Corrigendum: Acute Exercise-Induced Oxidative Stress Does Not Affect Immediate or Delayed Precursor Cell Mobilization in Healthy Young Males

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

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Exercise-Induced Oxidative Stress, Nitric Oxide and Plasma Amino Acid Profile in Recreational Runners with Vegetarian and Non-Vegetarian Dietary Patterns

Nutrients ◽

10.3390/nu11081875 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1875 ◽

Cited By ~ 1

Author(s):

Josefine Nebl ◽

Kathrin Drabert ◽

Sven Haufe ◽

Paulina Wasserfurth ◽

Julian Eigendorf ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Amino Acid ◽

Acute Exercise ◽

Amino Acid Profile ◽

Post Exercise ◽

Stable Isotope Dilution ◽

Amino Acid Profiles ◽

Recreational Runners ◽

Exercise Induced

This study investigated the exercise-induced changes in oxidative stress, nitric oxide (NO) metabolism and amino acid profile in plasma of omnivorous (OMN, n = 25), lacto-ovo-vegetarian (LOV, n = 25) and vegan (VEG, n = 23) recreational runners. Oxidative stress was measured as malondialdehyde (MDA), NO as nitrite and nitrate, and various amino acids, including homoarginine and guanidinoacetate, the precursor of creatine. All analytes were measured by validated stable-isotope dilution gas chromatographic-mass spectrometric methods. Pre-exercise, VEG had the highest MDA and nitrate concentrations, whereas nitrite concentration was highest in LOV. Amino acid profiles differed between the groups, with guanidinoacetate being highest in OMN. Upon acute exercise, MDA increased in the LOV and VEG group, whereas nitrate, nitrite and creatinine did not change. Amino acid profiles changed post-exercise in all groups, with the greatest changes being observed for alanine (+28% in OMN, +21% in LOV and +28% in VEG). Pre-exercise, OMN, LOV and VEG recreational runners differ with respect to oxidative stress, NO metabolism and amino acid profiles, in part due to their different dietary pattern. Exercise elicited different changes in oxidative stress with no changes in NO metabolism and closely comparable elevations in alanine. Guanidinoacetate seems to be differently utilized in OMN, LOV and VEG, pre- and post-exercise.

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Exercise-Induced Oxidative Stress and the Effects of Antioxidant Intake from a Physiological Viewpoint

Antioxidants ◽

10.3390/antiox7090119 ◽

2018 ◽

Vol 7 (9) ◽

pp. 119 ◽

Cited By ~ 44

Author(s):

Takuji Kawamura ◽

Isao Muraoka

Keyword(s):

Oxidative Stress ◽

Acute Exercise ◽

Animal Experiments ◽

Whole Body ◽

Oxygen Species ◽

Healthy Individuals ◽

Redox Biology ◽

Radical Production ◽

Antioxidant Intake ◽

Exercise Induced

It is well established that the increase in reactive oxygen species (ROS) and free radicals production during exercise has both positive and negative physiological effects. Among them, the present review focuses on oxidative stress caused by acute exercise, mainly on evidence in healthy individuals. This review also summarizes findings on the determinants of exercise-induced oxidative stress and sources of free radical production. Moreover, we outline the effects of antioxidant supplementation on exercise-induced oxidative stress, which have been studied extensively. Finally, the following review briefly summarizes future tasks in the field of redox biology of exercise. In principle, this review covers findings for the whole body, and describes human trials and animal experiments separately.

