Acute Exercise-Induced Oxidative Stress Does Not Affect Immediate or Delayed Precursor Cell Mobilization in Healthy Young Males.
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ABSTRACT:
SUBMITTER: Schmid M
PROVIDER: S-EPMC7606978 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The capacity to utilize ingested protein for optimal support of protein synthesis and lean body mass is described within the paradigm of anabolic competence. Protein synthesis can be stimulated by physical exercise, however, it is not known if physical exercise affects post-exercise protein oxidation. Characterization of the driving forces behind protein oxidation, such as exercise, can contribute to improved understanding of whole body protein metabolism. The purpose of this study is to determine the effect of two levels of aerobic exercise intensity on immediate post-exercise exogenous protein oxidation. Sixteen healthy males with a mean (SD) age of 24 (4) years participated. The subjects' VO2-max was estimated with the Åstrand cycling test. Habitual dietary intake was assessed with a three-day food diary. Exogenous protein oxidation was measured by isotope ratio mass spectrometry. These measurements were initiated after the ingestion of a 30 g 13C-milk protein test drink that was followed by 330 minutes breath sample collection. On three different days with at least one week in between, exogenous protein oxidation was measured: 1) during rest, 2) after 15 minutes of aerobic exercise at 30% of VO2-max (moderate intensity), and 3) after 15 minutes of aerobic exercise at 60% of VO2-max (vigorous intensity). After vigorous intensity aerobic exercise, 31.8%±8.0 of the 30 g 13C-milk protein was oxidized compared to 26.2%±7.1 during resting condition (p = 0.012), and 25.4%±7.6 after moderate intensity aerobic exercise compared to resting (p = 0.711). In conclusion, exogenous protein oxidation is increased after vigorous intensity aerobic exercise which could be the result of an increased protein turnover rate.
| S-EPMC6876877 | biostudies-literature
Project description:Although systemic sex-specific differences in cardiovascular responses to exercise are well established, the comparison of sex-specific cerebrovascular responses to exercise has gone under-investigated especially, during high intensity exercise. Therefore, our purpose was to compare cerebrovascular responses in males and females throughout a graded exercise test (GXT). Twenty-six participants (13 Females and 13 Males, 24 ± 4 yrs.) completed a GXT on a recumbent cycle ergometer consisting of 3-min stages. Each sex completed 50W, 75W, 100W stages. Thereafter, power output increased 30W/stage for females and 40W/stage for males until participants were unable to maintain 60-80 RPM. The final stage completed by the participant was considered maximum workload(Wmax ). Respiratory gases (End-tidal CO2 , EtCO2 ), middle cerebral artery blood velocity (MCAv), heart rate (HR), non-invasive mean arterial pressure (MAP), cardiac output (CO), and stroke volume (SV) were continuously recorded on a breath-by-breath or beat-by-beat basis. Cerebral perfusion pressure, CPP = MAP (0. 7,355 distance from heart-level to doppler probe) and cerebral vascular conductance index, CVCi = MCAv/CPP 100mmHg were calculated. The change from baseline (Δ) in MCAv was similar between the sexes during the GXT (p = .091, ωp 2 = 0.05). However, ΔCPP (p < .001, ωp 2 = 0.25) was greater in males at intensities ≥ 80% Wmax and ΔCVCi (p = .005, ωp 2 = 0.15) was greater in females at 100% Wmax . Δ End-tidal CO2 (ΔEtCO2 ) was not different between the sexes during exercise (p = .606, ωp 2 = -0.03). These data suggest there are sex-specific differences in cerebrovascular control, and these differences may only be identifiable at high and severe intensity exercise.
| S-EPMC7592493 | biostudies-literature
Project description:Dietary intake of vitamin D includes vitamin D3 (vitD3), 25-hydroxyvitamin D3 (25OH-D3), and vitamin D2 (vitD2). However, the bioactivity of the different species has not been scientifically established. The hypothesis in this study was that vitD3, 25OH-D3, and vitD2 have an equal effect on 25-hydroxyvitamin D in serum (vitamin D status). To test our hypothesis, we performed a randomized, crossover study. Twelve young males consumed 10 µg/day vitD3 during a four-week run-in period, followed by 3 × 6 weeks of 10 µg/day vitD3, 10 µg/day 25OH-D3, and 10 µg/day vitD2. The content of vitD3, vitD2, 25OH-D3, and 25-hydroxyvitamin D2 (25OH-D2) in serum was quantified by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The hypothesis that the three sources of vitamin D affect vitamin D status equally was rejected. Based on the assumption that 1 µg vitD3/day will show an increase in vitamin D status of 1.96 nmol/L, the results showed that 23 µg vitD2 and 6.8 µg 25OH-D3 was similar to 10 µg vitD3. These results demonstrate that further investigations are necessary to determine how to quantify the total vitamin D activity based on chemical quantification of the individual vitamin D metabolites to replace the total vitamin D activity assessed in biological rat models.
