The diving response is largely elicited by apnea (breath-holding) alone (Table 1.04). It is further intensified by face immersion, or submersion of the whole body in water. Apnea is directed by higher CNS centers which act on the medullary respiratory center. Under its influence and the peripheral chemoreceptors (carotid & aortic bodies), the vasomotor center increases peripheral sympathetic tone which causes systemic arteriolar vasoconstriction, and raises blood pressure. This transient modest hypertension acts on the baroreceptors, producing increased parasympathetic tone to the heart, resulting in bradycardia. The vasomotor center also acts directly on the cardio-inhibitory center to induce cardiac slowing.
The wetness, cold, etc. resulting from placing the face in water stimulates facial receptors reaching the CNS through the trigeminal nerve. This further intensifies the effects of breath-holding alone, as well as, further inhibiting ventilation. Neither the immersion of other parts of the body nor the depth of immersion have any effect on the diving response.
Cold (water) intensifies the response by producing increased cutaneous vasoconstriction, which further elevates blood pressure, inducing greater reflex cardiac slowing. Because the vasoconstriction associated with diving occurs in larger arterioles, the vasodilatation which one would anticipate as the result of tissue hypoxia acting through local control mechanisms, is blocked. Many organs (skeletal muscle, gut, kidney) are treated as expendible circulations during diving and receive reduced blood flow.
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