Nardone Massimo, Bommarito Julian C, Pfundt Kathryn N, Amanual Samuel, Chetty Yeshale, Millar Philip J
Human Cardiovascular Physiology Laboratory, Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Department of Kinesiology, University of Guelph-Humber, Toronto, Ontario, Canada.
Am J Physiol Regul Integr Comp Physiol. 2025 Jul 1;329(1):R195-R203. doi: 10.1152/ajpregu.00084.2025. Epub 2025 Jun 9.
Vascular conductance increases following a single bout of dynamic exercise, whereas sympathetic nerve traffic commonly appears unchanged. Discordance between vascular and sympathetic responses may reflect modulation in vasoconstrictor responsiveness. The primary study objective was to evaluate sympathetic neurovascular transduction following cycling exercise. The secondary objective was to explore mechanisms contributing to altered sympathetic neurovascular transduction by manipulating limb vascular conductance using local heating of the foot. We hypothesized that sympathetic neurovascular transduction would decrease following cycling exercise but would be unchanged by lower limb heating. Sixteen adults (22 ± 3 yr; 43 ± 8 mL·kg·min; 8 females) underwent measurements of heart rate (electrocardiography), mean arterial pressure (photoplethysmography), muscle sympathetic nerve activity (MSNA; microneurography), and femoral vascular conductance (FVC; duplex ultrasound) across three interventions: cycling exercise [60 min, 60% peak oxygen consumption (V̇O), = 16], time control (60 min, = 16), and lower limb heating (foot submersion into 40°C water, = 9). MSNA-FVC transduction was quantified using signal averaging. Compared with control, exercise did not alter MSNA ( = 0.72) but increased FVC ( < 0.01) and MSNA-FVC transduction (-8.6 ± 4.5 vs. -15.1 ± 5.7 mL/min/100 mmHg; < 0.01). Compared with exercise, heating did not alter MSNA ( = 0.71) and tended to increases FVC ( = 0.09). However, increases in MSNA-FVC transduction following exercise tended to persist when compared with heating (-8.7 ± 8.0 vs. -15.1 ± 5.9 mL/min/100 mmHg; = 0.06). Contrary to our hypothesis, these findings provide evidence for potentiated sympathetic neurovascular transduction following acute cycling exercise in healthy adults. The observed increase in neurovascular transduction appears independent of resting vasomotor tone. Following cycling exercise, leg vascular conductance increases, whereas sympathetic nerve traffic is unchanged in young healthy adults. Discordant vascular and sympathetic responses may reflect modulation in vasoconstrictor responsiveness. The current study demonstrated that signal-averaged sympathetic neurovascular transduction was increased by ∼75% following a single bout of cycling exercise. Secondary experiments using local heating suggest that potentiation in sympathetic neurovascular transduction after exercise may occur independent of changes in resting vascular conductance.
单次动态运动后血管传导性增加，而交感神经活动通常未见变化。血管反应与交感神经反应之间的不一致可能反映了血管收缩反应性的调节。本研究的主要目的是评估骑行运动后的交感神经血管转导。次要目的是通过足部局部加热来调节肢体血管传导性，从而探究导致交感神经血管转导改变的机制。我们假设骑行运动后交感神经血管转导会降低，但下肢加热不会使其改变。16名成年人（22±3岁；43±8 mL·kg·min；8名女性）在三种干预情况下接受了心率（心电图）、平均动脉压（光电容积描记法）、肌肉交感神经活动（MSNA；微神经ography）和股血管传导性（FVC；双功超声）的测量：骑行运动[60分钟，60%峰值耗氧量（V̇O），n = 16]、时间对照（60分钟，n = 16）和下肢加热（足部浸入40°C水中，n = 9）。使用信号平均法对MSNA-FVC转导进行量化。与对照组相比，运动未改变MSNA（P = 0.72），但增加了FVC（P < 0.01）和MSNA-FVC转导（-8.6±4.5 vs. -15.1±5.7 mL/min/100 mmHg；P < 0.01）。与运动组相比，加热未改变MSNA（P = 0.71），但有增加FVC的趋势（P = 0.09）。然而，与加热相比，运动后MSNA-FVC转导的增加仍有持续的趋势（-8.7±8.0 vs. -15.1±5.9 mL/min/100 mmHg；P = 0.06）。与我们的假设相反，这些发现为健康成年人急性骑行运动后交感神经血管转导增强提供了证据。观察到的神经血管转导增加似乎与静息血管运动张力无关。骑行运动后，年轻健康成年人的腿部血管传导性增加，而交感神经活动未改变。血管反应与交感神经反应的不一致可能反映了血管收缩反应性的调节。当前研究表明，单次骑行运动后信号平均交感神经血管转导增加了约75%。使用局部加热的二次实验表明，运动后交感神经血管转导的增强可能独立于静息血管传导性的变化而发生。
