Journal of Applied Physiology · 2015 · 116 citations · 42 references
Pv ContractionPhysiological ResearchExerciseHematologyApplied PhysiologyHealth SciencesHigh AltitudeAldosterone ConcentrationHypoxia (Medicine)Hemoglobin MassRespiration (Physiology)3,454-M AltitudeIntravascular Volume KineticsPhysiologyExercise PhysiologyTissue OxygenationMetabolismMedicineAnesthesiology
High altitude (HA) exposure facilitates a rapid contraction of plasma volume (PV) and a slower occurring expansion of hemoglobin mass (Hb mass ). The kinetics of the Hb mass expansion has never been examined by multiple repeated measurements, and this was our primary study aim. The second aim was to investigate the mechanisms mediating the PV contraction. Nine healthy, normally trained sea-level (SL) residents (8 males, 1 female) sojourned for 28 days at 3,454 m. Hb mass was measured and PV was estimated by carbon monoxide rebreathing at SL, on every 4th day at HA, and 1 and 2 wk upon return to SL. Four weeks at HA increased Hb mass by 5.26% (range 2.5-11.1%; P < 0.001). The individual Hb mass increases commenced with up to 12 days of delay and reached a maximal rate of 4.04 ± 1.02 g/day after 14.9 ± 5.2 days. The probability for Hb mass to plateau increased steeply after 20–24 days. Upon return to SL Hb mass decayed by −2.46 ± 2.3 g/day, reaching values similar to baseline after 2 wk. PV, aldosterone concentration, and renin activity were reduced at HA ( P < 0.001) while the total circulating protein mass remained unaffected. In summary, the Hb mass response to HA exposure followed a sigmoidal pattern with a delayed onset and a plateau after ∼3 wk. The decay rate of Hb mass upon descent to SL did not indicate major changes in the rate of erythrolysis. Moreover, our data support that PV contraction at HA is regulated by the renin-angiotensin-aldosterone axis and not by changes in oncotic pressure.
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