Abstract
ABSTRACTBackgroundProlonged past exposure to secondhand tobacco smoke (SHS) is associated with exercise limitation. Pulmonary factors including air trapping contribute to this limitation but the contribution of cardiovascular factors is unclear.MethodsTo determine contribution of cardiovascular mechanisms to SHS-associated exercise limitation, we examined the cardiovascular responses to maximum effort exercise testing in 166 never-smokers with remote but prolonged occupational exposure to SHS and no known history of cardiovascular disease except nine with medically-controlled hypertension. We estimated the contribution of oxygen-pulse (proxy for cardiac stroke volume) and changes in systolic (SBP) and diastolic blood pressures (DBP) and heart rate (HR) over workload towards exercise capacity, and examined whether the association of SHS with exercise capacity was mediated through these variables.ResultsOxygen consumption (VO2Peak) and oxygen-pulse (O2-PulsePeak) at peak exercise were 1,516±431mL/min (100±23 %predicted) and 10.6±2.8mL/beat (117±25 %predicted), respectively, with 91 (55%) and 43 (26%) of subjects not being able to achieve their maximum predicted values. Sixty-two percent showed hypertensive response to exercise by at least one established criterion. In adjusted models, VO2Peak was associated directly with O2-Pulse and inversely with rise of SBP and DBP over workload (all P<0.05). Moreover, SHS exposure association with VO2Peak was mainly (84%) mediated through its effect on oxygen-pulse (P=0.034). Notably, although not statistically significant, a large proportion (60%) of air trapping effect on VO2Peak seemed to be mediated through oxygen-pulse (P=0.066).DiscussionIn a never-smoker population with remote prolonged exposure to SHS, abnormal escalation of afterload and an SHS-associated reduction in cardiac output contributed to lower exercise capacity.
Publisher
Cold Spring Harbor Laboratory