Heavier smokers had lower TST measures of cardiore-spiratory fitness including peak exercise capacity, RPP (P
< .01, pack-years only), peak HR increase (P
< .05), and HR reserve (P
< .01). To our knowledge, this is the first large study to serrially evaluate maximum exercise responses in a large cohort of modern smokers. Our finding of a dose effect of cigarette smoke on TST parameters that are predictive of CVD risk and mortality is important, as it helps identify a mechanism by which increased smoking burden increases CVD risk, namely, reduced exercise capacity and impaired physiological responses to exercise. These findings are consistent with previous reports from smaller studies that compared certain exercise responses (eg, peak HR, exercise capacity) among smokers with nonsmokers and reports that described the longitudinal effects of continued smoking, the effects of acute exposure to smoke, or varying levels of smoke exposure in young adults.5,28-32
A recent report, however, suggested that younger smokers achieved a higher RPP during exercise than nonsmokers because of amplified BP changes.6
Second, we demonstrated that despite gaining weight, successful abstainers from smoking had greater improvements than continuing smokers in several TST parameters including RPP, peak HR increase, and HR reserve. These improvements were statistically significant even after adjusting for confounding variables, including baseline measures of smoking intensity, smoking burden, and CO levels. This is the first report, to our knowledge, of the longitudinal effects of smoking cessation on exercise parameters. Although exercise capacity and HR recovery did not improve significantly, the 3 parameters that did improve are important predictors of CVD and all-cause mortality.15,17-21
Our longitudinal findings are consistent with some small cross-sectional studies of the short-term effects of smoking cessation on certain exercise parameters30,33-35
and suggest that improved exercise physiology may be a mechanism for cessation-related reductions in CVD risk.
Importantly, the magnitude of improvement in TST parameters was not related to baseline smoking intensity or burden, suggesting that in the range of cigarette use reported in our subjects, TST parameters improve regardless of the degree of baseline smoking. That baseline smoking intensity and burden are not related to improvements in TST markers of CVD risk after cessation is consistent with our previous reports that improvements in HDL cholesterol36
and endothelial function8
in smokers who succesfully abstain are not related to baseline smoking intensity or burden either. This suggests a health benefit may be seen even amongst relatively light smokers. Also, older smokers who are able to quit may see the most improvement in TST parameters.
As expected, abstainers had larger increases in body mass index than individuals who continued to smoke cigarettes. Although increased weight is associated with reduced exercise capacity,37
the benefical effects of smoking cessation on several TST parameters still were observed among abstainers. We did not formally evaluate mechanisms for the improved TST parameters we observed. Ischemic responses were very rare, so our findings are unlikely to be caused by fewer individuals with myocardial ischemia. Exercise responses are influenced by catecholamines and vagal tone; however, we did not see a change in HR recovery or resting HR. Exercise responses can be affected by leisure time activities, but they did not predict changes in TST parameters in our study. We previously demonstrated improved flow-mediated vasodilation after smoking cessation, so it is possible that improved endothelial function with improved cardiac and skeletal blood flow may mediate some of the improvements we observed.8
Improved pulmonary function also may have contributed to our observations.
Because this was a randomized clinical trial of smoking cessation interventions, there were no nonsmoking controls. Therefore, we cannot determine the extent to which the exercise parameters that improved among abstainers approached normal values. Because stress tests were obtained only at baseline and after 3 years, we could not evaluate the time course of improvement with quitting. It is common for subjects in smoking cessation studies who relapse to drop out or miss follow-up visits,38-40
so we cannot exclude bias based on continued participation.
Although we observed longitudinal improvements in peak RPP, HR reserve, and HR increase with abstainence, we did not observe improvements in HR recovery or exercise capacity. Exercise capacity is a derived estimate of METs based on models related to VO2
max stress testing results and achieved treadmill stress test workloads. It has significant variability and imprecision, so it may be more difficult to show longitudinal improvements in this TST parameter than those that rely on more direct measurements. Vagal reactivation is the main determinant of the HR decrease seen immediately after exercise.15
It is possible that vagal tone does not improve quickly among individuals who abstain from smoking. Indeed, we did not observe differences in resting HR among eventual abstainers and continuing smokers. It also is possible that continued exposure to second-hand smoke among ex-smokers blunted the expected physiological improvement in this parameter.
In our study, 38.3% of subjects did not return for their 1-year follow-up visit, which is consistent with the 30% to 43% 1-year drop-out rates reported in other recent clinical trials of smoking cessation pharmacotherapy.38,39
Subjects who did not attend the 3-year visit were similar to subjects who only attended the baseline visit. Because second-hand smoke exposure was not quantified, the effects of smoking cessation on TST parameters may have been underestimated. Finally, the long-term effect of smoking cessation on CVD events was not evaluated, so the relationships between the changes in the TST parameters observed in this study and changes in long-term risk are not known.