Acute Exhaustive Exercise Research Articles

Intracerebroventricular administration of the exercise hormone irisin or acute strenuous exercise alleviates epileptic seizure-induced neuroinflammation and improves memory dysfunction in rats

BackgroundStatus epilepticus is a common and potentially life-threatening neurological emergency with a high risk for cognitive and neurobiological impairment. Our aim was to evaluate the neuroprotective effects of centrally administered irisin and acute exhausting exercise against oxidative brain injury and memory dysfunction due to a pentylenetetrazole (PTZ)-induced single seizure. Male Sprague Dawley rats with intracerebroventricular (icv) cannulas were randomly divided into intraperitoneally (ip) saline-injected control and PTZ-injected (45 mg/kg) seizure groups. Both the control and PTZ groups were then treated with irisin (7.5 µg/kg, 2 µl, icv), saline (2 µl, icv) or were forced to an acute bout of strenuous exercise before the ip injection of saline (control) or PTZ. Seizures were evaluated using the Racine score. To evaluate memory performance, a passive avoidance test was performed before and after PTZ injection. Following euthanasia at the 24th hour of seizure induction, brain tissues were removed for histopathological examination and for evaluating oxidative damage, antioxidant capacity, and neurotransmitter levels.ResultsGlutamate/GABA imbalance observed in PTZ rats was corrected by irisin administration (p < 0.001/p < 0.01), while irisin prevented the generation of reactive oxygen species and lipid peroxidation (p < 0.05 − 0.001) and replenished the antioxidant catalase and glutathione levels (p < 0.01–0.01) in the cerebral tissue, and reduced the histologically evident neuronal injury due to a single seizure (p < 0.05 − 0.01). Irisin also delayed the onset of seizures (p < 0.05) and improved memory dysfunction (p < 0.05), but did not affect the severity of seizures. The acute exhaustive swimming exercise completed before PTZ-seizure depressed glutamate level (p < 0.001), maintained the oxidant/antioxidant balance, alleviated neuronal injury (p < 0.05 − 0.01) and upregulated cerebral BDNF expression (p < 0.05).ConclusionIn conclusion, acute high-intensity exercise or exogenously administered irisin provides neuroprotection by maintaining the balance of excitatory/inhibitory neurotransmitters and oxidant/antioxidant systems.

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.

Effect Of Protein Sports Drink Supplementation On Fatigue Recovery After Acute Exhaustive Exercise In Table Tennis Players

Effect Of Protein Sports Drink Supplementation On Fatigue Recovery After Acute Exhaustive Exercise In Table Tennis Players

The effects of subtoxic dose of acetaminophen combined with exercise on the liver of rats.

Regular physical exercise is beneficial to the body. Acute exercise causes oxidant stress in many tissues including the liver by creating an unbalanced status between oxidant and antioxidant levels. Analgesic drugs are commonly consumed to reduce the pain after exercise. Acetaminophen (APAP), commonly used as an over-the-counter analgesic, can cause hepatotoxicity. The aim of this study was to investigate the effect and underlying mechanisms of APAP at subtoxic dose, which is given after the acute and exhaustive exercise on the rat livers. Male Wistar rats weighing 200-250 g were divided into 6 groups each consisting of 7 rats/group; Control, APAP (250 mg/kg, ip), Acute Exercise (AEx), Acute Exhaustive Exercise (AEEx), Acute Exercise and APAP (AEx+APAP) and Acute Exhaustive Exercise and APAP (AEEx+APAP) groups. Rats were exercised at moderate intensity or exhaustive on the treadmill and then received APAP. Tissue MDA levels were significantly increased in AEEx, AEx+APAP and AEEx+APAP groups compared with the control. There was no significant difference in GSH levels between groups. Tissue Sirtuin1 (Sirt1) levels of APAP, AEx and AEEx groups were significantly less than control. There was no significant difference between groups in VEGF levels. Liver damage score was significantly higher in all groups compared with control group. As a result, this study shows that subtoxic dose of APAP treatment alone or in combination with acute or exhaustive treadmill exercise can cause oxidative liver damage by affecting Sirt1 levels and without affecting VEGF levels.

Arı Sütünün Tüketici Egzersize Bağlı Oksidatif Stres Üzerindeki Rolü

In this study, the effects of Royal Jelly (RJ) on oxidative stress caused by exhaustive swimming exercise in rat tissues were evaluated. Methods: Twenty four male Wistar albino rats were indiscriminately distributed into four experimental groups: Sedentary control (SC); SC with administration of RJ (100 mg kg-1) (SC + RJ); exhaustive swimming exercise (E); Exhaustive swimming exercise with administration of RJ (100 mg kg-1) (E + RJ). 100 mg kg-1 of RJ were dissolved in drinking water. Rats in the SC+RJ and E+RJ groups supplemented with RJ (100 mg kg-1) orally once a day for two weeks. Rats in groups E and E+RJ subjected to acute exhaustive swimming exercise on the 14th day of the study, then some biochemical parameters related to oxidative stress of all groups were measured. Results: The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen (BUN) and creatinine (CRE) levels significantly raised in the exercised rats compared with the sedentary rats (P &lt; 0.05). The decreased superoxide dismutase (SOD), glutathione peroxidase (GSHPx), and catalase (CAT) activities of muscular and hepatic tissues significantly increased and the high malondialdehyde (MDA) levels of muscular, hepatic and kidney tissues significantly reduced in exercised rats treated with RJ (P &lt; 0.05). Conclucion: Collectively, in this study, protective effects of RJ on tissues against oxidative damage after exhaustive exercise were observed.

