Exercise-induced central and peripheral sympathetic activity in a community-based group of epilepsy patients differ from healthy controls.

Ictal and interictal activity within the autonomic nervous system is characterized by a sympathetic overshoot in people with epilepsy. This autonomic dysfunction is assumed to be driven by alterations in the central autonomic network. In this study, exercise-induced changes of the interrelation of central and peripheral autonomic activity in patients with epilepsy was assessed. 21 patients with epilepsy (16 seizure-free), and 21 healthy matched controls performed an exhaustive bicycle ergometer test. Immediately before and after the exercise test, resting state electroencephalography measurements (Brain Products GmbH, 128-channel actiCHamp) of 5 min were carried out to investigate functional connectivity assessed by phase locking value in source space for whole brain, central autonomic network and visual network. Additionally, 1-lead ECG (Brain products GmbH) was performed to analyze parasympathetic (root mean square of successive differences (RMSSD) of the heart rate variability) and sympathetic activity (electrodermal activity (meanEDA)). MeanEDA increased (p < 0.001) and RMSSD decreased (p < 0.001) from pre to post-exercise in both groups. Correlation coefficients of meanEDA and central autonomic network functional connectivity differed significantly between the groups (p = 0.004) after exercise. Both patients with epilepsy and normal control subjects revealed the expected physiological peripheral autonomic responses to acute exhaustive exercise, but alterations of the correlation between central autonomic and peripheral sympathetic activity may indicate a different sympathetic reactivity after exercise in patients with epilepsy. The clinical relevance of this finding and its modulators (seizures, anti-seizure medication, etc.) still needs to be elucidated.

The Contrasting Effects of Two Distinct Exercise Training Modalities on Exhaustive Exercise-Induced Muscle Damage in Mice May Be Associated with Alterations in the Gut Microbiota.

Exhaustive exercise is known to induce muscle damage characterized by inflammation and oxidative stress. Although "regular" and "weekend warrior" exercise regimens have been shown to confer comparable health benefits in human studies, such as reduced risks of all-cause, cardiovascular disease (CVD), and cancer mortality, their differential impacts on muscle damage post-exhaustive exercise remain unclear. This study aimed to compare the effects of long-term, moderate-intensity (LTMI) and short-term, high-intensity (STHI) training modalities, matched for total exercise volume, on gut microbiota, short-chain fatty acids (SCFAs), and exhaustive exercise-induced muscle damage in mice, as well as to evaluate the correlation between these factors. LTMI is considered a regular exercise regimen, while STHI shares some similarities with the "weekend warrior" pattern, such as promoting exercise intensity and condensing training sessions into a short period. Our findings indicate that LTMI training significantly enhanced the abundance of SCFA-producing bacteria, including Akkermansia, Prevotellaceae_NK3B31_group, Odoribacter, Alistipes, and Lactobacillus, thereby increasing SCFA levels and attenuating muscle damage following exhaustive swimming. In contrast, STHI training increased the abundance of opportunistic pathogens such as Staphylococcus and Bilophila, without altering SCFA levels, and was associated with exacerbated muscle damage. Moreover, we observed a significant negative correlation between the abundance of SCFA-producing bacteria and SCFA levels with the expression of inflammatory cytokines in the muscle of mice post-exhaustive exercise. Conversely, the abundance of Staphylococcus and Bilophila showed a notable positive correlation with these cytokines. Additionally, the effects of LTMI and STHI on exhaustive exercise-induced muscle damage were transmissible to untrained mice via fecal microbiota transplantation, suggesting that gut microbiota changes induced by these training modalities may contribute to their contrasting impacts on muscle damage. These results underscore the significance of selecting an appropriate training modality prior to engaging in exhaustive exercise, with implications for athletic training and injury prevention.

Effects of 3-(4-Hydroxy-3-methoxyphenyl)propionic Acid on Enhancing Grip Strength and Inhibiting Protein Catabolism Induced by Exhaustive Exercise.

