High-altitude (HA) natives have evolved some beneficial responses leading to superior work capacity at HA compared to native lowlanders. Our aim was to study two responses potentially protective against hypoxia: the spleen contraction elevating hemoglobin concentration (Hb) and the cardiovascular diving response in Sherpa highlanders, compared to lowlanders. Male participants were recruited from three groups: (1) 21 Sherpa living at HA (SH); (2) seven Sherpa living at low altitude (SL); and (3) ten native Nepalese lowlanders (NL). They performed three apneas spaced by a twomin rest at low altitude (1370 m). Their peripheral oxygen saturation (SpO 2), heart rate (HR), and spleen volume were measured across the apnea protocol. Spleen volume at rest was 198 ± 56 mL in SH and 159 ± 35 mL in SL (p = 0.047). The spleen was larger in Sherpa groups compared to the 129 ± 22 mL in NL (p < 0.001 compared to SH; p = 0.046 compared to SL). Spleen contraction occurred in all groups during apnea, but it was greater in Sherpa groups compared to NL (p < 0.001). HR was lower in Sherpa groups compared to NL both during rest (SL: p < 0.001; SH: p = 0.003) and during maximal apneas (SL: p < 0.001; SH: p = 0.06). The apnea-induced HR reduction was 8 ± 8% in SH, 10 ± 4% in SL (NS), and 18 ± 6% in NL (SH: p = 0.005; SL: p = 0.021 compared to NL). Resting SpO 2 was similar in all groups. The progressively decreasing baseline spleen size across SH, SL, and NL suggests a role of the spleen at HA and further that both genetic predisposition and environmental exposure determine human spleen size. The similar HR responses of SH and SL suggest that a genetic component is involved in determining the cardiovascular diving response.

Acute mountain sickness (AMS) is a potentially life-threatening illness that may develop during exposure to hypoxia at high altitude (HA). Susceptibility to AMS is highly individual, and the ability to predict it is limited. Apneic diving also induces hypoxia, and we aimed to investigate whether protective physiological responses, i.e., the cardiovascular diving response and spleen contraction, induced during apnea at low-altitude could predict individual susceptibility to AMS. Eighteen participants (eight females) performed three static apneas in air, the first at a fixed limit of 60 s (A1) and two of maximal duration (A2–A3), spaced by 2 min, while SaO 2 , heart rate (HR) and spleen volume were measured continuously. Tests were conducted in Kathmandu (1470 m) before a 14 day trek to mount Everest Base Camp (5360 m). During the trek, participants reported AMS symptoms daily using the Lake Louise Questionnaire (LLQ). The apnea-induced HR-reduction (diving bradycardia) was negatively correlated with the accumulated LLQ score in A1 ( r s = −0.628, p = 0.005) and A3 ( r s = −0.488, p = 0.040) and positively correlated with SaO 2 at 4410 m (A1: r = 0.655, p = 0.003; A2: r = 0.471, p = 0.049; A3: r = 0.635, p = 0.005). Baseline spleen volume correlated negatively with LLQ score ( r s = −0.479, p = 0.044), but no correlation was found between apnea-induced spleen volume reduction with LLQ score ( r s = 0.350, p = 0.155). The association between the diving bradycardia and spleen size with AMS symptoms suggests links between physiological responses to HA and apnea. Measuring individual responses to apnea at sea-level could provide means to predict AMS susceptibility prior to ascent.

Voluntary apnoea causes splenic contraction and reductions in heart rate (HR; bradycardia), and subsequent transient increases in haemoglobin concentration ([Hb]). Ascent to high altitude (HA) induces systemic hypoxia and reductions in oxygen saturation (S pO 2), which may cause tonic splenic contraction, which may contribute to haematological acclimatization associated with HA ascent. We measured resting cardiorespiratory variables (HR, S pO 2 , [Hb]) and resting splenic volume (via ultrasound) during incremental ascent from 1400 m (day 0) to 3440 m (day 3), 4240 m (day 7) and 5160 m (day 10) in non-acclimatized native lowlanders during assent to HA in the Nepal Himalaya. In addition, apnoea-induced responses in HR, S pO 2 and splenic volume were measured before and after two separate voluntary maximal apnoeas (A1

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Splenic contraction, which leads to ejection of stored erythrocytes, is greater in athletes involved in regular freediving or high-altitude activities. As this response facilitates oxygen carrying capacity, similar characteristics may be expected of elite endurance athletes. Therefore, our aims were to compare resting and apnea-induced splenic volume in endurance athletes and untrained individuals, and to assess the athletes' exercise-induced splenic volume. Twelve elite biathletes (7 women) and 12 controls (6 women) performed a maximal effort apnea in a seated position. In addition, the biathletes completed a maximal roller-skiing time trial. Splenic dimensions were measured by ultrasonic imaging for subsequent volume calculations, while Hb was analyzed from capillary blood samples and cardiorespiratory variables were monitored continuously. Baseline splenic volume was larger in the biathletes (214±56 mL) compared to controls (157±39 mL, p=0.008) and apnea-induced splenic contraction was also greater in the biathletes (46±20 mL versus 30±16 mL, p=0.035). Hb increased immediately after apnea in the biathletes (4.5±4.8%, p=0.029) but not the controls (-0.7±3.1%, p=0.999). Increases in exercise-induced splenic contraction (p=0.008) and Hb (p=0.001) were greater compared to the apnea-induced responses among the athletes. Baseline splenic volume tended to be correlated with V̇O2max (r=0.584, p=0.059). We conclude that elite biathletes have greater splenic volume with a greater ability to contract and elevate Hb compared to untrained individuals. These characteristics may transiently enhance O2-carrying capacity and possibly increase O2 uptake, thereby helping biathletes to cope with high intermittent O2 demands and severe O2 deficits that occur during biathlon training and competition.