Rezk C C, Marrache R C B, Tinucci T, Mion D, Forjaz C L M
Exercise Hemodynamic Laboratory, School of Physical Education and Sport, University of São Paulo, Av Prof Mello de Moraes, 65, Butantã, São Paulo, SP, Brazil.
Eur J Appl Physiol. 2006 Sep;98(1):105-12. doi: 10.1007/s00421-006-0257-y. Epub 2006 Aug 3.
The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C-40 min of rest), low- (E40%-40% of 1 repetition maximum, RM), and high-intensity (E80%-80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF(R-R)nu) and high-frequency (HF(R-R)nu) components of the R-R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (-6 +/- 1 and -8 +/- 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (-0.4 +/- 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (-11 +/- 2 vs. -17 +/- 2 ml/beat, and +17 +/- 2 vs. +21 +/- 2 bpm, P < 0.05). LF(R-R)nu increased, while ln HF(R-R)nu decreased in both exercise sessions.
Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.
抗阻运动后运动后低血压的发生存在争议，其机制尚不清楚。为了评估不同抗阻运动强度对运动后血压（BP）、血流动力学和自主神经机制的影响，17名血压正常者进行了三个实验阶段：对照（C - 休息40分钟）、低强度（E40% - 1次重复最大值的40%，RM）和高强度（E80% - 1次重复最大值的80%）抗阻运动。在干预前后，测量血压、心率（HR）和心输出量（CO）。通过R - R间期变异性的标准化低频（LF(R - R)nu）和高频（HF(R - R)nu）成分评估自主神经调节。与运动前相比，E40%和E80%组的收缩压均有类似程度的下降（分别为-6±1和-8±1 mmHg，P < 0.05）。E40%组舒张压下降，C组舒张压升高，E80%组舒张压无变化。所有阶段的心输出量均有类似程度的下降（-0.4±0.2 l/min，P < 0.05），而全身血管阻力（SVR）在C组升高，E40%组无变化，E80%组升高。两次运动后每搏输出量均下降，心率均升高，且这些变化在E80%组更为明显（分别为-11±2 vs. -17±2 ml/搏，以及+17±2 vs. +21±2次/分钟，P < 0.05）。两个运动阶段的LF(R - R)nu均升高，而ln HF(R - R)nu均下降。
低强度和高强度抗阻运动均可导致运动后收缩期低血压；然而，只有低强度运动可降低舒张压。血压下降是由于心输出量减少且未被全身血管阻力增加所代偿。血压下降伴随着心率增加，这是由于对心脏的交感神经调节增强所致。
