Influence of aerobic fitness on age-related lymphocyte DNA damage in humans: relationship with mitochondria respiratory chain and hydrogen peroxide production

Abstract

The aim of this study was to analyze the influence of aerobic fitness (AF) on age-related lymphocyte DNA damage in humans, giving special attention to the role of the mitochondrial respiratory chain and hydrogen peroxide production. Considering age and AF (as assessed by VO(2)max), 66 males (19-59 years old) were classified as high fitness (HF) or low fitness (LF) and distributed into one of the following groups: young adults (19-29 years old), adults (30-39 years old), and middle-aged adults (over 40 years old). Peripheral lymphocytes obtained at rest were used to assess DNA damage (strand breaks and formamidopyrimidine DNA glycosylase (FPG) sites through the comet assay), activity of mitochondrial complexes I and II (polarographically measured), and the hydrogen peroxide production rate (assayed by fluorescence). Results revealed a significant interaction between age groups and AF for DNA strand breaks (F = 8.415, p = .000), FPG sites (F = 11.766, p = .000), mitochondrial complex I activity (F = 7.555, p = .000), and H(2)O(2) production (F = 7.500, p = .000). Except for mitochondrial complex II activity, the age variation of the remaining parameters was significantly attenuated by HF. Considering each AF level, an increase in DNA strand breaks and FPG sites with age (r = 0.655, p = 0.000, and r = 0.738, p = 0.000, respectively) was only observed in LF. Moreover, decreased mitochondrial complex I activity with age (r = -.470, p = .009) was reported in LF. These results allow the conclusion that high AF seems to play a key role in attenuating the biological aging process.

Physical Activity and Total Antioxidant Capacity across an Adult Lifespan of Men

“…We did not observe significant differences of serum uric acid levels across the subjects' age. Moreover, aerobic fitness was previously described to decrease the mitochondrial rate of hydrogen peroxide production and to attenuate age-related DNA damage (28). These can be explanations of similar TAC values in subgroups with different ages noted in our study.…”

Effects of combined physical exercise training on DNA damage and repair capacity: role of oxidative stress changes

“…Considering this, it is expected that exercise may decrease nuclear DNA damage, reducing the risk of developing cell mutations associated to several diseases. Although physical fitness has already been inversely related with DNA damage and mitochondria ROS production, revealing a positive effect on mitochondria function (Mota et al 2010), it is not possible to conclude that exercise is responsible for these changes since no physical exercise training was implemented. It is likely that aerobic fitness is related to higher antioxidant capacity, reduced DNA damage, or with increased DNA repair capacity, which would favor a lower nuclear DNA damage.…”

Effects of physical exercise training in DNA damage and repair activity in humans with different genetic polymorphisms of hOGG1 (Ser326Cys)

“…Such as in our study, Siu et al have already found an increase in antioxidant capacity and a decrease in oxidative damage to DNA after physical exercise training. Also, a higher cardiorespiratory fitness has been associated with the lower DNA damage in humans . Indeed, several studies have reported an up‐regulation of the antioxidant capacity after exercise training, in different tissues suggesting the antioxidant effects of regular physical exercise.…”

“…Also, a higher cardiorespiratory fitness has been associated with the lower DNA damage in humans. 17,22 Indeed, several studies have reported an up-regulation of the antioxidant capacity after exercise training, in different tissues 23,24 suggesting the antioxidant effects of regular physical exercise. Nevertheless, concerning DNA repair activity, this study is to our knowledge the first one searching for the effects of exercise training in DNA damage and DNA repair activity considering the hOGG1 Ser326Cys polymorphism.…”