Breath‐Hold Diving

Abstract

Breath-hold diving is practiced by recreational divers, seafood divers, military divers, and competitive athletes. It involves highly integrated physiology and extreme responses. This article reviews human breath-hold diving physiology beginning with an historical overview followed by a summary of foundational research and a survey of some contemporary issues. Immersion and cardiovascular adjustments promote a blood shift into the heart and chest vasculature. Autonomic responses include diving bradycardia, peripheral vasoconstriction, and splenic contraction, which help conserve oxygen. Competitive divers use a technique of lung hyperinflation that raises initial volume and airway pressure to facilitate longer apnea times and greater depths. Gas compression at depth leads to sequential alveolar collapse. Airway pressure decreases with depth and becomes negative relative to ambient due to limited chest compliance at low lung volumes, raising the risk of pulmonary injury called "squeeze," characterized by postdive coughing, wheezing, and hemoptysis. Hypoxia and hypercapnia influence the terminal breakpoint beyond which voluntary apnea cannot be sustained. Ascent blackout due to hypoxia is a danger during long breath-holds, and has become common amongst high-level competitors who can suppress their urge to breathe. Decompression sickness due to nitrogen accumulation causing bubble formation can occur after multiple repetitive dives, or after single deep dives during depth record attempts. Humans experience responses similar to those seen in diving mammals, but to a lesser degree. The deepest sled-assisted breath-hold dive was to 214 m. Factors that might determine ultimate human depth capabilities are discussed. © 2018 American Physiological Society. Compr Physiol 8:585-630, 2018.

Arterial Blood Gas Analysis in Breath-Hold Divers at Depth

“…Surprisingly, in two subjects out of 6 (who had the same training and experience as the others), paO 2 was lower than predicted, 75 and 61 mmHg, respectively (Figure 3 ). We hypothesize that in these two subjects the lower than expected paO 2 was due to ventilation/perfusion mismatch and right-to-left intrapulmonary shunt due to atelectasis caused by the significant reduction in lung volume at 40 m (20% of the pre-dive volume), ( Fitz-Clarke, 2018 ). Blood flow through an atelectatic area would likely be augmented by pulmonary vasodilatation caused by the combination of immersion ( Cherry et al, 2009 ) and pulmonary vascular engorgement due to pressure differential between pulmonary blood vessels and alveolar gas as lung volume during descent approaches residual volume.…”

“…Dynamic apnea: swimming a horizontal distance on a single breath of air while submerged, either with or without fins ( Fitz-Clarke, 2018 ).…”

Exercise with End-expiratory Breath Holding Induces Large Increase in Stroke Volume

“…The drop in HR during breath holding would be due to an oxygenconserving effect that aims at maintaining perfusion to the brain and at reducing cardiac work in order to lower the overall O 2 uptake [32,33]. This effect would be partly mediated by the degree of hypoxaemia through chemoreceptor stimulation [34].…”

Investigation of changes in electrocardiography before and after free diving

“…Increased vagal tone causes bradycardia, but increased sympathetic tone leads to ectopy. [16] Apart from static apnea, increased metabolic activity and oxygen consumption in muscles related to the use of extremities during dive performances such as dynamic apnea have been found to cause more hypoxemic stress in the body. The degree of hypoxemia is also associated with the development of arrhythmia.…”