Single Bout Of Endurance Exercise Research Articles

Plasma-derived extracellular vesicles released after endurance exercise exert cardioprotective activity through the activation of antioxidant pathways

Cardiovascular diseases (CVD) can cause various conditions, including an increase in reactive oxygen species (ROS) levels that can decrease nitric oxide (NO) availability and promote vasoconstriction, leading to arterial hypertension. Physical exercise (PE) has been found to be protective against CVD by helping to maintain redox homeostasis through a decrease in ROS levels, achieved by increased expression of antioxidant enzymes (AOEs) and modulation of heat shock proteins (HSPs). Extracellular vesicles (EVs) circulating in the body are a major source of regulatory signals, including proteins and nucleic acids. Interestingly, the cardioprotective role of EVs released after PE has not been fully described.The aim of this study was to investigate the role of circulating EVs, obtained through Size Exclusion Chromatography (SEC) of plasma samples from healthy young males (age: 26.95 ± 3.07; estimated maximum oxygen consumption rate (VO2max): 51.22 ± 4.85 (mL/kg/min)) at basal level (Pre_EVs) and immediately after a single bout of endurance exercise (30’ treadmill, 70% heart rate (HR) -Post_EVs). Gene ontology (GO) analysis of proteomic data from isolated EVs, revealed enrichment in proteins endowed with catalytic activity in Post_EVs, compare to Pre_EVs, with MAP2K1 being the most significantly upregulated protein. Enzymatic assays on EVs derived from Pre and Post samples showed increment in Glutathione Reductase (GR) and Catalase (CAT) activity in Post_EVs. At functional level, Post_EVs, but not Pre_EVs, enhanced the activity of antioxidant enzymes (AOEs) and reduced oxidative damage accumulation in treated human iPS-derived cardiomyocytes (hCM) at basal level and under stress conditions (Hydrogen Peroxide (H2O2) treatment), resulting in a global cardioprotective effect.In conclusion, our data demonstrated, for the first time, that a single 30-min endurance exercise is able to alter the cargo of circulating EVs, resulting in cardioprotective effect through antioxidant activity.

A single bout of endurance exercise decreases oxidative stress in young adults with overweight

This study aims to prove the effects of a single bout of endurance exercise on decreased oxidative stress in young adults with overweight. This study used the true experimental method with a pretest-posttest control group design. Twenty overweight women between the ages of 20 and 23 were recruited from college students and randomly divided into CON (n = 10, control group without exercise) and EEx (n = 10, endurance exercise group). The endurance exercise intervention is carried out once by running on a treadmill with an intensity of 60-70% HRmax for 40 minutes/exercise sessions. Malondialdehyde (MDA) levels as a biomarker of oxidative stress were measured 30 minutes pre-exercise and 24 hours post-exercise using the Thiobarbituric Acid Reactive Substance (TBARs) method. The results showed that MDA levels significantly decreased in the endurance training group compared to the control group. Results of analysis of MDA levels between pre-exercise and post-exercise in CON (819.00±66.47 vs. 853.00±113.55 ng/mL; (P > 0.05), EEx (810.00±120.19 vs. 596.00±67.57 ng/mL; (P < 0.05). Based on the results of this study, it was concluded that a single session of endurance exercise at an intensity of 60-70% HRmax for 40 minutes reduces oxidative stress in overweight adolescent females.

Effects of a Single Bout of Endurance Exercise on Brain-Derived Neurotrophic Factor in Humans: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

We aimed to investigate the impact of a single bout of endurance exercise on the brain-derived neurotrophic factor (BDNF) in humans and analyze how a single bout of endurance exercise impacts the peripheral BDNF types by age group. We performed a systematic literature review by searching PubMed, Elsevier, and Web of Science for studies that included a single bout of endurance exercise in the experimental group and other exercise types in the control group. Eight interventions were included in the study. Overall, a single bout of endurance exercise significantly increased BDNF expression (SMD = 0.30; 95% CI = [0.08, 0.52]; p = 0.001), which was confirmed in the serum BDNF (SMD = 0.30; 95% CI = [0.04, 0.55]; p < 0.001). A non-significant trend was observed in the plasma BDNF (SMD = 0.31; 95% CI = [-0.13, 0.76]; p = 0.017). The serum and plasma BDNF levels significantly increased regardless of age (SMD = 0.35; 95% CI = [0.11, 0.58]; p = 0.004; I2 = 0%). In conclusion, a single bout of endurance exercise significantly elevates BDNF levels in humans without neurological disorders, regardless of age. The serum BDNF is a more sensitive index than the plasma BDNF in evaluating the impact of a single bout of endurance exercise on the BDNF.