| S-EPMC5793240 | biostudies-literature
Project description:Regular physical exercise can positively influence cardiac function; however, investigations have shown an increase of myocardial damage biomarkers after acute prolonged endurance exercises. We investigated the effect of repeated sprint vs. moderate long duration exercise on markers of myocardial necrosis, as well as cardiac dimensions and functions. Thirteen healthy males performed two different running sessions (randomized, single blinded cross-over design): 60 minutes moderate intensity continuous training (MCT, at 70% of peak heart rate (HRpeak)) and two series of 12 × 30-second sprints with set recovery periods in-between (RST, at 90% HRpeak). Venous blood samples for cardiac troponin T (cTnT), creatine kinase (CK) and MB isoenzyme (CK-MB) were taken 1 and 4 hours after exercise sessions. After each session electrocardiographic (ECG) and transthoracic echocardiographic (TTE) data were recorded. Results showed that all variables - average heart rate, serum lactate concentration during RST, subjective exertion and cTnT after RST - were significantly higher compared to MCT. CK and CK-MB significantly increased regardless of exercise protocol, while ECG and TTE indicated normal cardiac function. Our results provide evidence that RST contributes significantly to cTnT and CK release. This biomarker increase seems to reflect a physiological rather than a pathological phenomenon in healthy, exercising subjects.
| S-EPMC4835763 | biostudies-other
Project description:Hypoxia-induced insulin resistance appears to suppress exogenous glucose oxidation during metabolically matched aerobic exercise during acute (<8 h) high-altitude (HA) exposure. However, a better understanding of this metabolic dysregulation is needed to identify interventions to mitigate these effects. The objective of this study was to determine if differences in metabolomic profiles during exercise at sea level (SL) and HA are reflective of hypoxia-induced insulin resistance. Native lowlanders (n = 8 males) consumed 145 g (1.8 g/min) of glucose while performing 80-min of metabolically matched treadmill exercise at SL (757 mmHg) and HA (460 mmHg) after 5-h exposure. Exogenous glucose oxidation and glucose turnover were determined using indirect calorimetry and dual tracer technique ([13C]glucose and [6,6-2H2]glucose). Metabolite profiles were analyzed in serum as change (Δ), calculated by subtracting postprandial/exercised state SL (ΔSL) and HA (ΔHA) from fasted, rested conditions at SL. Compared with SL, exogenous glucose oxidation, glucose rate of disappearance, and glucose metabolic clearance rate (MCR) were lower (P < 0.05) during exercise at HA. One hundred and eighteen metabolites differed between ΔSL and ΔHA (P < 0.05, Q < 0.10). Differences in metabolites indicated increased glycolysis, tricarboxylic acid cycle, amino acid catabolism, oxidative stress, and fatty acid storage, and decreased fatty acid mobilization for ΔHA. Branched-chain amino acids and oxidative stress metabolites, Δ3-methyl-2-oxobutyrate (r = -0.738) and Δγ-glutamylalanine (r = -0.810), were inversely associated (P < 0.05) with Δexogenous glucose oxidation. Δ3-Hydroxyisobutyrate (r = -0.762) and Δ2-hydroxybutyrate/2-hydroxyisobutyrate (r = -0.738) were inversely associated (P < 0.05) with glucose MCR. Coupling global metabolomics and glucose kinetic data suggest that the underlying cause for diminished exogenous glucose oxidative capacity during aerobic exercise is acute hypoxia-mediated peripheral insulin resistance.
