In conclusion, our data show that CS exposure or vitamin D deficiency alone did not attenuate the hypertrophic response of overloaded plantaris muscles, but this hypertrophic response was weakened when both conditions were combined. In situ fatigue resistance was elevated in hypertrophied plantaris, irrespective of vitamin D deficiency and/or CS exposure. The increase in plantaris muscle fiber cross-sectional area in response to overload was attenuated in vitamin D-deficient CS-exposed mice (smoking × diet interaction for hypertrophy, P = 0.03). Maximal exercise capacity, whole body strength, in situ plantaris muscle force, and key markers of hypertrophic signaling (Akt, 4EBP1, and FoxO1) were not significantly affected by smoking or diet. CS exposure instigated loss of body and muscle mass, and increased lung inflammatory cell infiltration ( P < 0.05), independently of diet. Twelve weeks later, the hypertrophic response was assessed. The right leg served as internal control. Six weeks after initiation of smoke or air exposure, sham surgery or denervation of the agonists of the left plantaris muscle was performed. Male C57Bl/6JolaH mice on a normal or vitamin D-deficient diet were exposed to CS or room air for 18 wk. We examined whether cigarette smoke (CS) exposure and/or vitamin D deficiency impairs the skeletal muscle hypertrophic response to overload. Vitamin D deficiency, which is highly prevalent in the general population, exerts similar deleterious effects on skeletal muscles to those induced by cigarette smoking.
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