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      A comparison of the metabolic effects of treadmill and wheel running exercise in mouse model

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          Abstract

          Aerobic exercise is well known to have a positive impact on body composition, muscle strength, and oxidative capacity. In animal model, both treadmill and wheel running exercise modalities have become more popular, in order to study physiological adaptation associated with aerobic exercise. However, few studies have compared physiological adaptations in response to either treadmill exercise (TE), or voluntary wheel running exercise (WE). We therefore compared each exercise intervention on body composition and oxidative markers in male C57BL/6 N mice. The total distance run was remarkably higher in the WE group than in the TE group. Both forms of exercise resulted in the reduction of body weight, fat mass, and adipocyte size. However, the average for grip strength of WE was higher than for control and TE. Interestingly, PGC-1α expression was increased in the gastrocnemius (glycolytic-oxidative) and soleus (oxidative) muscle of TE group, whereas WE showed a significant effect on PGC-1α expression only in the soleus muscle. However, muscle fiber type composition was not shifted remarkably in either type of exercise. These results suggest that TE and WE may exert beneficial effects in suppressing metabolic risks in mouse model through attenuating body weight, fat mass, size, and increase in mitochondria biogenesis marker, PGC-1α.

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          The role of exercise and PGC1alpha in inflammation and chronic disease.

          Inadequate physical activity is linked to many chronic diseases. But the mechanisms that tie muscle activity to health are unclear. The transcriptional coactivator PGC1alpha has recently been shown to regulate several exercise-associated aspects of muscle function. We propose that this protein controls muscle plasticity, suppresses a broad inflammatory response and mediates the beneficial effects of exercise.
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            Exercise-induced mitochondrial biogenesis begins before the increase in muscle PGC-1alpha expression.

            Exercise results in rapid increases in expression of the transcription coactivator peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) and in mitochondrial biogenesis in skeletal muscle. PGC-1alpha regulates and coordinates mitochondrial biogenesis, and overexpression of PGC-1alpha in muscle cells results in increases in mitochondrial content. In this context, it has been proposed that the increase in PGC-1alpha protein expression mediates the exercise-induced increase in mitochondrial biogenesis. However, we found that mitochondrial proteins with a short half-life increase as rapidly as, or more rapidly than, PGC-1alpha protein. This finding led us to hypothesize that activation, rather than increased expression, of PGC-1alpha mediates the initial phase of the exercise-induced increase in mitochondria. In this study, we found that most of the PGC-1alpha in resting skeletal muscle is in the cytosol. Exercise resulted in activation of p38 MAPK and movement of PGC-1alpha into the nucleus. In support of our hypothesis, binding of the transcription factor nuclear respiratory factor 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cytochrome oxidase subunit 4 promoter increased in response to exercise prior to an increase in PGC-1alpha protein. Furthermore, exercise-induced increases in the mRNAs of cytochrome c, delta-aminolevulinate synthase, and citrate synthase also occurred before an increase in PGC-1 protein. Thus, it appears that activation of PGC-1alpha may mediate the initial phase of the exercise-induced adaptive increase in muscle mitochondria, whereas the subsequent increase in PGC-1alpha protein sustains and enhances the increase in mitochondrial biogenesis.
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              Voluntary exercise alters the cytoarchitecture of the adult dentate gyrus by increasing cellular proliferation, dendritic complexity, and spine density.

              Voluntary exercise produces a dramatic increase in the number of bromodeoxyuridine (BrdU)-positive cells in the adult dentate gyrus (DG); however, it has never been determined whether this increase reflects neurogenic activity or some exercise-induced change in the metabolic processing of systemically injected BrdU. In these experiments, we show that 1) 200 mg/kg is a saturating dose for single injections of BrdU in both control and voluntary exercise animals; 2) there is significantly more cell labeling in animals that exercise when saturating doses of BrdU are employed; 3) high doses of BrdU do not affect the number, appearance, or distribution of labeled cells; 4) voluntary exercise leads to similar increases in the number of cells expressing Ki67, an intrinsic marker of cellular proliferation; 5) both dendritic length and complexity are significantly increased in the DG of animals that exercise; and 6) spine density is significantly greater on dendrites in the DG following voluntary exercise. This study demonstrates that exercise up-regulates neurogenic activity in the DG of adult rats, independently of any putative changes in altered BrdU metabolism, and that it also substantially alters the morphology of dentate granule cell dendrites. The dramatic changes in the cytoarchitecture of the DG induced by voluntary exercise might underlie the enhancement of hippocampal long-term potentiation and hippocampal-dependent memory that our group has previously described. These results suggest that exercise may be an effective component of therapeutic regimes aimed at improving the functioning of individuals with neuropathologies that involve the degradation of cells in the hippocampus. (c) 2005 Wiley-Liss, Inc.
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                Author and article information

                Contributors
                jun151169@gmail.com
                snumouse@snu.ac.kr
                Journal
                Lab Anim Res
                Lab Anim Res
                Laboratory Animal Research
                BioMed Central (London )
                1738-6055
                2233-7660
                7 February 2020
                7 February 2020
                2020
                : 36
                : 3
                Affiliations
                [1 ]GRID grid.31501.36, ISNI 0000 0004 0470 5905, Laboratory of Developmental Biology and Genomics, BK21 Program for Veterinary Science, College of Veterinary Medicine, , Seoul National University, ; Seoul, South Korea
                [2 ]GRID grid.31501.36, ISNI 0000 0004 0470 5905, The Research Institute for Veterinary Science, College of Veterinary Medicine, , Seoul National University, ; Seoul, 08826 Republic of Korea
                [3 ]GRID grid.31501.36, ISNI 0000 0004 0470 5905, Korea Mouse Phenotyping Center (KMPC), , Seoul National University, ; 08826 Seoul, Republic of Korea
                [4 ]GRID grid.15444.30, ISNI 0000 0004 0470 5454, Severance Biomedical Science Institute, , Yonsei University College of Medicine, ; Seoul, 03722 South Korea
                [5 ]GRID grid.31501.36, ISNI 0000 0004 0470 5905, Interdisciplinary Program for Bioinformatics, Program for Cancer Biology, BIO-MAX/N-Bio Institute, , Seoul National University, ; 08826 Seoul, Republic of Korea
                Author information
                http://orcid.org/0000-0003-1177-6958
                Article
                35
                10.1186/s42826-019-0035-8
                7081706
                32206610
                69337ec7-916a-4f65-bf3c-77ae5c06d535
                © The Author(s) 2020

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 13 November 2019
                : 27 December 2019
                Funding
                Funded by: Korea Mouse Phenotyping Center
                Award ID: NRF-2013M3A9D5072550
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2020

                Life sciences
                exercise,treadmill,wheel running,physiology,adipocyte,muscle fiber
                Life sciences
                exercise, treadmill, wheel running, physiology, adipocyte, muscle fiber

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