3-(4-Hydroxy-3-methoxyphenyl)propionic acid (HMPA), also known as dihydroferulic acid, is a hydroxycinnamic acid derivative that can be derived from the microbial transformation of dietary polyphenols or naturally obtained from fermented foods. Although numerous studies have documented its antioxidant and anti-obesity effects, the effect of HMPA on muscle function remains unknown. This study investigated the effects of HMPA on muscle strength and exercise endurance capacity. Mice were orally administered low and high doses of HMPA for 14 days and subjected to grip force and treadmill exhaustion tests to evaluate muscle function. Our results showed that HMPA-administered groups significantly enhanced absolute grip strength (p = 0.0256) and relative grip strength (p = 0.0209), and low-dose HMPA decreased the plasma level of blood urea nitrogen after exercise (p = 0.0183), but HMPA did not affect endurance performance. Low-dose HMPA administration increased Myf5 expression in sedentary mice (p = 0.0106), suggesting that low-dose HMPA may promote muscle development. Additionally, HMPA improved hepatic glucose and lipid metabolism, and inhibited muscular lipid metabolism and protein catabolism, as indicated by changes in mRNA expression levels of related genes. These findings suggest that HMPA may be a promising dietary supplement for muscle health and performance.

Experimental hyperoxia (O2 supersaturation) reveals a gill diffusion limitation of maximum aerobic performance in fish.

Several studies have demonstrated that hyperoxia increases the maximal O2 consumption rate (MO2max) in fish, but exactly how this occurs remains to be explained. Here, we tested the hypothesis that hyperoxia improves arterial oxygenation in rainbow trout during exhaustive exercise. We demonstrate a 35% higher MO2max in hyperoxia (200% air saturation) relative to normoxia, which was achieved through a combined 15% increase in cardiac output due to elevated peak heart rate, and a 19% increase of the arterial-venous (A-V) O2 content difference. While arterial O2 partial pressure (PaO2) and O2 saturation of haemoglobin declined post-exhaustive exercise in normoxia, this did not occur in hyperoxia. This protective effect of hyperoxia on arterial oxygenation led to a 22% higher arterial O2 content post-exhaustive exercise, thereby allowing a higher A-V O2 content difference. These findings indicate that MO2max is gill diffusion limited in exhaustively exercised rainbow trout. Moreover, as previous studies in salmonids have demonstrated collapsing PaO2 in normoxia at maximal swimming speed and at acutely high temperatures, a diffusion limitation may constrain MO2 in other situations eliciting peak metabolic demand. These findings, along with the fact that hyperoxia increases MO2max in several other fishes, suggest that gill diffusion limitations of MO2max may be widespread in fishes.

Neuromuscular fatigability during repeated sprints assessed with an innovative cycle ergometer.

PURPOSE: Repeated sprint ability is an integral component of team sports. This study aimed to evaluate fatigability development and its aetiology during and immediately after a cycle repeated sprint exercise performed until a given fatigability threshold. METHODS: On an innovative cycle ergometer, 16 healthy males completed an RSE (10-s sprint/28-s recovery) until task failure (TF): a 30% decrease in sprint mean power (Pmean). Isometric maximum voluntary contraction of the quadriceps (IMVC), central alterations [voluntary activation (VA)], and peripheral alterations [twitch (Pt)] were evaluated before (pre), immediately after each sprint (post), at TF and 3 min after. Sprints were expressed as a percentage of the total number of sprints to TF (TSTF). Individual data were extrapolated at 20, 40, 60, and 80% TSTF. RESULTS: Participants completed 9.7 ± 4.2 sprints before reaching a 30% decrease in Pmean. Post-sprint IMVCs were decreased from pre to 60% TSTF and then plateaued (pre: 345 ± 56 N, 60% 247 ± 55 N, TF: 233 ± 57 N, p < 0.001). Pt decreased from 20% and plateaued after 40% TSTF (p < 0.001, pre-TF = - 45 ± 13%). VA was not significantly affected by repeated sprints until 60% TSTF (pre-TF = - 6.5 ± 8.2%, p = 0.036). Unlike peripheral parameters, VA recovered within 3 min (p = 0.042). CONCLUSION: During an RSE, Pmean and IMVC decreases were first concomitant to peripheral alterations up to 40% TSTF and central alterations was only observed in the second part of the test, while peripheral alterations plateaued. The distinct recovery kinetics in central versus peripheral components of fatigability further confirm the necessity to reduce traditional delays in neuromuscular fatigue assessment post-exercise.

Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats.

The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.

Normoxic limitation of maximal oxygen consumption rate, aerobic scope and cardiac performance in exhaustively exercised rainbow trout (Oncorhynchus mykiss).

