Decreased Circulating mtDNA Levels in Professional Male Volleyball Players

Nasi, Milena; Cristani, A; Lamberti, I; Gibellini, Lara; Biasi, Sara De; Guazzaloca, Alessandro; Trenti, Tommaso; Cossarizza, Andrea

doi:10.1123/ijspp.2014-0461

Cited by 21 publications

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“…On the other hand, prolonged moderate exercise (90 min treadmill run at 60% of VO2 max) caused the decrease in cf mt-DNA in healthy moderately trained young men [15]. In addition, professional male volleyball players presented lower circulating cf mt-DNA levels in comparison to non-athlete male volunteers [17]. These two afore mentioned reports on exercise–induced decline in cf mt-DNA are also consistent to our finding of gradual decrease in pre-exercise cf mt-DNA over the study period involving three bouts of exhaustive treadmill exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Ten highly trained men were included for investigation of exercise-induced changes of circulating DNAse [13], and kinetics of post-exercise increase in cf-DNA was studied in a group of 11 men [19]. In addition, changes of cf mt-DNA related to seasonal training were described in 12 professional volleyball players [17]. The exercise-induced increase in cf-DNA was very high and this may explain the relatively low size of studied groups [11,12,14].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, studies on the association between exercise and circulating levels of cf mt-DNA gave controversial results. Exhaustive exercises related to 10 km cross-country run and treadmill running workout did not alter plasma cf mt-DNA levels [15,16], while in other trials involving treadmill runners and professional male volleyball players, exercise surprisingly caused the decline in cf mt-DNA [17]. Although the cellular source of exercise-induced cf DNA is still an unresolved question (apoptotic or necrotic cells, skeletal muscles, blood mononuclear cells, cells of the hematopoietic lineage) [18,19], this phenomenon is supposed to be the predictor of muscle damage, immunological alterations, inflammatory response, and even the overtraining syndrome in elite athletes [6–14].…”

Section: Introductionmentioning

confidence: 99%

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Repeated bouts of exhaustive exercise increase circulating cell free nuclear and mitochondrial DNA without development of tolerance in healthy men

et al. 2017

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ObjectiveAcute single strenuous exercise increases circulating cell free DNA (cf DNA). We tested whether three repeated bouts of exhaustive exercise induced the cf DNA response without development of tolerance in healthy men.MethodsEleven average-trained men (age 34.0±5.2 years, body mass index 26.2±3.1 kg/m2, maximal oxygen consumption—VO2max 49.6±4.5 ml/kg*min) performed three treadmill exercise tests to exhaustion at speed corresponding to 70% VO2max separated by 72 hours of resting. Blood was collected before and after each bout of exercise for determination of cell free nuclear and mitochondrial DNA (cf n-DNA, cf mt-DNA) by real-time PCR, selected markers of muscle damage, and blood cell count.ResultsEach bout induced the increase (p<0.05) in plasma cf n-DNA: from 3.4±1.4 to 38.5±27.5, from 4.1±3.3 to 48.5±26.2, and 3.1±1.6 to 53.8±39.9 ng/mL after the first, second, and third exercise, respectively. In a congruent way, cf mt-DNA rose significantly after the second (from 229±216 to 450±228*103 GE/mL) and third bout of exercise (from 173±120 to 462±314*103 GE/mL).Pre-exercise cf mt-DNA decreased (p<0.05) by 2-times (from 355±219 before the first bout to 173±120*103 GE/mL before the third bout) over the study period and were accompanied by significant increase in white blood cells, platelets, creatine kinase, creatinine and lactate after each bout. However, the exercise induced percentage increment of cf n-DNA was always many times higher than corresponding increments of the afore-mentioned markers at any occasion.ConclusionsRepeated bouts of exhaustive exercise induced remarkable increase in circulating cf n-DNA without signs of tolerance development. Baseline cf mt-DNA decreased in response to series of strenuous exercise. Since percentage increments of cf n-DNA in response to exercise were many times higher than those observed for other markers, measurement of circulating cf n-DNA could be a sensitive tool for monitoring acute exercise effects in human body.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Repeated bouts of exhaustive exercise increase circulating cell free nuclear and mitochondrial DNA without development of tolerance in healthy men

et al. 2017

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“…cfDNA release via apoptosis does not occur so rapidly. (c) Changes in blood components that result in anti‐inflammatory effects include a reduction in the expression of monocyte and macrophage Toll‐like receptors (TLRs) (Nasi et al, ). (d) The production and release of anti‐inflammatory cytokines from contracting skeletal muscles can result in anti‐inflammatory effects (Nasi et al, ).…”

