Abnormal heart rate (HR) rise during physical activity does not impair exercise capacity for patients with chronic heart failure (CHF), a multifaceted study found. Although a link between exercise capacity and chronotropic incompetence was evident in this population (r2=0.366 for those with mild-to-moderate left ventricular systolic dysfunction and r2=0.179 for those with severe dysfunction), it was weak compared with that seen among patients with normal left ventricular function (r2=0.420) in a retrospective cohort. In a randomized intervention crossover study, adjusting heart rate up or down with rate-adaptive pacemaker programming was not associated with better oxygen consumption, exercise times, or other exercise capacity metrics. In a second such experiment, HR-lowering by ivabradine (Corlanor) was not tied to worse exercise capacity either, found Klaus K. Witte, MD, of University of Leeds in the U.K., and colleagues, who reported the findings together in a paper online in the Journal of the American College of Cardiology. “This finding has widespread implications for pacemaker programming and the use of heart-rate lowering agents,” they noted. In particular, “although chronotropic incompetence and exercise tolerance are related, correcting this in CHF patients is unnecessary and might have adverse metabolic effects,” they wrote, adding that “physicians and their patients should be reassured that optimal doses of HR-lowering agents with the aim of achieving the best prognostic outcomes are unlikely to objectively worsen exercise capacity.” Rate-adaptive cardiac pacing mode for chronotropic incompetence has been tied to inconsistent improvements in exercise capacity. In fact, that same pacing program has also been thought to worsen cardiac function. In an accompanying editorial, Neal A. Chatterjee, MD, and Gregory D. Lewis, MD, both of Boston’s Massachusetts General Hospital, agreed that the findings “cast significant doubt on the causative role of chronotropic incompetence in exercise intolerance in HF and on a uniform strategy aiming for higher exercise HRs among unselected HF patients,” concluding that that “‘faster is not better’ for exercise HR in patients with heart failure and reduced ejection fraction.” However, “we believe there are ample opportunities to better define subphenotypes of exercise intolerance in heart failure,” the editorialists noted. “Such a mechanistic, precision medicine approach to exercise intolerance will help to refine selection of those who may benefit most from our expanding armamentarium of pharmacologic and device-based interventions,” they wrote. Witte’s investigation of CHF patients consisted of an observational component (n=195) and two prospective, randomized crossover studies (n=79 and 40). Participants in the two interventional HR substudies had prior pacemaker implantation. Disclosures The study was supported by an unrestricted grant from Servier. Witte declared no relevant conflicts of interest. Lewis reported support by the NIH, American Heart Association, and receipt of the Hassenfeld Clinical Scholar Award.