In fish, maximum O2 consumption rate (MO2,max) and aerobic scope can be expanded following exhaustive exercise in hyperoxia; however, the mechanisms explaining this are yet to be identified. Here, in exhaustively exercised rainbow trout (Oncorhynchus mykiss), we assessed the influence of hyperoxia on MO2,max, aerobic scope, cardiac function and blood parameters to address this knowledge gap. Relative to normoxia, MO2,max was 33% higher under hyperoxia, and this drove a similar increase in aerobic scope. Cardiac output was significantly elevated under hyperoxia at MO2,max because of increased stroke volume, indicating that hyperoxia released a constraint on cardiac contractility apparent with normoxia. Thus, hyperoxia improved maximal cardiac performance, thereby enhancing tissue O2 delivery and allowing a higher MO2,max. Venous blood O2 partial pressure (PvO2) was elevated in hyperoxia at MO2,max, suggesting a contribution of improved luminal O2 supply in enhanced cardiac contractility. Additionally, despite reduced haemoglobin and higher PvO2, hyperoxia treated fish retained a higher arterio-venous O2 content difference at MO2,max. This may have been possible because of hyperoxia offsetting declines in arterial oxygenation that are known to occur following exhaustive exercise in normoxia. If this occurs, increased contractility at MO2,max with hyperoxia may also relate to an improved O2 supply to the compact myocardium via the coronary artery. Our findings show MO2,max and aerobic scope may be limited in normoxia following exhaustive exercise as a result of constrained maximal cardiac performance and highlight the need to further examine whether or not exhaustive exercise protocols are suitable for eliciting MO2,max and estimating aerobic scope in rainbow trout.

Paraoxonase and oxidative stress changes in left and right ventricles of exhaustively exercised rats.

Exhaustive exercise can cause subclinical inflammation to the heart, as it is an oxidative tissue that works continuously. The effect of exhaustive exercise on left and right ventricles (LVs, RVs) may be different. It is claimed that paraoxonase-1 (PON1), an antioxidant enzyme, has a cardioprotective effect on oxidative stress. Rats were separated as non-exercised controls (Con), those euthanized immediately after (E-0) and 24 h after exhaustive exercise (E-24). Cardiac troponin-I (cTnI), total antioxidant status (TAS), total oxidant status (TOS), PON1 activities, and histological findings in LV and RV of the exhausted rats were evaluated. TAS and PON1 levels were lower in LVs compared with RVs of all groups. TOS levels were high in LVs compared with RVs of all groups. In LVs, TAS levels decreased significantly in the E-0 group while PON1 activity decreased in E-0 and E-24 groups compared with controls. In LVs, TOS levels decreased significantly in E-0 and E-24 groups, but in RVs a decrease was seen only in the E-0 group. cTnI levels increased significantly in the E-0 group and decreased to control levels in the E-24 group. Considering the histological and biochemical findings, exhaustive exercise affected the heart to the maximum during and just after exhaustion, and LV was influenced more than RV.

Study on the time-effectiveness of exercise preconditioning on heart protection in exhausted rats.

To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague-Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.

The effect of prolonged intense physical exercise of special forces volunteers on their plasma protein denaturation profile examined by differential scanning calorimetry.

The human blood plasma proteome profile has been an area of intensive investigation and differential scanning calorimetry (DSC) has come forward as a novel tool in analyzing plasma heat capacity changes to monitor various physiological responses in health and disease. This study used DSC to assess potential alterations in the plasma heat capacity profile of albumin and globulins during extremely demanding physical exercise. We monitored the changes in denaturation profiles of those plasma proteins for five consecutive days of an extraordinary exercise training schedule in 14 young male Special Forces volunteers, as well as after a 30-day recovery period. The major effect of the prolonged intense exercise was the continuous upward shift of the albumin peak by 2°-3 °C on the initial days of exercise, with a tendency to plateau circa the 5th day of exercise. In addition, some redistribution of the denaturational enthalpy was observed upon exercise, where the globulins peak increased relative to the albumin peak. Noteworthy, the alterations in the plasma proteome denaturational profiles were not persistent, as virtually full recovery of the initial status was observed after 30 days of recovery. Our findings indicate that 5 days of exhaustive physical exercise of highly trained individuals enhanced the thermal stability of plasma albumin shifting its denaturational transition to higher temperatures. We surmise that these effects may be a result of increased blood oxygenation during the prolonged intense exercise and, consequently, of albumin oxidation as part of the overall adaptation mechanisms of the body to extreme physical and/or oxidative stress.

