Why the study?
Trained apneists have an augmented apnea-induced bradycardic response compared to novices, but whether short-term apnea training alters apnea phases and bradycardia via central command mechanisms remained to be tested.
Does 13 days of apnea training improve apnea duration and physiological responses in novice apneists?
Does 13 days of apnea training improve apnea duration and physiological responses in novice apneists?
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Short-term apnea training in novices significantly increases apnea duration and augments the bradycardic response, while attenuating the heart rate response to psychological stress.
Trained apneists such as freedivers have an augmented apnea-induced bradycardic response compared to novice apneists. We hypothesized that (1) our short-term apnea training protocol would extend the duration of the easy-going and struggle apnea phases while augmenting bradycardia, (2) central command is the mechanism responsible for augmented bradycardia, and (3) the response to a psychological stressor would be attenuated post-training. 22 participants without previous apnea training underwent 13 days of training, which included daily apneas alongside targeted psychological coaching, with in-lab assessments pre- and post-training. In-lab assessment involved a maximal apnea, static handgrip with post-exercise circulatory occlusion to assess central command, and a Stroop test used as a psychological stressor. Heart rate, blood pressure, oxygen saturation, and muscle sympathetic nerve activity were measured continuously throughout in-lab testing. Overall apnea duration (44 ± 21 vs. 75 ± 33 s, p < 0.001) and struggle phase duration (18 ± 18 vs. 45 ± 34 s, p < 0.001) were increased post-training, while the easy-going phase did not increase (26 ± 12 vs. 30 ± 17 s, p = 0.329). The bradycardic response during in-lab apneas was larger post-training (−10 ± 11 vs. −20 ± 13 bpm, p < 0.001). No difference in the heart rate response to handgrip was found post-training (19 ± 15 vs. 16 ± 12 bpm, p = 0.122). The heart rate response to the Stroop test was attenuated post-training (10 ± 7 vs. 6 ± 5 bpm, p = 0.009). The lack of attenuated heart rate response to handgrip indicates decreased central command signalling is not the mechanism responsible for augmented apnea bradycardia. Stroop test results highlight an improved response to a psychological stressor.
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O’Croinin et al. (2025) studied this question.
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