Department of Biomedical Informatics and Medical Education, University of Washington, Seattle, Washington, USA.
Pulmonary and Critical Care Section, San Francisco Veterans Affairs Health Care System, San Francisco, California, USA.
BMJ Open Respir Res. 2022 May;9(1). doi: 10.1136/bmjresp-2022-001217.
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.
To determine the contribution of cardiovascular mechanisms to SHS-associated exercise limitation.
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.
At peak exercise (highest workload completed (Watts)=156±46 watts (135±33 %predicted)), oxygen consumption and oxygen-pulse (O-Pulse) 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 was associated directly with O-Pulse, HR and SBP 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 was substantially (41%) mediated through its effect on O-Pulse (p=0.038). Although not statistically significant, a considerable proportion (36%) of air trapping effect on Watts seemed to be mediated through O-Pulse (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).
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.
既往接触二手烟（SHS）与运动受限有关。包括空气潴留在内的肺部因素对此受限有一定影响，但心血管因素的影响尚不清楚。
确定心血管机制在 SHS 相关运动受限中的作用。
我们检查了 245 名从未吸烟的个体在经历过远程、长期职业性 SHS 暴露且无已知心血管疾病史时进行最大努力运动的心血管反应。我们估计了氧脉冲（心输出量的代理）和收缩压（SBP）、舒张压和心率（HR）变化对运动能力的贡献，并检查了 SHS 与运动能力的关联是否通过这些变量介导。
在峰值运动时（完成的最高工作量（瓦特）=156±46 瓦特（100±24%预测值）），耗氧量和氧脉冲（O-Pulse）分别为 1557±476ml/min（100±24%预测值）和 11.0±3.0ml/beat（116±25%预测值），分别有 29%和 3%的参与者未达到其预测的正常范围。峰值运动时的氧饱和度为 98%±1%，所有参与者的氧饱和度均保持在>93%。66%的人表现出运动时的高血压反应。在调整了协变量的模型中，瓦特与 O-Pulse、HR 和 SBP 直接相关，与 SHS、空气潴留（残气量/总肺容量）和 SBP 随工作量的升高呈负相关（均<0.01）。此外，SHS 暴露与瓦特的关联主要通过其对 O-Pulse 的影响（p=0.038）而发生中介作用（41%）。虽然没有统计学意义，但空气潴留对瓦特的影响有相当大的比例（36%）似乎通过 O-Pulse 发生中介作用（p=0.078）。基线时有呼吸症状（改良医学研究委员会评分≥1）的可能性与 SBP 随工作量的增加呈更陡峭的上升有关（p<0.01）。
在经历远程 SHS 暴露的从不吸烟人群中，血压的异常升高和 SHS 相关的心输出量减少导致了运动能力的下降。
