scholarly journals Physical Training Status Determines Oxidative Stress and Redox Changes in Response to an Acute Aerobic Exercise

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Farnaz Seifi-skishahr ◽  
Arsalan Damirchi ◽  
Manoochehr Farjaminezhad ◽  
Parvin Babaei

Objective. To assess the influence of different physical training status on exercise-induced oxidative stress and changes in cellular redox state.Methods. Thirty male subjects participated in this study and were assigned as well-trained (WT), moderately trained (MT), and untrained (UT) groups. The levels of cortisol, creatine kinase, plasma reduced glutathione to oxidized glutathione (GSH/GSSG), cysteine/cystine (Cys/CySS), and GSH/GSSG ratio in red blood cells (RBCs) were measured immediately and 10 and 30 min after exercise.Results. Following the exercise, plasma GSH/GSSG (p=0.001) and Cys/CySS (p=0.005) were significantly reduced in all groups. Reduction in plasma GSH/GSSG ratio in all groups induced a transient shift in redox balance towards a more oxidizing environment without difference between groups (p=0.860), while RBCs GSH/GSSG showed significant reduction (p=0.003) and elevation (p=0.007) in UT and MT groups, respectively. The highest level of RBCs GSH/GSSG ratio was recorded in MT group, and the lowest one was recorded in the WT group.Conclusion. Long term regular exercise training with moderate intensity shifts redox balance towards more reducing environment, versus intensive exercise training leads to more oxidizing environment and consequently development of related diseases.

2019 ◽  
Vol 127 (3) ◽  
pp. 858-866 ◽  
Author(s):  
Alex J. Wadley ◽  
Gary Keane ◽  
Tom Cullen ◽  
Lynsey James ◽  
Jordan Vautrinot ◽  
...  

Redox enzymes modulate intracellular redox balance and are secreted in response to cellular oxidative stress, potentially modulating systemic inflammation. Both aerobic and resistance exercise are known to cause acute systemic oxidative stress and inflammation; however, how redox enzyme concentrations alter in extracellular fluids following bouts of either type of exercise is unknown. Recreationally active men ( n = 26, mean ± SD: age 28 ± 8 yr) took part in either: 1) two separate energy-matched cycling bouts: one of moderate intensity (MOD) and a bout of high intensity interval exercise (HIIE) or 2) an eccentric-based resistance exercise protocol (RES). Alterations in plasma (study 1) and serum (study 2) peroxiredoxin (PRDX)-2, PRDX-4, superoxide dismutase-3 (SOD3), thioredoxin (TRX-1), TRX-reductase and interleukin (IL)-6 were assessed before and at various timepoints after exercise. There was a significant increase in SOD3 (+1.5 ng/mL) and PRDX-4 (+5.9 ng/mL) concentration following HIIE only, peaking at 30- and 60-min post-exercise respectively. TRX-R decreased immediately and 60 min following HIIE (−7.3 ng/mL) and MOD (−8.6 ng/mL), respectively. In non-resistance trained men, no significant changes in redox enzyme concentrations were observed up to 48 h following RES, despite significant muscle damage. IL-6 concentration increased in response to all trials, however there was no significant relationship between absolute or exercise-induced changes in redox enzyme concentrations. These results collectively suggest that HIIE, but not MOD or RES increase the extracellular concentration of PRDX-4 and SOD3. Exercise-induced changes in redox enzyme concentrations do not appear to directly relate to systemic changes in IL-6 concentration. NEW & NOTEWORTHY Two studies were conducted to characterize changes in redox enzyme concentrations after single bouts of exercise to investigate the emerging association between extracellular redox enzymes and inflammation. We provide evidence that SOD3 and PRDX-4 concentration increased following high-intensity aerobic but not eccentric-based resistance exercise. Changes were not associated with IL-6. The results provide a platform to investigate the utility of SOD3 and PRDX-4 as biomarkers of oxidative stress following exercise.


