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Training effects on ROS production determined by electron paramagnetic resonance in master swimmers.

Mrakic-Sposta S, Gussoni M, Porcelli S, Pugliese L, Pavei G, Bellistri G, Montorsi M, Tacchini P, Vezzoli A - Oxid Med Cell Longev (2015)

Bottom Line: A significant (P < 0.01) increase of ROS production from REST to the END of IE in PRE Trg (2.82 ± 0.66 versus 3.28 ± 0.66 µmol·min(-1)) was observed.HIDT increased peak oxygen consumption (36.1 ± 4.3 versus 40.6 ± 5.7 mL·kg(-1)·min(-1) PRE and POST Trg, resp.) and the antioxidant capacity (+13%) while it significantly decreased the ROS production both at REST (-20%) and after IE (-25%).The observed link between ROS production, adaptive antioxidant defense mechanisms, and peak oxygen consumption provides new insight into the correlation between ROS response pathways and muscle metabolic function.

View Article: PubMed Central - PubMed

Affiliation: Istituto di Bioimmagini e di Fisiologia Molecolare, Consiglio Nazionale delle Ricerche, Via Fratelli Cervi 93, 20090 Segrate, Italy.

ABSTRACT
Acute exercise induces an increase in Reactive Oxygen Species (ROS) production dependent on exercise intensity with highest ROS amount generated by strenuous exercise. However, chronic repetition of exercise, that is, exercise training, may reduce exercise-induced oxidative stress. Aim of this study was to evaluate the effects of 6-weeks high-intensity discontinuous training (HIDT), characterized by repeated variations of intensity and changes of redox potential, on ROS production and antioxidant capacity in sixteen master swimmers. Time course changes of ROS generation were assessed by Electron Paramagnetic Resonance in capillary blood by a microinvasive approach. An incremental arm-ergometer exercise (IE) until exhaustion was carried out at both before (PRE) and after (POST) training (Trg) period. A significant (P < 0.01) increase of ROS production from REST to the END of IE in PRE Trg (2.82 ± 0.66 versus 3.28 ± 0.66 µmol·min(-1)) was observed. HIDT increased peak oxygen consumption (36.1 ± 4.3 versus 40.6 ± 5.7 mL·kg(-1)·min(-1) PRE and POST Trg, resp.) and the antioxidant capacity (+13%) while it significantly decreased the ROS production both at REST (-20%) and after IE (-25%). The observed link between ROS production, adaptive antioxidant defense mechanisms, and peak oxygen consumption provides new insight into the correlation between ROS response pathways and muscle metabolic function.

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Related in: MedlinePlus

Panel plots of relationship between ROS production rate (μmol·min−1) and (a) antioxidant capacity (nW) and (b) peak ROS production rate (μmol·min−1·kg−1) and V′O2  peak (mL·kg−1·min−1) recorded at the end of IE in the two sessions: before (PRE Trg, full squares) and after (POST Trg, empty squares) training. The linear regression fit (solid line) is also shown and so is the correlation coefficient (r2) reported in each panel. A significant linear relationship in the ROS production between antioxidant capacity (P < 0.0001) and V′O2 peak (P < 0.0001) values was estimated.
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fig5: Panel plots of relationship between ROS production rate (μmol·min−1) and (a) antioxidant capacity (nW) and (b) peak ROS production rate (μmol·min−1·kg−1) and V′O2  peak (mL·kg−1·min−1) recorded at the end of IE in the two sessions: before (PRE Trg, full squares) and after (POST Trg, empty squares) training. The linear regression fit (solid line) is also shown and so is the correlation coefficient (r2) reported in each panel. A significant linear relationship in the ROS production between antioxidant capacity (P < 0.0001) and V′O2 peak (P < 0.0001) values was estimated.

Mentions: Lastly, a possible correlation between ROS production rate levels, antioxidant capacity, and metabolic data was investigated. An inverse significant relationship between (i) ROS production rate (μmol·min−1) and antioxidant capacity (nW) (r2 = 0.48, P < 0.0001) at baseline (see Figure 5(a)) and (ii) ROS peak production rate (μmol·kg−1·min−1) and V′O2  peak (mL·kg−1·min−1) (r2 = 0.61, P < 0.0001) (see Figure 5(b)) was found by Pearson's product-moment correlation.


