Intermittent hypoxic resistance training: Is metabolic stress the key moderator?
Scott, B.R., Slattery, K.M. and Dascombe, B.J. (2015) Intermittent hypoxic resistance training: Is metabolic stress the key moderator? Medical Hypotheses, 84 (2). pp. 145-149.
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Traditionally, researchers and practitioners have manipulated acute resistance exercise variables to elicit the desired responses to training. However, recent research indicates that altering the muscular environment during resistance training, namely by implementing a hypoxic stimulus, can augment muscle hypertrophy and strength. Intermittent hypoxic resistance training (IHRT), whereby participants inspire hypoxic air during resistance training, has been previously demonstrated to increase muscle cross-sectional area and maximum strength by significantly greater amounts than the equivalent training in normoxia. However, some recent evidence has provided conflicting results, reporting that the use of systemic hypoxia during resistance training provided no added benefit. While the definitive mechanisms that may augment muscular responses to IHRT are not yet fully understood, an increased metabolic stress is thought to be important for moderating many downstream processes related to hypertrophy. It is likely that methodological differences between conflicting IHRT studies have resulted in different degrees of metabolic stress during training, particularly when considering the inter-set recovery intervals used. Given that the most fundamental physiological stresses resulting from hypoxia are disturbances to oxidative metabolism, it becomes apparent that resistance training may only benefit from additional hypoxia if the exercise is structured to elicit a strong metabolic response. We hypothesize that for IHRT to be more effective in producing muscular hypertrophy and increasing strength than the equivalent normoxic training, exercise should be performed with relatively brief inter-set recovery periods, with the aim of providing a potent metabolic stimulus to enhance anabolic responses.
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|Copyright:||© 2014 Elsevier Ltd|
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