Polyphenols prevent ageing-related impairment in skeletal muscle mitochondrial function through decreased reactive oxygen species production

Ageing is associated with skeletal muscle impairment. Changes in mitochondrial homeostasis are thought to play a key role in this process. This study examined whether chronic intake of polyphenols (PPs), which are known to be modulators of oxidative stress, might prevent the age-related decline of mitochondrial functions in skeletal muscle. Three groups of 10 Wistar rats were investigated. Rats aged 16 weeks were compared with rats aged 40 weeks that were given 75 mg kg(-1) day(-1) PPs or solvent in the drinking water starting at week 16. Mitochondrial respiratory chain complex activities were measured in saponin-skinned fibres of soleus muscles using glutamate-malate (V-max), succinate (V-succ) and N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride-ascorbate (V-TMPD). Production of reactive oxygen species was assessed using dihydroethidium staining. Transcript levels of genes involved in antioxidant defence were determined using RT-PCR. Ageing reduced muscle V-max (from 8.8 +/- 0.45 to 6.17 +/- 0.51 mu mol O-2 min(-1) g(-1), -30.5%, P < 0.01), V-TMPD (from 20.67 +/- 1.24 to 16.55 +/- 1.16 mu mol O2 min(-1) g(-1), -19.9%, P < 0.05), increased production of reactive oxygen species (from 100 +/- 9.9 to 351.1 +/- 31.7%) and decreased transcripts of mitochondrial superoxide dismutase 2 (-59.3%, P < 0.01), peroxisome proliferator-activated receptor. coactivator-1 beta (PGC-1 beta; -61.5%, P < 0.05) and sirtuin 1 (-54.2%, P < 0.05). Chronic PP intake normalized V-max (8.63 +/- 0.63 mu mol O-2 min(-1) g(-1)), decreased production of reactive oxygen species (141.7 +/- 16.7%, P < 0.001) and enhanced antioxidant defence (superoxide dismutase 2 expression, +151.3%, P < 0.05) and PGC-1 beta expression (+185.7%, P < 0.05) in comparison to age-matched untreated rats. The present data indicate that regular intake of PPs starting at a young age prevents age-related mitochondrial respiratory impairment in skeletal muscle, probably through decreased oxidative stress and enhancement of PGC-1 beta expression.