What is the Combined Effects of Ginkgo Biloba Extract (EGb761) and Acute Exhaustive Exercise on the Thiol-Disulfide Homeostasis in Rats?

What is the Combined Effects of Ginkgo Biloba Extract (EGb761) and Acute Exhaustive Exercise on the Thiol-Disulfide Homeostasis in Rats?

Body Surface Potential Mapping during Ventricular Depolarization in Rats after Acute Exhaustive Exercise.

Exhaustive physical exercise can cause substantial changes in the electrical properties of the myocardium. To evaluate, using body surface potential mapping, the electrical activity of the heart in rats during ventricular depolarization after acute exhaustive exercise. Twelve-week-old male rats were submitted to acute treadmill exercise at 36 m/min until exhaustion. Unipolar electrocardiograms (ECGs) from the torso surface were recorded in zoletil-anesthetized rats three to five days before (Pre-Ex), 5 and 10 minutes after exhaustive exercise (Post-Ex 5 and Post-Ex 10, respectively) simultaneously with ECGs in limb leads. The instantaneous body surface potential maps (BSPMs) were analyzed during ventricular depolarization. P values <0.05 were considered statistically significant. Compared with Pre-Ex, an early completion of the second inversion of potential distributions, an early completion of ventricular depolarization, as well as a decrease in the duration of the middle phase and the total duration of ventricular depolarization on BSPMs were revealed at Post-Ex 5. Also, compared with Pre-Ex, an increase in the amplitude of negative BSPM extremum at the R-wave peak on the ECG in lead II (RII-peak) and a decrease in the amplitude of negative BSPM extremum at 3 and 4 ms after RII-peak were showed at Post-Ex 5. At Post-Ex 10, parameters of BSPMs did not differ from those at Pre-Ex. In rats, acute exhaustive exercise causes reversible changes in the temporal and amplitude characteristics of BSPMs during ventricular depolarization, most likely related to alterations in the excitation of the main mass of the ventricular myocardium.

Low Vitamin D Status Relates to the Poor Response of Peripheral Pulse Wave Velocity Following Acute Maximal Exercise in Healthy Young Men.

The primary objective of this study was to determine the effects of vitamin D levels on peripheral pulse wave velocity (pPWV) following acute maximal exercise in healthy young adults. Fifty male healthy adults from National Chung Cheng University participated in the study. Participants were divided into the 25-hydroxyvitamin D (25(OH)D) sufficiency group (n = 28, 25(OH)D ≥ 50 nmol/L) and deficiency group (n = 22, 25(OH)D < 50 nmol/L). The acute maximal exercise was performed using an incremental cycling test to exhaustion. Additionally, the pPWV and blood pressure were obtained at rest and 0, 15, 30, 45, 60 min after acute maximal exercise. The results show that 25(OH)D deficiency group had higher pPWV at post-exercise (5.34 ± 0.71 vs. 4.79 ± 0.81 m/s, p < 0.05), post-exercise 15 min (5.13 ± 0.53 vs. 4.48 ± 0.66 m/s, p < 0.05) and post-exercise 30 min (5.26 ± 0.84 vs. 4.78 ± 0.50 m/s, p < 0.05) than the sufficiency group. Furthermore, there was a significant inverse correlation between 25(OH)D levels and pPWV following acute maximal exercise. Our study demonstrated that low vitamin D status relates to the poor response of pPWV following maximal exercise in healthy young men. Vitamin D deficiency may increase the risk of incident cardiovascular events after acute exhaustive exercise, even in healthy and active adults.

Sulforaphane enhances Nrf2-mediated antioxidant responses of skeletal muscle induced by exhaustive exercise in HIIT mice

Nuclear factor erythroid-derived 2-like 2 (Nrf2) is the master regulator of antioxidant defenses. High-intensity interval training (HIIT) has been proposed as a time-efficient training program and has become a substantial component of modern training program. In the present study, we evaluated the effects of sulforaphane (SFN), a dietary isothiocyanate derived from cruciferous vegetables and a potent Nrf2 activator, on Nrf2-mediated antioxidant defense responses of skeletal muscle induced by exhaustive exercise in HIIT mice. Male C57BL/6J mice were randomly allocated into control group, HIIT group, and HIIT pretreated with SFN (HIIT+SFN) group. On the third day after completion of a 6-weeks HIIT protocol, an exhaustive treadmill test was conducted in all mice. Mice were intraperitoneally injected with SFN (HIIT+SFN group) or PBS (HIIT and control mice) 4 times in 3 days prior to the exhaustive treadmill test. The results indicated that the 6-weeks HIIT protocol did not increase the antioxidative capacity of skeletal muscle during exhaustive exercise. Importantly, SFN treatment improved antioxidative capacity of skeletal muscle in response to the acute exhaustive exercise by increasing mRNA and nucleoprotein expression of Nrf2 and these genes involved in antioxidant generation and decreasing blood creatine kinase (CK) and 4-hydroxy-2-nonenal (4-HNE)-modified protein levels in the HIIT mice.

