Key result
Muscle afferent stimulation in rabbits increases cardiac output and pulmonary ventilation without altering PCO2.
Stimulation of thin fiber muscle afferents in rabbits produces distinct cardiorespiratory response patterns depending on stimulation frequency, both characterized by isocapnic hyperpnea.
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Muscle afferent stimulation coordinates cardiorespiratory responses in rabbits; hypothesis-generating for exercise hyperpnea mechanisms but leaves open human translation.
The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).
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Raimondi et al. (1996) studied this question. Electrical stimulation of the central end of the gastrocnemius nerves was evaluated on Cardiorespiratory responses (mean arterial pressure, systemic vascular resistance, cardiac output, stroke volume, pulmonary ventilation). Low- and high-frequency electrical stimulation of muscle afferents in rabbits induced isocapnic hyperpnea, characterized by increased cardiac output and pulmonary ventilation without changes in PCO2.
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