Abstract

Muscle dysfunction is thought to contribute to exercise intolerance in smokers with COPD. In this study, cigarette smoke (CS) was hypothesized to impair skeletal muscle fatigue resistance. To test this hypothesis, adult C57Bl6 mice were exposed via a nose‐only system to daily periods of CS (5 cigarettes/period for 2 periods, 5 days/week) for 8 weeks and compared to mice delivered CS‐extract (weekly, i.p) and control, unexposed mice. Body weights were recorded each week. Gastrocnemius complex fatigue resistance was evaluated by measuring the time to reach 50% of maximal force when electrically stimulated to contract in situ. Compared to control mice, body weights were decreased in CS‐exposed mice, but not CS‐extract mice, at 3‐weeks (7.4%, p<0.05), 7‐weeks (7.9%, p<0.05), and 8‐weeks (12.4%, p<0.001). However, gastrocnemius, soleus, and plantaris mass / body weight ratios were not different between groups. A trend to earlier fatigue was seen in CS‐extract mice (Con. 342 ± 72 sec., CS‐exposed 310 ± 111 sec., CS‐extract 177 ± 16 sec., p=0.06). These data suggest the route or amount of CS that circulates in the blood may influence the extent of peripheral skeletal muscle dysfunction.Grant Funding Source: Supported by NIH 1 PO1 HL091830‐01A1

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