School of Kinesiology, Faculty of Education, University of British Columbia, Vancouver, BC, Canada.
Research Center of Health, Physical Fitness and Sports, Nagoya University, Nagoya, Japan.
Exp Physiol. 2020 Dec;105(12):1984-1989. doi: 10.1113/EP088103. Epub 2020 Mar 16.
What is the topic of this review? Elevated demand is placed on the respiratory muscles during whole-body exercise-induced hyperpnoea. What is the role of elevated demand in neural modulation of cardiovascular control in respiratory and locomotor skeletal muscle, and what are the mechanisms involved? What advances does it highlight? There is a sympathetic restraint of blood flow to locomotor muscles during near-maximal exercise, which might function to maintain blood pressure. During submaximal exercise, respiratory muscle blood flow might be also be reduced if ventilatory load is sufficiently high. Methodological advances (near-infrared spectroscopy with indocyanine green) confirm that blood flow is diverted away from respiratory muscles when the work of breathing is alleviated.
It is known that the respiratory muscles have a significant increasing oxygen demand in line with hyperpnoea during whole-body endurance exercise and are susceptible to fatigue, in much the same way as locomotor muscles. The act of ventilation can itself be considered a form of exercise. The manipulation of respiratory load at near-maximal exercise alters leg blood flow significantly, demonstrating a competitive relationship between different skeletal muscle vascular beds to perfuse both sets of muscles adequately with a finite cardiac output. In recent years, the question has moved towards whether this effect exists during submaximal exercise, and the use of more direct measurements of respiratory muscle blood flow itself to confirm assumptions that uphold the concept. Evidence thus far has shown that there is a reciprocal effect on blood flow redistribution during ventilatory load manipulation observed at the respiratory muscles themselves and that the effect is observable during submaximal exercise, where active limb blood flow was reduced in conditions that simulated a high work of breathing. This has clinical applications for populations with respiratory disease and heart failure, where the work of breathing is remarkably high, even during submaximal efforts.
这篇综述的主题是什么？全身运动引起的过度通气会对呼吸肌产生高需求。在呼吸和运动骨骼肌肉的心血管控制的神经调节中，高需求扮演什么角色？涉及哪些机制？它强调了哪些进展？在接近最大运动时，运动骨骼肌肉的血流会受到交感神经的抑制，这可能有助于维持血压。在次最大运动时，如果通气负荷足够高，呼吸肌的血流也可能减少。方法学进展（近红外光谱与吲哚菁绿）证实，当呼吸功减轻时，血流会从呼吸肌转移。
众所周知，在全身耐力运动中，随着通气量的增加，呼吸肌的耗氧量显著增加，并且与运动骨骼肌肉一样容易疲劳。通气本身可以被视为一种运动形式。在接近最大运动时，呼吸负荷的改变会显著改变腿部血流，表明不同骨骼肌血管床之间存在竞争关系，以有限的心输出量充分灌注两组肌肉。近年来，问题已经转向这种效应是否存在于次最大运动中，以及使用更直接的呼吸肌血流测量来证实支持这一概念的假设。到目前为止的证据表明，在通气负荷操纵期间，在呼吸肌本身观察到的血流再分配上存在一种相互影响，并且这种影响在次最大运动中是可见的，在模拟高呼吸功的情况下，主动肢体血流减少。这对于呼吸疾病和心力衰竭患者具有临床应用价值，因为即使在次最大运动时，呼吸功也非常高。
