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 approximately 4000 m, PIO(2) approximately 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 (V(0), -31% with pamitoylCoA + carnitine and -21% with palmitoylcarnitine, P < 0.05) and maximal (V(max), -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 V(0), mCPT-1 activity index and mCPT-1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, V(max) reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O(2). min(-1) . mg(-1) for hypoxic training vs. 19.9 nmol O(2) . 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.
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 approximately 4000 m, PIO(2) approximately 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 (V(0), -31% with pamitoylCoA + carnitine and -21% with palmitoylcarnitine, P < 0.05) and maximal (V(max), -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 V(0), mCPT-1 activity index and mCPT-1 protein content values back to sedentary normoxic levels. Moreover, in the group trained in hypoxia, V(max) reached a higher level than in the group that maintained a sedentary lifestyle in normoxia (24.2 nmol O(2). min(-1) . mg(-1) for hypoxic training vs. 19.9 nmol O(2) . 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.
Authors: Elie Farhat; Maiah E M Devereaux; Matthew E Pamenter; Jean-Michel Weber Journal: Am J Physiol Regul Integr Comp Physiol Date: 2020-06-17 Impact factor: 3.619
Authors: Vladimir Essau Martinez-Bello; Fabian Sanchis-Gomar; Ana Lucia Nascimento; Federico V Pallardo; Sandra Ibañez-Sania; Gloria Olaso-Gonzalez; Jose Antonio Calbet; Mari Carmen Gomez-Cabrera; Jose Viña Journal: Eur J Appl Physiol Date: 2010-12-01 Impact factor: 3.078