Training effects on ROS production determined by electron paramagnetic resonance in master swimmers.

Mrakic-Sposta S, Gussoni M, Porcelli S, Pugliese L, Pavei G, Bellistri G, Montorsi M, Tacchini P, Vezzoli A - Oxid Med Cell Longev (2015)

Panel plots of relationship between ROS production rate (μmol·min−1) and (a) antioxidant capacity (nW) and (b) peak ROS production rate (μmol·min−1·kg−1) and V′O2  peak (mL·kg−1·min−1) recorded at the end of IE in the two sessions: before (PRE Trg, full squares) and after (POST Trg, empty squares) training. The linear regression fit (solid line) is also shown and so is the correlation coefficient (r2) reported in each panel. A significant linear relationship in the ROS production between antioxidant capacity (P < 0.0001) and V′O2 peak (P < 0.0001) values was estimated.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4385700&req=5

fig5: Panel plots of relationship between ROS production rate (μmol·min−1) and (a) antioxidant capacity (nW) and (b) peak ROS production rate (μmol·min−1·kg−1) and V′O2  peak (mL·kg−1·min−1) recorded at the end of IE in the two sessions: before (PRE Trg, full squares) and after (POST Trg, empty squares) training. The linear regression fit (solid line) is also shown and so is the correlation coefficient (r2) reported in each panel. A significant linear relationship in the ROS production between antioxidant capacity (P < 0.0001) and V′O2 peak (P < 0.0001) values was estimated.
Mentions: Lastly, a possible correlation between ROS production rate levels, antioxidant capacity, and metabolic data was investigated. An inverse significant relationship between (i) ROS production rate (μmol·min−1) and antioxidant capacity (nW) (r2 = 0.48, P < 0.0001) at baseline (see Figure 5(a)) and (ii) ROS peak production rate (μmol·kg−1·min−1) and V′O2  peak (mL·kg−1·min−1) (r2 = 0.61, P < 0.0001) (see Figure 5(b)) was found by Pearson's product-moment correlation.

Bottom Line: A significant (P < 0.01) increase of ROS production from REST to the END of IE in PRE Trg (2.82 ± 0.66 versus 3.28 ± 0.66 µmol·min(-1)) was observed.HIDT increased peak oxygen consumption (36.1 ± 4.3 versus 40.6 ± 5.7 mL·kg(-1)·min(-1) PRE and POST Trg, resp.) and the antioxidant capacity (+13%) while it significantly decreased the ROS production both at REST (-20%) and after IE (-25%).The observed link between ROS production, adaptive antioxidant defense mechanisms, and peak oxygen consumption provides new insight into the correlation between ROS response pathways and muscle metabolic function.

View Article: PubMed Central - PubMed

Affiliation: Istituto di Bioimmagini e di Fisiologia Molecolare, Consiglio Nazionale delle Ricerche, Via Fratelli Cervi 93, 20090 Segrate, Italy.

ABSTRACT
Acute exercise induces an increase in Reactive Oxygen Species (ROS) production dependent on exercise intensity with highest ROS amount generated by strenuous exercise. However, chronic repetition of exercise, that is, exercise training, may reduce exercise-induced oxidative stress. Aim of this study was to evaluate the effects of 6-weeks high-intensity discontinuous training (HIDT), characterized by repeated variations of intensity and changes of redox potential, on ROS production and antioxidant capacity in sixteen master swimmers. Time course changes of ROS generation were assessed by Electron Paramagnetic Resonance in capillary blood by a microinvasive approach. An incremental arm-ergometer exercise (IE) until exhaustion was carried out at both before (PRE) and after (POST) training (Trg) period. A significant (P < 0.01) increase of ROS production from REST to the END of IE in PRE Trg (2.82 ± 0.66 versus 3.28 ± 0.66 µmol·min(-1)) was observed. HIDT increased peak oxygen consumption (36.1 ± 4.3 versus 40.6 ± 5.7 mL·kg(-1)·min(-1) PRE and POST Trg, resp.) and the antioxidant capacity (+13%) while it significantly decreased the ROS production both at REST (-20%) and after IE (-25%). The observed link between ROS production, adaptive antioxidant defense mechanisms, and peak oxygen consumption provides new insight into the correlation between ROS response pathways and muscle metabolic function.

Show MeSH
Related in: MedlinePlus