Heart rate transient at the onsset of active and passive dynamic exercise

CLAUDIO, ANTONIO; N??BREGA, L; Gil, Claudio; ARA??JO, S

doi:10.1249/00005768-199301000-00007

Cited by 66 publications

(13 citation statements)

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“…Thus, HR responses to passive and active cycling could reflect redundancy. In support of that view, the present study showed a similar increase in HR during passive and active cycling, which has been previously reported (38), indicating that the HR response at the onset of cycling is not affected when central command is absent. In this sense, we reasoned that the GABAergic mechanisms involved in the cardiac vagal withdrawal at the onset of exercise is primarily mediated by muscle mechanoreceptor afferents.…”

Section: Discussionsupporting

confidence: 93%

“…The immediate increase in HR at the onset of exercise can be evoked by central command (16,30,63) and by isolated muscle mechanoreflex stimulation with passive movement (38,58,63) or muscle stretch (12,22). Thus, HR responses to passive and active cycling could reflect redundancy.…”

Section: Discussionmentioning

confidence: 99%

“…Each exercise bout was performed at the end-expiratory breath to avoid the possible confounding influence of respiratory sinus arrhythmia (17,24,41,49,60). Passive movement was carried out by the experimenter manually cycling the subject's legs in which visual and auditory feedback from EMG were provided to the subjects throughout passive cycling trials to help him/her keep leg muscles relaxed (38,39,60,63). Figure 1 show a schematic illustration of the experimental setup ( Fig.…”

Section: Subjectsmentioning

confidence: 99%

“…It has been proposed that the isolation of muscle mechanoreflex can be evoked by passive movement (11,25,38,39,60,63) or muscle stretch (9,12,22). Interestingly, Nóbrega and Araújo (38) observed a similar increase in HR during voluntary and passive cycling, indicating that the HR response at the onset of exercise is not affected when central command and muscle metaboreflex are absent.…”

Section: Introductionmentioning

confidence: 99%

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GABAergic contribution to the muscle mechanoreflex-mediated heart rate responses at the onset of exercise in humans

Teixeira

Ramos

Samora

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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Previous studies have indicated that central GABAergic mechanisms are involved in the heart rate (HR) responses at the onset of exercise. On the basis of previous research that showed similar increases in HR during passive and active cycling, we reasoned that the GABAergic mechanisms involved in the HR responses at the exercise onset are primarily mediated by muscle mechanoreceptor afferents. Therefore, in this study, we sought to determine whether central GABA mechanisms are involved in the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. Twenty-eight healthy subjects (14 men and 14 women) aged between 18 and 35 yr randomly performed three bouts of 5-s passive and active cycling under placebo and after oral administration of diazepam (10 mg), a benzodiazepine that produces an enhancement in GABA activity. Beat-to-beat HR (electrocardiography) and arterial blood pressure (finger photopletysmography) were continuously measured. Electromyography of the vastus lateralis was obtained to confirm no electrical activity during passive trials. HR increased from rest under placebo and further increased after administration of diazepam in both passive (change: 12 ± 1 vs. 17 ± 1 beats/min, P < 0.01) and active (change: 14 ± 1 vs. 18 ± 1 beats/min, P < 0.01) cycling. Arterial blood pressure increased from rest similarly during all conditions ( P > 0.05). Importantly, no sex-related differences were found in any variables during experiments. These findings demonstrate, for the first time, that the GABAergic mechanisms significantly contribute to the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. NEW & NOTEWORTHY We found that passive and voluntary cycling evokes similar increases in heart rate and that these responses were enhanced after diazepam administration, a benzodiazepine that enhances GABA activity. These findings suggest that the GABAergic system may contribute to the muscle mechanoreflex-mediated vagal withdrawal at the onset of exercise in humans.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

GABAergic contribution to the muscle mechanoreflex-mediated heart rate responses at the onset of exercise in humans

Teixeira

Ramos

Samora

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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“…The sensory component of the exercise pressor reflex comprises group III and IV skeletal muscle afferents that respond to both mechanical (i.e., muscle mechanoreflex) and metabolic (i.e., muscle metaboreflex) stimuli (28). In humans, the muscle mechanoreflex can be activated by mechanical stretch (22) or passive movement (35,52,56); however, its effects on cardiovascular responses appear small and transient. On the other hand, Alam and Smirk (2) first reported that the increases in arterial BP observed during isometric handgrip (IHG) exercise were partially maintained when the circulation of blood through the working skeletal muscles was arrested by suprasystolic cuff occlusion just before the cessation of exercise.…”

Section: Introductionmentioning

confidence: 99%

Muscle metaboreflex activation via postexercise ischemia as a tool for teaching cardiovascular physiology for undergraduate students

Teixeira

Samora

Vianna

2019

Advances in Physiology Education

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The cardiovascular responses to exercise are mediated by several interactive neural mechanisms, including central command, arterial baroreflex, and skeletal muscle mechano- and metaboreflex. In humans, muscle metaboreflex activation can be isolated via postexercise ischemia (PEI), which increases sympathetic nerve activity and partially maintains the exercise-induced increase in arterial blood pressure. Here, we describe a practical laboratory class using PEI as a simple and useful technique to teach cardiovascular physiology. In an undergraduate exercise physiology class ( n = 47), a traditional 4-h lecture was conducted discussing the neural control mechanisms of cardiovascular regulation during exercise. Thereafter, eight students (4 men and 4 women) were selected to participate as a volunteer of a practical laboratory class. Each participant performed 90 s of isometric handgrip exercise at 40% of maximal voluntary contraction, followed by 3 min of PEI. Arterial blood pressure and heart rate were measured by digital monitors at rest and during isometric handgrip, PEI, and recovery. In addition, blood samples were collected from the tip of the exercising finger for blood lactate analyses. After the laboratory class, a survey was given to determine the perceptions of the students. The findings demonstrate that this laboratory class has proved to be highly popular with students, who self-reported a significant improvement in their understanding of several aspects of cardiovascular regulation during exercise.

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Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

180

193

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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Heart rate transient at the onsset of active and passive dynamic exercise

Cited by 66 publications

References 0 publications

GABAergic contribution to the muscle mechanoreflex-mediated heart rate responses at the onset of exercise in humans

GABAergic contribution to the muscle mechanoreflex-mediated heart rate responses at the onset of exercise in humans

Muscle metaboreflex activation via postexercise ischemia as a tool for teaching cardiovascular physiology for undergraduate students

Control of Breathing During Exercise

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