title: Effects of acute hypoxia on metabolic and hormonal responses to resistance exercise.
abstract: BACKGROUND
  Several recent studies have shown that resistance exercise combined with vascular occlusion effectively causes increases in muscular size and strength. Researchers speculated that the vascular occlusion-induced local hypoxia may contribute to the adaptations via promoting anabolic hormone secretions stimulated by local accumulation of metabolic subproducts. Here, we examined whether acute systemic hypoxia affects metabolic and hormonal responses to resistance exercise.
  
  
  METHODS
  Twelve male subjects participated in two experimental trials: 1) resistance exercise while breathing normoxic air [normoxic resistance exercise (NR)] and 2) resistance exercise while breathing 13% oxygen [hypoxic resistance exercise (HR)]. The resistance exercises (bench press and leg press) consisted of 10 repetitions for five sets at 70% of maximum strength with 1-min rest between sets. Blood lactate, serum growth hormone (GH), epinephrine (E), norepinephrine (NE), insulin-like growth factor 1, testosterone, and cortisol concentrations were measured before normoxia and hypoxia exposures, 15 min after the exposures, and at 0, 15, 30, and 60 min after the exercises.
  
  
  RESULTS
  Lactate significantly increased after exercises in both trials (P < 0.05). In the HR trial, GH and cortisol significantly increased after the exercise (P < 0.05) but not in the NR trial. The E, NE, insulin-like growth factor 1, and testosterone significantly increased after the exercises in both trials (P < 0.05). The mean values of lactate, GH, E, and NE after exercises were significantly higher in the HR trial than those in the NR trial (P < 0.05).
  
  
  CONCLUSIONS
  These findings suggest that resistance exercise in hypoxic condition caused greater accumulation of metabolites and strong anabolic hormone response.
authors.affiliation: Department of Sports Sciences, Japan Institute of Sports Sciences, Tokyo, Japan. kon.michihiro@jiss.naash.go.jp
authors.forename: Michihiro
authors.initials: M
authors.lastname: Kon
authors.forename: Tatsuaki
authors.initials: T
authors.lastname: Ikeda
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Homma
authors.forename: Takayuki
authors.initials: T
authors.lastname: Akimoto
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Takashi
authors.initials: T
authors.lastname: Kawahara
mesh_terms: D000328:Adult; D004837:Epinephrine / Q000378:metabolism*; D015444:Exercise / Q000502:physiology*; D019382:Human Growth Hormone / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D055070:Resistance Training; D013739:Testosterone / Q000378:metabolism
chemical_list: D019382:Human Growth Hormone; D019344:Lactic Acid; D013739:Testosterone; D007334:Insulin-Like Growth Factor I; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine