Ba Abdoulaye, Delliaux Stephane, Bregeon Fabienne, Levy Samuel, Jammes Yves
UMR MD2 (P2COE), IFR Jean Roche, Faculty of Medicine, University of Mediterranee, Bd. Pierre Dramard, 13916, Marseille Cedex 20, France.
Clin Res Cardiol. 2009 Jan;98(1):52-8. doi: 10.1007/s00392-008-0723-0. Epub 2008 Oct 13.
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.
由于血液酸中毒和动脉氧合（PaO₂）在心脏活动的化学反射控制中起关键作用，我们推测最大运动后心率（HR）衰减率可能与运动后血乳酸（LA）水平升高和/或静息PaO₂有关。20名健康受试者和35名有心血管疾病风险的患者（20名肥胖者；15名慢性阻塞性肺疾病患者，COPD）进行了最大强度的自行车运动。在恢复期，连续10秒测量心率，以计算线性或二阶多项式方程，并计算与峰值心率值（ΔHR）相比每分钟的心率变化。测量静息时的PaO₂，并确定运动后最大LA水平。二阶多项式方程（y = a₂x² + b₂x + c）最适合运动后心率衰减率。a₂和b₂系数以及ΔHR不依赖于年龄、性别和体重指数。尽管心率衰减率存在很大差异，即使在健康受试者中也是如此，但肥胖者和COPD患者的a₂和ΔHR显著较低。在整个人群中，a₂系数和ΔHR均与运动后最大LA水平呈负相关。低氧血症患者的ΔHR降低。因此，在运动后LA升高峰值最高或存在低氧血症的受试者中，测量到的运动后心率衰减率最慢。因此，即使在健康受试者中，运动后LA升高加剧和/或存在低氧血症的个体运动后心率衰减率也会降低。运动后心率恢复延迟的机制仅为推测，因为显著相关性无法评估因果关系。
