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

Galbes, Olivier; Goret, Lucie; Caillaud, Corinne; Mercier, Jacques; Obert, Philippe; Candau, Robin; Py, Guillaume

doi:10.1111/j.1748-1716.2007.01794.x

Cited by 20 publications

(26 citation statements)

References 40 publications

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“…In general, most studies of human and non-human skeletal muscles point to decreased mitochondrial oxidative capacity after chronic hypoxia [21;29;30]. Mitochondrial oxygen consumption rates decrease in rodent hind limb muscles after acute (state 3 and 4) and chronic hypoxia (state 2 and 3) [18;35]. Our results concur: mitochondria from triceps surae had lower respiration rates after 4 weeks of hypoxia.…”

Section: Discussionsupporting

confidence: 82%

Muscle endurance and mitochondrial function after chronic normobaric hypoxia: contrast of respiratory and limb muscles

Gamboa

Andrade

2011

Pflugers Arch - Eur J Physiol

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Skeletal muscle adaptation to chronic hypoxia includes loss of oxidative capacity and decrease in fiber size. However, the diaphragm may adapt differently since its activity increases in response to hypoxia. Thus, we hypothesized that chronic hypoxia would not affect endurance, mitochondrial function or fiber size in the mouse diaphragm. Adult male mice were kept in normoxia (Control) or hypoxia (Hypoxia, FIO2= 10%) for 4 weeks. After that time, muscles were collected for histological, biochemical and functional analyses. Hypoxia soleus muscles fatigued faster (fatigue index higher in Control, 21.5±2.6% vs. 13.4±2.4%, p<0.05), but there was no difference between Control and Hypoxia diaphragm bundles. Mean fiber cross sectional area was unchanged in Hypoxia limb muscles, but it was 25% smaller in diaphragm (p<0.001). Ratio of capillary length contact to fiber perimeter was significantly higher in Hypoxia diaphragm (28.6±1.2 vs. 49.3±1.4, Control and Hypoxia, p<0.001). Mitochondrial respiration rates in Hypoxia limb muscles were lower: state 2 decreased 19%, state 3 31% and state 4 18% vs. Control, p<0.05 for all comparisons. There were similar changes in Hypoxia diaphragm: state 3 decreased 29% and state 4 17%, p<0.05. After 4 weeks of hypoxia limb muscle mitochondria had lower content of complex IV (cytochrome c oxidase), while diaphragm mitochondria had higher content of complexes IV and V (F1/F0 ATP synthase) and less uncoupling protein 3 (UCP-3). These data demonstrate that diaphragm retains its endurance during chronic hypoxia, apparently due to a combination of morphometric changes and optimization of mitochondrial energy production.

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Section: Discussionsupporting

confidence: 82%

Muscle endurance and mitochondrial function after chronic normobaric hypoxia: contrast of respiratory and limb muscles

Gamboa

Andrade

2011

Pflugers Arch - Eur J Physiol

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“…Altogether, this confirms that regulation of redox status under reduced O 2 availability is of key importance. Mitochondrial function is depreciated in rodents exposed to simulated altitude, even when O 2 consumption was normalized to mitochondrial protein content [86][87][88]. Unexpectedly, mitochondrial respiration was only modestly altered in humans exposed to 4550 m with slight reduction in maximal oxidative phosphorylation capacity [89].…”

Section: Mitochondrial Remodelling and Regulation Of Ros Productionmentioning

confidence: 99%

HIF-1-driven skeletal muscle adaptations to chronic hypoxia: molecular insights into muscle physiology

Favier

Britto

Freyssenet

et al. 2015

Cell. Mol. Life Sci.

