Drouin Patrick J, Forbes Stacey P A, Zedic Abby K, Mladen Stuart P S, Tschakovsky Michael E
Human Vascular Control Laboratory, School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada.
Exp Physiol. 2025 May;110(5):708-721. doi: 10.1113/EP091436. Epub 2025 Mar 25.
Sympathetic restraint in exercising muscle is currently viewed as required to prevent 'excess' vasodilatation from exceeding the cardiac output ( ) response, even in submaximal exercise. Certainly, muscle vasodilatory capacity dictates the requirement for sympathetic restraint when cardiac pumping capacity is approached. However, a similar role in submaximal exercise has at least two important implications for integrated cardiovascular control in exercise that have not been considered. First, such a role means that there is a 'set' response to a given exercise challenge that dictates the cardiovascular circuit flow and therefore the vasodilatation allowed such that -peripheral blood flow balance and target arterial blood pressure are achieved. This represents a 'cardiocentric' model of integrated cardiovascular control, whereby the heart leads and the peripheral resistance vessel tone is modulated accordingly. Second, what is commonly described as 'tight' matching of exercising muscle oxygen delivery relative to demand would therefore require that the response is closely 'calibrated' to exercising muscle metabolic demand. This would require a means of driving cardiac activation via precise communication of exercising muscle metabolic demand. However, considerable evidence demonstrates that 'excess' vasodilatation in a healthy system simply leads to a matching increased without arterial blood pressure compromise. This review re-examines the evidence for existence of sympathetic restraint in exercising muscle and its currently proposed role. We propose that key questions remain unanswered and that renewed investigation into sympathetic restraint and its role can lead to important advances in understanding integrated cardiovascular control in exercise.
目前认为,即使在次最大运动时,运动肌肉中的交感神经抑制对于防止“过度”血管舒张超过心输出量( )反应是必要的。当然,当接近心脏泵血能力时,肌肉血管舒张能力决定了对交感神经抑制的需求。然而,在次最大运动中的类似作用对于运动中综合心血管控制至少有两个未被考虑的重要影响。首先,这样的作用意味着对给定运动挑战存在一种“设定”的 反应,该反应决定了心血管回路流量,从而决定了允许的血管舒张,以便实现 -外周血流平衡和目标动脉血压。这代表了一种“以心脏为中心”的综合心血管控制模型,即心脏起主导作用,外周阻力血管张力相应地受到调节。其次,通常所说的运动肌肉氧输送相对于需求的“紧密”匹配,因此需要 反应与运动肌肉代谢需求紧密“校准”。这将需要一种通过精确传达运动肌肉代谢需求来驱动心脏激活的方法。然而,大量证据表明,健康系统中的“过度”血管舒张只会导致匹配的 增加而不会损害动脉血压。本综述重新审视了运动肌肉中交感神经抑制存在的证据及其目前提出的作用。我们提出关键问题仍未得到解答,对交感神经抑制及其作用的重新研究可以在理解运动中综合心血管控制方面取得重要进展。