Key result
Sciatic-stimulated exercise raises PaCO2 ~3 Torr, showing humoral pathways alone fail to maintain isocapnic hyperpnea.
Why the study?
The role of neural pathways in the ventilatory response to exercise was unclear, particularly when neural connections from limbs to CNS are severed.
The significant increase in PaCO2 during exercise in dogs with severed sciatic nerves suggests that neural pathways play a fundamental role in the normal ventilatory response to exercise.
Answers are grounded in this paper and cite their sources.
Neural drive is required for isocapnic hyperpnea in this canine model; leaves open its primacy and translation to humans.
The ventilatory response to exercise induced by stimulation of the peripheral ends of severed sciatic nerves was studied in seven anesthetized dogs. In response to exercise (n = 23) there were increases in expired minute ventilation (delta VE = 4.09 l/min), arterial CO2 partial pressure (delta PaCO2 = 3.06 Torr), and carotid artery temperature (delta Tca = 0.26 degrees C). There was also a concomitant decrease in mean arterial blood pressure (delta MAP = -6.28 Torr). Since the neural pathways from the exercising limbs to the central nervous system had been eliminated by nerve section, the significant increase in PaCO2 during exercise indicates that humoral factors alone cannot produce the normal exercise response, i.e., an isocapnic hyperpnea. Therefore, neural pathways may play a fundamental role in the ventilatory response to exercise in intact animals.
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F.M. Bennett (1984) studied Exercise hyperpnea (n=7). Exercise induced by stimulation of severed sciatic nerves was evaluated on Ventilatory response to exercise (expired minute ventilation, arterial CO2 partial pressure). Exercise induced by sciatic nerve stimulation in dogs with severed neural pathways increased PaCO2 (delta 3.06 Torr), indicating humoral factors alone cannot produce normal isocapnic hyperpnea.
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