Mittuniversitetet

Apnea is physiologically stressful and can within a short time frame pose a threat to survival. To sustain prolonged apnea, oxygen use should be minimized and its storage maximized. Two mechanisms known to have this effect are the cardiovascular diving response, directing the available oxygen selectively to the heart and brain, and spleen contraction increasing the circulating erythrocyte volume and thereby gas storage capacity. Spleen contraction is also observed after maximal exercise, and is thought to enhance aerobic performance. While the cardiovascular diving response is known to be more pronounced after apnea training, spleen contraction has not been studied in conjunction with apnea training or other types of training. The aim of the present investigation is to study the hematological responses to apnea performed during rest by elite apneic divers, by elite cross-country skiers and by untrained subjects. After 20 min of rest, subjects performed 3 maximal apneas spaced by 2 min normal breathing intervals. Blood samples were drawn before, directly after, and 10 min after the apnea series and hemoglobin concentration was measured. All groups responded to maximal apneas with an increase in hemoglobin concentration, which had disappeared after 10 min of recovery. The increase in hemoglobin concentration was more pronounced in the apneic divers (4g/L) than in skiers (3g/L) and untrained subjects (2g/L; P < 0.05). All groups prolonged their apneic times through the series, but the increase was most evident for the divers versus both the skiers (P < 0.05) and untrained subjects (P < 0.01). The results suggest that these responses could be more pronounced as a result of apnea training.

Spleen contraction resulting in an increase in circulating erythrocytes has been shown to occur during apnea. This effect, however, has not previously been studied during normobaric hypoxia whilst breathing. After 20 min of horizontal rest and normoxic breathing, five subjects underwent 20-min of normobaric hypoxic breathing (12.8% oxygen) followed by 10 min of normoxic breathing. Ultrasound measurements of spleen volume and samples for venous hemoglobin concentration (Hb) and hematocrit (Hct) were taken simultaneously at short intervals from 20 min before until 10 min after the hypoxic period. Heart rate, arterial oxygen saturation (SaO2) and respiration rate were recorded continuously. During hypoxia, a reduction in SaO2 by 34% (P < 0.01) was accompanied by an 18% reduction in spleen volume and a 2.1% increase in both Hb and Hct (P < 0.05). Heart rate increased 28% above baseline (P < 0.05). Within 3 min after hypoxia SaO2 had returned to pre-hypoxic levels, and spleen volume, Hb and Hct had all returned to pre-hypoxic levels within 10 min. Respiratory rate remained stable throughout the protocol. This study of short-term exposure to eupneic normobaric hypoxia suggests that hypoxia plays a key role in triggering spleen contraction and subsequent release of stored erythrocytes in humans. This response could be beneficial during early altitude acclimatization.

Increased hemoglobin concentration (Hb) and hematocrit (Hct) attributable to spleen contraction raises blood gas storage capacity during apnea, but the mechanisms that trigger this response have not been clarified. We focused on the role of hypoxia in triggering these Hb and Hct elevations. After horizontal rest for 20 min, 10 volunteers performed 3 maximal apneas spaced by 2 min, each preceded by a deep inspiration of air. The series was repeated using the same apneic durations but after 1 min of 100% oxygen breathing and oxygen inspiration prior to apneas. Mean apneic durations were 150s, 171s, and 214s for apneas 1, 2, and 3, respectively. Relative to pre-apnea values, the mean post-apneic arterial oxygen saturation nadir was 84.7% after air and 98% after oxygen. A more pronounced elevation of both Hb and Hct occurred during the air trial: after apnea 1 with air, mean Hb had increased by 1.5% (P<0.01), but no clear increase was found after the first apnea in with oxygen. After the third apnea with air Hb had increased by 3.0% (P<0.01), and with oxygen by 2.0% (P<0.01). After the first apnea with air Hct had increased by 1.9% (P<0.01) and after 3 apneas by 3.0% (P<0.01), but Hct did not change significantly in the oxygen trial. In both trials, Hb and Hct were at pre-apneic levels 10 min after apneas. Diving bradycardia during apnea was the same in both trials. We concluded that hypoxia is essential in inducing spleen-related Hb and Hct increase during apnea.