Muscle sympathetic nerve responses to passive and active one-legged cycling: insights into the contributions of central command

• Published in: American journal of physiology. Heart and circulatory physiology 2018-01, Vol.314 (1), p.H3-H10
• Main Authors: Doherty, Connor J, Incognito, Anthony V, Notay, Karambir, Burns, Matthew J, Slysz, Joshua T, Seed, Jeremy D, Nardone, Massimo, Burr, Jamie F, Millar, Philip J
• Format: Article
• Language: English
• Subjects: Active control; Adult; Arterial Pressure; Baroreceptors; Baroreflex; Bicycling; Blood pressure; Brain - physiology; Bursting strength; Cardiac Output; Conductance; Cycles; Efferent Pathways - physiology; Exercise; Exercise - physiology; Female; Heart diseases; Heart rate; Humans; Leg; Legs; Lower Extremity; Male; Microneurography; Muscle Contraction; Muscle Strength; Muscle, Skeletal - blood supply; Muscle, Skeletal - innervation; Muscles; Muscular system; Nervous system; Physical training; Reflexes; Stroke; Stroke volume; Sympathetic Nervous System - physiology; Vasoconstriction; Young Adult
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00494.2017

The contribution of central command to the peripheral vasoconstrictor response during exercise has been investigated using primarily handgrip exercise. The purpose of the present study was to compare muscle sympathetic nerve activity (MSNA) responses during passive (involuntary) and active (voluntary) zero-load cycling to gain insights into the effects of central command on sympathetic outflow during dynamic exercise. Hemodynamic measurements and contralateral leg MSNA (microneurography) data were collected in 18 young healthy participants at rest and during 2 min of passive and active zero-load one-legged cycling. Arterial baroreflex control of MSNA burst occurrence and burst area were calculated separately in the time domain. Blood pressure and stroke volume increased during exercise ( P < 0.0001) but were not different between passive and active cycling ( P > 0.05). In contrast, heart rate, cardiac output, and total vascular conductance were greater during the first and second minute of active cycling ( P < 0.001). MSNA burst frequency and incidence decreased during passive and active cycling ( P < 0.0001), but no differences were detected between exercise modes ( P > 0.05). Reductions in total MSNA were attenuated during the first ( P < 0.0001) and second ( P = 0.0004) minute of active compared with passive cycling, in concert with increased MSNA burst amplitude ( P = 0.02 and P = 0.005, respectively). The sensitivity of arterial baroreflex control of MSNA burst occurrence was lower during active than passive cycling ( P = 0.01), while control of MSNA burst strength was unchanged ( P > 0.05). These results suggest that central feedforward mechanisms are involved primarily in modulating the strength, but not the occurrence, of a sympathetic burst during low-intensity dynamic leg exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity burst frequency decreased equally during passive and active cycling, but reductions in total muscle sympathetic nerve activity were attenuated during active cycling. These results suggest that central command primarily regulates the strength, not the occurrence, of a muscle sympathetic burst during low-intensity dynamic leg exercise.