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Published on: April 30, 2020
Effect of Moderate Exercise on Mitochondrial Proteome in Heart Tissue of Spontaneous Hypertensive Rats
Luiz Antonio de Oliveira Rocha1, Kleber Souza Oliveira2, Ludovico Migliolo2
1Curso de Educação Física, Universidade Católica de Brasilia, Brasília, DF, Brazil; Curso de pós-graduação em Patologia Molecular, Universidade de Brasília, Brasília, DF, Brazil; Centro de Analises Proteomicas e Bioquimicas, Curso de Pós-graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília, Brasília, DF, Brazil;
Background:
Hypertension is a multifactorial disease and an important independent risk factor for cardiovascular diseases. Exercise training is one of the most important non-pharmacological therapeutic strategies for treating hypertension; however, mitochondrial adaptations in the hypertensive heart as a result of exercise remain obscure.
Methods:
Aiming to explore the effects of exercise training of moderate intensity on the mitochondrial proteome in hypertensive animal models before and after the pathology developed, 20 isogenic male spontaneous hypertensive rats (SHRs) were randomly divided into 2 groups, 1 with animals of 6 and 40 weeks of age. Animals were submitted to exercise training on a treadmill for 30 minutes, 5 days per week for 4 weeks at 90% of the anaerobic threshold (AT). A mitochondrial sample extract from the left ventricle was prepared and further analyzed using LC-MS/MS.
Results:
Proteomics analyses led to the identification of 143 proteins in all groups. The data showed a considerable and clear increase in the abundance of NADH dehydrogenase and ATP synthase, as well as voltage-dependent anion channel (VDAC) type 1 decrease in exercise groups. When exercise effects were compared, differential proteins expressed only in exercise increased, such as cytochrome c oxidase, alcohol dehydrogenase, and NADH dehydrogenase [ubiquinone] 1 alpha subcomplex.
Conclusions:
The results support the proposition that moderate exercise induces a beneficial adaptation in left ventricle myocardial mitochondria in order to attenuate the decrease in ATP production in hypertensive models.
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