Central command activation during exercise is essential for the bradycardic response to diving
Authors: Araujo Marcela , Lima Adamor , Guerrero Rosa , Vianna Lauro 
Published: May 2024

Mammalian diving response evokes complex cardiovascular adjustments, including bradycardia during sustained muscular activity. This is intriguing because voluntary exercise involves the activation of central command and skeletal muscle afferents, known to provoke tachycardia by reducing vagal outflow and increasing cardiac sympathetic activity. Nonetheless, it is currently unknown how diving-induced bradycardia can override the exercise tachycardia. Given this, we aimed to test the hypothesis that central and peripheral afferent mechanisms interact to modulate this physiological phenomenon. In three visits, 32 healthy subjects (15 women; 22±3 yr) were exposed to trigeminal nerve stimulation (i.e., facial cooling; TGS) to partially activate the diving reflex at rest (semi-recumbent position) and under three protocols: 1) during voluntary light (resting heart rate+20 beats.min−1) and moderate (resting heart rate+50 beats.min−1) steady-state cycling exercise; 2) during isolation of peripheral afferent reflexes via passive exercise (muscle mechanoreceptors) and cold pressor test (nociceptors; CPT), and; 3) during CPT with concurrent light exercise. The exercise intensities were assumed to provide different levels of central command activation, while both passive exercise and CPT were used to provide insights into the contribution of central command to diving bradycardia. TGS was performed for at least 90 seconds in all conditions. Beat-to-beat heart rate (HR, by electrocardiography) and blood pressure (finger photoplethysmography) were continuously measured, and surface electromyography was used to ensure the lack of volitional component during passive exercise. TGS elicited significant bradycardia at rest (Δ-12±0.9 beats·min−1; P<0.001), and this response was increased during voluntary light exercise (Δ-15±1.2 beats·min−1; P=0.002), but unaffected during voluntary moderate exercise when compared to rest (Δ-11±1.3 beats·min−1; P=0.536). In contrast, compared to rest, the HR response to TGS during passive exercise was significantly attenuated (Δ-13±1.2 beats·min−1 vs. Δ-9±1.7 beats·min−1; P=0.039), whereas CPT completely abolish the diving bradycardic response (Δ0±1.6 beats·min−1; P<0.001). However, when the volitional component was restored during CPT with concurrent light exercise, TGS provoked a significant bradycardic response, when compared to CPT condition (Δ1±1.6 beats·min−1 vs. Δ-10±2.1 beats·min−1; P=0.004). Notably, our findings were not affected by sex. In conclusion, these findings suggest that 1) central command activation during cycling exercise is essential for the bradycardic response to diving; 2) isolated peripheral afferent reflexes exert inhibitory feedback to modulate diving-induced bradycardia, and; 3) central and peripheral afferent feedback are important mechanisms by which exercise modulates the dive response.

CNPq 307764/2022-2; CAPES (001).

This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.