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Effects of Acute Hypoxia on Metabolic and Hormonal Responses to Resistance Exercise


Medicine & Science in Sports & Exercise: July 2010 - Volume 42 - Issue 7 - p 1279-1285
doi: 10.1249/MSS.0b013e3181ce61a5
BASIC SCIENCES: Contrasting Perspectives

Introduction: 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.

1Department of Sports Sciences, Japan Institute of Sports Sciences, Tokyo, JAPAN; and 2Laboratory of Regenerative Medical Engineering, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, JAPAN

Address for correspondence: Michihiro Kon, Ph.D., Department of Sports Sciences, Japan Institute of Sports Sciences, 3-15-1 Nishigaoka, Kita, Tokyo, 115-0056, Japan; E-mail:

Submitted for publication October 2009.

Accepted for publication December 2009.

©2010The American College of Sports Medicine