Mitochondrial Adaptations in Aged Skeletal Muscle: Effect of Exercise Training

Ziaaldini, Mohammad Mosaferi; Hosseini, S Ra; Fathi, Mehrdad

doi:10.33549/physiolres.933329

Cited by 12 publications

(10 citation statements)

References 135 publications

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“…Besides mitochondrial biogenesis, the control of mitochondrial quantity and quality depends on the integration of coordinated events such as fusion, fission, and mitophagy. Studies have shown that proper mitochondrial dynamics are impaired during aging (Marzetti et al, 2014) and that exercise is an important strategy for counteracting such effects (Marzetti et al, 2014;Ziaaldini, Hosseini, & Fathi, 2017). In this study, RT did not acutely change any of the proteins related to mitochondrial dynamics.…”

Section: Discussionmentioning

confidence: 40%

Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults

et al. 2020

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Section: Discussionmentioning

confidence: 40%

Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults

et al. 2020

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“…7-9 weeks) endurance training adjuvant to T therapy in mice, 93,94 we showed RET coupled to T therapy augmented PGC1-α/Tfam mRNA, mitochondrial CS activity, 2 and protein levels of complex IV (cytochrome c oxidase subunit 85 ) and V (ATP synthase subunit) 85 (not mtDNA copy number). Possible mechanisms include heightened activation of IGF-1/MAPK pathways 87,95 and augmented MRFs mRNA (e.g. Myogenin) 96 during RET, as observed in the T study group, which consequently mediate mitochondrial gene expression.…”

Section: Discussionmentioning

confidence: 95%

“…For instance, it was reported that ageing is associated with decreases in PGC1-α mRNA (a main regulator of mitochondrial biogenesis and oxidative capacity 86 ), OxPhos capacity, mitochondria enzyme activity (e.g. CS), mtDNA content, and increases in oxidative stress, which all result in an impaired mitochondrial function 87 . Crucially, exercise, including RET, is known to induce mitochondrial adaptations.…”

Section: Discussionmentioning

confidence: 99%

Testosterone therapy induces molecular programming augmenting physiological adaptations to resistance exercise in older men

Gharahdaghi

Rudrappa

Brook

et al. 2019

J cachexia sarcopenia muscle

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BackgroundThe andropause is associated with declines in serum testosterone (T), loss of muscle mass (sarcopenia), and frailty. Two major interventions purported to offset sarcopenia are anabolic steroid therapies and resistance exercise training (RET). Nonetheless, the efficacy and physiological and molecular impacts of T therapy adjuvant to short‐term RET remain poorly defined.MethodsEighteen non‐hypogonadal healthy older men, 65–75 years, were assigned in a random double‐blinded fashion to receive, biweekly, either placebo (P, saline, n = 9) or T (Sustanon 250 mg, n = 9) injections over 6 week whole‐body RET (three sets of 8–10 repetitions at 80% one‐repetition maximum). Subjects underwent dual‐energy X‐ray absorptiometry, ultrasound of vastus lateralis (VL) muscle architecture, and knee extensor isometric muscle force tests; VL muscle biopsies were taken to quantify myogenic/anabolic gene expression, anabolic signalling, muscle protein synthesis (D2O), and breakdown (extrapolated).ResultsTestosterone adjuvant to RET augmented total fat‐free mass (P=0.007), legs fat‐free mass (P=0.02), and appendicular fat‐free mass (P=0.001) gains while decreasing total fat mass (P=0.02). Augmentations in VL muscle thickness, fascicle length, and quadriceps cross‐section area with RET occured to a greater extent in T (P < 0.05). Sum strength (P=0.0009) and maximal voluntary contract (e.g. knee extension at 70°) (P=0.002) increased significantly more in the T group. Mechanistically, both muscle protein synthesis rates (T: 2.13 ± 0.21%·day−1 vs. P: 1.34 ± 0.13%·day−1, P=0.0009) and absolute breakdown rates (T: 140.2 ± 15.8 g·day−1 vs. P: 90.2 ± 11.7 g·day−1, P=0.02) were elevated with T therapy, which led to higher net turnover and protein accretion in the T group (T: 8.3 ± 1.4 g·day−1 vs. P: 1.9 ± 1.2 g·day−1, P=0.004). Increases in ribosomal biogenesis (RNA:DNA ratio); mRNA expression relating to T metabolism (androgen receptor: 1.4‐fold; Srd5a1: 1.6‐fold; AKR1C3: 2.1‐fold; and HSD17β3: two‐fold); insulin‐like growth factor (IGF)‐1 signalling [IGF‐1Ea (3.5‐fold) and IGF‐1Ec (three‐fold)] and myogenic regulatory factors; and the activity of anabolic signalling (e.g. mTOR, AKT, and RPS6; P < 0.05) were all up‐regulated with T therapy. Only T up‐regulated mitochondrial citrate synthase activity (P=0.03) and transcription factor A (1.41 ± 0.2‐fold, P=0.0002), in addition to peroxisome proliferator‐activated receptor‐γ co‐activator 1‐α mRNA (1.19 ± 0.21‐fold, P=0.037).ConclusionsAdministration of T adjuvant to RET enhanced skeletal muscle mass and performance, while up‐regulating myogenic gene programming, myocellular translational efficiency and capacity, collectively resulting in higher protein turnover, and net protein accretion. T coupled with RET is an effective short‐term intervention to improve muscle mass/function in older non‐hypogonadal men.