Exercise Preconditioning Increases Beclin1 and Induces Autophagy to Promote Early Myocardial Protection via Intermittent Myocardial Ischemia-Hypoxia.

Exercise preconditioning (EP) provides protective effects for acute cardiovascular stress; however, its mechanisms need to be further investigated. Autophagy is a degradation pathway essential for myocardium health. Therefore, we investigated whether intermittent myocardial ischemia-hypoxia affected Beclin1 and whether the changes in autophagy levels contribute to EP-induced early myocardial protective effects. Rats were trained on a treadmill using an EP model (four cycles of 10 minutes of running/10 minutes of rest). Exhaustive exercise (EE) was performed to induce myocardial injury. Cardiac troponin I (cTnI) and ischemia-hypoxia staining were used to evaluate myocardial injury and protection. Double-labeled immunofluorescence staining and western blot analysis were employed to examine related markers. EP attenuated the myocardial ischemic-hypoxic injury induced by EE. Compared with the control (C) group, the dissociations of Beclin1/Bcl-2 ratio and Beclin1 expression were both higher in all other groups. Compared with the C group, PI3KC3 and the LC3-II/LC3-I ratio were higher in all other groups, whereas LC3-II was higher in the EE and EEP + EE groups. p62 was higher in the EE group than in the C group but lower in the EEP + EE group than in the EE group. We concluded that EP increases Beclin1 via intermittent myocardial ischemia-hypoxia and induces autophagy, which exerts early myocardial protective effects and reduces the myocardial ischemic-hypoxic injury induced by exhaustive exercise.

Effect of Genistein Supplementation on Exercise-Induced Inflammation and Oxidative Stress in Mice Liver and Skeletal Muscle.

Background and objectives: The purpose of this study was to investigate the influences of oral high-dose genistein (GE) administration on exercise-induced oxidative stress, inflammatory response and tissue damage. Materials and Methods: Thirty-two mice were randomly divided into control group (Con; sedentary/0.5% CMC-Na), GE administrated group (GE; sedentary/GE dosed), exercise group (Ex; exercise/0.5% CMC-Na), or GE administrated plus exercise group (GE + Ex; exercise/GE dosed), mice in the GE and GE + Ex group were given GE orally at the dose of 200 mg/kg weight. Results: Plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, liver interleukin (IL)-6, IL-1ß, superoxide dismutase 1 (SOD1), catalase (CAT), hemeoxygenase-1 (HO-1) gene expression levels and skeletal muscle IL-6, nuclear factor erythroid 2-related factor (Nrf2), and HO-1 gene expression levels increased immediately after exhaustive exercise. GE supplementation increased liver protein carbonyl concentrations. On the other hand, GE supplementation significantly decreased SOD1, CAT gene expression levels in the liver and Nrf2, and HO-1 gene expression levels in the skeletal muscles. Conclusions: Acute exercise induced organ damage, inflammation, and oxidative stress in skeletal muscles and the liver. However, a single dose of GE supplementation before exercise did not lead to favorable antioxidant and anti-inflammatory effects in this study.

TIGAR regulates mitochondrial functions through SIRT1-PGC1α pathway and translocation of TIGAR into mitochondria in skeletal muscle.