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Skeletal muscle is a metabolically active tissue and the major body protein reservoir. Drop in ambient oxygen pressure likely results in a decrease in muscle cells oxygenation, reactive oxygen species (ROS) overproduction and stabilization of the oxygen-sensitive hypoxia-inducible factor (HIF)-1α. However, skeletal muscle seems to be quite resistant to hypoxia compared to other organs, probably because it is accustomed to hypoxic episodes during physical exercise. Few studies have observed HIF-1α accumulation in skeletal muscle during ambient hypoxia probably because of its transient stabilization. Nevertheless, skeletal muscle presents adaptations to hypoxia that fit with HIF-1 activation, although the exact contribution of HIF-2, I kappa B kinase and activating transcription factors, all potentially activated by hypoxia, needs to be determined. Metabolic alterations result in the inhibition of fatty acid oxidation, while activation of anaerobic glycolysis is less evident. Hypoxia causes mitochondrial remodeling and enhanced mitophagy that ultimately lead to a decrease in ROS production, and this acclimatization in turn contributes to HIF-1α destabilization. Likewise, hypoxia has structural consequences with muscle fiber atrophy due to mTOR-dependent inhibition of protein synthesis and transient activation of proteolysis. The decrease in muscle fiber area improves oxygen diffusion into muscle cells, while inhibition of protein synthesis, an ATP-consuming process, and reduction in muscle mass decreases energy demand. Amino acids released from muscle cells may also have protective and metabolic effects. Collectively, these results demonstrate that skeletal muscle copes with the energetic challenge imposed by O2 rarefaction via metabolic optimization.

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“…These genes are involved in angiogenesis, glycolysis, lipid metabolism, carbohydrate metabolism, and protein amino acid phosphorylation (Baze et al, 2010). Endurance training lessens chronic hypoxiainduced impairments in mitochondrial fatty acid oxidation mostly mediated by the activity of the long chain mitochondrial fatty acid transporter muscle carnitine palmitoyl transferase 1 (mCPT-1) rather than by mCPT-1 content (Galbès et al, 2008). Hypoxic training for three weeks regulated the lipid metabolism by reducing the mRNA and protein expression of sterol regulatory element binding protein-1c in the obese rat liver (Wang et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Effects of hypoxic exercise training on microRNA expression and lipid metabolism in obese rat livers

Wen

Feng

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:To investigate the effects of hypoxic exercise training on microRNA (miRNA) expression and the role of miRNA expression in regulating lipid metabolism, 20 dietary-induced obese SD rats were divided into a normoxic sedentary group (N, n=10) and a hypoxic exercise training group (H, n=10). After four weeks, measurements were taken of body weight, body length, fat mass, serum lipid concentration, miRNAs differentially expressed in rat liver, and gene and protein expression levels of peroxisome proliferator activated receptor α (PPARα), fatty acid synthetase (FAS), and carnitine palmitoyl transferase 1A (CPT1A) in rat liver. Body weight, Lee's index, fat mass, fat/weight ratio, and serum levels of total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) were all significantly lower in the H group than in the N group (P<0.01). Six miRNAs expressed significantly differently in the liver (P<0.05). Specifically, expression levels of miR-378b were significantly lower in the H group than in the N group (P<0.05). Compared with the normoxic sedentary group, hypoxic exercise training resulted in a lower ratio of FAS mRNA to CPT1A mRNA (P<0.05), as well as lower CPT1A protein levels (P<0.01), while a higher ratio of FAS to CPT1A protein levels (P<0.01) was observed. In conclusion, hypoxic training may elevate the resistance of high fat diet induced obesity in rats by reducing the expression of miR-378b, and decrease the fatty acid mitochondrial oxidation in obese rat livers by decreasing the protein expression of CPT1A and increasing the protein expression ratio of FAS/CPT1A.

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

Abstract: 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.

Cited by 20 publications

References 40 publications

Muscle endurance and mitochondrial function after chronic normobaric hypoxia: contrast of respiratory and limb muscles

Muscle endurance and mitochondrial function after chronic normobaric hypoxia: contrast of respiratory and limb muscles

HIF-1-driven skeletal muscle adaptations to chronic hypoxia: molecular insights into muscle physiology

Effects of hypoxic exercise training on microRNA expression and lipid metabolism in obese rat livers

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