Bentley Robert F, Kellawan J Mikhail, Moynes Jackie S, Poitras Veronica J, Walsh Jeremy J, Tschakovsky Michael E
School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada.
School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada
J Appl Physiol (1985). 2014 Aug 15;117(4):392-405. doi: 10.1152/japplphysiol.01155.2013. Epub 2014 Jun 26.
The primary objective of this study was to determine whether cardiovascular compensatory response phenotypes exist in the face of a reduced perfusion pressure challenge to exercising muscle oxygen delivery (O2D), and whether these responses might be exercise intensity (EI) dependent. Ten healthy men (19.5 ± 0.4 yr) completed two trials of progressive forearm isometric handgrip exercise to exhaustion (24.5 N increments every 3.5 min) in each of forearm above and below heart level [forearm arterial perfusion pressure (FAPP) difference of 29.5 ± 0.97 mmHg]. At the end of each EI, measurements of forearm blood flow (FBF; ml/min) via brachial artery Doppler and echo ultrasound, mean arterial blood pressure (MAP; mmHg) via finger photoplethysmography, and exercising forearm venous effluent via antecubital vein catheter revealed distinct cardiovascular response groups: n = 6 with compensatory vasodilation vs. n = 4 without compensatory vasodilation. Compensatory vasodilators were able to blunt the perfusion pressure-evoked reduction in submaximal O2D in the arm-above-heart condition, whereas nonvasodilators did not (-22.5 ± 13.6 vs. -65.4 ± 14.1 ml O2/min; P < 0.05), and in combination with being able to increase O2 extraction, nonvasodilators defended submaximal V̇o2 and experienced less of an accumulated submaximal O2D deficit (-80.7 ± 24.7 vs. -219.1 ± 36.0 ml O2/min; P < 0.05). As a result, the compensatory vasodilators experienced less of a compromise to peak EI than nonvasodilators (-24.5 ± 3.5 N vs. -52.1 ± 8.9 N; P < 0.05). In conclusion, in the forearm exercise model studied, vasodilatory response phenotypes exist that determine individual susceptibility to hypoperfusion and the degree to which aerobic metabolism and exercise performance are compromised.
本研究的主要目的是确定面对运动肌肉氧输送（O2D）的灌注压力挑战降低时，心血管代偿反应表型是否存在，以及这些反应是否可能依赖于运动强度（EI）。10名健康男性（19.5±0.4岁）在心脏水平以上和以下的每只前臂完成了两次渐进性前臂等长握力运动试验，直至力竭（每3.5分钟增加24.5N）[前臂动脉灌注压力（FAPP）差值为29.5±0.97mmHg]。在每个EI结束时，通过肱动脉多普勒和超声心动图测量前臂血流量（FBF；ml/min），通过手指光电容积描记法测量平均动脉血压（MAP；mmHg），并通过肘前静脉导管测量运动前臂静脉流出量，结果显示出不同的心血管反应组：6例有代偿性血管舒张，4例无代偿性血管舒张。在心脏以上手臂的情况下，代偿性血管舒张剂能够减轻灌注压力引起的次最大O2D降低，而非血管舒张剂则不能（-22.5±13.6 vs.-65.4±14.1 ml O2/min；P<0.05），并且与能够增加O2提取相结合，非血管舒张剂维持了次最大V̇o2，并且积累的次最大O2D deficit较小（-80.7±24.7 vs.-219.1±36.0 ml O2/min；P<0.05）。因此，与非血管舒张剂相比，代偿性血管舒张剂在峰值EI时受到的影响较小（-24.5±3.5 N vs.-52.1±8.9 N；P<0.05）。总之，在所研究的前臂运动模型中，存在血管舒张反应表型，这些表型决定了个体对低灌注的易感性以及有氧代谢和运动表现受损的程度。
