Burtscher 2012 Abstract Bioblast

From Bioblast
Burtscher M (2012) Strategies for improving exercise tolerance: Targeting the skeletal muscles and/or the brain? Mitochondr Physiol Network 17.12.

Link: MiPNet17.12 Bioblast 2012 - Open Access

Burtscher M (2012)

Event: Bioblast 2012

Martin Burtscher

The individual level of exercise tolerance is closely associated with mortality and quality of life. Thus, to maintain or improve exercise tolerance is one of the most important goals in the elderly or those suffering from various diseases. Exercise training has been evidenced as the most effective way to achieve this goal. Exercise tolerance is related to the ability to use a high percentage of the individual maximum oxygen uptake which is thought predominantly to result from chronic adaptations in skeletal muscle. These adaptations include the increase of key enzyme activities of the mitochondrial electron transport chain and an associated increase in mitochondrial protein accumulation and increased capillary supply. The resulting improvements in performance seem mainly due to a higher rate of fat oxidation and a concomitant reduction in glycolytic flux, and a tighter control of the acid-base status. However, in certain cases, the rapid development of fatigue which cannot simply be explained by metabolic aspects of working muscles affects exercise performance. Recent studies suggest that exercise increases not only muscle but also brain mitochondrial biogenesis thereby likely contributing to reduced fatigue and improved exercise performance [1]. Beside exercise training, repeated passive exposures to short-term hypoxia (interval hypoxia) have also been demonstrated to increase exercise tolerance, e.g. in patients suffering from respiratory or heart diseases [2]. Similar to exercise, transient hypoxia with and without exercise may be capable to stimulate mitochondrial biogenesis in the skeletal muscle as well as the brain [3], thereby contributing to the observed changes in muscle metabolism and the rating of perceived exertion after interval hypoxia [2]. Our observations, derived from measurements of cerebral and muscle oxygenation by NIRS, indicate that beneficial effects on exercise tolerance following exercise training might rather be due to reduced peripheral fatigue and following interval hypoxia due to diminished central fatigue.

  1. Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM (2011) Exercise training increases mitochondrial biogenesis in the brain. J Appl Physiol 111: 1066-1071.
  2. Burtscher M, Gatterer H, Szubski C, Pierantozzi E, Faulhaber M (2010) Effects of interval hypoxia on exercise tolerance: special focus on patients with CAD or COPD. Sleep Breath 14: 209-220.
  3. Gutsaeva DR, Carraway MS, Suliman HB, Demchenko IT, Shitara H, Yonekawa H, Piantadosi CA (2008) Transient hypoxia stimulates mitochondrial biogenesis in brain subcortex by a neuronal nitric oxide synthase-dependent mechanism. J Neurosci 28: 2015-2204.

β€’ Keywords: Exercise tolerance, Exercise training, Intermittent hypoxia

β€’ O2k-Network Lab: AT Innsbruck Burtscher M

Labels: MiParea: mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine 

Organism: Human  Tissue;cell: Skeletal muscle, Nervous system 

Affiliations and author contributions

Martin Burtscher1

(1) Department of Sport Science, Medical Section, University of Innsbruck; Austria; Email: [email protected]


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