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Date: September 29, 2016 Author: admin Comments: 0
  • Category Clinical studies

Mitochondria changes in human muscle after prolonged exercise, endurance training and selenium supplementation.

The functional and structural responses to acute exercise (E) and training, (T) with or without selenium supplementation (Sel), were investigated in a double-blind study on 24 young male subjects. The Sel or the placebo were given over 10 weeks of an endurance training programme. Prior to the programme and on its conclusion muscle biopsies were taken from the vastus lateralis muscle before and after an exhausting treadmill test of maximal endurance capacity (Capmax). The muscle samples were examined by electron microscopy to make a quantitative analysis of the mitochondria population in the muscle fibres. The number of mitochondria per area (QA) and the relative surface occupied by the total mitochondria profile area (AA) were estimated. The mean area per mitochondrion (â) was obtained by the quotient AA/QA. The effects of the isolated or combined independent variables T, E and Sel were analysed by nonparametric tests. Training induced significant increases in both QA (30%, P < 0.001) and AA (52%, P < 0.001), without changing â; T + Sel produced a slight rise of AA (27%, P < 0.001), which resulted in larger (24%, P < 0.001) â. The E produced an enlargement of â resembling swelling. This phenomenon was also found for the combinations E + T and E + T + Sel, but it was then far more pronounced in E + T. The training effects observed are in agreement with previous descriptions. In contrast, the changes observed after acute exercise seem to indicate a remarkable short-term plasticity of muscle mitochondria. The results in Sel would seem to suggest a dampening effect of the selenium on the mitochondria changes, both in chronic and acute exercise. The mechanism of this action on mitochondrial turnover is uncertain, but might be related to a higher efficiency of the selenium-dependent enzyme glutathione peroxidase.

Source: www.ncbi.nlm.nih.gov

 

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