Massimo Nardone, Julian C Bommarito, Kathryn N Pfundt, Samuel Amanual, Yeshale Chetty, Philip J Millar
{"title":"正常血压成人运动后交感神经血管传导增强的证据。","authors":"Massimo Nardone, Julian C Bommarito, Kathryn N Pfundt, Samuel Amanual, Yeshale Chetty, Philip J Millar","doi":"10.1152/ajpregu.00084.2025","DOIUrl":null,"url":null,"abstract":"<p><p>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<sup>-1</sup>·min<sup>-1</sup>; 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<sub>2peak</sub>), <i>n</i> = 16], time control (60 min, <i>n</i> = 16), and lower limb heating (foot submersion into 40°C water, <i>n</i> = 9). MSNA-FVC transduction was quantified using signal averaging. Compared with control, exercise did not alter MSNA (<i>P</i> = 0.72) but increased FVC (<i>P</i> < 0.01) and MSNA-FVC transduction (-8.6 ± 4.5 vs. -15.1 ± 5.7 mL/min/100 mmHg; <i>P</i> < 0.01). Compared with exercise, heating did not alter MSNA (<i>P</i> = 0.71) and tended to increases FVC (<i>P</i> = 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; <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> 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.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. 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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<sup>-1</sup>·min<sup>-1</sup>; 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<sub>2peak</sub>), <i>n</i> = 16], time control (60 min, <i>n</i> = 16), and lower limb heating (foot submersion into 40°C water, <i>n</i> = 9). MSNA-FVC transduction was quantified using signal averaging. Compared with control, exercise did not alter MSNA (<i>P</i> = 0.72) but increased FVC (<i>P</i> < 0.01) and MSNA-FVC transduction (-8.6 ± 4.5 vs. -15.1 ± 5.7 mL/min/100 mmHg; <i>P</i> < 0.01). Compared with exercise, heating did not alter MSNA (<i>P</i> = 0.71) and tended to increases FVC (<i>P</i> = 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; <i>P</i> = 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.<b>NEW & NOTEWORTHY</b> Following cycling exercise, leg vascular conductance increases, whereas sympathetic nerve traffic is unchanged in young healthy adults. 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引用次数: 0
摘要
单次动态运动后,血管导度增加,而交感神经流量似乎不变。血管反应和交感反应之间的不一致可能反映了血管收缩剂反应的调节。主要目的是评估骑车运动后交感神经血管的转导。次要目的是探索通过局部加热足部来控制肢体血管传导,从而改变交感神经血管传导的机制。我们假设骑车运动后交感神经血管传导会减少,但下肢加热不会改变。成人16例(22±3岁);43±8ml /kg/min;8名女性)接受心率(心电图)、平均动脉压(MAP;光容积脉搏图),肌肉交感神经活动(MSNA;微神经造影)和股血管传导(FVC;三种干预措施:循环运动(60分钟,60% vo2峰值,n=16)、时间控制(60分钟,n=16)和下肢加热(足部浸入40°C水中,n=9)。用信号平均法量化MSNA-FVC转导。与对照组相比,运动没有改变MSNA (P=0.72),但增加了FVC (PPP=0.71),并倾向于引起静息FVC的更大增加(P=0.09)。然而,与加热相比,运动后MSNA-FVC转导的增加倾向于持续存在(-8.7±8.0 vs -15.1±5.9 mL/min/100mmHg;P = 0.06)。与我们的假设相反,这些发现为健康成人急性骑车运动后交感神经血管转导的增强提供了证据。观察到的神经血管转导的增加似乎与静息血管舒张性张力无关。
Evidence for potentiation in sympathetic neurovascular transduction following exercise in normotensive adults.
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-1·min-1; 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 (V̇O2peak), n = 16], time control (60 min, n = 16), and lower limb heating (foot submersion into 40°C water, n = 9). MSNA-FVC transduction was quantified using signal averaging. Compared with control, exercise did not alter MSNA (P = 0.72) but increased FVC (P < 0.01) and MSNA-FVC transduction (-8.6 ± 4.5 vs. -15.1 ± 5.7 mL/min/100 mmHg; P < 0.01). Compared with exercise, heating did not alter MSNA (P = 0.71) and tended to increases FVC (P = 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; P = 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.NEW & NOTEWORTHY 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.
期刊介绍:
The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. Major areas of emphasis include regulation in genetically modified animals; model organisms; development and tissue plasticity; neurohumoral control of circulation and hypertension; local control of circulation; cardiac and renal integration; thirst and volume, electrolyte homeostasis; glucose homeostasis and energy balance; appetite and obesity; inflammation and cytokines; integrative physiology of pregnancy-parturition-lactation; and thermoregulation and adaptations to exercise and environmental stress.