Steiner 2011 J Appl Physiol: Difference between revisions
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|title=Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM (2011) Exercise training increases mitochondrial biogenesis in the brain. J Appl Physiol doi:10.1152/japplphysiol.00343.2011. | |title=Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM (2011) Exercise training increases mitochondrial biogenesis in the brain. J Appl Physiol doi:10.1152/japplphysiol.00343.2011. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21817111 PMID: 21817111] | |||
|authors=Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM | |authors=Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM | ||
|year=2011 | |year=2011 | ||
|journal=J Appl Physiol | |journal=J Appl Physiol | ||
|abstract=Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training. However, very little attention has been given to the likely benefits of increased brain mitochondria in this regard. We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions (''n''=16-19/gr). EX mice performed 8 weeks of treadmill running for 1 hr/d, 6 d/wk at 25 m/min and a 5% incline. Twenty-four hours after the last training bout a subgroup of mice (''n''=9-11/gr) were sacrificed and brain (brainstem, cerebellum, cortex, frontal lobe, hippocampus, hypothalamus, and midbrain), and muscle (soleus) tissues were isolated for analysis of mRNA expression of peroxisome proliferator activated receptor gamma coactivator-1-alpha (PGC-1ฮฑ), Silent Information Regulator T1 (SIRT1), citrate synthase (CS), and mitochondrial DNA (mtDNA) using RT-PCR. A different sub-group of EX and SED mice (''n''=7-8/gr), performed a treadmill RTF test. Exercise training increased PGC-1ฮฑ, SIRT1 and CS mRNA and mtDNA, in most brain regions in addition to the soleus (''P''<0.05). Mean treadmill RTF increased from 74.0ยฑ9.6 min to 126.5ยฑ16.1 min following training (''P''<0.05). These findings suggest that exercise training increases brain mitochondrial biogenesis which may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction. | |abstract=Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training. However, very little attention has been given to the likely benefits of increased brain mitochondria in this regard. We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions (''n''=16-19/gr). EX mice performed 8 weeks of treadmill running for 1 hr/d, 6 d/wk at 25 m/min and a 5% incline. Twenty-four hours after the last training bout a subgroup of mice (''n''=9-11/gr) were sacrificed and brain (brainstem, cerebellum, cortex, frontal lobe, hippocampus, hypothalamus, and midbrain), and muscle (soleus) tissues were isolated for analysis of mRNA expression of peroxisome proliferator activated receptor gamma coactivator-1-alpha (PGC-1ฮฑ), Silent Information Regulator T1 (SIRT1), citrate synthase (CS), and mitochondrial DNA (mtDNA) using RT-PCR. A different sub-group of EX and SED mice (''n''=7-8/gr), performed a treadmill RTF test. Exercise training increased PGC-1ฮฑ, SIRT1 and CS mRNA and mtDNA, in most brain regions in addition to the soleus (''P''<0.05). Mean treadmill RTF increased from 74.0ยฑ9.6 min to 126.5ยฑ16.1 min following training (''P''<0.05). These findings suggest that exercise training increases brain mitochondrial biogenesis which may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction. | ||
|keywords=PGC-1ฮฑ, SIRT1, citrate synthase, endurance exercise, central fatigue | |keywords=[[PGC-1ฮฑ]], SIRT1, citrate synthase, endurance exercise, central fatigue | ||
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{{Labeling | {{Labeling | ||
Revision as of 13:06, 12 June 2012
| Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM (2011) Exercise training increases mitochondrial biogenesis in the brain. J Appl Physiol doi:10.1152/japplphysiol.00343.2011. |
Steiner JL, Murphy EA, McClellan JL, Carmichael MD, Davis JM (2011) J Appl Physiol
Abstract: Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training. However, very little attention has been given to the likely benefits of increased brain mitochondria in this regard. We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions (n=16-19/gr). EX mice performed 8 weeks of treadmill running for 1 hr/d, 6 d/wk at 25 m/min and a 5% incline. Twenty-four hours after the last training bout a subgroup of mice (n=9-11/gr) were sacrificed and brain (brainstem, cerebellum, cortex, frontal lobe, hippocampus, hypothalamus, and midbrain), and muscle (soleus) tissues were isolated for analysis of mRNA expression of peroxisome proliferator activated receptor gamma coactivator-1-alpha (PGC-1ฮฑ), Silent Information Regulator T1 (SIRT1), citrate synthase (CS), and mitochondrial DNA (mtDNA) using RT-PCR. A different sub-group of EX and SED mice (n=7-8/gr), performed a treadmill RTF test. Exercise training increased PGC-1ฮฑ, SIRT1 and CS mRNA and mtDNA, in most brain regions in addition to the soleus (P<0.05). Mean treadmill RTF increased from 74.0ยฑ9.6 min to 126.5ยฑ16.1 min following training (P<0.05). These findings suggest that exercise training increases brain mitochondrial biogenesis which may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction. โข Keywords: PGC-1ฮฑ, SIRT1, citrate synthase, endurance exercise, central fatigue
Labels:
Organism: Mouse
Tissue;cell: Skeletal muscle, Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Regulation: Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
