UCSF

Background

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.

Objective

To determine the contribution of cardiovascular mechanisms to SHS-associated exercise limitation.

Methods

We examined the cardiovascular responses to maximum-effort exercise in 245 never-smokers with remote, prolonged occupational exposure to SHS and no known history of cardiovascular disease. We estimated the contribution of oxygen-pulse (proxy for cardiac stroke volume) and changes in systolic blood pressures (SBP), diastolic blood pressures and heart rate (HR) towards exercise capacity, and examined whether the association of SHS with exercise capacity was mediated through these variables.

Results

At peak exercise (highest workload completed (Watts_Peak)=156±46 watts (135±33 %predicted)), oxygen consumption and oxygen-pulse (O₂-Pulse_Peak) were 1557±476 mL/min (100±24 %predicted) and 11.0±3.0 mL/beat (116±25 %predicted), respectively, with 29% and 3% participants not achieving their predicted normal range. Oxygen saturation at peak exercise was 98%±1% and remained >93% in all participants. Sixty-six per cent showed hypertensive response to exercise. In models adjusted for covariates, Watts_Peak was associated directly with O₂-Pulse_Peak, HR_Peak and SBP_Peak and inversely with SHS, air trapping (residual volume/total lung capacity) and rise of SBP over workload (all p<0.01). Moreover, SHS exposure association with Watts_Peak was substantially (41%) mediated through its effect on O₂-Pulse_Peak (p=0.038). Although not statistically significant, a considerable proportion (36%) of air trapping effect on Watts_Peak seemed to be mediated through O₂-Pulse_Peak (p=0.078). The likelihood of having baseline respiratory symptoms (modified Medical Research Council score ≥1) was associated with steeper rise in SBP over workload (p<0.01).

Conclusion

In a never-smoker population with remote exposure to SHS, abnormal escalation of blood pressure and an SHS-associated reduction in cardiac output contributed to lower exercise capacity.