Cardiovascular responses to active and passive cycling movements

Nobrega, A. C. L.; Williamson, Jon W.; Friedman, D. B.; Araújo, Claudio G.S.; Mitchell, Jerf

doi:10.1249/00005768-199406000-00009

Cited by 92 publications

(107 citation statements)

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“…Using this experimental approach, previous investigations have implicated cardioacceleration (30,31) and CO in the hyperemic response to passive limb movement (26,30,31,33,43). By pharmacologically altering the HR response to passive movement, the present study supports these previous findings and provides further evidence that the immediate increase in HR is obligatory for the initial magnitude and timing of the hyperemic response to limb movement.…”

Section: Contribution Of Co and Analytic Approach To The Hyperemic Resupporting

confidence: 88%

“…Other variables, such as LBF and LVC, although slightly elevated above baseline, were not different between the two conditions during the second minute of movement. It is our contention that studies that failed to document a significant increase in LBF or contribution of CO to the hyperemic response likely did not have adequate time resolution for the measurements of LBF and CO, as the first measurements were made several minutes after the onset of passive movement (12,31,40).…”

Section: Contribution Of Co and Analytic Approach To The Hyperemic Rementioning

confidence: 99%

“…As the passive movement continued, MAP returned toward baseline values, as did HR and CO. Coinciding with the return of MAP, HR, and CO to baseline, input from the afferent fibers likely accommodated to the limb movement, thereby relaying less sensory information to the cardiovascular control center. An inability of mechanoreceptor feedback to sustain the central hemodynamic response to passive exercise has been reported (30,31).…”

Section: Partitioning the Central And Peripheral Hemodynamic Contribumentioning

confidence: 99%

“…Previous work blocking (25) or stimulating (36) the group III and IV fibers in cats revealed a crucial role of these fibers in regards to the cardiovascular and/or respiratory response to exercise. Work in humans during passive cycling has determined that peripheral afferent reflexes from exercising muscles are likely involved in cardioacceleration at the onset of passive movement (30,31,33); however, these studies did not pharmacologically inhibit the afferent fibers.…”

Section: Afferent Skeletal Muscle Feedback and The Hemodynamic Responsesmentioning

confidence: 99%

“…Recently, our group (26, 43) and others (30,31,33) have highlighted the role of cardioacceleration in the hyperemic responses to passive movement. Wray et al (43) reported that passive knee extension resulted in significant tachycardia and increased leg blood flow (LBF) during the first 5 s of movement.…”

mentioning

confidence: 99%

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Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Trinity

Amann²,

McDaniel

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study. Am J Physiol Heart Circ Physiol 299: H1693-H1700, 2010. First published August 27, 2010; doi:10.1152/ajpheart.00482.2010.-The purpose of this investigation was to partially remove feedback from type III/IV skeletal muscle afferents and determine how this feedback influences the central and peripheral hemodynamic responses to passive leg movement. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure, leg vascular conductance (LVC), and leg blood flow (LBF) were measured during 2 min of passive knee extension in eight young men before and after intrathecal fentanyl injection. Passive movement increased HR by 14 beats/min from baseline to maximal response during control (CON) (65 Ϯ 4 to 79 Ϯ 5 beats/min, P Ͻ 0.05), whereas HR did not significantly increase with the fentanyl block (BLK). LBF and LVC increased in both conditions; however, these increases were attenuated and delayed during BLK [%change from baseline to maximum, LBF: CON 295 Ϯ 109 vs. BLK 210 Ϯ 86%, (P Ͻ 0.05); LVC: CON 322 Ϯ 40% vs. BLK 231 Ϯ 32%, (P Ͻ 0.04)]. In CON, HR, SV, CO, and LVC increased contributing to the hyperemic response. However, under BLK conditions, statistically insignificant increases in HR and SV combined to yield a small, but significant, increase in CO and an attenuated hyperemic response. Therefore, partially blocking skeletal muscle afferent feedback blunts the central hemodynamic response due to passive limb movement, which then results in an attenuated and delayed movement-induced hyperemia. In combination, these findings provide evidence that limb movement-induced hyperemia has a significant central hemodynamic component induced by peripheral nerve activation. afferent nerve fiber; blood flow; hemodynamics CENTRAL AND PERIPHERAL HEMODYNAMIC factors contribute to the hyperemic response at the onset of exercise. These factors include the muscle pump (24, 38) mechanically induced vasodilation (6,19,41), mechanical deformation of arterioles (37), flow-mediated vasodilation (22, 34), and cardioacceleration (26, 30 -33, 43) due to stimulation of afferent mechanosensitive and metabosensitive fibers in the working muscles (25,36). Isolating the relative importance of these numerous mechanisms is difficult and requires a systematic approach to understand the nature of any single mechanism.One approach to study the movement-induced central and peripheral hemodynamic responses to the onset of exercise is to perform passive movement, thereby minimizing the metabolic contribution of voluntary exercise. Recently, our group (26, 43) and others (30,31,33) have highlighted the role of cardioacceleration in the hyperemic responses to passive movement. Wray et al. (43) reported that passive knee extension resulted in significant tachycardia and increased leg blood flow (LBF) during the first 5 s of movement. However, in this study, stroke volume (SV) was not measured, and cardiac output (CO) was assumed to r...

