Cardiovascular responses to brief static contractions in man with topical nervous blockade.

Lassen, Anders; Mitchell, Jere H.; Reeves, Deborah; Rogers, H. B.; Secher, Niels H.

doi:10.1113/jphysiol.1989.sp017500

Cited by 25 publications

(9 citation statements)

References 10 publications

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“…This view has been supported by further human studies where anaesthesia of muscle afferents was shown to reduce the heart rate response despite the fact that the force of contraction was maintained (e.g. Lassen, Mitchell, Reeves, Rogers & Secher, 1989). In contrast, the results of other human studies have stressed the importance of central mechanisms (e.g.…”

Section: Introductionmentioning

confidence: 43%

Changes in R‐R interval at the start of muscle contraction in the decerebrate cat.

McMahon

McWilliam

1992

The Journal of Physiology

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SUMMARY1. The effect on R-R interval of a brief hindlimb contraction, elicited by electrical stimulation of L7 ventral roots, was investigated in decerebrate cats. The first series of experiments was performed at both low and high carotid sinus pressure to vary the level of vagal tone. When carotid sinus pressure was elevated to increase vagal tone, contraction commenced 1 s later.2. The change in R-R interval at low carotid sinus pressure was expressed as the difference between the mean of the five R-R intervals immediately preceding contraction and the mean of the last five R-R intervals at the end of a 5 s contraction. At high carotid sinus pressure, the change was expressed as the difference between the mean of the last five R-R intervals at the end of a 5 s contraction and the mean of five R-R intervals at an equivalent time after raising pressure alone.3. Hindlimb contraction at low carotid sinus pressure produced a significant reduction in R-R interval from 359+25 (mean+s.E.M. n = 8) to 336+24 ms (P < 0005). At high carotid sinus pressure the response was enhanced with contraction producing a reduction in R-R interval from 474 + 45 to 419 + 47 ms (P < 0-001).4. The shortening of R-R interval produced by hindlimb contraction at high carotid sinus pressure, 55 + 8 ms, was significantly greater than that observed at low sinus pressure, 23 + 5 ms (P < 0-001, n = 8, paired t test). This pattern of response was also seen at stimulation frequencies as low as 10 Hz.5. In a second series of experiments, designed to determine the latency of the cardiac acceleration, the minimum latency between the onset of L7 ventral root stimulation and the end of the first shortened R-R interval was 687 + 29 ms (n = 5).6. Atropine (0-4 mg kg-', i.v.) prevented a 5 s contraction from producing any change in R-R interval.7. These results indicate that afferent information originating from receptors in contracting muscles is responsible for producing an immediate shortening of R-R interval, which is mediated by vagal withdrawal. The possibility that the shortening of R-R interval at the start of contraction is linked to a reduction in arterial baroreceptor reflex sensitivity, possibly via inhibitory effects on neurones forming the central pathway of the baroreceptor reflex, is discussed.

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Section: Introductionmentioning

confidence: 43%

Changes in R‐R interval at the start of muscle contraction in the decerebrate cat.

McMahon

McWilliam

1992

The Journal of Physiology

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“…8). Although such a relationship is not as clear during high intensity isometric contractions (107,184) and maximal dynamic exercise (104). Studies employing additional strategies to modulate central command input such as electrical stimulation of resting skeletal muscle (180), hypnosis (49,339,370,379,380), muscle tendon vibration (113,155,246), and patients with unilateral limb weakness (151,385) or sensory neuropathies (61) have also demonstrated a role for central command in mediating the cardiac acceleration and increases in BP in response to exercise.…”

Section: Central Command During Steady-state Exercisementioning

confidence: 95%

Autonomic Adjustments to Exercise in Humans

Fisher

Young

Fadel

2015

Comprehensive Physiology

227

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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“…neural inputs from higher centres of the brain, possibly the motor cortex, influencing those regions of the brain controlling the cardiovascular system, whereas the peripheral theory proposes that sensory information from receptors in exercising muscle is responsible for the cardiovascular response to exercise (Alam & Smirk, 1937). Studies in humans seem to indicate that the initial immediate increase in heart rate, due to vagal withdrawal (Freyschuss, 1970), is due entirely to afferent activity originating in the contracting muscles (Lassen, Mitchell, Reeves, Rogers & Secher, 1989).…”

Section: Discussionmentioning

confidence: 99%

Changes in the baroreceptor reflex at the start of muscle contraction in the decerebrate cat.

McWilliam

Yang

Chen

1991

The Journal of Physiology

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SUMMARY1. The action of muscle contraction on the sensitivity of the cardiac vagal component of the baroreceptor reflex was examined in decerebrate cats.2. The sensitivity of the baroreceptor reflex was expressed as the difference between the maximum prolongation of the R-R interval in response to carotid sinus baroreceptor stimulation and the mean of ten R-R intervals immediately before carotid sinus pressure elevation.3. Muscle contraction elicited by electrical stimulation of L7 ventral roots (50 Hz) significantly reduced the sensitivity of the baroreceptor reflex by reducing the prolongation of the R-R interval from 269 + 31 to 159 + 22 ms.4. Inhibition of the cardiac vagal component of the baroreceptor reflex was seen just 1 s after the onset of contraction and with stimulation frequencies as low as 10 Hz.5. These results show for the first time that changes in the sensitivity of the baroreceptor reflex during exercise result in part from afferent information originating in the contracting muscles.

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Cardiovascular responses to brief static contractions in man with topical nervous blockade.

Cited by 25 publications

References 10 publications

Changes in R‐R interval at the start of muscle contraction in the decerebrate cat.

Changes in R‐R interval at the start of muscle contraction in the decerebrate cat.

Autonomic Adjustments to Exercise in Humans

Changes in the baroreceptor reflex at the start of muscle contraction in the decerebrate cat.

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