TP53-induced glycolysis and apoptosis regulator (TIGAR), a glycolytic inhibitor, plays vital roles in regulating cellular metabolism and oxidative stress. However, the role of highly expressed TIGAR in skeletal muscle remains unexplored. In the present study, TIGAR levels varied in different skeletal muscles and fibers. An exhaustive swimming test with a load corresponding to 5% of body weight was utilized in mice to assess the effects of TIGAR on exercise-induced fatigue and muscle damage. The running time and metabolic indicators were significantly greater in wild-type (WT) mice compared with TIGAR knockout (KO) mice. Poor exercise capacity was accompanied by decreased type IIA fibers in TIGAR KO mice. Decreased mitochondrial number and mitochondrial oxidative phosphorylation were observed more in TIGAR KO mice than in WT mice, which were involved in sirtuin 1 (SIRT1)-mediated deacetylation of peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α), and resveratrol treatment in TIGAR KO mice can increase mitochondrial content and exercise time. Much more TIGAR was also detected in mitochondria during exhaustive exercise. In addition, TIGAR, rather than mitochondria-targeted TIGAR achieved by in vitro plasmid transfection, promoted SIRT1-PGC1α pathway. Glutathione S-transferase-TIGAR pull-down assay followed by liquid chromatography mass spectrometry found that TIGAR interacted with ATP synthase F1 subunit α (ATP5A1), and its binding to ATP5A1 increased during exhaustive exercise. Overexpression of mitochondrial-TIGAR enhanced ATP generation, maintained mitochondrial membrane potential and reduced mitochondrial oxidative stress under hypoxia condition. Taken together, our results uncovered a novel role for TIGAR in mitochondrial regulation in fast-twitch oxidative skeletal muscle through SIRT1-PGC1α and translocation into mitochondria, which contribute to the increase in exercise endurance of mice.-Geng, J., Wei, M., Yuan, X., Liu, Z., Wang, X., Zhang, D., Luo, L., Wu, J., Guo, W., Qin, Z.-H. TIGAR regulates mitochondrial functions through SIRT1-PGC1α pathway and translocation of TIGAR into mitochondria in skeletal muscle.

Interactive effects of osmotic stress and burrowing activity on protein metabolism and muscle capacity in the soft shell clam Mya arenaria.

Bioturbators such as sediment-dwelling marine bivalves are ecosystem engineers that enhance sediment-water exchange and benthic-pelagic coupling. In shallow coastal areas, bivalves are exposed to frequent disturbance and salinity stress that might negatively affect their activity and physiological performance; however, the mechanisms underlying these effects are not fully understood. We investigated the effects of osmotic stress (low and fluctuating salinity) and repeated burrowing on aerobic and contractile capacity of the foot muscle (assessed by the activity of succinate dehydrogenase and myosin ATPase) as well as the levels of organic osmolytes (free amino acids) and biochemical markers of protein synthesis and proteolysis in key osmoregulatory and energy storing tissues (gills and hepatopancreas, respectively) in a common bioturbator, the soft shell clam Mya arenaria. Osmotic stress and exhaustive exercise altered the foot muscle capacity of soft shell clams and had a strong impact on protein and amino acid homeostasis in tissues not directly involved in locomotion. Acclimation to constant low salinity (5 practical salinity units) depleted the whole-body free amino acid pool and affected protein synthesis but not protein breakdown in the gill. In contrast, fluctuating (5-15) salinity increased protein breakdown rate, suppressed protein synthesis, caused oxidative damage to proteins in the gill and selectively depleted whole-body glycine pool. Clams acclimated to normal salinity (15) increased the aerobic capacity of the foot muscle upon repeated burrowing, whereas acclimation to low and fluctuating salinity reduced this adaptive muscle plasticity. Under the normal and low salinity conditions, exhaustive exercise induced protein conservation pathways (indicated by suppression of protein synthesis and catabolism), but this effect was disrupted by fluctuating salinity. These findings indicate that exhaustive exercise and osmotic stress interactively affect whole-body protein homeostasis and functional capacity of the foot muscle in soft shell clams which might contribute to reduced burrowing activity of bivalve bioturbators in osmotically challenging environments such as estuaries and shallow coastal zones.

Changes in Autophagy Levels in Rat Myocardium During Exercise Preconditioning-Initiated Cardioprotective Effects.