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Section: Contribution Of Co and Analytic Approach To The Hyperemic Resupporting

confidence: 88%

Section: Contribution Of Co and Analytic Approach To The Hyperemic Rementioning

confidence: 99%

Section: Partitioning the Central And Peripheral Hemodynamic Contribumentioning

confidence: 99%

Section: Afferent Skeletal Muscle Feedback and The Hemodynamic Responsesmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Trinity

Amann²,

McDaniel

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Autonomic Adjustments to Exercise in Humans

Fisher

Young

Fadel

2015

Comprehensive Physiology

204

224

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Autonomic nervous system adjustments to the heart and blood vessels are necessary for mediating the cardiovascular responses required to meet the metabolic demands of working skeletal muscle during exercise. These demands are met by precise exercise intensity-dependent alterations in sympathetic and parasympathetic nerve activity. The purpose of this review is to examine the contributions of the sympathetic and parasympathetic nervous systems in mediating specific cardiovascular and hemodynamic responses to exercise. These changes in autonomic outflow are regulated by several neural mechanisms working in concert, including central command (a feed forward mechanism originating from higher brain centers), the exercise pressor reflex (a feed-back mechanism originating from skeletal muscle), the arterial baroreflex (a negative feed-back mechanism originating from the carotid sinus and aortic arch), and cardiopulmonary baroreceptors (a feed-back mechanism from stretch receptors located in the heart and lungs). In addition, arterial chemoreceptors and phrenic afferents from respiratory muscles (i.e., respiratory metaboreflex) are also capable of modulating the autonomic responses to exercise. Our goal is to provide a detailed review of the parasympathetic and sympathetic changes that occur with exercise distinguishing between the onset of exercise and steady-state conditions, when appropriate. In addition, studies demonstrating the contributions of each of the aforementioned neural mechanisms to the autonomic changes and ensuing cardiac and/or vascular responses will be covered.

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Integration of Central and Peripheral Regulation of the Circulation during Exercise: Acute and Chronic Adaptations

Mueller

Clifford

Crandall

et al. 2017

Comprehensive Physiology

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Physical movement lasting any more than a few seconds (e.g., exercise), requires coordination of motor control with concomitant changes in the cardiovascular and respiratory support necessary to respond to the rapid increases in metabolic demand. Without such coordination, delivery of oxygen and removal of waste products become rate limiting and will restrict the duration, speed, and quality of movement. Fortunately, under healthy conditions, the central and peripheral nervous systems contribute importantly to this remarkable level of coordination via complex mechanisms that remain to be fully elucidated. The purposes of this review are to present the current state of knowledge regarding: (i) mechanisms by which the body maintains appropriate perfusion pressure to all organs during acute bouts of exercise, and (ii) alterations occurring in these mechanisms via central nervous system adaptations when exercise is performed or not performed on a regular basis (e.g., physically active versus sedentary lifestyle, respectively). Results from studies performed in humans and laboratory animals provide the reader a well-rounded knowledge base. They are intended to instill an appreciation of what is known, and not known, about how the brain regulates the cardiovascular system during acute bouts of exercise, and the adaptations that occur when individuals exercise regularly versus when chronically sedentary. Discussion of the latter is intended to provide novel mechanisms for the increased incidence of cardiovascular disease in sedentary individuals versus a reduced incidence in individuals who are regularly active. © 2018 American Physiological Society. Compr Physiol 8:103-151, 2018.

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Cardiovascular responses to active and passive cycling movements

Cited by 92 publications

References 0 publications

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Autonomic Adjustments to Exercise in Humans

Integration of Central and Peripheral Regulation of the Circulation during Exercise: Acute and Chronic Adaptations

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