The effects of normoxic endurance exercise on erythropoietin (EPO) production and the impact of selective β1 and non-selective β1 + β2 adrenergic receptor blockade

Habitual endurance exercise results in increased erythropoiesis, which is primarily controlled by erythropoietin (EPO), yet studies demonstrating upregulation of EPO via a single bout of endurance exercise have been equivocal. This study compares the acute EPO response to 30min of high versus 90min of moderate-intensity endurance exercise and whether that response can be upregulated via selective adrenergic receptor blockade. Using a counterbalanced, cross-over design, fifteen participants (age 28 ± 8) completed two bouts of running (30-min, high intensity vs 90-min, moderate intensity) matched for overall training stress. A separate cohort of fourteen participants (age 31 ± 6) completed three bouts of 30-min high-intensity cycling after ingesting the preferential β1-adrenergic receptor (AR) antagonist bisoprolol, the non-preferential β1 + β2 antagonist nadolol or placebo. Venous blood was collected before, during, and after exercise, and serum EPO levels were determined by ELISA. No detectable EPO response was observed during or after high intensity running, however, in the moderate-intensity trial EPO was significantly elevated at both during-exercise timepoints (+ 6.8% ± 2.3% at 15min and + 8.7% ± 2.2% at 60min). No significant change in EPO was observed post-cycling or between the trials involving βAR blockade. Neither training mode (running or cycling), nor beta-blockade significantly influenced the EPO response to 30min of high-intensity exercise, however, 90min of moderate-intensity running elevated EPO during exercise, returning to baseline immediately post-exercise. Identifying the optimal mode, duration and intensity required to evoke an EPO response to exercise may help tailor exercise prescriptions designed to maximize EPO response for both performance and clinical applications.

Nicotinamide riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise.

Acute nicotinamide riboside (NR) supplementation does not alter substrate metabolism at rest, during or in recovery from endurance exercise. NR does not alter NAD+ -sensitive signalling pathways in human skeletal muscle. NR supplementation and acute exercise influence the NAD+ metabolome. Oral supplementation of the NAD+ precursor nicotinamide riboside (NR) has been reported to alter metabolism alongside increasing sirtuin (SIRT) signalling and mitochondrial biogenesis in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study assessed the effect of 7-day NR supplementation on whole-body metabolism and exercise-induced mitochondrial biogenic signalling in skeletal muscle. Eight male participants (age: 23±4years, 46.5±4.4mlkg-1 min-1 ) received 1week of NR or cellulose placebo (PLA) supplementation (1000mgday-1 ). Muscle biopsies were collected from the medial vastus lateralis prior to supplementation and pre-, immediately post- and 3h post-exercise (1h of 60% Wmax cycling) performed following the supplementation period. There was no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Global acetylation, auto-PARylation of poly ADP-ribose polymerase 1 (PARP1), acetylation of Tumour protein 53 (p53)Lys382 and Manganese superoxide dismutase (MnSOD)Lys122 were also unaffected by NR supplementation or exercise. NR supplementation did not increase skeletal muscle NAD+ concentration, but it did increase the concentration of deaminated NAD+ precursors nicotinic acid riboside (NAR) and nicotinic acid mononucleotide (NAM) and methylated nicotinamide breakdown products (Me2PY and Me4PY), demonstrating the skeletal muscle bioavailability of NR supplementation. In summary, 1week of NR supplementation does not alter whole-body metabolism or skeletal muscle signal transduction pathways implicated in the mitochondrial adaptation to endurance exercise.

