At the end of maximal exercise, heart rate drops exponentially in healthy humans, as vagal tone returns from its profound exertional withdrawal and sympathetic activation wanes.1–4 After Bruce protocol exercise, for example, the healthy heart slows by > 10 to 12 beats/min, 60 s after end-exercise (18 beats/min for stress echocardiography).5– A delayed heart rate recovery (HRR) has been associated with increased all-cause mortality in most studies,6–11 but not all.12 Cole et al6 reported that the 6-year mortality rate from all causes was 19% in patients with an HRR of < 13 beats/min, at 1 min after end-exercise (relative risk, 4.0; 95% confidence interval [CI], 3.0 to 5.2). Later, patients studied by Nishime et al8 who had an abnormal HRR experienced a 5-year all-cause mortality rate of 8% (risk ratio, 4.16; 95% CI, 3.33 to 5.19), and a mortality rate of 9% in patients whose abnormal HRR was coupled with chronotropic incompetence. When both of these abnormalities occurred in persons with Duke treadmill scores of 4 or worse, the 5-year all-cause mortality rate was 18%.13– The report of Seshadri et al in this issue of CHEST (see page 1287) raises the possibility that some of this excess mortality is due to underlying pulmonary disease rather than to cardiovascular causes. Their retrospective analysis of 627 treadmill patients identified 229 (36.5%) with an abnormal HRR, while 188 (30%) had an abnormal chronotropic index. These HRR and chronotropic index abnormalities appear to be closely correlated (r = 0.86 for the respective means, as percentages of abnormal values, when analyzed by quartiles of FEV1 percent predicted [Table 2 of Sheshadri et al]). One wonders how many patients had abnormal Duke treadmill scores.15 Perhaps future publications will let us know whether the prognostic implications of these observations in patients with lung disease are as gloomy as they are in patients suspected of having cardiovascular conditions.