Breath-Hold Diving

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.