turnover rates, intracellular signalling, and mRNA response in skeletal muscle was investigated 0.5-5 h after quadriceps resistance exercise. Each trial was preceded by a four-day lead-in treatment period. Leg protein turnover rates were assessed by infusion of [13 C6 ]-phenylalanine and sampling of arterial and venous blood as well as vastus lateralis muscle biopsies 0.5 and 5 h after exercise. Furthermore, myofibrillar fractional synthesis rate (FSR), intracellular signalling and mRNA response were measured in muscle biopsies. Mean (±95%CI) myofibrillar FSR was higher for salbutamol than placebo [0.079(±0.007) vs. 0.066(±0.004)% × h-1 ](P < 0.05). Mean net leg phenylalanine balance 0.5-5 h after exercise was 3.6(±2.6) nmol × min-1 × 100 gLeg Lean Mass-1 higher for salbutamol than placebo (P < 0.01). Phosphorylation of Akt2, CREB and PKA-substrate 0.5 and 5 h after exercise as well as phosphorylation of eEF2 5 h after exercise was higher (P < 0.05) for salbutamol than placebo. Calpain-1, FoxO1, myostatin and Smad3 mRNA content was higher (P < 0.01) for salbutamol than placebo 0.5 h after exercise, and FoxO1 and myostatin mRNA content 5 h after, whereas ActivinRIIB mRNA content was lower (P < 0.01) for salbutamol 5 h after. These observations suggest that beta2 -agonist increases protein turnover rates in skeletal muscle after resistance exercise in humans, with concomitant cAMP/PKA and Akt2 signalling, and modulation of mRNA response of growth-regulating proteins. This article is protected by copyright. All rights reserved.

OriginalsprogEngelsk
TidsskriftThe Journal of physiology
Vol/bind596
Udgave nummer17
Sider (fra-til)4121-4139
Antal sider18
ISSN0022-3751
DOI
StatusUdgivet - 2018

ID: 54718915