Because blood acidosis and arterial oxygenation (PaO2) 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 PaO2. 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 (ΔHR). PaO2 was measured at rest and post-exercise maximal LA level was determined. A second order polynomial equation (y = a2x2 + b2x + c) best fitted the post-exercise HR decay rate. The a2 and b2 coefficients and ΔHR did not depend on age, sex, and body mass index. Despite a large scattering of HR decay rate, even present in healthy subjects, a2 and ΔHR were significantly lower in obeses and COPDs. In the whole population, both a2 coefficient and ΔHR were negatively correlated with maximal post-exercise LA level. ΔHR 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.
exercise recovery cardiac function lactic acid normal subjects obesity COPD