Physical exercise improves mitochondrial function in ovariectomized rats

in Journal of Endocrinology
Authors:
Daniele Leão IgnacioSchool of Physical Education and Sports, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Faculdades Integradas IESGO, Formosa, Goiás, Brazil

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Rodrigo Soares FortunatoInstitute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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Diego SilvestreSchool of Physical Education and Sports, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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Leonardo MattaInstitute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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Andressa Lima de VansconcelosInstitute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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Denise Pires CarvalhoInstitute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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Antonio GalinaInstitute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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João Pedro Werneck-de-CastroSchool of Physical Education and Sports, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Division of Endocrinology, Diabetes and Metabolism, University of Miami, Miller School of Medicine, Miami, Florida, USA

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João Paulo Cavalcanti-de-AlbuquerqueInstitute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

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https://orcid.org/0000-0002-1894-9658
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Correspondence should be addressed to J P Cavalcanti-de-Albuquerque: albuquerquejp@biof.ufrj.br
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Estrogen deficiency causes metabolic disorders in humans and rodents, including in part due to changes in energy expenditure. We have shown previously that skeletal muscle mitochondrial function is compromised in ovariectomized (Ovx) rats. Since physical exercise is a powerful strategy to improve skeletal muscle mitochondrial content and function, we hypothesize that exercise training would counteract the deficiency-induced skeletal muscle mitochondrial dysfunction in Ovx rats. We report that exercised Ovx rats, at 60–65% of maximal exercise capacity for 8 weeks, exhibited less fat accumulation and body weight gain compared with sedentary controls. Treadmill exercise training decreased muscle lactate production, indicating a shift to mitochondrial oxidative metabolism. Furthermore, reduced soleus muscle mitochondrial oxygen consumption confirmed that estrogen deficiency is detrimental to mitochondrial function. However, exercise restored mitochondrial oxygen consumption in Ovx rats, achieving similar levels as in exercised control rats. Exercise-induced skeletal muscle peroxisome proliferator-activated receptor-γ coactivator-1α expression was similar in both groups. Therefore, the mechanisms by which exercise improves mitochondrial oxygen consumption appears to be different in Ovx-exercised and sham-exercised rats. While there was an increase in mitochondrial content in sham-exercised rats, demonstrated by a greater citrate synthase activity, no induction was observed in Ovx-exercised rats. Normalizing mitochondrial respiratory capacity by citrate synthase activity indicates a better oxidative phosphorylation efficiency in the Ovx-exercised group. In conclusion, physical exercise sustains mitochondrial function in ovarian hormone-deficient rats through a non-conventional mitochondrial content-independent manner.

 

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