2012 ◽  
Vol 109 (2) ◽  
pp. 293-301 ◽  
Author(s):  
Mark C. Fogarty ◽  
Ciara M. Hughes ◽  
George Burke ◽  
John C. Brown ◽  
Gareth W. Davison

Pharmacological antioxidant vitamins have previously been investigated for a prophylactic effect against exercise-induced oxidative stress. However, large doses are often required and may lead to a state of pro-oxidation and oxidative damage. Watercress contains an array of nutritional compounds such as β-carotene and α-tocopherol which may increase protection against exercise-induced oxidative stress. The present randomised controlled investigation was designed to test the hypothesis that acute (consumption 2 h before exercise) and chronic (8 weeks consumption) watercress supplementation can attenuate exercise-induced oxidative stress. A total of ten apparently healthy male subjects (age 23 (sd4) years, stature 179 (sd10) cm and body mass 74 (sd15) kg) were recruited to complete the 8-week chronic watercress intervention period (and then 8 weeks of control, with no ingestion) of the experiment before crossing over in order to compete the single-dose acute phase (with control, no ingestion). Blood samples were taken at baseline (pre-supplementation), at rest (pre-exercise) and following exercise. Each subject completed an incremental exercise test to volitional exhaustion following chronic and acute watercress supplementation or control. The main findings show an exercise-induced increase in DNA damage and lipid peroxidation over both acute and chronic control supplementation phases (P< 0·05v.supplementation), while acute and chronic watercress attenuated DNA damage and lipid peroxidation and decreased H2O2accumulation following exhaustive exercise (P< 0·05v.control). A marked increase in the main lipid-soluble antioxidants (α-tocopherol, γ-tocopherol and xanthophyll) was observed following watercress supplementation (P< 0·05v.control) in both experimental phases. These findings suggest that short- and long-term watercress ingestion has potential antioxidant effects against exercise-induced DNA damage and lipid peroxidation.


Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle


1995 ◽  
Vol 79 (3) ◽  
pp. 675-686 ◽  
Author(s):  
C. K. Sen

There is consistent evidence from human and animal studies that strenuous physical exercise may induce a state wherein the antioxidant defenses of several tissues are overwhelmed by excess reactive oxygen. A wide variety of physiological and dietary antioxidants act in concert to evade such a stress. Submaximal long-duration exercise training may augment the physiological antioxidant defenses in several tissues; however, this enhanced protection may not be sufficient to completely protect highly fit individuals from exhaustive exercise-induced oxidative stress. Regular physical activity in association with dietary habits that ensure adequate supply of a combination of appropriate antioxidants may be expected to yield desirable results. The significance of this area of research, current state of information, and possibilities of further investigation are briefly reviewed.


2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


2014 ◽  
Vol 46 (7) ◽  
pp. 256-267 ◽  
Author(s):  
Milène Catoire ◽  
Marco Mensink ◽  
Eric Kalkhoven ◽  
Patrick Schrauwen ◽  
Sander Kersten

Endurance exercise is associated with significant improvements in cardio-metabolic risk parameters. A role for myokines has been hypothesized, yet limited information is available about myokines induced by acute endurance exercise in humans. Therefore, the aim of the study was to identify novel exercise-induced myokines in humans. To this end, we carried out a 1 h one-legged acute endurance exercise intervention in 12 male subjects and a 12 wk exercise training intervention in 18 male subjects. Muscle biopsies were taken before and after acute exercise or exercise training and were subjected to microarray-based analysis of secreted proteins (secretome). For acute exercise, secretome analysis resulted in a list of 86 putative myokines, which was reduced to 29 by applying a fold-change cut-off of 1.5. Based on that shortlist, a selection of putative myokines was measured in the plasma by ELISA or multiplex assay. From that selection, CX3CL1 (fractalkine) and CCL2 (MCP-1) increased at both mRNA and plasma levels. From the known myokines, only IL-6 and FGF 21 changed at the mRNA level, whereas none of the known myokines changed at the plasma level. Secretome analysis of exercise training intervention resulted in a list of 69 putative myokines. Comparing putative myokines altered by acute exercise and exercise training revealed a limited overlap of only 13 genes. In conclusion, this study identified CX3CL1 and CCL2 as myokines that were induced by acute exercise at the gene expression and plasma level and that may be involved in communication between skeletal muscle and other organs.


