Trangmar Steven J, Chiesa Scott T, Stock Christopher G, Kalsi Kameljit K, Secher Niels H, González-Alonso José
Centre for Sports Medicine and Human Performance, Brunel University, London, UK.
Centre for Sports Medicine and Human Performance, Brunel University, London, UK Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
J Physiol. 2014 Jul 15;592(14):3143-60. doi: 10.1113/jphysiol.2014.272104. Epub 2014 May 16.
Intense exercise is associated with a reduction in cerebral blood flow (CBF), but regulation of CBF during strenuous exercise in the heat with dehydration is unclear. We assessed internal (ICA) and common carotid artery (CCA) haemodynamics (indicative of CBF and extra-cranial blood flow), middle cerebral artery velocity (MCA Vmean), arterial-venous differences and blood temperature in 10 trained males during incremental cycling to exhaustion in the heat (35°C) in control, dehydrated and rehydrated states. Dehydration reduced body mass (75.8 ± 3 vs. 78.2 ± 3 kg), increased internal temperature (38.3 ± 0.1 vs. 36.8 ± 0.1°C), impaired exercise capacity (269 ± 11 vs. 336 ± 14 W), and lowered ICA and MCA Vmean by 12-23% without compromising CCA blood flow. During euhydrated incremental exercise on a separate day, however, exercise capacity and ICA, MCA Vmean and CCA dynamics were preserved. The fast decline in cerebral perfusion with dehydration was accompanied by increased O2 extraction (P < 0.05), resulting in a maintained cerebral metabolic rate for oxygen (CMRO2). In all conditions, reductions in ICA and MCA Vmean were associated with declining cerebral vascular conductance, increasing jugular venous noradrenaline, and falling arterial carbon dioxide tension (P aCO 2) (R(2) ≥ 0.41, P ≤ 0.01) whereas CCA flow and conductance were related to elevated blood temperature. In conclusion, dehydration accelerated the decline in CBF by decreasing P aCO 2 and enhancing vasoconstrictor activity. However, the circulatory strain on the human brain during maximal exercise does not compromise CMRO2 because of compensatory increases in O2 extraction.
高强度运动与脑血流量(CBF)减少有关,但在炎热环境下进行剧烈运动且伴有脱水时脑血流量的调节尚不清楚。我们评估了10名训练有素的男性在炎热环境(35°C)中进行递增式骑行至力竭时,在对照、脱水和补液状态下的颈内动脉(ICA)和颈总动脉(CCA)血流动力学(反映CBF和颅外血流)、大脑中动脉速度(MCA Vmean)、动静脉差异和体温。脱水使体重减轻(75.8±3 vs. 78.2±3 kg),体温升高(38.3±0.1 vs. 36.8±0.1°C),运动能力受损(269±11 vs. 336±14 W),ICA和MCA Vmean降低12 - 23%,但不影响CCA血流。然而,在另一天的等容递增运动中,运动能力以及ICA、MCA Vmean和CCA动力学得以保持。脱水导致脑灌注快速下降,同时氧摄取增加(P < 0.05),从而使脑氧代谢率(CMRO2)维持不变。在所有情况下, ICA和MCA Vmean的降低与脑血管传导性下降、颈静脉去甲肾上腺素增加以及动脉二氧化碳分压(P aCO 2)降低有关(R(2)≥0.41,P≤0.01),而CCA血流和传导性与体温升高有关。总之,脱水通过降低P aCO 2和增强血管收缩活性加速了CBF的下降。然而,由于氧摄取的代偿性增加,最大运动时人脑的循环应激不会损害CMRO2。