Hypoxia preconditioning by cobalt chloride enhances endurance performance and protects skeletal muscles from exercise‐induced oxidative damage in rats

Saxena, Sanjeev; Shukla, Dhananjay; Khan, Yasir Akhtar; Singh, Mrinalini; Bansal, Anju; Sairam, M.; Jain, Swatantra Kumar

doi:10.1111/j.1748-1716.2010.02136.x

Cited by 45 publications

(38 citation statements)

References 83 publications

(147 reference statements)

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“…As ROS are involved in HIF-1a stabilization (see above), this reduction would suppress HIF-1a accumulation consistently with its transient up-regulation observed in vitro [34]. Muscle proteome of highlanders is characterized by reinforced protection against ROS compared to control subjects permanently residing at low altitude [84], and hypoxia preconditioning by CoCl 2 in rats reduced exercise-induced skeletal muscle oxidative damages [85]. Altogether, this confirms that regulation of redox status under reduced O 2 availability is of key importance.…”

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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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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“…Eventually, also the MSC-, HSC-, and EPC-derived mature cells are affected by HO-1. Antiapoptotic, anti-inflammatory, and proproliferative effects of HO-1 were reported in osteoclasts (179,256), osteoblasts (34,41,43), myoblasts (80,168,182), leukocytes (234), and endothelial cells (133).…”

Section: Heme Oxygenase-1mentioning

confidence: 99%

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

Kozakowska

Szade

Dulak

et al. 2014

Antioxidants & Redox Signaling

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Significance: Heme oxygenase-1 (HO-1) converts heme to biliverdin, carbon monoxide, and ferrous ions, but its cellular functions are far beyond heme metabolism. HO-1 via heme removal and degradation products acts as a cytoprotective, anti-inflammatory, immunomodulatory, and proangiogenic protein, regulating also a cell cycle. Additionally, HO-1 can translocate to nucleus and regulate transcription factors, so it can also act independently of enzymatic function. Recent Advances: Recently, a body of evidence has emerged indicating a role for HO-1 in postnatal differentiation of stem and progenitor cells. Maturation of satellite cells, skeletal myoblasts, adipocytes, and osteoclasts is inhibited by HO-1, whereas neurogenic differentiation and formation of cardiomyocytes perhaps can be enhanced. Moreover, HO-1 influences a lineage commitment in pluripotent stem cells and maturation of hematopoietic cells. It may play a role in development of osteoblasts, but descriptions of its exact effects are inconsistent. Critical Issues: In this review we discuss a role of HO-1 in cell differentiation, and possible HO-1-dependent signal transduction pathways. Among the potential mediators, we focused on microRNA (miRNA). These small, noncoding RNAs are critical for cell differentiation. Recently we have found that HO-1 not only influences expression of specific miRNAs but also regulates miRNA processing enzymes. Future Directions: It seems that interplay between HO-1 and miRNAs may be important in regulating fates of stem and progenitor cells and needs further intensive studies.

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“…Furthermore, strenuous exercise is known to cause oxidative stress and inflammatory responses in skeletal muscles which leads to muscle damage. Previous studies carried out in our laboratory have shown that preconditioning by oral cobalt supplementation, a hypoxia mimetic, enhances endurance performance and also protects muscle from exercise induced oxidative damage in rat skeletal muscle 8 . Most importantly, supplementation of hypoxia mimetics is practical and feasible way of inducing hypoxia to enhance physical performance.…”

mentioning

confidence: 88%

Untitled

2015

IJPSR

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ABSTRACT:Training under hypoxic conditions is known to enhance physical performance. The possible mechanism might be the stabilization of Hypoxia Inducible Factor (HIF), which otherwise is degraded under normoxia by the action of Prolyl Hydroxylase domain enzymes (PHD). Stabilization of HIF leads to upregulation of its target genes leading to improved erythropoiesis, angiogenesis and antioxidant status as an adaptation to combat training induced stress. Present study investigates efficacy of Ethyl 3, 4 Dihydroxybenzoate (EDHB) in stabilizing HIF-1α which leads to elevated levels of Vascular Endothelial Growth Factor, Erythropoetin, Hb and Hct, indicating improved angiogenesis and blood oxygen carrying capacity. In the present study we have reported 1.5 times increase in endurance performance in rats supplemented with EDHB with or without training as compared to respective controls. Significant improvement in antioxidant status as observed by increase in GSH, SOD, GST and decrease in MDA and protein oxidation, enhanced expression of anti-oxidative proteins Heme-Oxygenase, Metallothionein, Nuclear Factor Erythroid 2-Related Factor contributed in decreasing exercise training induced oxidative stress in EDHB supplemented trained rats. Enhanced levels of anti-inflammatory and reduced levels of pro-inflammatory cytokines might be additional factors responsible in decreasing muscle damage as observed by histopathological studies. The major outcome of the study is preconditioning with PHD inhibitor EDHB results in stabilization of HIF-1α, thus boosting erythropoiesis, antioxidant status and anti-inflammatory response which, in concert result in improvement of physical performance. The study thus underscores the potential of EDHB as a therapeutic agent for improving endurance performance by facilitating hypoxia adaptation in the skeletal muscle.

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Hypoxia preconditioning by cobalt chloride enhances endurance performance and protects skeletal muscles from exercise‐induced oxidative damage in rats

Abstract: Our study provides strong evidence that hypoxic preconditioning with cobalt chloride enhances physical performance and protects muscle from exercise-induced oxidative damage via GSH, HO-1 and MT-mediated antioxidative capacity.

Cited by 45 publications

References 83 publications

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

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

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

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