2020 ◽  
Vol 9 (5) ◽  
pp. 1379
Author(s):  
Katarzyna Hojan ◽  
Danuta Procyk ◽  
Dorota Horyńska-Kęstowicz ◽  
Ewa Leporowska ◽  
Maria Litwiniuk

Cardiotoxicity is known as a severe clinical problem in oncological practice that reduces the options for cancer therapy. Physical exercise is recognized as a well-established protective measure for many heart and cancer diseases. In our study, we hypothesized that supervised and moderate-intensity exercise training would prevent heart failure and its consequences induced by trastuzumab therapy. The aim of this study was to examine the effect of physical training on ventricular remodeling, serum cardiac markers, and exercise performance in women with human epidermal growth receptor 2 (HER2+) breast cancer (BC) undergoing trastuzumab therapy. This was a prospective, randomized, clinical controlled trial. Forty-six BC women were randomized into either an intervention group (IG) or a control group (CG). An exercise program (IG) was performed after 3–6 months of trastuzumab therapy at 5 d/week (to 80% maximum heart rate (HRmax)) for 9 weeks. We then evaluated their cardiac function using echocardiography, a 6-Minute Walk Test (6MWT), and plasma parameters (C-reactive protein (CRP), myoglobin (MYO), interleukin-6 (IL-6), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatine kinase (CK)). After the physical training program, we did not observe any significant changes in the left ventricular (LV) ejection fraction (LVEF) and 6MWT (p > 0.05) in the IG compared to the CG (decrease p < 0.05). The differences in the blood parameters were not significant (p < 0.05). To conclude, moderate-intensity exercise training prevented a decrease in the LVEF and physical capacity during trastuzumab therapy in HER2+ BC. Further research is needed to validate our results.


2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Ewin B. Almeida ◽  
Juliana M. B. Santos ◽  
Vitória Paixão ◽  
Jonatas B. Amaral ◽  
Roberta Foster ◽  
...  

Although regular combined aerobic-resistance exercises can ameliorate the inflammatory status and redox balance in elderly population, it is unclear whether protein or specific amino acid supplementation could improve such benefits. Therefore, we aimed to evaluate the inflammatory status and redox indexes through of the saliva of 34 elderly subject nonpractitioners (NP group, 73.3±6.6 years) and 49 elderly subject practitioners of a combined-exercise training in moderate intensity (CET group, 71.9±5.8 years) before (pre) and after (post) 30 days of supplementation with L-glutamine (Gln) or placebo (PL). Our results showed that, both in pre- and postsupplementation, the salivary levels of nitric oxide (NO⋅) and TNF-α were lower, whereas the levels of uric acid and IL-10 (as well as IL-10/TNF-α ratio) were higher in the CET groups than in the NP groups. In postsupplementation, both groups supplemented with Gln (NP-Gln and CET-Gln) showed higher salivary uric acid levels compared to baseline. In addition, lower NO⋅ levels were found in the CET-Gln group postsupplementation than presupplementation values. Whereas the CET-Gln group showed lower GSH levels postsupplementation, NP-Gln subjects showed lower GSSG levels at the same time point, both compared to baseline. Interestingly, salivary peroxidase activity was lower only in NP groups (NP-PL and NP-Gln) postsupplementation than baseline values. A positive significant correlation between salivary peroxidase activity and GSH levels, and also between salivary peroxidase activity and uric acid levels were observed in the CET-Gln group both pre- and postsupplementation. No differences were found in albumin, total antioxidant activity (TEAC), and reducing power analysis between groups, pre- or postsupplementation. In conclusion, the elderly subjects from the CET group showed a better inflammatory response and redox balance and, for the first time, it was shown that daily supplementation with Gln for 30 days can improve these benefits with putative association with a healthy aging.


2008 ◽  
Vol 40 (Supplement) ◽  
pp. S245
Author(s):  
Kelsey H. Fisher-Wellman ◽  
David E. Ferebee ◽  
Richard J. Bloomer

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S122
Author(s):  
K Koyama ◽  
D Ando ◽  
J Yokouchi ◽  
Y Ono ◽  
M Kaya ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document