Proceedings of The Physiological Society

University College London December 2005 (2006) Proc Physiol Soc 1, PC24

Poster Communications

The effects of smoking on contractile properties and fatigue resistance of human quadriceps muscle

Wust, R C I; Morse, C I; Jones, D A; de Haan, A; Degens, H;

1. Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Alsager, Cheshire, United Kingdom. 2. Institute for Fundamental and Clinical Human Movement Sciences, Faculty of Human Movement Sciences, Vrije University, Amsterdam, Netherlands.

Smoking is a major cause of chronic obstructive pulmonary disease (COPD) but while COPD is often accompanied by skeletal muscle dysfunction, it is not known whether smoking itself has a negative effect on muscle function. We have measured the contractile properties and fatigue resistance of the quadriceps muscles of eight smokers (2 female, 6 male; mean (range) age: 25.6 (21-37) years), average smoking volume of 5.8 (1.515) pack years together with 13 age- and physical activity-matched controls (2 female, 11 male; age: 27.2 (2240) years) using voluntary and electrically stimulated isometric contractions at optimum knee angle. No differences were observed in maximal voluntary torque, torque-frequency relationship and muscle speed, the latter measured as contraction and half-relaxation times of a 100 Hz tetanus, nor was there a difference in the force oscillation amplitude at 10 Hz. During a 2 min period of repeated isometric contractions (1 s on, 1 s off) at 30 Hz, with intact circulation, greater fatigue was observed in smokers: torque declining to 58.4% (SD: 7.5%) and 67.8% (6.5%) of the starting value in smokers and control subjects, respectively (p<0.01, Students t test). We conclude that smoking reduces fatigue resistance. Since the electrical stimulation activated only about 30% of one quadriceps muscle, it is unlikely that the higher fatigueability was a result of cardio-respiratory changes but rather indicates a peripheral change in either the capillary supply or the oxidative capacity of the muscle. These changes may represent an early sign of the pathological muscle changes seen in COPD.

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