title: High twin resemblance for sensitivity to hypoxia.
abstract: OBJECTIVE
  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·kg) 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˙O2max (-39%), HRmax (HR, -8%), maximal pulmonary ventilation (V˙Emax, -11%), and urinary norepinephrine excretion (-31%) were reduced (P < 0.05) whereas HR at rest (25%) and during EXSUB (16%) and V˙E at rest (38%) and during EXSUB (70%) were increased (P < 0.05). However, hypoxia-induced changes (Δ) were not randomly distributed between subjects. Between-pair variance was substantially larger than within-pair variance (P < 0.05) for Δ%SpO2 at rest (approximately threefold) and during exercise (approximately fourfold), ΔV˙O2max (approximately fourfold), ΔHR during exercise (approximately seven- to eightfold), hypoxic ventilatory response (approximately sixfold), and Δ 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.
authors.affiliation: 1Exercise Physiology Research Group, Department of Kinesiology, KU Leuven, Leuven, BELGIUM; and 2Physical Activity, Sports and Health Research Group, Department of Kinesiology, KU Leuven, Leuven, BELGIUM.
authors.forename: Evi
authors.initials: E
authors.lastname: Masschelein
authors.forename: Ruud
authors.initials: R
authors.lastname: Van Thienen
authors.forename: Martine
authors.initials: M
authors.lastname: Thomis
authors.forename: Peter
authors.initials: P
authors.lastname: Hespel
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics; D000293:Adolescent; D000328:Adult; D000399:Air Pressure; D000531:Altitude; D000532:Altitude Sickness / Q000235:genetics* / Q000503:physiopathology; D005080:Exercise Test; D017079:Exercise Tolerance / Q000235:genetics; D006339:Heart Rate; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000652:urine; D010100:Oxygen / Q000008:administration & dosage* / Q000097:blood; D010101:Oxygen Consumption; D005082:Physical Exertion / Q000502:physiology*; D012123:Pulmonary Ventilation; D012146:Rest / Q000502:physiology; D014430:Twins, Monozygotic; D055815:Young Adult
chemical_list: D010100:Oxygen; D009638:Norepinephrine