Sex‐based differences after a single bout of exercise on PGC1α isoforms in skeletal muscle: A pilot study

To date, there are limited and incomplete data on possible sex-based differences in fiber-types of skeletal muscle and their response to physical exercise. Adult healthy male and female mice completed a single bout of endurance exercise to examine the sex-based differences of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), heat shock protein 60 (Hsp60), interleukin 6 (IL-6) expression, as well as the Myosin Heavy Chain (MHC) fiber-type distribution in soleus and extensor digitorum longus (EDL) muscles. Our results showed for the first time that in male soleus, a muscle rich of type IIa fibers, endurance exercise activates specifically genes involved in mitochondrial biogenesis such as PGC1 α1 isoform, Hsp60 and IL-6, whereas the expression of PGC1 α2 and α3 was significantly upregulated in EDL muscle, a fast-twitch skeletal muscle, independently from the gender. Moreover, we found that the acute response of different PGC1α isoforms was muscle and gender dependent. These findings add a new piece to the huge puzzle of muscle response to physical exercise. Given the importance of these genes in the physiological response of the muscle to exercise, we strongly believe that our data could support future research studies to personalize a specific and sex-based exercise training protocol.

Hepatic LC3 II/I ratio is not modulated in exercised mice

Autophagy plays an essential role in body homeostasis achievement. One of the main proteins involved in this process is the LC3I, which, after lipidation, leads to the formation of LC3II that participates in the formation and maturation of autophagosome. This descriptive study verified the responses of LC3II to LC3I proteins, as well as the time-course of this ratio in mice livers after different types of acute physical exercise protocols. Eight-week-old male C57BL/6 mice were maintained three per cage with controlled temperature (22±2 °C) on a 12:12-h light-dark normal cycle with food (Purina chow) and water ad libitum. Mice were randomly divided into four groups: control (CT, sedentary mice), resistance (RE, submitted to a single bout of resistance exercise), endurance (EE, submitted to a single bout of endurance exercise), and concurrent (CE, submitted to a single bout of endurance combined with resistance exercise). The mice livers were extracted and used for the immunoblotting technique. The hepatic LC3B II/I ratio for the RE and EE groups were not altered during the different time-points. For the CE group, there was a decrease in this ratio 12h after exercise compared to time 0 and 18h. Also, the hepatic LC3B II/I ratios were not different among the acute physical exercise protocols along the time-course. The hepatic LC3B II/I ratio was not influenced by the endurance and resistance protocols but decreased in response to the concurrent protocol at 12h after the stimulus.

Time-of-day dependent effects of contractile activity on the phase of the skeletal muscle clock.

Key points Disruptions in circadian rhythms across an organism are associated with negative health outcomes, such as cardiometabolic and neurodegenerative diseases.Exercise has been proposed as a time cue for the circadian clock in rodents and humans.In this study, we assessed the effect of a single bout of endurance exercise on the skeletal muscle clock in vivo and a bout of muscle contractions in vitro.Timing of exercise or contractions influences the directional response of the muscle clock phase in vivo and in vitro.Our findings demonstrate that muscle contractions, as a component of exercise, can directly modulate the expression of muscle clock components in a time‐of‐day dependent manner. Exercise has been proposed to be a zeitgeber for the muscle circadian clock mechanism. However, this is not well defined and it is unknown if exercise timing induces directional shifts of the muscle clock. Our purpose herein was to assess the effect of one bout of treadmill exercise on skeletal muscle clock phase changes. We subjected PERIOD2::LUCIFERASE mice (n = 30F) to one 60 min treadmill exercise bout at three times of day. Exercise at ZT5, 5 h after lights on, induced a phase advance (100.2 ± 25.8 min; P = 0.0002), whereas exercise at ZT11, 1 h before lights off, induced a phase delay (62.1 ± 21.1 min; P = 0.0003). Exercise at ZT17, middle of the dark phase, did not alter the muscle clock phase. Exercise induces diverse systemic changes so we developed an in vitro model system to examine the effects of contractile activity on muscle clock phase. Contractions applied at peak or trough Bmal1 expression induced significant phase delays (applied at peak: 27.2 ± 10.2 min; P = 0.0017; applied at trough: 64.6 ± 6.5 min, P < 0.0001). Contractions applied during the transition from peak to trough Bmal1 expression induced a phase advance (49.8 ± 23.1 min; P = 0.0051). Lastly, contractions at different times of day resulted in differential changes of core clock gene expression, demonstrating an exercise and clock interaction, providing insight into potential mechanisms of exercise‐induced phase shifts. These data demonstrate that muscle contractions, as part of exercise, are sufficient to shift the muscle circadian clock phase, likely through changes in core clock gene expression. Additionally, our findings that exercise induces directional muscle clock phase changes confirms that exercise is a bona fide environmental time cue for skeletal muscle.

