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Central oxytocin modulates exercise-induced tachycardia.
1Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, 05508-900 Sao Paulo, Brazil.
Summary
Oxytocin in the brainstem restrains heart rate during exercise in trained rats. Blocking oxytocin receptors amplified exercise tachycardia in trained rats, suggesting a novel regulatory mechanism.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Exercise Physiology
Background:
- Vasopressinergic projections in the dorsal brainstem are known to activate during exercise and influence heart rate.
- Differential heart rate responses to exercise exist between trained and sedentary individuals.
Purpose of the Study:
- To investigate the role of oxytocinergic projections to the nucleus of the solitary tract-dorsal motor nucleus of the vagus (NTS/DMV) complex in the differential heart rate response to exercise.
- To determine if oxytocin (OT) release in the NTS/DMV influences exercise-induced tachycardia in trained (T) versus sedentary (S) rats.
Main Methods:
- Compared arterial pressure (AP) and heart rate (HR) responses to dynamic exercise in S and T rats.
- Administered vehicle, oxytocin (OT), or OT-receptor antagonist (OT(ant)) into the NTS/DMV.
- Measured OT content in brain regions and plasma at rest and post-exercise.
- Administered OT-receptor antagonist or OT into the fourth cerebral ventricle.
Main Results:
- Exercise increased OT content in the dorsal and ventral brainstem and spinal cord exclusively in T rats.
- Blockade of NTS/DMV OT receptors potentiated exercise-induced tachycardia by 26% in T rats but not S rats.
- Exogenous OT administration into the NTS/DMV blunted exercise tachycardia in both S and T rats.
- Neither OT receptor blockade nor OT administration into the fourth cerebral ventricle affected cardiovascular responses.
Conclusions:
- Oxytocinergic projections to the NTS/DMV are activated during exercise in trained rats.
- Oxytocin released in the NTS/DMV acts on OT receptors to restrain exercise-induced tachycardia.
- This suggests a novel central neural mechanism for regulating heart rate during exercise.