Smoking impairs muscle protein synthesis and increases the expression of myostat

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Am J Physiol Endocrinol Metab. 2007 Jul 3

Smoking impairs muscle protein synthesis and increases the

expression of myostatin and MAFbx in muscle.

sen AM, Magkos F, Atherton P, Selby A, K, Rennie MJ,

Pedersen BK, Mittendorfer B.

Copenhagen Muscle Research Center, Copenhagen, Denmark.

Smoking causes multiple organ dysfunction. The effect of smoking on

skeletal muscle protein metabolism is unknown. We hypothesized that

the skeletal muscle protein synthesis rate is depressed in smokers

compared with non-smokers.

We studied eight smokers (>/=20 cigarettes/day for >/=20 years) and

eight non-smokers matched for sex (4 men and 4 women per group), age

(65+/-3 and 63+/-3y, respectively; means+/-SEM) and body mass index

(25.9+/-0.9 and 25.1+/-1.2 kg/m(2), respectively). Each subject

underwent an intravenous infusion of stable isotope-labeled leucine

in conjunction with blood and muscle tissue sampling to measure the

mixed muscle protein fractional synthesis rate (FSR) and whole-body

leucine rate of appearance (Ra) in plasma (an index of whole-body

proteolysis), the expression of genes involved in the regulation of

muscle mass (myostatin, a muscle growth inhibitor; MAFBx and MuRF-1,

which encode E3 ubiquitin ligases in the proteasome proteolytic

pathway) and that for the inflammatory cytokine tumor necrosis

factor-alpha (TNFalpha) in muscle, and the concentration of

inflammatory markers in plasma which are associated with muscle

wasting in other conditions.

There were no differences between non-smokers and smokers in leucine

Ra and plasma concentrations of inflammatory markers, or TNFalpha

mRNA in muscle, but muscle protein FSR was much less (0.037+/-0.005

vs. 0.059+/-0.005 %/h, respectively; P=0.004) and myostatin and

MAFBx (but not MuRF-1) expression was much greater (by ~33% and 45%,

respectivley; P<0.05) in the muscle of smokers than of non-smokers.

We conclude that smoking impairs the muscle protein synthesis

process and increases the expression of genes associated with

impaired muscle maintenance.