Resting EEG Microstates and Autonomic Heart Rate Variability Do Not Return to Baseline One Hour After a Submaximal Exercise.

Recent findings suggest that an acute physical exercise modulates the temporal features of the EEG resting microstates, especially the microstate map C duration and relative time coverage. Microstate map C has been associated with the salience resting state network, which is mainly structured around the insula and cingulate, two brain nodes that mediate cardiovascular arousal and interoceptive awareness. Heart rate variability (HRV) is dependent on the autonomic balance; specifically, an increase in the sympathetic (or decrease in the parasympathetic) tone will decrease variability while a decrease in the sympathetic (or increase in the parasympathetic) tone will increase variability. Relying on the functional interaction between the autonomic cardiovascular activity and the salience network, this study aims to investigate the effect of exercise on the resting microstate and the possible interplay with this autonomic cardiovascular recovery after a single bout of endurance exercise. Thirty-eight young adults performed a 25-min constant-load cycling exercise at an intensity that was subjectively perceived as “hard.” The microstate temporal features and conventional time and frequency domain HRV parameters were obtained at rest for 5 min before exercise and at 5, 15, 30, 45, and 60 min after exercise. Compared to the baseline, all HRV parameters were changed 5 min after exercise cessation. The mean durations of microstate B and C, and the frequency of occurrence of microstate D were also changed immediately after exercise. A long-lasting effect was found for almost all HRV parameters and for the duration of microstate C during the hour following exercise, indicating an uncompleted recovery of the autonomic cardiovascular system and the resting microstate. The implication of an exercise-induced afferent neural traffic is discussed as a potential modulator of both the autonomic regulation of heart rate and the resting EEG microstate.

P-151 - A single bout of endurance exercise induces αB-crystallin (CRYAB) modulation in cardiac muscle as it happens in oxidative skeletal muscle fibers

CRYAB is a small Heat Shock Protein, expressed in various tissues such as skeletal and cardiac muscles, activated as phosphorylated CRYAB (pCRYAB) and involved in several pathophysiological processes. In mammals there are no reports to date on CRYAB activation following an acute endurance exercise, so the aim of my study was to explore in mouse cardiac tissue the pCRYAB levels as effect of this exercise at 0’, 15’ and 120’ of recovery. H2O2 - treated HL-1 cardiomyocytes have been utilized as in vitro model to identify the underlying molecular mechanism/s. Both in vivo and in vitro models showed no changes in CRYAB protein expression level but its phosphorylation state was significantly increased at short time, paralleled by oxidative stress markers’ modulation (i.e. 4-HNE), indicating a correlation between CRYAB activation and redox perturbation. Our previous results in skeletal muscles where exercise modulated CRYAB only in oxidative fiber types supported these data. All together these results suggest a role for CRYAB in the defense system against ROS production. Further experiments are in progress to study the possible interactors, the cellular localization and the eventual release of CRYAB in extracellular vesicles as a mean for a cross talk between tissues

NADPH Oxidase and Xanthine Oxidase Inhibition Attenuates the Activation of AMPK Signaling After a Single Bout of Endurance Exercise in Mouse Skeletal Muscle

NADPH Oxidase and Xanthine Oxidase Inhibition Attenuates the Activation of AMPK Signaling After a Single Bout of Endurance Exercise in Mouse Skeletal Muscle

Effects of age and sex on epigenetic modification induced by an acute physical exercise.

