Relation between resting spleen volume and apnea-induced increases in hemoglobin mass.

Introduction: Indigenous populations renowned for apneic diving have comparatively large spleen volumes. It has been proposed that a larger spleen translates to heightened apnea-induced splenic contraction and elevations in circulating hemoglobin mass (Hbmass), which, in theory, improves O2 carrying and/or CO2/pH buffering capacities. However, the relation between resting spleen volume and apnea- induced increases in Hbmass is unknown. Therefore, we tested the hypothesis that resting spleen volume is positively related to apnea-induced increases in total Hbmass. Methods: Fourteen healthy adults (six women; 29 ± 5 years) completed a two-minute carbon monoxide rebreathe procedure to measure pre-apneas Hbmass and blood volume. Spleen length, width, and thickness were measured pre-and post-five maximal apneas via ultrasound. Spleen volume was calculated via the Pilström equation (test-retest CV:2 ± 2%). Hemoglobin concentration ([Hb]; g/dl) and hematocrit (%) were measured pre- and post-apneas via capillary blood samples. Post-apneas Hbmass was estimated as post-apnea [Hb] x pre-apnea blood volume. Data are presented as mean ± SD. Results: Spleen volume decreased from pre- (247 ± 95 mL) to post- (200 ± 82 mL, p<0.01) apneas. [Hb] (14.6 ± 1.2 vs. 14.9 ± 1.2 g/dL, p<0.01), hematocrit (44 ± 3 vs. 45 ± 3%, p=0.04), and Hbmass (1025 ± 322 vs. 1046 ± 339 g, p=0.03) increased from pre- to post-apneas. Pre-apneas spleen volume was unrelated to post-apneas increases in Hbmass (r=-0.02, p=0.47). O2 (+28 ± 31 mL, p<0.01) and CO2 (+31 ± 35 mL, p<0.01) carrying capacities increased post-apneas. Conclusion: Larger spleen volume is not associated with a greater rise in apneas-induced increases in Hbmass in non-apnea-trained healthy adults.

Acute moderate normobaric hypoxia does not modify circulating thyroid hormone concentrations induced by 1 h of head-out cold-water immersion.

This study tested the hypothesis that acute moderate normobaric hypoxia augments circulating thyroid hormone concentrations during and following 1 h of cold head-out water immersion (HOWI), compared with when cold HOWI is completed during normobaric normoxia. In a randomized crossover single-blind design, 12 healthy adults (27 ± 2 yr, 2 women) completed 1 h of cold (22.0 ± 0.1°C) HOWI breathing either normobaric normoxia ([Formula: see text] = 0.21) or normobaric hypoxia ([Formula: see text] = 0.14). Free and total thyroxine (T3) and triiodothyronine (T4), and thyroid-stimulating hormone (TSH) concentrations were measured in venous blood samples obtained before (baseline), during (15-, 30-, and 60 min), and 15 min following HOWI (post-), and were corrected for changes in plasma volume. Arterial oxyhemoglobin saturation and core (rectal) temperature were measured continuously. Arterial oxyhemoglobin saturation was lower during hypoxia (90 ± 3%) compared with normoxia (98 ± 1%, P < 0.001). Core temperature fell from baseline (normoxia: 37.2 ± 0.4°C, hypoxia: 37.2 ± 0.4°C) to post-cold HOWI (normoxia: 36.4 ± 0.5°C, hypoxia: 36.3 ± 0.5°C, P < 0.001) in both conditions but did not change differently between conditions (condition × time: P = 0.552). Circulating TSH, total T3, free T4, total T3, and free T4 concentrations demonstrated significant main effects of time (all P ≤ 0.024), but these changes did not differ between normoxic and hypoxic conditions (condition × time: all P ≥ 0.163). These data indicate that acute moderate normobaric hypoxia does not modify the circulating thyroid hormone response during 1 h of cold HOWI.NEW & NOTEWORTHY Acute head-out cold (22°C) water immersion (HOWI) decreased core temperature and increased thermogenesis. This thermogenic response was paralleled by the activation of the hypothalamic-pituitary-thyroid axis, as evidenced by changes in thyroid hormones. However, cold HOWI in combination with moderate normobaric hypoxia did not modify the thermogenic nor the circulating thyroid hormone response. This finding suggests that hypoxia-induced alterations in thyroid hormone concentrations are unlikely to acutely contribute to adaptations resulting from repeated cold-water exposures.