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Effects of Exercise-Induced ROS on the Pathophysiological Functions of Skeletal Muscle

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/3846122 ◽

2021 ◽

Vol 2021 ◽

pp. 1-5

Author(s):

Fan Wang ◽

Xin Wang ◽

Yiping Liu ◽

Zhenghong Zhang

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Acute Exercise ◽

Redox System ◽

The Body ◽

Muscle Adaptation ◽

Exercise Induced ◽

And Function ◽

Stress Fatigue

Oxidative stress is the imbalance of the redox system in the body, which produces excessive reactive oxygen species, leads to multiple cellular damages, and closely relates to some pathological conditions, such as insulin resistance and inflammation. Meanwhile, exercise as an external stimulus of oxidative stress causes the changes of pathophysiological functions in the tissues and organs, including skeletal muscle. Exercise-induced oxidative stress is considered to have different effects on the structure and function of skeletal muscle. Long-term regular or moderate exercise-induced oxidative stress is closely related to the formation of muscle adaptation, while excessive free radicals produced by strenuous or acute exercise can cause muscle oxidative stress fatigue and damage, which impacts exercise capacity and damages the body’s health. The present review systematically summarizes the relationship between exercise-induced oxidative stress and the adaptions, damage, and fatigue in skeletal muscle, in order to clarify the effects of exercise-induced oxidative stress on the pathophysiological functions of skeletal muscle.

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The Effect of Acute Intense Exercise on Activity of Antioxidant Enzymes in Smokers and Non-smokers

10.20944/preprints202008.0363.v1 ◽

2020 ◽

Author(s):

Hadi Nobari ◽

Hamzeh Abdi nejad ◽

Mina Ahmadi ◽

Soghra Mohseni ◽

Mehdi Kargarfard ◽

...

Keyword(s):

Oxidative Stress ◽

Recovery Time ◽

Acute Exercise ◽

Smoking Habit ◽

Antioxidant Enzyme Activity ◽

Intense Exercise ◽

Significant Difference ◽

Post Test ◽

Total Antioxidant ◽

Exercise Induced

Acute intense exercise causes significant oxidative stress and consequently an increase in total antioxidant capacity; however, the mechanisms and combined effects of intense exercise and smoking on oxidative stress among active and non-active smokers are not clear. The aim of this study was to investigate the effect of acute intense exercise on antioxidant enzyme activity responses in active and non-active individuals exposed to cigarette smoke. The study included 40 subjects who were equally classified as: smokers that did exercise (SE), smokers that did not do exercise (SnE), non-smokers that did exercise (NSE), and non-smokers that did not do exercise (NSnE). The adjusted Astrand test was used to exhaust the subjects. Salivary enzymes of peroxidase (POX), catalase (CAT), and superoxide dismutase (SOD) were measured, by spectrophotometry methods, at 3 different time points: pre-test (TP1), post-test (TP2), and one hour after finishing the test (TP3). Significant (p<0.05) group x time interactions were found for the three enzymes. Salivary POX, CAT and SOD increased in all groups from TP1 to TP2 and decreased from TP2 to TP3. Only the NSE showed a significant difference between TP1 to TP3 in POX and SOD by +0.011 ± 0.007 and +0.075 ± 0.02 (U/ml), respectively. The NSE showed significantly higher levels of POX, CAT and SOD in TP2 compared to the other groups. Furthermore, NSE and NSnE had higher levels of POX, CAT and SOD in TP1 and TP3 (p<0.05) compared with SE and SnE. Only in the NSnE, were no differences observed in CAT compared with SE and SnE in TP3. These results showed that the antioxidant level at rest and in the recovery time after the acute intense exercise was lower in SE and SnE compared with NSE and NSnE, suggesting that smoking habit may reduce the ameliorating effect of regular physical activity on acute exercise-induced oxidative stress.

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MiRNA126 – RGS16 – CXCL12 Cascade as a Potential Mechanism of Acute Exercise-Induced Precursor Cell Mobilization

Frontiers in Physiology ◽

10.3389/fphys.2021.780666 ◽

2021 ◽

Vol 12 ◽

Author(s):

Michelle Schmid ◽

Helena Caria Martins ◽

Gerhard Schratt ◽

Julia M. Kröpfl ◽

Christina M. Spengler

Keyword(s):