It has been observed that, after 2 hours of aerobic exercise, plasma interleukin-6 (IL-6) increases whereas nuclear concentrations of enzyme DNA methyltransferase (DNMT) 3B significantly decreased in peripheral blood mononuclear cells (PBMCs), with no change observed in DNMT3A. The aim of the present study was to detect differences in these changes induced by exercise in plasma IL-6 levels as well as in PBMC nuclear concentrations of DNMT3A and DNMT3B, in relation to age and sex. Four groups were studied: 12 young men (24.8 ± 1.77 years old), 12 young women (23.8 ± 1.81 years old), 12 adult men (45.8 ± 1.82 years old), 12 adult women (mean 44.5 ± 2.07 years old). Participants had to run at 60% of maximal oxygen consumption (VO2max) for 120 minutes, interspersed with sprints at 90% of VO2max for the last 30 seconds of every 10 minutes. About 250 μL of PBMCs (1 × 106 cells) were treated with 100 μL of either pre-exercise plasma or post-exercise plasma and nuclear DNMT3A and DNMT3B concentrations were quantified. No change in nuclear concentration of DNMT3A following the exercise was observed. Conversely, nuclear concentrations of DNMT3B significantly decreased, with a reduction of about 78% in young men, 72% in young women, 61% in adult men, and 53% in adult women. Moreover, a strong positive correlation between the nuclear concentration of DNMT3B in PBMC following stimulation with post-exercise plasma and post-exercise plasma concentrations of IL-6 was observed in all the 4 studied groups. This study confirms that a single bout of endurance exercise is sufficient to decrease nuclear concentrations of DNMT3B and thus protein upregulation. Moreover, the epigenetic mechanisms induced by exercise apparently cause more intense changes in men than in women and that, in both of them, this effect seems to decrease with age.

Autophagy regulation in human skeletal muscle during exercise.

Autophagy regulation in human skeletal muscle during exercise.

More than mitochondrial biogenesis: alternative roles of PGC-1α in exercise adaptation.

More than mitochondrial biogenesis: alternative roles of PGC-1α in exercise adaptation.

Control of GLUT4 biogenesis through PPARδ and MEF2 axis with single bout of endurance exercise in rodent skeletal muscle

Control of GLUT4 biogenesis through PPARδ and MEF2 axis with single bout of endurance exercise in rodent skeletal muscle

FoxO transcription factors and endurance training: a role for FoxO1 and FoxO3 in exercise-induced angiogenesis.

FoxO transcription factors and endurance training: a role for FoxO1 and FoxO3 in exercise-induced angiogenesis.

Autophagy is essential to support skeletal muscle plasticity in response to endurance exercise.

Physical exercise is a stress that can substantially modulate cellular signaling mechanisms to promote morphological and metabolic adaptations. Skeletal muscle protein and organelle turnover is dependent on two major cellular pathways: Forkhead box class O proteins (FOXO) transcription factors that regulate two main proteolytic systems, the ubiquitin-proteasome, and the autophagy-lysosome systems, including mitochondrial autophagy, and the MTORC1 signaling associated with protein translation and autophagy inhibition. In recent years, it has been well documented that both acute and chronic endurance exercise can affect the autophagy pathway. Importantly, substantial efforts have been made to better understand discrepancies in the literature on its modulation during exercise. A single bout of endurance exercise increases autophagic flux when the duration is long enough, and this response is dependent on nutritional status, since autophagic flux markers and mRNA coding for actors involved in mitophagy are more abundant in the fasted state. In contrast, strength and resistance exercises preferentially raise ubiquitin-proteasome system activity and involve several protein synthesis factors, such as the recently characterized DAGK for mechanistic target of rapamycin activation. In this review, we discuss recent progress on the impact of acute and chronic exercise on cell component turnover systems, with particular focus on autophagy, which until now has been relatively overlooked in skeletal muscle. We especially highlight the most recent studies on the factors that can impact its modulation, including the mode of exercise and the nutritional status, and also discuss the current limitations in the literature to encourage further works on this topic.

Regulation of ubiquitin proteasome pathway molecular markers in response to endurance and resistance exercise and training.

