Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits

OʼHagan, K. P.; Bell, Leonard; Mittelstadt, Scott W.; Clifford, Philip S.

doi:10.1152/jappl.1993.74.5.2099

Cited by 46 publications

(34 citation statements)

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“…This study, which was performed on conscious rabbits, demonstrated that renal vasoconstriction was increased within 10 s of initiation of dynamic exercise in the innervated kidney, whereas no such response was seen in the denervated kidney. Other studies on cats and rabbits have also found that renal sympathetic nerve activity increases within seconds after the onset of muscle contraction (11,15,18).…”

Section: Protocol 2: Static Handgrip Exercise At Graded Intensitymentioning

confidence: 84%

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

Momen

Bower

Leuenberger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Static exercise causes activation of the sympathetic nervous system, which results in increased blood pressure (BP) and renal vascular resistance (RVR). The question arises as to whether renal vasoconstriction that occurs during static exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal blood flow velocity (RBV) responses to two different handgrip (HG) exercise paradigms in 7 kidney transplant recipients (RTX) and 11 age-matched healthy control subjects. Transplanted kidneys are functionally denervated. Beat-by-beat analyses of changes in RBV (observed via duplex ultrasound), BP, and heart rate were performed during HG exercise in all subjects. An index of RVR was calculated as BP/RBV. In protocol 1, fatiguing HG exercise (40% of maximum voluntary contraction) led to significant increases in RVR in both groups. However, at the end of exercise, RVR was more than fourfold higher in control subjects than in the RTX group (88 vs. 20% increase over baseline; interaction, P Ͻ 0.001). In protocol 2, short bouts of HG exercise (15 s) led to significant increases in RVR at higher workloads (50 and 70% of maximum voluntary contraction) in the control subjects (P Ͻ 0.001). RVR did not increase in the RTX group. In conclusion, we observed grossly attenuated renal vasoconstrictor responses to exercise in RTX subjects, in whom transplanted kidneys were considered functionally denervated. Our results suggest that renal vasoconstrictor responses to exercise in conscious humans are mainly dependent on activation of a neural mechanism.kidney; blood flow; autoregulation; handgrip; vasoconstriction; transplant DURING EXERCISE, THE SYMPATHETIC nervous system is activated, and this results in increases in heart rate (HR), blood pressure (BP), and peripheral vasoconstriction. As part of this process, renal vasoconstriction occurs and serves to maintain BP as well as to redistribute blood flow to the contracting skeletal muscle bed.Of note, the observed increase in renal vascular resistance (RVR) is associated with an increase in arterial pressure. Thus the question arises as to whether renal vasoconstriction that occurs during static exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal hemodynamic responses during two different handgrip exercise paradigms in a group of kidney transplant recipients (RTX) and in age-matched healthy control subjects. Previous reports (7,8,16) suggest that transplanted kidneys remain functionally denervated for several months after transplantation. In studies measuring tissue norepinephrine in rat kidney grafts (7), researchers found grossly diminished norepinephrine levels compared with native kidneys 9 mo after transplantation. Similarly, necropsy specimens from human renal allografts demonstrate a reduction in sympathetic ganglia synaptic density 3 yr after transplantation (16). In addition, the resea...

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Section: Protocol 2: Static Handgrip Exercise At Graded Intensitymentioning

confidence: 84%

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

Momen

Bower

Leuenberger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…These findings are consistent with work in cats in which pharmacological blockade of skeletal muscle stretch activated ion channels did not influence early increases in BP during spontaneous muscle contractions (i.e., central command induced pressor response) (201). However, the autonomic contribution to potential central command induced early increases in BP has yet to be fully determined, although in support of a sympathetic contribution, BP and renal SNA have been shown to increase prior to and at the onset of static exercise (206), locomotion (277), grooming (203) and treadmill exercise (237) in animals. Although not specifically designed to examine the onset of exercise, work from Victor and colleagues using brief rhythmic handgrip exercise and partial neuromuscular blockade lends some additional insight (355).…”

