Resumen de High Twin Resemblance for Sensitivity to Hypoxia.
Evi Masschelein, Peter Hespel, Ruud van Thienen, Martine Thomis
AB Purpose: Physiological responses to hypoxia vary between individuals, and genetic factors are conceivably involved. Using a monozygotic twin design, we investigated the role of genetic factors in physiological responses to acute hypoxia. Methods: Thirteen pairs of monozygotic twin brothers participated in two experimental sessions in a normobaric hypoxic facility with a 2-wk interval. In one session, fraction of inspired O2 (FiO2) was gradually reduced to 10.7% (approximately 5300 m altitude) over 5 h. During the next 3 h at 10.7%, FiO2 subjects performed a 20-min submaximal exercise bout (EXSUB, 1.2 W[middle dot]kg-1) and a maximal incremental exercise test (EXMAX). An identical control experiment was done in normoxia. Cardiorespiratory measurements were continuously performed, and 8-h urine output was collected. Results: Compared with normoxia, hypoxia decreased (P < 0.05) arterial O2 saturation (%SpO2) at rest (-22%) and during exercise (-28%). Furthermore, V[spacing dot above]O2max (-39%), HRmax (HR, -8%), maximal pulmonary ventilation (V[spacing dot above]Emax, -11%), and urinary norepinephrine excretion (-31%) were reduced (P < 0.05) whereas HR at rest (25%) and during EXSUB (16%) and V[spacing dot above]E at rest (38%) and during EXSUB (70%) were increased (P < 0.05). However, hypoxia-induced changes ([DELTA]) were not randomly distributed between subjects. Between-pair variance was substantially larger than within-pair variance (P < 0.05) for [DELTA]%SpO2 at rest (approximately threefold) and during exercise (approximately fourfold), [DELTA]V[spacing dot above]O2max (approximately fourfold), [DELTA]HR during exercise (approximately seven- to eightfold), hypoxic ventilatory response (approximately sixfold), and [DELTA] urinary norepinephrine output (approximately threefold). Incidence of acute mountain sickness (AMS) also yielded significant twin similarity (P < 0.05). AMS+ subjects showed approximately 50% greater drop in urinary norepinephrine and lower hypoxic ventilator response than AMS- individuals. Conclusions: Our data suggest that genetic factors regulate cardiorespiratory responses, exercise tolerance, and pathogenesis of AMS symptoms in acute severe hypoxia. Hypoxia-induced sympathetic downregulation was associated with AMS.