Peripheral Blood ◽

Acute Exercise ◽

Mononuclear Cells ◽

Strongly Correlated ◽

Potential Mechanism ◽

Clinical Trial Registration ◽

Peripheral Blood Mononuclear ◽

Time Points ◽

Cell Mobilization ◽

Exercise Induced

Acute exercise enhances circulating stem and precursor cells (CPCs) in the peripheral blood. The responsible mechanisms and molecular pathways, however, have not been fully identified. The aim of the present study was to investigate a pathway related to elevated levels of apoptotic peripheral blood mononuclear cells (MNCs) and their secretome. An increased uptake of miRNA126 in MNCs was suggested to lead to reduced levels of RGS16 mRNA and, in turn, an enhanced translation and secretion of CXCL12. Eighteen healthy, young men underwent two identical incremental cycling exercises of which the first served as control while the second was preceded by a 7-day-long antioxidative supplementation. Blood samples were collected at baseline (−10min) and several time points after exercise (0, 30, 90, 180, and 270min). Relative concentrations of miRNA126 in MNCs and CXCL12 levels in plasma were determined at all time points while RGS16 mRNA was assessed in MNCs at baseline and 30min after exercise. CXCL12 increased after exercise and strongly correlated with CPC numbers. MiRNA126 increased 30min and, to a lesser extent, also 180 and 270min after exercise but only with supplementation. RGS16 mRNA decreased 30min after exercise independent of the intervention. The amount of RGS16 mRNA inversely correlated with levels of miRNA126, but not with plasma CXCL12. In conclusion, even though plasma CXCL12 correlated with CPC numbers, the increase in CXCL12 cannot be explained by the increased concentration of miRNA126 and lower RGS16 mRNA in MNCs that would have allowed for an enhanced translation of CXCL12.Clinical Trial Registration: ClinicalTrials.gov, NCT03747913. Registered 20 November 2018, https://clinicaltrials.gov/ct2/show/NCT03747913.

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Intermittent hypoxic training: implications for lipid peroxidation induced by acute normoxic exercise in active men

Clinical Science ◽

10.1042/cs1010465 ◽

2001 ◽

Vol 101 (5) ◽

pp. 465-475 ◽

Cited By ~ 65

Author(s):

Damian M. BAILEY ◽

Bruce DAVIES ◽

Ian S. YOUNG

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Acute Exercise ◽

Mass Action ◽

Lipid Hydroperoxides ◽

Double Blind ◽

Intermittent Hypoxic Training ◽

Hypoxic Conditions ◽

Hypoxic Training ◽

Exercise Induced

Oxidant generation during regular physical exercise training may influence the adaptive responses that have been shown to confer protection against oxidative stress induced by subsequent acute exercise. To examine this, we randomly assigned 32 males to either a normoxic (n = 14) or a hypoxic (n = 18) group. During the acute phase, subjects in the hypoxic group performed two maximal cycling tests in a randomized double-blind fashion: one under conditions of normoxia and the other under hypoxic conditions (inspired fraction of O2 = 0.21 and 0.16 respectively). During the intermittent phase, the normoxic and hypoxic groups each trained for 4 weeks at the same relative exercise intensity, under conditions of normoxia and hypoxia respectively. During acute exercise under hypoxic conditions, the venous concentrations of lipid hydroperoxides and malondialdehyde were increased, despite a comparatively lower maximal oxygen uptake (o2max) (P < 0.05 compared with normoxia). The increases in lipid hydroperoxides and malondialdehyde were correlated with the exercise-induced decrease in arterial haemoglobin oxygen saturation (r =-0.61 and r =-0.50 respectively; P < 0.05), but not with o2max. Intermittent hypoxic training attenuated the increases in lipid hydroperoxides and malondialdehyde induced by acute normoxic exercise more effectively than did normoxic training, due to a selective mobilization of α-tocopherol (P < 0.05). The latter was related to enhanced exercise-induced mobilization/oxidation of blood lipids due to a selective increase in o2max (P < 0.05 compared with normoxic group). We conclude that lipid peroxidation induced by acute exercise (1) increases during hypoxia; (2) is not regulated exclusively by a mass action effect of o2; and (3) is selectively attenuated by regular hypoxic training. Oxidative stress may thus be considered as a biological prerequisite for adaptation to physical stress in humans.

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