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

• Published in: Acta Physiologica 2008-06, Vol.193 (2), p.163-173
• Main Authors: Galbès, O, Goret, L, Caillaud, C, Mercier, J, Obert, P, Candau, R, Py, G
• Format: Article
• Language: English
• Subjects: 3-Hydroxyacyl CoA Dehydrogenases - metabolism; Altitude; Animals; Biological and medical sciences; Body Weight; Carnitine O-Palmitoyltransferase - metabolism; Cell Respiration; Chronic Disease; chronic hypoxia; Citrate (si)-Synthase - metabolism; Computer Science; endurance training; fatty acid oxidation; Fatty Acids - metabolism; Fundamental and applied biological sciences. Psychology; Hemoglobins - metabolism; Hypoxia - metabolism; Life Sciences; Lipid Metabolism; Male; mCPT-1; mitochondria; Mitochondria, Muscle - metabolism; Muscle, Skeletal - metabolism; Oxidation-Reduction; Physical Conditioning, Animal - methods; Physical Conditioning, Animal - physiology; Rats; Rats, Wistar; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 1748-1708; 0001-6772; 1748-1716; 1365-201X
• DOI: 10.1111/j.1748-1716.2007.01794.x

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). Male Wistar rats were exposed either to hypobaric hypoxia (at a simulated altitude of [almost equal to]4000 m, PIO₂ [almost equal to] 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. 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). 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.