Exercise-Induced Mitochondrial Biogenesis in Skeletal Muscle

Hood, David A.; Chabi, Béatrice; Menzies, Keir J.; O'Leary, Michael F. N.; Walkinshaw, Donald R.

doi:10.1007/978-88-470-0376-7_3

Cited by 84 publications

(108 citation statements)

References 137 publications

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“…Thus, to identify genotypes related to mitochondriogenesis (involving the PPARD-PPARGC1A-NRF-TFAM pathway) is of interest from a broader health perspective in aged people because these genotypes theoretically could be associated with muscle capacity and frailty in the elderly. Indeed, mitochondriogenesis is critical for the normal function of cells and the PPARD-PPARGC1A-NRF-TFAM pathway is impaired by chronic physical inactivity (Vina, Gomez-Cabrera, Borras, Froio, Sanchis-Gomar, Martinez-Bello & Pallardo, 2009a) and ageing (Hood, 2009). Reduced mitochondriogenesis can result in reduced muscle aerobic capacity (which is in itself an important health indicator), increased tendency for mitochondrially-mediated apoptosis, and, ultimately, accelerated sarcopenia (Hood, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Growing interest has focused on elucidating the factors that can affect the PPARD-PPARGC1A-NRF-TFAM pathway. This pathway is impaired by ageing, leading to increased tendency for mitochondrially-mediated apoptosis and thus eventually to sarcopenia (Hood, 2009). Genetic variants could also affect the PPARD-PPARGC1A-NRF-TFAM pathway and several important health-related phenotypes.…”

Section: Introductionmentioning

confidence: 99%

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Genetic variants in the PPARD-PPARGC1A-NRF-TFAM mitochondriogenesis pathway are neither associated with muscle characteristics nor physical performance in elderly. [Variaciones genéticas en la vía de la mitocondriogénesis PPARD-PPARGC1A-NRF-TFAM no están asociadas ni con características musculares ni con rendimiento físico en personas mayores].

Garatachea¹,

Santiago²,

Yvert³

et al. 2015

Rev. int. cienc. deporte

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Variaciones genéticas en la vía de la mitocondriogénesis PPARD-PPARGC1A-NRF-TFAM no están asociadas ni con características musculares ni con rendimiento físico en personas mayores We studied the influence of genetic polymorphisms involved in the PPARD-PPARGC1A-NRF-TFAM mitochondriogenesis pathway (rs6949152, rs12594956, rs2267668, rs8192678, and rs1937) on muscle phenotypes (thigh muscles' cross-sectional, maximal handgrip-strength and 30-second chair stand-test) and Barthel index in Caucasian (Spanish) community-dwelling old people (n=75, 21 men, 54 women; 71-94 years). We found no significant genetic associations with the studied phenotypes. Multiple, complex gene-environment and gene-gene interactions which are yet to be determined are likely to play a more determinant role.Key words: ageing; mitochondria; muscle. AbstractCorrespondence/correspondencia: Nuria Garatachea-Vallejo Faculty of Health and Sport Science, Universidad de Zaragoza. Spain Email: nuria.garatachea@unizar.es Se estudió la influencia de los polimorfismos genéticos implicados en la vía de mitocondriogénesis PPARD-PPARGC1A-NRF-TFAM (rs6949152, rs12594956, rs2267668, rs8192678 y rs1937) en distintos fenotipos musculares (sección transversal muscular del muslo, fuerza máxima de prensión manual y 30 segundos de sentarse-levantarse de una silla) y en el índice de Barthel en personas mayores caucási-cas (españoles) (n = 75, 21 hombres, 54 mujeres; 71 a 94 años). No se encontraron asociaciones gené-ticas significativas con los fenotipos estudiados. Interacciones múltiples, complejos gen-ambiente y relaciones gen-gen aún no determinadas podrían desempeñar un papel más determinante.Palabras clave: envejecimiento; mitocondrias; músculo.Resumen Received: July 11, 2014 / Accepted: January 17, 2015 http://dx.doi.org/10.5232/ricyde2015.04101 Garatachea, N.; Santiago, C.; Yvert, T.; Verde-Rello, Z.; Fiuza-Luces, C.; . Genetic variants in the PPARD-PPARGC1A-NRF-TFAM mitochondriogenesis pathway are not associated neither muscle characteristics nor physical performance in elderly. RICYDE. Revista internacional de ciencias del deporte, 41(11),[196][197][198][199][200][201][202][203][204][205][206][207][208]

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genetic variants in the PPARD-PPARGC1A-NRF-TFAM mitochondriogenesis pathway are neither associated with muscle characteristics nor physical performance in elderly. [Variaciones genéticas en la vía de la mitocondriogénesis PPARD-PPARGC1A-NRF-TFAM no están asociadas ni con características musculares ni con rendimiento físico en personas mayores].