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“…Muscle mitochondria are subject to age‐related remodelling; for instance, ageing is associated with decreases in mitochondrial biogenesis and oxidative capacity 38 and mitochondrial enzyme activity (e.g. CS), resulting in impaired mitochondrial function 39 (especially in individuals older than 80 years suffering from severe muscle loss, chronic diseases, or orthopaedic issues 40 ). Exercise, including HIIT, is well known to induce mitochondrial adaptations.…”

Section: Discussionmentioning

confidence: 99%

The physiological impact of high‐intensity interval training in octogenarians with comorbidities

Blackwell

Gharahdaghi

Brook

et al. 2021

J cachexia sarcopenia muscle

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Background Declines in cardiorespiratory fitness (CRF) and fat‐free mass (FFM) with age are linked to mortality, morbidity and poor quality of life. High‐intensity interval training (HIIT) has been shown to improve CRF and FFM in many groups, but its efficacy in the very old, in whom comorbidities are present is undefined. We aimed to assess the efficacy of and physiological/metabolic responses to HIIT, in a cohort of octogenarians with comorbidities (e.g. hypertension and osteoarthritis). Methods Twenty‐eight volunteers (18 men, 10 women, 81.2 ± 0.6 years, 27.1 ± 0.6 kg·m−2) with American Society of Anaesthesiology (ASA) Grade 2–3 status each completed 4 weeks (12 sessions) HIIT after a control period of equal duration. Before and after each 4 week period, subjects underwent body composition assessments and cardiopulmonary exercise testing. Quadriceps muscle biopsies (m. vastus lateralis) were taken to quantify anabolic signalling, mitochondrial oxidative phosphorylation, and cumulative muscle protein synthesis (MPS) over 4‐weeks. Results In comorbid octogenarians, HIIT elicited improvements in CRF (anaerobic threshold: +1.2 ± 0.4 ml·kg−1·min−1, P = 0.001). HIIT also augmented total FFM (47.2 ± 1.4 to 47.6 ± 1.3 kg, P = 0.04), while decreasing total fat mass (24.8 ± 1.3 to 24 ± 1.2 kg, P = 0.0002) and body fat percentage (33.1 ± 1.5 to 32.1 ± 1.4%, P = 0.0008). Mechanistically, mitochondrial oxidative phosphorylation capacity increased after HIIT (i.e. citrate synthase activity: 52.4 ± 4 to 67.9 ± 5.1 nmol·min−1·mg−1, P = 0.005; membrane protein complexes (C): C‐II, 1.4‐fold increase, P = 0.002; C‐III, 1.2‐fold increase, P = 0.03), as did rates of MPS (1.3 ± 0.1 to 1.5 ± 0.1%·day−1, P = 0.03). The increase in MPS was supported by up‐regulated phosphorylation of anabolic signalling proteins (e.g. AKT, p70S6K, and 4E‐BP1; all P < 0.05). There were no changes in any of these parameters during the control period. No adverse events were reported throughout the study. Conclusions The HIIT enhances skeletal muscle mass and CRF in octogenarians with disease, with up‐regulation of MPS and mitochondrial capacity likely underlying these improvements. HIIT can be safely delivered to octogenarians with disease and is an effective, time‐efficient intervention to improve muscle mass and physical function in a short time frame.

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Mitochondrial Adaptations in Aged Skeletal Muscle: Effect of Exercise Training

Cited by 12 publications

References 135 publications

Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults

Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults

Testosterone therapy induces molecular programming augmenting physiological adaptations to resistance exercise in older men

The physiological impact of high‐intensity interval training in octogenarians with comorbidities

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