Effect of smoking and smoking cessation on muscle and vascular function-a pilot study

Smoking is a preventable risk factor for the development of chronic diseases in the lungs, brain, heart and kidneys, but smoking can also affect vascular and muscle function. It has been observed, for instance, that the smokers suffer from an earlier onset skeletal muscle fatigue that may at least partly be caused by toxins, such as carbon monoxide (CO), in the blood. The impact of smoking and smoking cessation on skeletal muscle and vascular function however are unknown. Methodology. After obtaining ethical approval and informed written consent, we investigated the impact of smoking and 2 weeks smoking cessation on muscle and arterial function in 13 participants (8 smokers (S); 5 controls (C)). We measured blood CO with a smokelyser and nicotine using an ELISA. In the right femoral artery (FA) we measured flow and vasodilation induced by contractile activity and a short occlusion with 2D US. The muscle strength, fatigability of the right Vastus lateralis muscle were determined with a dynamometer. Results. The blood CO (S: 4 ± 0.9%; C: 0.0 ± 0.0 %, P < 0.003) and cotinine levels (179 ± 24 vs 27 ± 16 ng·ml-1, P < 0.001) were significantly higher, whereas maximal torque (208 ± 21 vs 259 ± 14 Nm, P < 0.03), flow (548 ± 42 vs 714 ± 80 ml·min-¹ P < 0.01) and FA diameter (6.8 ± 0.3 vs 7.6 ± 0.2 mm, P < 0.01) were significantly lower in smokers than non-smokers. After 2 weeks of smoking cessation, CO decreased to 0.3 ± 0.2% (P < 0.01) and cotinine to 30 ± 13 ng·ml-1 (P < 0.02) while there were no significant changes in FA diameter, flow, maximal torque or fatigue resistance. Conclusion Our data suggests that the reduced muscle and arterial function in smokers does not revert to normal after a short cessation period, although CO/Cotinine levels decline and may require a longer cessation period, supplemented with antioxidants to stabilize, improve or recover function.