Combined effects of hypoxia and endurance training on lipid metabolism in rat skeletal muscle.

Saved in:

Bibliographic Details
Title:	Combined effects of hypoxia and endurance training on lipid metabolism in rat skeletal muscle.
Authors:	Galbès, O., Goret, L., Caillaud, C., Mercier, J., Obert, P., Candau, R., Py, G.
Source:	Acta Physiologica. Jun2008, Vol. 193 Issue 2, p163-173. 11p. 1 Chart, 6 Graphs.
Subjects:	Exercise, Hypoxemia, Fatty acids, Transferases, Lipid metabolism, Quadriceps muscle
Abstract:	Aim: To determine whether endurance training can counterbalance the negative effects of hypoxia on mitochondrial phosphorylation and expression of the long chain mitochondrial fatty acid transporter muscle carnitine palmitoyl transferase 1 (mCPT-1). Methods: Male Wistar rats were exposed either to hypobaric hypoxia (at a simulated altitude of ≈4000 m, PIO2 ≈ 90 mmHg) or to normoxia (sea level) for 5 weeks. In each environment, rats were randomly assigned to two groups. The trained group went through a 5-week endurance training programme. The control group remained sedentary for the same time period. Muscle fatty acid oxidation capacity was evaluated after the 5-week period on isolated mitochondria prepared from quadriceps muscles with the use of palmitoylcarnitine or pamitoylCoA + carnitine. Results: Chronic hypoxia decreased basal ( V0, −31% with pamitoylCoA + carnitine and −21% with palmitoylcarnitine, P < 0.05) and maximal ( Vmax, −31% with pamitoylCoA + carnitine, P < 0.05) respiration rates, hydroxyacylCoA dehydrogenase activity (−48%, P < 0.05), mCPT-1 activity index (−34%, P < 0.05) and mCPT-1 protein content (−34%, P < 0.05). Five weeks of endurance training in hypoxia brought V0, mCPT-1 activity index and mCPT-1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, Vmax reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O2· min−1 · mg−1 for hypoxic training vs. 19.9 nmol O2 · min−1 · mg−1 for normoxic sedentarity, P < 0.05). Conclusion: Endurance training can attenuate chronic hypoxia-induced impairments in mitochondrial fatty acid oxidation. This training effect seems mostly mediated by mCPT-1 activity rather than by mCPT-1 content. [ABSTRACT FROM AUTHOR]
	Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database:	Psychology and Behavioral Sciences Collection

Description
Abstract:	Aim: To determine whether endurance training can counterbalance the negative effects of hypoxia on mitochondrial phosphorylation and expression of the long chain mitochondrial fatty acid transporter muscle carnitine palmitoyl transferase 1 (mCPT-1). Methods: Male Wistar rats were exposed either to hypobaric hypoxia (at a simulated altitude of ≈4000 m, PIO2 ≈ 90 mmHg) or to normoxia (sea level) for 5 weeks. In each environment, rats were randomly assigned to two groups. The trained group went through a 5-week endurance training programme. The control group remained sedentary for the same time period. Muscle fatty acid oxidation capacity was evaluated after the 5-week period on isolated mitochondria prepared from quadriceps muscles with the use of palmitoylcarnitine or pamitoylCoA + carnitine. Results: Chronic hypoxia decreased basal ( V0, −31% with pamitoylCoA + carnitine and −21% with palmitoylcarnitine, P < 0.05) and maximal ( Vmax, −31% with pamitoylCoA + carnitine, P < 0.05) respiration rates, hydroxyacylCoA dehydrogenase activity (−48%, P < 0.05), mCPT-1 activity index (−34%, P < 0.05) and mCPT-1 protein content (−34%, P < 0.05). Five weeks of endurance training in hypoxia brought V0, mCPT-1 activity index and mCPT-1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, Vmax reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O2· min−1 · mg−1 for hypoxic training vs. 19.9 nmol O2 · min−1 · mg−1 for normoxic sedentarity, P < 0.05). Conclusion: Endurance training can attenuate chronic hypoxia-induced impairments in mitochondrial fatty acid oxidation. This training effect seems mostly mediated by mCPT-1 activity rather than by mCPT-1 content. [ABSTRACT FROM AUTHOR]
ISSN:	17481708
DOI:	10.1111/j.1748-1716.2007.01794.x