Maintenance of the adaptation of skeletal muscle mitochondria to exercise in old rats

Jc, Young; M, Chen; Jo, Holloszy

doi:10.1249/00005768-198315030-00011

Cited by 32 publications

(23 citation statements)

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“…There are many human (28,43,45,54) and rodent studies (14,53,63) that have shown beneficial improvements from endurance exercise training in late middle age, both in terms of whole body aerobic capacity and muscle mitochondrial enzyme activity. We have also previously shown that treadmill exercise training in late-middle-aged F344BN rats can restore muscle aerobic function and enzyme activity levels to young adult levels (9).…”

Section: Impact Of Endurance Training On Skeletal Muscle Aerobic Funcmentioning

confidence: 99%

“…Age-related declines in physical activity do not entirely explain the decreases in aerobic capacity at the whole body level, since chronically trained older individuals and master athletes still show evidence of a decline with aging (27, 39, 46 -48, 61). Nonetheless, many studies in middle-to late-middle-aged individuals have shown a maintained capacity to increase whole body maximal oxygen uptake (V O 2 max ) (28,42,43) and mitochondrial enzyme activity (14,63) following exercise training relative to young adults. Very few studies have examined whole body aerobic responses to endurance training in very advanced age (Ն80 yr of age; senescence) (20,41), and none has assessed adaptability of the skeletal muscle aerobic machinery specifically.…”

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confidence: 99%

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Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Betik¹,

Thomas²,

Wright³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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We previously showed that 7 wk of treadmill exercise training in late-middle-aged rats can reverse the modest reductions in skeletal muscle aerobic function and enzyme activity relative to values in young adult rats (Exp Physiol 93: 863-871, 2008). The purpose of the present study was to determine whether extending this training program into senescence would attenuate the accelerated decline in the muscle aerobic machinery normally seen at this advanced age. For this purpose, 29-mo-old Fisher 344 Brown-Norway rats underwent 5 or 7 mo of treadmill exercise training. Training resulted in greater exercise capacity during an incremental treadmill exercise test and reduced percent body fat in 34- and 36-mo-old rats and improved survival. Despite these benefits at the whole body level, in situ muscle aerobic capacity and muscle mass were not greater in the trained groups at 34 mo or 36 mo of age. Similarly, the trained groups did not have higher activities of citrate synthase (CS) or Complex IV in homogenates of either the plantaris (fast twitch) or the soleus (slow twitch) muscles at either age. Finally, protein expression of CS (a marker of mitochondrial content) and peroxisome proliferator-activated receptor-gamma coactivator-1 (relating to the drive on mitochondrial biogenesis) were not higher in the trained groups. Therefore, although treadmill training from late middle age into senescence had significant benefits on running capacity, survival, and body fat, it did not prevent the declines in muscle mass, muscle aerobic capacity, or mitochondrial enzyme activities normally seen across this age, revealing a markedly diminished plasticity of the aerobic machinery in response to endurance exercise at advanced age.

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Section: Impact Of Endurance Training On Skeletal Muscle Aerobic Funcmentioning

confidence: 99%

mentioning

confidence: 99%

Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Betik¹,

Thomas²,

Wright³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This represents the most common morphological change associated with impaired oxidative phosphorylation (Bresolin et al 1987;Bua et al 2002) as a result of mtDNA defects. While it is known that endurance training can ameliorate the decline in enzyme activities evident in older individuals (Young et al 1983), the role of exercise-induced mitochondrial biogenesis in other agerelated mitochondrial processes, as noted above, is currently unknown.…”

Section: Implication Of Mitochondrial Biogenesis For Mtdna Defects Anmentioning

confidence: 99%

“…It remains to be determined whether this is the result of a greater production of ROS. In addition, while it is established that various forms of exercise training can produce mitochondrial biogenesis in aged individuals (Young et al 1983;Jubrias et al 2001), it is not known whether this can exert a beneficial, or detrimental effect on the progression of aged muscle towards cell death.…”

Section: Implication Of Mitochondrial Biogenesis For Mtdna Defects Anmentioning

confidence: 99%

Plasticity of Skeletal Muscle Mitochondria in Response to Contractile Activity

Adhihetty

Irrcher

Joseph

et al. 2003

Experimental Physiology

143

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Regularly performed exercise in the form of endurance training produces a well-established adaptation in skeletal muscle termed mitochondrial biogenesis. The physiological benefit of this is an enhanced performance of muscle when subject to endurance exercise. This is not only of great advantage for athletic endeavours, but it also clearly improves the quality of life of previously sedentary individuals and those involved in injury rehabilitation. Here we review the molecular basis for mitochondrial biogenesis in muscle, from the initial signals arising in contracting muscle, to the transcription factors involved in mitochondrial and nuclear DNA transcription, as well as the post-translational import mechanisms required for the synthesis of the organelle. We discuss specific protein components associated with reactive oxygen species production, and suggest some questions which remain unanswered with respect to the role of exercise-induced mitochondrial biogenesis in ageing, apoptosis and disease. Experimental Physiology (2003) 88.1, 99-107. 2505

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“…As documented by electron microscopic studies in different tissues, the ultrastructural features of a given mitochondrial population are coupled to the organelles' functional performances and can undergo significant adaptations to the changing environmental conditions (8)(9)(10)(11). Thus, quantitation of mitochondrial morphological parameters, e.g.…”

Section: Introductionmentioning

confidence: 99%

A morphometric study on human muscle mitochondria in aging

Bertoni–Freddari

Fattoretti

Caselli

et al. 2002

AGE

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Mitochondria are dynamic organelles capable of significant changes of their ultrastructural features according to the tissue-specific energy demands. In human biopsies of vastus lateralis and anterior tibialis muscles from young (25.0 _+ 4.4 years), middle-aged (50.4 _+ 7.5 years) and old (75.5+_3.9 years) healthy volunteers, we carried out a morphometric study on subsarcolemmal and intermyofibrillar mitochondria to assess whether age-related alterations of the morphology of these organelles contribute to the muscle performance decay in aging. By computer-assisted methods, we measured: the average area (MAA), the longer diameter (Dmax) and the ratio perimeter to area (pleomorphic index: Plei) of mitochondria. No significant age-related ultrastructural differences were found either in subsarcolemmal or intermyofibrillar organelles. However, in middle-aged as well as in the old group of patients vs. the young one, MAA and Dmax showed a clear trend to decrease, while Plei showed a marked, age-related tendency to increase. Higher percentages of less pleomorphic organelles were found in the youngest group of patients and this was particularly evident in the subsarcolemmal mitochondrial population. In addition to reporting on discrete aspects of mitochondrial ultrastructure, MAA, Dmax and Plei are closely related to each other and provide a reliable index of the muscle mitochondria adaptive response to age. Thus, we interpret our results as indicating a substantial preservation of muscle mitochondrial ultrastructure during aging.

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Maintenance of the adaptation of skeletal muscle mitochondria to exercise in old rats

Cited by 32 publications

References 0 publications

Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Plasticity of Skeletal Muscle Mitochondria in Response to Contractile Activity

A morphometric study on human muscle mitochondria in aging

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