Section: Causes Of Circulating Cfdna Releasementioning

confidence: 99%

The diverse origins of circulating cell‐free DNA in the human body: a critical re‐evaluation of the literature

et al. 2018

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Since the detection of cell-free DNA (cfDNA) in human plasma in 1948, it has been investigated as a non-invasive screening tool for many diseases, especially solid tumours and foetal genetic abnormalities. However, to date our lack of knowledge regarding the origin and purpose of cfDNA in a physiological environment has limited its use to more obvious diagnostics, neglecting, for example, its potential utility in the identification of predisposition to disease, earlier detection of cancers, and lifestyle-induced epigenetic changes. Moreover, the concept or mechanism of cfDNA could also have potential therapeutic uses such as in immuno- or gene therapy. This review presents an extensive compilation of the putative origins of cfDNA and then contrasts the contributions of cellular breakdown processes with active mechanisms for the release of cfDNA into the extracellular environment. The involvement of cfDNA derived from both cellular breakdown and active release in lateral information transfer is also discussed. We hope to encourage researchers to adopt a more holistic view of cfDNA research, taking into account all the biological pathways in which cfDNA is involved, and to give serious consideration to the integration of in vitro and in vivo research. We also wish to encourage researchers not to limit their focus to the apoptotic or necrotic fraction of cfDNA, but to investigate the intercellular messaging capabilities of the actively released fraction of cfDNA and to study the role of cfDNA in pathogenesis.

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“…While to our knowledge the effect of exercise on mtDNA–TLR9 signalling has not been explored in skeletal muscle, a very recent study of professional male athletes (volleyball players) reported lower levels of circulating mtDNA when compared to non‐athlete volunteers (Nasi et al . ). These preliminary findings indicate that increased TLR signalling may be correlated with physical inactivity and a sedentary lifestyle and supports the potentially important influence of mitochondria‐driven inflammation pathways in the beneficial adaptations observed with training (Gleeson et al .…”

Section: Introductionmentioning

confidence: 97%

Beneficial effects of exercise on age‐related mitochondrial dysfunction and oxidative stress in skeletal muscle

Joseph

Adhihetty

Leeuwenburgh

2015

The Journal of Physiology

124

107

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Mitochondria are negatively affected by ageing leading to their inability to adapt to higher levels of oxidative stress and this ultimately contributes to the systemic loss of muscle mass and function termed sarcopenia. Since mitochondria are central mediators of muscle health, they have become highly sought-after targets of physiological and pharmacological interventions. Exercise is the only known strategy to combat sarcopenia and this is largely mediated through improvements in mitochondrial plasticity. More recently a critical role for mitochondrial turnover in preserving muscle has been postulated. Specifically, cellular pathways responsible for the regulation of mitochondrial turnover including biogenesis, dynamics and autophagy may become dysregulated during ageing resulting in the reduced clearance and accumulation of damaged organelles within the cell. When mitochondrial quality is compromised and homeostasis is not re-established, myonuclear cell death is activated and muscle atrophy ensues. In contrast, acute and chronic exercise attenuates these deficits, restoring mitochondrial turnover and promoting a healthier mitochondrial pool that leads to the preservation of muscle. Additionally, the magnitude of these exercise-induced mitochondrial adaptations is currently debated with several studies reporting a lower adaptability of old muscle relative to young, but the processes responsible for this diminished training response are unclear. Based on these observations, understanding the molecular details of how advancing age and exercise influence mitochondria in older muscle will provide invaluable insight into the development of exercise protocols that will maximize beneficial adaptations in the elderly. This information will also be imperative for future research exploring pharmacological targets of mitochondrial plasticity.

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Decreased Circulating mtDNA Levels in Professional Male Volleyball Players

Abstract: Regular physical activity appeared associated with lower levels of circulating mtDNA, further confirming the protective, anti-inflammatory effect of exercise.

Cited by 21 publications

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Repeated bouts of exhaustive exercise increase circulating cell free nuclear and mitochondrial DNA without development of tolerance in healthy men

Repeated bouts of exhaustive exercise increase circulating cell free nuclear and mitochondrial DNA without development of tolerance in healthy men

The diverse origins of circulating cell‐free DNA in the human body: a critical re‐evaluation of the literature

Beneficial effects of exercise on age‐related mitochondrial dysfunction and oxidative stress in skeletal muscle

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