Section: Central Command At Exercise Onsetmentioning

confidence: 99%

“…The increase in skin SNA at exercise onset appears proportional to the exercise intensity and remains elevated throughout exercise (267,283,344,358,359). Likewise, animal investigations demonstrated immediate increases in renal and cardiac SNA at the onset of dynamic exercise (54,237,346). Overall, the onset of dynamic exercise does not appear to produce mass, uniform sympathetic discharge to all tissues, rather the majority of studies suggest selective sympathetic activation at exercise onset.…”

Section: Peripheral Sympathetic Activity At Exercise Onsetmentioning

confidence: 99%

Autonomic Adjustments to Exercise in Humans

Fisher

Young

Fadel

2015

Comprehensive Physiology

226

253

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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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“…Cardiac, renal, and lumbar sympathetic nerve activities also demonstrate a rapid increase at the beginning of dynamic exercise or natural body movement in cats (13,20,22,30,48), rabbits (37), and rats (6). Central command is the most likely to cause the prompt sympathoexcitation, which in turn contributes to the cardiovascular adaptation at the beginning of static or dynamic exercise.…”

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confidence: 97%

Central command blunts the baroreflex bradycardia to aortic nerve stimulation at the onset of voluntary static exercise in cats

Komine

Matsukawa

Tsuchimochi

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Komine, Hidehiko, Kanji Matsukawa, Hirotsugu Tsuchimochi, and Jun Murata. Central command blunts the baroreflex bradycardia to aortic nerve stimulation at the onset of voluntary static exercise in cats. Am J Physiol Heart Circ Physiol 285: H516-H526, 2003. First published May 1, 2003 10.1152/ajpheart.00013.2003.-To examine whether the central characteristics of the aortic baroreflex alter from moment to moment during static exercise, we identified the dynamic changes in the sizes of the bradycardia and depressor response evoked by stimulation of the aortic depressor nerve (ADN). Three conscious cats were trained to voluntarily extend the right forelimb and press a bar for 31 Ϯ 1 s with a peak force of 337 Ϯ 22 g while maintaining a sitting posture. The ADN stimulation-induced bradycardia was attenuated at the initial period of exercise (up to 8 s from the exercise onset) to 62 Ϯ 5% of the preexercise bradycardia and remained blunted until the end of exercise. The most blunted bradycardia was observed immediately before or when the forelimb was extended before force development. The baroreflex-induced bradycardia was suppressed again at cessation of exercise when the forelimb was retracted and recovered within a few seconds. In contrast, static exercise did not affect the ADN stimulation-induced depressor response. The ADN stimulation-induced bradycardia was also blunted at the beginning of naturally occurring body movement such as spontaneous postural change or grooming behavior. Thus it is likely that the central characteristics of the aortic baroreflex dynamically change from moment to moment during voluntary static exercise and during natural body movement and that particularly a central inhibition of the cardiac component of the aortic baroreflex is induced by central command at the onset of static exercise, whereas the central property of the vasomotor component of the baroreflex is preserved.aortic depressor nerve; aortic baroreceptors; baroreflex sensitivity; baroreflex depressor response; central modulation of the arterial baroreflex ARTERIAL BLOOD PRESSURE (AP) is sensed by arterial baroreceptors in the carotid sinus and aortic arch regions, whose activities transmit the beat-to-beat changes in AP to the central nervous system and evoke the baroreflex responses of autonomic efferent nerve activities to the heart and blood vessels. For example, if AP increases during resting, arterial baroreceptors are stimulated in proportion to the rise in AP, which elicits reflex bradycardia and depressor response and thereby restores AP to the control level. However, it is well known that heart rate (HR) and AP increase simultaneously during static or dynamic exercise in humans and conscious animals, indicating that arterial baroreflex function is modulated by exercise.The effect of exercise on the arterial baroreflexes has been extensively studied in humans and animals. When baroreflex sensitivity was assessed as a ratio of the change in R-R interval or HR in response to an alteration in AP, it was reduced during d...

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Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits

Cited by 46 publications

References 0 publications

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

Autonomic Adjustments to Exercise in Humans

Central command blunts the baroreflex bradycardia to aortic nerve stimulation at the onset of voluntary static exercise in cats

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