Post-exercise heart rate recovery in healthy, obeses, and COPD subjects: relationships with blood lactic acid and PaO2 levels

Abstract

Because blood acidosis and arterial oxygenation (PaO(2)) play key roles in the chemoreflex control of cardiac activity, we hypothesized that heart rate (HR) decay rate after maximal exercise may be linked to post-exercise increase in blood lactate (LA) level and/or the resting PaO(2). Twenty healthy subjects and thirty five patients at risks of cardiovascular diseases (20 obeses; 15 patients with chronic obstructive pulmonary disease, COPD) performed a maximal cycling exercise. During the recovery period, HR was continuously measured for consecutive 10-s epochs allowing to compute linear or second order polynomial equations and to calculate every minute HR variations compared to peak HR value (DeltaHR). PaO(2) was measured at rest and post-exercise maximal LA level was determined. A second order polynomial equation (y = a(2) x (2) + b(2) x + c) best fitted the post-exercise HR decay rate. The a(2) and b(2) coefficients and DeltaHR did not depend on age, sex, and body mass index. Despite a large scattering of HR decay rate, even present in healthy subjects, a(2) and DeltaHR were significantly lower in obeses and COPDs. In the whole population, both a(2) coefficient and DeltaHR were negatively correlated with maximal post-exercise LA level. DeltaHR was lowered in hypoxemic patients. Thus, the slowest post-exercise HR decay rate was measured in subjects having the highest peak LA increase or hypoxemia. Thus, even in healthy subjects, the post-exercise HR decay rate is lowered in individuals having an accentuated exercise-induced LA increase and/or hypoxemia. The mechanisms of delayed post-exercise HR recovery are only suspected because significant correlations cannot assess cause-to-effect relationships.