| S-EPMC8321788 | biostudies-literature
Project description:This study was aimed at examining the impact of common types of physical efforts used to determine the aerobic and anaerobic performance of the participants on the complement system in their peripheral blood. Fifty-one physically active young males aged 16 years old (range 15-21 years) were divided into two age groups (younger, 15-17 years old and older, 18-21 years old) and performed two types of intensive efforts: aerobic (endurance; 20-m shuttle run test; Beep) and anaerobic (speed; repeated speed ability test; RSA). Venous blood samples were collected before and after each exercise (5 and 60 min) to profile the complement system components, namely the levels of C2, C3, C3a, iC3b, and C4. The endurance effort caused a decrease in the post-test C3 (p < 0.001 for both age groups) and increase in post-test C3a (p < 0.001 and p < 0.01 for the younger and older group, respectively), recovery iC3b (p < 0.001 and p < 0.05 for younger and older group, respectively), recovery C2 (p < 0.01 for both age groups), and post-test C4 (p < 0.05 and p < 0.01 for the younger and older group, respectively) levels, while the speed effort caused a decrease only in the post-test C2 (p < 0.05 for younger participants) and post-test C4 levels (p < 0.001 and p < 0.01 for the younger and older group, respectively) and an increase in the recovery C3a level (p < 0.05). Our study provides evidence that different types of physical effort promote different immune responses in physically active young men. Aerobic exercise induced the activation of an alternative pathway of the complement system, whilst the anaerobic effort had little influence. A better understanding of the post-exercise immune response provides a framework to prescribe physical activity to achieve different health outcomes.
| S-EPMC7464301 | biostudies-literature
Project description:BackgroundAerobic exercise benefits health but increases inhalation of fine particles (PM2.5) in ambient air. Acute cardiopulmonary responses to PM2.5 exposure in individuals with different exercise habits, especially in areas with severe air pollution, are not well understood.MethodsTo examine acute cardiopulmonary responses to PM2.5 exposure modified by exercise habits, a panel of 20 healthy non-smoking male subjects, recruited in Beijing, China, completed seven visits. The exercise frequency per week and preferred exercise place were recorded using a baseline questionnaire to describe exercise habits. Fractional exhaled nitric oxide (FeNO), cytokines in exhaled breath condensate, blood pressure, and pulse-wave analysis (PWA) indices were measured during each visit as biomarkers of acute cardiopulmonary responses. The hourly average mass concentration of PM2.5 and black carbon (BC), and the number concentrations of ultrafine particles (UFP) and accumulation mode particles (AMP) were monitored throughout the follow-up period at an outdoor fixed monitoring station beginning 14 days prior to each visit. Linear mixed-effects models were used to evaluate the associations between acute changes in biomarker levels and exposure to PM2.5 and its constituents. The primary aim was to assess the modification of long-term exercise habits on these associations.ResultsFeNO concentration, systolic blood pressure, ejection duration, aortic augmentation pressure, and aortic pressure index were positively associated with exposure to PM2.5 and its constituents. However, no associations with cytokine levels or diastolic blood pressure were observed. In a stratified analysis, we found that acute cardiopulmonary responses were modified by exercise habit. Specifically, the interquartile ranges (IQR) of increases in the 6-12-h moving average (MA) PM2.5 and AMP exposure were associated with 19-21% and 24-26% increases in FeNO, respectively, in subjects with high exercise frequency; these associations were significantly stronger than those in subjects with low exercise frequency. An IQR increase in 3-11-d MA AMP exposure was associated with a 10-26% increase in aortic augmentation pressure in subjects with low exercise frequency; this association was significantly stronger than that in subjects with high exercise frequency. An IQR increase in 9-13-d MA UFP exposure was associated with a 13-17% increase in aortic augmentation pressure in subjects who preferred outdoor exercise; this association was stronger than that in subjects who preferred indoor exercise.ConclusionsIn highly polluted areas, frequent exercise might protect against PM2.5-associated arterial stiffness but exacerbate airway inflammation.
| S-EPMC6293663 | biostudies-literature
Project description:BackgroundInadequate sleep is associated with many detrimental health effects, including increased risk of developing insulin resistance and type 2 diabetes. These effects have been associated with changes to the skeletal muscle transcriptome, although this has not been characterised in response to a period of sleep restriction. Exercise induces a beneficial transcriptional response within skeletal muscle that may counteract some of the negative effects associated with sleep restriction. We hypothesised that sleep restriction would down-regulate transcriptional pathways associated with glucose metabolism, but that performing exercise would mitigate these effects.Methods20 healthy young males were allocated to one of three experimental groups: a Normal Sleep (NS) group (8 h time in bed per night (TIB), for five nights (11 pm - 7 am)), a Sleep Restriction (SR) group (4 h TIB, for five nights (3 am - 7 am)), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB, for five nights (3 am - 7 am) and three high-intensity interval exercise (HIIE) sessions (performed at 10 am)). RNA sequencing was performed on muscle samples collected pre- and post-intervention. Our data was then compared to skeletal muscle transcriptomic data previously reported following sleep deprivation (24 h without sleep).ResultsGene set enrichment analysis (GSEA) indicated there was an increased enrichment of inflammatory and immune response related pathways in the SR group post-intervention. However, in the SR+EX group the direction of enrichment in these same pathways occurred in the opposite directions. Despite this, there were no significant changes at the individual gene level from pre- to post-intervention. A set of genes previously shown to be decreased with sleep deprivation was also decreased in the SR group, but increased in the SR+EX group.ConclusionThe alterations to inflammatory and immune related pathways in skeletal muscle, following five nights of sleep restriction, provide insight regarding the transcriptional changes that underpin the detrimental effects associated with sleep loss. Performing three sessions of HIIE during sleep restriction attenuated some of these transcriptional changes. Overall, the transcriptional alterations observed with a moderate period of sleep restriction were less evident than previously reported changes following a period of sleep deprivation.