Garatachea¹,

Santiago²,

Yvert³

et al. 2015

Rev. int. cienc. deporte

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“…12 mtDNA abundance has been associated with a beneficial muscle response to endurance exercise as well as senescence and states of oxidative stress. [13][14][15] It is indeed conceivable that an increase in mtDNA copy number in the latter situations could occur as a feedback response that compensates for defective mitochondria or mutated mtDNA.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial DNA Injury and Mortality in Hemodialysis Patients

Madhumathi

Demello

et al. 2009

Journal of the American Society of Nephrology

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The role of mitochondrial injury in the pathogenesis of complications of uremia is incompletely defined, although diminished bioenergetic capacity and the accumulation of mitochondrial DNA (mtDNA) mutations have been reported. This study was undertaken to evaluate the prevalence of mtDNA injury in 180 patients who had ESRD and were enrolled into the baseline phase of the HEMO study and to relate these markers to all-cause mortality. The mitochondrial injury markers studied in peripheral blood mononuclear cells were the mtDNA copy number per cell, measured by quantitative PCR, and the presence of the mtDNA 4977 mutation. After frequency-matching healthy control subjects for age, mtDNA copy number was lower among older dialysis patients compared with older healthy subjects (P ϭ 0.01). A one-log increase in mtDNA copy number was independently associated with a decreased hazard for mortality (adjusted hazard ratio 0.64; 95% confidence interval 0.46 to 0.89). The mtDNA 4977 deletion was present in 48 (31%) patients and was independently associated with a decreased hazard for mortality (adjusted hazard ratio 0.33; 95% confidence interval 0.19 to 0.56). In summary, the mtDNA 4977 seems to predict survival in ESRD, but a reduced mitochondrial copy number seems to predict a poor outcome. Although further exploration of these associations is needed, evaluation of mitochondrial DNA copy number and somatic mtDNA mutations may provide simple genomic biomarkers to predict clinical outcomes among patients with ESRD. The uremic syndrome is characterized by abnormalities in energy metabolism, manifest as changes in basal metabolic rate, relative catabolism, negative nitrogen balance, protein energy malnutrition, insulin resistance, and dyslipidemia. 1 Mitochondria are integral to these metabolic processes, which they probably influence through cytokine-and adipokine-mediated mechanisms. 2 Early studies with 31-phosphorus nuclear magnetic resonance demonstrated that mitochondrial oxidative capacity was diminished in muscle of patients established on dialysis. 3 More recent studies showed a high prevalence of somatic mitochondrial DNA (mtDNA) mutations, specifically the "common deletion" (a 4977-bp deletion between nucleotide positions 8470 and 13,447 [mtDNA 4977 ]) in skeletal muscle of patients with ESRD. 4 Human mtDNA is particularly prone to oxidant injury because mitochondria generate reactive oxygen species during ATP production. 5 mtDNA injury may be qualitativedeletion or point mutations-or quantitative-abnormalities of mtDNA copy number per cell, mtDNA being polyploid. 6 mtDNA mutations are classically studied in skeletal muscle tissue, but recent observations suggested that the use of periph-

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“…We postulated that the hyperactivity in SPORTS rats resulted from upregulated enzymes of the mitochondrial respiratory chain [11]. We measured levels of D-loop gene expression in the SOL and EDL muscles of SED SPORTS and SED Wistar rats to estimate mitochondrial biogenesis since D-loop copy number is indicative of mtDNA replication intensity [8].…”

Section: Gene Expression In the Respiratory Chain In Sports Rat Musclementioning

confidence: 99%

Distinct Gene Expression Profile Distinguishes Increased Metabolic Activity in Spontaneously Hyperactive Rats While Sedentary from That Induced by Exercise

Abe¹,

Matsuo²,

Harada-Sukeno³

et al. 2018

ABC

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The Spontaneously-Running Tokushima Shikoku (SPORTS) strain is an original line derived from Wistar rats, which spontaneously runs >6 km/day on wheels, and has better glucose tolerance and less fat than Wistar rats. However, the molecular mechanism that contributes to the increased metabolic activity in SPORTS rats is unknown. The present study aimed to characterize the gene expression profiles of skeletal muscles in SPORTS rats housed under sedentary (SED) conditions. We found that the expression levels of genes encoding mitochondrial respiratory chain enzymes such as ATP synthase 6 (mt-Atp6) and cytochrome c oxidase subunit 6c (Cox6c), were higher in the soleus (SOL) muscles of SED SPORTS than in SED Wistar rats. The ratio of type IIa myofibers was higher and glucose tolerance was better in SED SPORTS than in Wistar rats that were sedentary and trained daily on treadmills, respectively. We then investigated candidate genes that might contribute to the better glucose tolerance of SED SPORTS rats using DNA microarray analysis. Among 116 upregulated genes in the SOL muscles of SED SPORTS rats, only 19 were also increased in trained Wistar rats. We focused on v-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (Erbb3), which How to cite this paper: Abe, M., Matsuo, Y., Harada-Sukeno, A., Uchida, T., Kitahata, K., Tomida, C., Hirasaka, K., TeshimaKondo, S., Harada, N., Nakaya, Y., Sakaue, H., Nakao, R. and Nikawa, T. (2018) was associated with glucose transport in myocytes, and found higher expression levels in the SOL muscles of SED SPORTS than in SED Wistar rats. The SOL muscles of SED SPORTS rats also contained more activity of β-hydroxyacylCoA dehydrogenase, a key enzyme of β-oxidation, indicating enhanced lipid oxidation. These findings suggest that increased metabolic activity in skeletal muscle (especially the SOL muscle) of SPORTS rats is congenital and that gene expression profiles of SPORTS rats and Trained Wistar rats are different.

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Exercise-Induced Mitochondrial Biogenesis in Skeletal Muscle

Cited by 84 publications

References 137 publications

Mitochondrial DNA Injury and Mortality in Hemodialysis Patients

Distinct Gene Expression Profile Distinguishes Increased Metabolic Activity in Spontaneously Hyperactive Rats While Sedentary from That Induced by Exercise

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