Knowledge on the effects of divergent exercise on ostensibly protein degradation pathways may be valuable for counteracting muscle wasting and for understanding muscle remodelling. This study examined mRNA and/or protein levels of molecular markers of the ubiquitin proteasome pathway (UPP), including FBXO32 (atrogin-1), MURF-1, FBXO40, FOXO1 and FOXO3. Protein substrates of atrogin-1-including EIF3F, MYOG and MYOD1-and of MURF-1-including PKM and MHC-were also measured. Subjects completed 10 weeks of endurance training (ET) or resistance training (RT) followed by a single-bout of endurance exercise (EE) or resistance exercise (RE). Following training, atrogin-1, FBXO40, FOXO1 and FOXO3 mRNA increased independently of exercise mode, whereas MURF-1 mRNA and FOXO3 protein increased following ET only. No change in other target proteins occurred post-training. In the trained state, single-bout EE, but not RE, increased atrogin-1, MURF-1, FBXO40, FOXO1, FOXO3 mRNA and FOXO3 protein. In contrast to EE, FBXO40 mRNA and protein decreased following single-bout RE. MURF-1 and FOXO1 protein levels as well as the protein substrates of atrogin-1 and MURF-1 were unchanged following training and single-bout exercise. This study demonstrates that the intracellular signals elicited by ET and RT result in an upregulation of UPP molecular markers, with a greater increase following ET. However, in the trained state, the expression levels of UPP molecular markers are increased following single-bout EE, but are less responsive to single-bout RE. This suggests that adaptations following endurance exercise training are more reliant on protein UPP degradation processes than adaptations following resistance exercise training.

Increased Stearoyl-CoA Desaturase Index and Triglyceride Content in the Liver of Rats after a Single Bout of Swimming Exercise

Up-regulation of stearoyl-CoA desaturase (SCD) is closely related to improved insulin resistance. We investigated whether the SCD indices in tissues were influenced by a single-endurance exercise and low content of dietary medium-chain fatty acid (FA). Wistar rats were fed a long-chain (S) or medium- and long-chain FA (M) diet for 2 weeks. At the end of the experiment, the rats were further assigned to two sub-groups (sedentary, Sed; exercise, Ex). These groups were defined as S-Sed, S-Ex, M-Sed, and M-Ex. The rats in the exercise groups were subjected to swimming exercise for 4 h, and tissue samples were obtained. The exercise significantly increased the triglyceride (TG) content and SCD index only in the liver. In contrast, no such changes were apparent by intake of the M diet. A single bout of endurance exercise increased the hepatic TG content and SCD index which might be effective in protecting against insulin resistance.

Preferential utilization of perilipin 2‐associated intramuscular triglycerides during 1 h of moderate‐intensity endurance‐type exercise

The lipid droplet (LD)-associated protein perilipin 2 (PLIN2) appears to colocalize with LDs in human skeletal muscle fibres, although the function of PLIN2 in the regulation of intramuscular triglyceride (IMTG) metabolism is currently unknown. Here we investigated the hypothesis that the presence of PLIN2 in skeletal muscle LDs is related to IMTG utilisation during exercise. We therefore measured exercise-induced changes in IMTG and PLIN2 distribution and changes in their colocalization. Muscle biopsies from the vastus lateralis were obtained from seven lean, untrained men (22 ± 2 years old, body mass index 24.2 ± 0.9 kg m(-2) and peak oxygen uptake 3.35 ± 0.13 l min(-1)) before and after 1 h of moderate-intensity cycling at ~65% peak oxygen uptake. Cryosections were stained for perilipin 2, IMTG and myosin heavy chain type I and viewed using wide-field and confocal fluorescence microscopy. Exercise induced a 50 ± 7% decrease in IMTG content in type I fibres only (P < 0.05), but no change in PLIN2 content. Colocalization analysis showed that the fraction of PLIN2 associated with IMTG was 0.67 ± 0.03 before exercise, which was reduced to 0.51 ± 0.01 postexercise (P < 0.05). Further analysis revealed that the number of PLIN2-associated LDs was reduced by 31 ± 10% after exercise (P < 0.05), whereas the number of PLIN2-null LDs was unchanged. No such changes were seen in type II fibres. In conclusion, this study shows that PLIN2 content in skeletal muscle is unchanged in response to a single bout of endurance exercise. Furthermore, the PLIN2 and IMTG association is reduced postexercise, apparently due to preferential utilization of PLIN2-associated LDs. These results confirm the hypothesis that the PLIN2 association with IMTG is related to the utilization of IMTG as a fuel during exercise.