Burtscher 2012 Abstract Bioblast
| Burtscher M (2012) Strategies for improving exercise tolerance: Targeting the brain and/or the skeletal muscles? Mitochondr Physiol Network 17.12. |
Link: MiPNet17.12 Bioblast 2012 - Open Access
Burtscher M (2012)
Event: Bioblast 2012
DRAFT
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 to result primarily from chronic adaptations in skeletal muscle. These adaptations include the increase of key enzyme activities of the mitochondrial electron transfer system and an associated increase in mitochondrial density 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]. Besides 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 thereby contributing to the observed changes in muscle metabolism and the rating of perceived exertion after interval hypoxia. Thus, exercise tolerance may be improved by the use of passive and active strategies targeting both the skeletal muscle and the brain.
- 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.
- 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.
• Keywords: Exercise tolerance, Exercise training, Intermittent hypoxia
• O2k-Network Lab: AT Innsbruck Burtscher M
Labels:
Organism: Human
Tissue;cell: Skeletal muscle, Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Regulation: Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
Affiliations and author contributions
Martin Burtscher1
(1) Institut für Sportwissenschaften, Leopold Franzens Univ. Innsbruck, Innsbruck, Austria; Email: [email protected]