The role of autophagy in the cardioprotection conferred by ischemic preconditioning (IPC) has been well described. This study aimed to investigate the changes in autophagy levels during the cardioprotective effects initiated by exercise preconditioning (EP).Rats were randomly divided into 4 groups: group C (control), group EP, group EE (exhaustive exercise), and group EP + EE (EP pretreatment at 0.5 hours before EE). The EP protocol included 4 periods of 10 minutes of treadmill running each at 30 m/minute with intervening 10 minute periods of rest. Hematoxylin-basic fuchsin-picric acid (HBFP) staining and plasma levels of cardiac troponin I (cTnI) were used to evaluate the ischemia-hypoxia injury in rat myocardium. Alteration levels in several autophagy proteins in the left ventricular myocardium were analyzed by Western blot. The phasic alterations of autophagy levels during EP-initiated cardioprotective phase were also examined.Compared with group C, the ischemia-hypoxia positive areas and IOD value in HBFP-staining and cTnI plasma levels increased significantly in group EE. Compared with group EE, the ischemia-hypoxia injury was markedly attenuated in group EP + EE. Compared with group C, the LC3-II/LC3-I ratio, a marker of autophagosome formation, was reduced in group EE, but the LC3-II/LC3-I ratio remained unaltered in group EP + EE. Furthermore, the LC3-II/LC3-I ratio increased significantly at 2 hours during the cardioprotective phase after EP.These results suggest that the activated autophagy level during the EP-initiated cardioprotective phase may be partly involved in the cardioprotective effects by maintaining a normal autophagy basal level during the subsequent exhaustive exercise in rat myocardium.

The Effect of Exhaustive Exercise on Plasma Metabolic Profiles of Male and Female Rats.

The objective of the study was to evaluate the alteration in biochemical composition and gender difference within exhaustive exercise in male and female rats using a metabolomics strategy. Sixty male and female rats were randomly assigned to control, exhaustive exercise and one-week recovery groups, respectively. The metabolic profiles of plasma were investigated by gas chromatograph-mass spectrometry (GC-MS) and data further underwent orthogonal partial least-squares (OPLS) analysis. The current study found that gender was a significant determinant of the effects of exhaustive exercise on the cortisol, blood urea nitrogen, creatine kinase, and the ratio of reduced glutathione to oxidized glutathione, whereas, no significant interaction effects between gender and exhaustive exercise were found on the levels of testosterone, malonaldehyde, reduced glutathione, oxidized glutathione and lactic dehydrogenase. In male rats, the altered metabolites within exhaustive exercise included increased tricarboxylic acid cycle intermediates (citric acid, fumaric acid, butanedioic acid), branch-chain amino acids (valine, leucine), fatty acids and metabolite (oleic acid, linoleic acid, 3-hydroxybutyric acid), phosphate and decreased glucose, lactic acid, serine, and glutamic acid. In female rats, the levels of fatty acids and metabolite (linoleic acid, oleic acid, arachidonic acid, 3-hydroxybutyric acid), amino acids (valine, leucine, glutamic acid, 5-oxo-proline, methionine, ornithine), other metabolites urea, myo-inositol and phosphate were increased. The results indicated that exhaustive exercise increased the rates of energy metabolism, glucose metabolism, amino acid catabolism and fatty acid metabolism in male rats, whereas, female rats showed an increased propensity to oxidize lipid and conserve carbohydrate and protein metabolism against physical stress. Disordered urea cycle and inositol metabolism also occurred in female rats with exhaustive exercise. Exhaustive exercise affected the balance of hormone adjustment and caused oxidative stress, subsequent cell membrane damage both in male and female rats. A significant gender-related difference in the metabolic profiles was also found between male and female rats within exhaustive exercise.

Exhaustive-exercise-induced oxidative stress alteration of erythrocyte oxygen release capacity.

The aim of the present study was to explore the effect of exhaustive running exercise in the oxygen release capacity of rat erythrocytes. Rats were divided into sedentary control, moderate running exercise, and exhaustive running exercise groups. The thermodynamic and kinetic properties of the erythrocyte oxygen release process of the different groups were tested. We also determined the degree of band-3 oxidation and phosphorylation, anion transport activity, and carbonic anhydrase isoform II activity. Biochemical studies suggested that exhaustive running significantly increased oxidative injury parameters in thiobarbituric acid reactive substances and methaemoglobin levels. Furthermore, exhaustive running significantly decreased anion transport activity and carbonic anhydrase isoform II activity. Thermodynamic analysis indicated that erythrocytes oxygen release ability also significantly increased due to elevated 2,3-DPG level after exhaustive running. Kinetic analysis indicated that exhaustive running resulted in significantly decreased T50 value. We presented evidence that exhaustive running remarkably impacted thermodynamic and kinetic properties of RBC oxygen release. In addition, changes in 2,3-DPG levels and band-3 oxidation and phosphorylation could be the driving force for exhaustive-running-induced alterations in erythrocyte oxygen release thermodynamic and kinetic properties.

