This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O(2) consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N(2) narcosis is also illuminated.

Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.

The ability of the pulmonary circulation of the fetal lamb to respond to a rise in oxygen tension was studied from 94 to 146 days of gestation. The unanesthetized ewe breathed room air at normal atmospheric pressure, followed by 100% oxygen at three atmospheres absolute pressure in a hyperbaric chamber. In eleven near-term lambs (132 to 146 days of gestation), fetal arterial oxygen tension (PaO2) increased from 25 +/- 1 to 55 +/- 6 Torr (mean +/- SE), which increased the proportion of right ventricular output distributed to the fetal lungs from 8 +/- 1 to 59 +/- 5%. In five very immature lambs (94 to 101 days of gestation), fetal PaO2 increased from 27 +/- 1 to 174 +/- 70 Torr, but the proportion of right ventricular output distributed to the lung did not change, 8 +/- 1 to 9 +/- 1%. In five of the near-term lambs, pulmonary blood flow was measured. It increased from 34 +/- 3 to 298 +/- 35 ml.kg fetal wt-1.min-1, an 8.8-fold increase. We conclude that the pulmonary circulation of the fetal lamb does not respond to an increase in oxygen tension before 101 days of gestation; however, near term an increase in oxygen tension alone can induce the entire increase in pulmonary blood flow that normally occurs after the onset of breathing at birth.

Pendergast DR, Lundgren CE. The underwater environment: cardiopulmonary, thermal, and energetic demands. J Appl Physiol 106: 276 -283, 2009. First published November 26, 2008 doi:10.1152/japplphysiol.90984.2008.-Water covers over 75% of the earth, has a wide variety of depths and temperatures, and holds a great deal of the earth's resources. The challenges of the underwater environment are underappreciated and more short term compared with those of space travel. Immersion in water alters the cardio-endocrine-renal axis as there is an immediate translocation of blood to the heart and a slower autotransfusion of fluid from the cells to the vascular compartment. Both of these changes result in an increase in stroke volume and cardiac output. The stretch of the atrium and transient increase in blood pressure cause both endocrine and autonomic changes, which in the short term return plasma volume to control levels and decrease total peripheral resistance and thus regulate blood pressure. The reduced sympathetic nerve activity has effects on arteriolar resistance, resulting in hyperperfusion of some tissues, which for specific tissues is time dependent. The increased central blood volume results in increased pulmonary artery pressure and a decline in vital capacity. The effect of increased hydrostatic pressure due to the depth of submersion does not affect stroke volume; however, a bradycardia results in decreased cardiac output, which is further reduced during breath holding. Hydrostatic compression, however, leads to elastic loading of the chest wall and negative pressure breathing. The depthdependent increased work of breathing leads to augmented respiratory muscle blood flow. The blood flow is increased to all lung zones with some improvement in the ventilation-perfusion relationship. The cardiac-renal responses are time dependent; however, the increased stroke volume and cardiac output are, during head-out immersion, sustained for at least hours. Changes in water temperature do not affect resting cardiac output; however, maximal cardiac output is reduced, as is peripheral blood flow, which results in reduced maximal exercise performance. In the cold, maximal cardiac output is reduced and skin and muscle are vasoconstricted, resulting in a further reduction in exercise capacity. respiratory; renal; immersion; exercise; aging; sex differences; submersion; pressure; energy cost THE UNDERWATER ENVIRONMENT is unique, and while it is a magical place with great history and beauty and plant and animal life and holds a wealth of resources, it also imposes pronounced physiological stresses on humans and animals. This brief review offers an overview of how the major environmental challenges, i.e., the pressure, temperature extremes, and the unbreathable ambient medium, of the "Silent World" affect circulation, renal system and water balance, breathing, exercise, and thermal balance and how it imposes some threats due to pharmacological or toxic effects of respired gases at high pressure, i.e., great depths. Adaptations to ...

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.