Splenic contraction and cardiovascular responses are augmented during apnea compared to rebreathing in humans.

The spleen contracts during apnea, releasing stored erythrocytes, thereby increasing systemic hemoglobin concentration (Hb). We compared apnea and rebreathing periods, of equal sub-maximal duration (mean 137 s; SD 30), in eighteen subjects to evaluate whether respiratory arrest or hypoxic and hypercapnic chemoreceptor stimulation is the primary elicitor of splenic contraction and cardiovascular responses during apnea. Spleen volume, Hb, cardiovascular variables, arterial (SaO2), cerebral (ScO2), and deltoid muscle oxygen saturations (SmO2) were recorded during the trials and end-tidal partial pressure of oxygen (PETO2) and carbon dioxide (PETCO2) were measured before and after maneuvers. The spleen volume was smaller after apnea, 213 (89) mL, than after rebreathing, 239 (95) mL, corresponding to relative reductions from control by 20.8 (17.8) % and 11.6 (8.0) %, respectively. The Hb increased 2.4 (2.0) % during apnea, while there was no significant change with rebreathing. The cardiovascular responses, including bradycardia, decrease in cardiac output, and increase in total peripheral resistance, were augmented during apnea compared to during rebreathing. The PETO2 was higher, and the PETCO2 was lower, after apnea compared to after rebreathing. The ScO2 was maintained during maneuvers. The SaO2 decreased 3.8 (3.1) % during apnea, and even more, 5.4 (4.4) %, during rebreathing, while the SmO2 decreased less during rebreathing, 2.2 (2.8) %, than during apnea, 8.3 (6.2) %. We conclude that respiratory arrest per se is an important stimulus for splenic contraction and Hb increase during apnea, as well as an important initiating factor for the apnea-associated cardiovascular responses and their oxygen-conserving effects.

Suspected arterial gas embolism after glossopharyngeal insufflation in a breath-hold diver.

INTRODUCTION: Many competitive breath-hold divers employ the technique of glossopharyngeal insufflation in order to increase their lung gas volume for a dive. After a maximal inspiration, using the oral and pharyngeal muscles repeatedly, air in the mouth is compressed and forced into the lungs. Such overexpansion of the lungs is associated with a high transpulmonary pressure, which could possibly cause pulmonary barotrauma. CASE REPORT: We report a case of transient neurological signs and symptoms occurring within 1 min after glossopharyngeal insufflation in a breath-hold diver. He complained of paresthesia of the right shoulder and a neurological exam revealed decreased sense of touch on the right side of the neck as compared to the left side. Motor function was normal. The course of events in this case is suggestive of arterial gas embolism. DISCUSSION: Although the diver recovered completely within a few minutes, the perspective of a more serious insult raises concerns in using the glossopharyngeal insufflation technique. In addition to a neurological insult, damage to other organs of the body has to be considered. Both acute and long-term negative health effects are conceivable.

Hypoxic syncope in a competitive breath-hold diver with elevation of the brain damage marker S100B.

INTRODUCTION: Competitive breath-hold divers can accomplish previously unbelievable performances; e.g., the current world record for apnea during rest ("static apnea") is 11 min 35 s. However, whether such performances are associated with a risk for hypoxic brain damage has not been established. CASE REPORT: A breath-hold diver's competitive performance resulted in a loss of consciousness, after which he was subjected to a medical examination by the event physician. Blood samples were collected for analysis of the brain damage marker S100B in serum. The S100B in serum was 0.100 microg x L(-1) in the blood sample collected 15 min after the loss of consciousness. At 1 and 5 d after the incident it was 0.097 microg x L(-1) and 0.045 microg x L(-1) respectively. DISCUSSION: The elevated level of S100B, close to the upper reference limit (0.105 microg x L(-1)) indicates that the incident affected the integrity of the central nervous system. Even though this case does not establish that hypoxic brain damage is an inherent risk with loss of consciousness in competitive breathhold diving, the observation raises concerns. We suggest that it should be considered that repetitive exposures to prolonged apneas leading to severe hypoxia may be associated with negative long-term effects.

Asystole and increased serum myoglobin levels associated with 'packing blackout' in a competitive breath-hold diver.

Many competitive breath-hold divers use 'glossopharyngeal insufflation', also called 'lung packing', to overfill their lungs above normal total lung capacity. This increases intrathoracic pressure, decreases venous return, compromises cardiac pumping, and reduces arterial blood pressure, possibly resulting in a syncope breath-hold divers call 'packing blackout'. We report a case with a breath-hold diver who inadvertently experienced a packing blackout. During the incident, an electrocardiogram (ECG) and blood pressure were recorded, and blood samples for determinations of biomarkers of cardiac muscle perturbation (creatine kinase-MB isoenzyme (CK-MB), cardiac troponin-T (TnT), and myoglobin) were collected. The ECG revealed short periods of asystole during the period of 'packing blackout', simultaneous with pronounced reductions in systolic, diastolic, and pulse pressures. Serum myoglobin concentration was elevated 40 and 150 min after the incident, whereas there were no changes in CK-MB or TnT. The ultimate cause of syncope in this diver probably was a decrease in cerebral perfusion following glossopharyngeal insufflation. The asystolic periods recorded in this diver could possibly indicate that susceptible individuals may be put at risk of a serious cardiac incident if the lungs are excessively overinflated by glossopharyngeal insufflation. This concern is further substantiated by the observed increase in serum myoglobin concentration after the event.

Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations.

The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281-403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O(2) and CO(2) (Pa(O(2)) and Pa(CO(2))) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with Pa(O(2)) and Pa(CO(2)) reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 microg/l at the start of apnea to 0.083 microg/l after the apnea (P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.

Pulmonary edema after competitive breath-hold diving.

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.

Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans.

The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10 degrees C) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion. Oxygen uptake from the lungs decreased during apnea in air (-22% compared with eupneic control) and was further reduced during apnea with face immersion (-25% compared with eupneic control). The plasma lactate concentration increased from control (11%) after apnea in air and even more after apnea with face immersion (20%), suggesting an increased anaerobic metabolism during apneas. The lung oxygen store was depleted more slowly during apnea with face immersion because of the augmented diving response, probably including a decrease in cardiac output. Venous oxygen stores were probably reduced by the cardiovascular responses. The turnover times of these gas stores would have been prolonged, reducing their effect on the oxygen uptake in the lungs. Thus the human diving response has an oxygen-conserving effect.

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.