Omega-3 polyunsaturated fatty acid docosahexaenoic acid and its role in exhaustive-exercise-induced changes in female rat ovulatory cycle.

Exhaustive exercises can cause delayed menarche or menstrual cycle irregularities in females. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) are incorporated into a wide range of benefits in many physiological systems. Our work aimed to assess the role of ω-3 PUFA docosahexaenoic acid (DHA) on the deleterious effects of exhaustive exercise on the female reproductive system in rats. Virgin female rats were randomly divided into 4 groups (12 rats in each): control group, omega-3 group treated with DHA, exhaustive exercise group, and exhaustive exercised rats treated with DHA. Omega-3 was given orally to the rats once daily for 4 estrous cycles. Exhaustive exercises revealed lower levels in progesterone and gonadotropins together with histopathological decrease in number of growing follicles and corpora lutea. Moreover, the exercised rats showed low levels of ovarian antioxidants with high level of caspase-3 and plasma cortisol level that lead to disruption of hypothalamic-pituitary-gonadal axis. ω-3 PUFA DHA has beneficial effects on the number of newly growing follicles in both sedentary and exercised rats with decreasing the level of caspase-3 and increasing the antioxidant activity in ovaries. Exhaustive exercises can cause ovulatory problems in female rats that can be improved by ω-3 supplementation.

Alterations of Cardiac KATP Channels and Autophagy Contribute in the Late Cardioprotective Phase of Exercise Preconditioning.

The cardiac effects of exercise preconditioning (EP) are well established; however, the mechanisms involving cardiac ATP-sensitive potassium channel (KATP channel) subunits and autophagy are yet to be fully established. The present work aims to investigate the alterations of cardiac KATP channel subunits Kir6.2, SUR2A, and autophagy-related LC3 during the late cardioprotective phase of EP against exhaustive exercise-induced myocardial injury. Rats run on treadmill for four running time intervals, each with 10 minutes running and rest. Exhaustive exercise was performed 24 h after EP. Cardiac biomarkers, cTnI and NT-proBNP, along with the histological stain, were served as indicators of myocardial injury. Cardiac KATP channel subunits Kir6.2 and SUR2A were analyzed in this study, and autophagy was evaluated by LC3. The results revealed that EP reduced the exhaustive exercise-induced high level of serum cTnI and myocardial ischemia/hypoxia; however, it did not reveal any changes in the serum NT-proBNP level or cardiac BNP. Cardiac SUR2A mRNA significantly upregulated during the exhaustive exercise. The high levels of Kir6.2, SUR2A, LC3IIpuncta and LC3II turnover observed after exhaustive exercise were significantly mitigated by EP in the late phase. These results suggest that EP alleviates myocardial injury induced by exhaustive exercise through the downregulation of cardiac KATP channels and autophagy.

The effect of probiotic yoghurt consumption on oxidative stress and inflammatory factors in young females after exhaustive exercise.

OBJECTIVE: To evaluate the effect of probiotic yoghurt consumption on oxidative stress and inflammatory factors in young females after exhaustive exercise. METHODS: TThis study included 27 healthy participants with an age range of 18-25. For two weeks, 450 grams of probiotic yoghurt and 450 grams of ordinary yoghurt were given to the supplement and control groups, respectively. Fasting blood samples were taken at baseline and at the end of study. At the end of the intervention, the participants were given one exhaustive exercise and then fasting blood samples were taken to test for blood antioxidant enzymes, inflammatory markers, and oxidative markers. Data were analyzed using descriptive statistics as well as paired and independent samples t-test. RESULTS: In supplement group, the glutathione peroxidise (GPX) blood levels and serum levels of total antioxidant capacity (TAC) significantly increased at the end of two weeks of intervention (p<0.05). After intense physical activity, the blood levels of superoxide dismutase (SOD), GPX and serum levels of TAC significantly increased, whereas the serum level of tumour necrosis factor alpha (TNF-?), matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), and malondialdehyde (MDA) significantly decreased in the supplement group compared to the control group (p<0.05). Besides, there were no significant changes in other biochemical factors. CONCLUSIONS: Regular probiotic yoghurt consumption significantly modulated MMP2, MMP9 and some inflammatory factors, and thus guarded against exhaustive exercise-inducing oxidative injury in young healthy females.