Bispebjerg Hospital Research Unit for Anaesthesia and Intensive Care, University of Copenhagen, Copenhagen, Denmark.
J Appl Physiol (1985). 2011 May;110(5):1327-33. doi: 10.1152/japplphysiol.01497.2010. Epub 2011 Mar 3.
Aerobic fitness may be associated with reduced orthostatic tolerance. To investigate whether trained individuals have less effective regulation of cerebral vascular resistance, we studied the middle cerebral artery (MCA) mean blood velocity (V(mean)) response to a sudden drop in mean arterial pressure (MAP) after 2.5 min of leg ischemia in endurance athletes and untrained subjects (maximal O(2) uptake: 69 ± 7 vs. 42 ± 5 ml O(2)·min(-1)·kg(-1); n = 9 for both, means ± SE). After cuff release when seated, endurance athletes had larger drops in MAP (94 ± 6 to 62 ± 5 mmHg, -39%, vs. 99 ± 5 to 73 ± 4 mmHg, -26%) and MCA V(mean) (53 ± 3 to 37 ± 2 cm/s, -30%, vs. 58 ± 3 to 43 ± 2 cm/s, -25%). The athletes also had a slower recovery to baseline of both MAP (25 ± 2 vs. 16 ± 1 s, P < 0.01) and MCA V(mean) (15 ± 1 vs. 11 ± 1 s, P < 0.05). The onset of autoregulation, determined by the time point of increase in the cerebrovascular conductance index (CVCi = MCA V(mean)/MAP) appeared later in the athletes (3.9 ± 0.4 vs. 2.7 ± 0.4s, P = 0.01). Spectral analysis revealed a normal MAP-to-MCA V(mean) phase in both groups but ~40% higher normalized MAP to MCA V(mean) low-frequency transfer function gain in the trained subjects. No significant differences were detected in the rates of recovery of MAP and MCA V(mean) and the rate of CVCi regulation (18 ± 4 vs. 24 ± 7%/s, P = 0.2). In highly trained endurance athletes, a drop in blood pressure after the release of resting leg ischemia was more pronounced than in untrained subjects and was associated with parallel changes in indexes of cerebral blood flow. Once initiated, the autoregulatory response was similar between the groups. A delayed onset of autoregulation with a larger normalized transfer gain conforms with a less effective dampening of MAP oscillations, indicating that athletes may be more prone to instances of symptomatic cerebral hypoperfusion when MAP declines.
有氧适能可能与直立耐量降低有关。为了研究训练有素的个体是否具有更有效的脑血管阻力调节功能，我们研究了 9 名耐力运动员和 9 名未经训练的受试者在腿部缺血 2.5 分钟后，平均动脉压（MAP）突然下降时大脑中动脉（MCA）平均血流速度（V（mean））的反应（最大摄氧量：69 ± 7 比 42 ± 5 ml O2·min-1·kg-1；均为 ± SE）。当穿着袖口坐着时，耐力运动员的 MAP 下降幅度更大（94 ± 6 至 62 ± 5 mmHg，-39%，相比之下，99 ± 5 至 73 ± 4 mmHg，-26%），MCA V（mean）（53 ± 3 至 37 ± 2 cm/s，-30%，相比之下，58 ± 3 至 43 ± 2 cm/s，-25%）。运动员的 MAP（25 ± 2 比 16 ± 1 s，P < 0.01）和 MCA V（mean）（15 ± 1 比 11 ± 1 s，P < 0.05）恢复到基线的速度也较慢。由脑血管传导指数（CVCi = MCA V（mean）/MAP）的增加时间点确定的自动调节开始时间在运动员中较晚（3.9 ± 0.4 比 2.7 ± 0.4 s，P = 0.01）。频谱分析显示两组的 MAP 与 MCA V（mean）之间存在正常的相位，但在训练有素的受试者中，归一化的 MAP 到 MCA V（mean）低频传递函数增益高约 40%。在 MAP 和 MCA V（mean）的恢复率以及 CVCi 调节率（18 ± 4 比 24 ± 7%/s，P = 0.2）方面未检测到显著差异。在高度训练有素的耐力运动员中，腿部缺血休息后血压下降比未经训练的受试者更为明显，并且与脑血流指数的平行变化相关。自动调节反应一旦开始，两组之间就相似。自动调节开始时间延迟，归一化传递增益较大，表明 MAP 波动的阻尼作用降低，这表明当 MAP 下降时，运动员可能更容易出现症状性脑灌注不足。