| S-EPMC9355502 | biostudies-literature
Project description:This study investigated the endurance exercise-induced changes in lesser known adipokines (visfatin, chemerin, apelin, semaphorin 3?C) related to obesity and metabolism, and their correlations with the changes in the parameters of obesity and glucose homeostasis. Forty metabolically healthy obese young males were randomly assigned to control group (C, n?=?12) or exercise group (Ex, n?=?28). The subjects in Ex participated in a 8-week supervised endurance exercise training program, comprised of four sessions of treadmill running at 65-70% of VO2max per week. Serum levels of visfatin, chemerin, apelin, and semaphorin 3?C were significantly decreased in Ex. At baseline, apelin and semaphorin 3?C appeared to be correlated with obesity measures, including body mass index, % total fat and trunk fat, and waist circumference. Exercise-induced changes in these obesity measures significantly correlated with the changes in chemerin and semaphorin 3?C. Basal chemerin, apelin and semaphorin 3?C correlated with glucose homeostasis parameters, including fasting plasma glucose, fasting plasma insulin, homeostasis model assessment of insulin resistance and ?-cell function, and quantitative insulin-sensitivity check index to different extents. Furthermore, the changes in apelin and semaphorin 3?C well predicted the improvements in glycemic parameters. We suggest that semaphorin 3?C is a novel adipokine involved in pathophysiology of obesity and metabolism, and that it is a biomarker representing an exercise-induced improvement in metabolically healthy obese young males.
| S-EPMC7305109 | biostudies-literature
Project description:The primary objective of the current study was to determine the effect of moderate normobaric hypoxia exposure during constant load cycling on post-exercise energy metabolism recorded in normoxia. Indirect calorimetry was used to examine whole body substrate oxidation before, during, 40-60 min post, and 22 h after performing 60 min of cycling exercise at two different fractions of inspired oxygen (FIO2): (i) FIO2 = 0.2091 (normoxia) and (ii) FIO2 = 0.15 (hypoxia). Seven active healthy male participants (26 ± 4 years of age) completed both experimental trials in randomized order with a 7-day washout period to avoid carryover effects between conditions. Resting energy expenditure was initially elevated following cycling exercise in normoxia and hypoxia (Δ 0.14 ± 0.05, kcal min-1, p = 0.037; Δ 0.19 ± 0.03 kcal min-1, p < 0.001, respectively), but returned to baseline levels the next morning in both conditions. Although, the same absolute workload was used in both environmental conditions (157 ± 10 W), a shift in resting substrate oxidation occurred after exercise performed in hypoxia while post-exercise measurements were similar to baseline after cycling exercise in normoxia. The additional metabolic stress of hypoxia exposure was sufficient to increase the rate of lipid oxidation (Δ 42 ± 11 mg min-1, p = 0.019) and tended to suppress carbohydrate oxidation (Δ -55 ± 26 mg min-1, p = 0.076) 40-60 min post-exercise. This shift in substrate oxidation persisted the next morning, where lipid oxidation remained elevated (Δ 9 ± 3 mg min-1, p = 0.0357) and carbohydrate oxidation was suppressed (Δ -22 ± 6 mg min-1, p = 0.019). In conclusion, prior exercise performed under moderate normobaric hypoxia alters post-exercise energy metabolism. This is an important consideration when evaluating the metabolic consequences of hypoxia exposure during prolonged exercise, and future studies should evaluate its role in the beneficial effects of intermittent hypoxia training observed in persons with obesity and insulin resistance.
| S-EPMC5434119 | biostudies-literature