Genetic deletion of IL-6 increases CK-MB, a classic cardiac damage marker, and decreases UPRmt genes after exhaustive exercise.

The intensity, duration, type of contraction, and muscle damage influence interleukin-6 (IL-6) response to acute exercise. However, in response to an exhaustive exercise session, the upregulation of IL-6 in the serum and heart is associated with an inflammatory condition and can inhibit autophagy. This study aimed to investigate the role of IL-6 in autophagy pathway responses and mitochondrial function in the heart of mice submitted to acute exhaustive physical exercise. The mice were allocated into three groups, five animals per group, for the wild type (WT) and the IL-6 knockout (IL-6 KO): Basal (sedentary; Basal), 1 h (after 1 h of the acute exercise; 1 h), and 3 h (after 3 h of the acute exercise; 3 h). After the specific time for each group, the blood was collected, each mouse heart was removed, and the left ventricle (LV) was isolated. In summary, under basal conditions, without the influence of the acute exercise, the IL-6 KO group showed lower number of nuclei in the cardiac tissue, but higher collagen deposition; lower messenger RNA(mRNA) levels of Prkaa1 and Mtco1, but higher mRNA levels of Ulk1; and higher protein levels of the ratio p-AMPK/AMPK in the heart when compared to WT at the same time point. After the acute exercise (1and 3 h), the IL-6 KO group had lower mRNA levels of Tfam, Mtnd1, Mtco1, and Nampt in the heart when compared to WT after exercise; higher serum levels of creatine kinase(CK), CK-MB, and lactate dehydrogenase for the IL-6 group when compared to the WT group after the exercise. Specifically, the heat-shock protein 60protein levels in the heart increased 3 h after exhaustive exercise in the WT group, but not in the IL-6 KO group. The study emphasizes that IL-6 may offer cardioprotective effects, including mitochondrial adaptations in response to acute exhaustive exercise.

Impaired oxidative stress in Thalassemia-Hemoglobin E traits after acute exhaustive exercise

Impaired oxidative stress in Thalassemia-Hemoglobin E traits after acute exhaustive exercise

Ubiquinol-cytochrome c reductase core protein 1 contributes to cardiac tolerance to acute exhaustive exercise.

Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) is an indispensable component of mitochondrial complex III. It plays a key role in cardioprotection and maintaining mitochondrion function. However, the exact role of UQCRC1 in maintaining cardiac function has not been reported by in vivo models. Also, the exact biological functions of UQCRC1 are far from fully understood. UQCRC1+/- mice had decreased both mRNA and protein expression of UQCRC1 in the left ventricular myocardia, and these mice had reduced tolerance to acute exhaustive exercise including decreased time and distance with higher apoptosis rate, higher expression level of cleaved CASPASE 3, and higher ratio of cleaved PARP1 to full-length PARP1. Moreover, UQCRC1 knockdown led to increased LV interventricular septal thicknesses both at systole and diastole, as well as decreased LV volume both at end-systole and end-diastole. Finally, UQCRC1 gene disruption resulted in mitochondrial vacuolation, fibril disarrangement, and more severe morphological and structural changes in mitochondria after acute exhaustive exercise. In conclusion, UQCRC1 contributes to cardiac tolerance to acute exhaustive exercise in mice, and it may be an essential component of complex III, playing a crucial role in maintaining cardiac functions.

Molecular and physiological responses predict acclimation limits in juvenile brook trout (Salvelinus fontinalis).

Understanding the resilience of ectotherms to high temperatures is essential because of the influence of climate change on aquatic ecosystems. The ability of species to acclimate to high temperatures may determine whether populations can persist in their native ranges. We examined physiological and molecular responses of juvenile brook trout (Salvelinus fontinalis) to six acclimation temperatures (5, 10, 15, 20, 23 and 25°C) that span the thermal distribution of the species to predict acclimation limits. Brook trout exhibited an upregulation of stress-related mRNA transcripts (heat shock protein 90-beta, heat shock cognate 71 kDa protein, glutathione peroxidase 1) and downregulation of transcription factors and osmoregulation-related transcripts (nuclear protein 1, Na+/K+/2Cl- co-transporter-1-a) at temperatures ≥20°C. We then examined the effects of acclimation temperature on metabolic rate (MR) and physiological parameters in fish exposed to an acute exhaustive exercise and air exposure stress. Fish acclimated to temperatures ≥20°C exhibited elevated plasma cortisol and glucose, and muscle lactate after exposure to the acute stress. Fish exhibited longer MR recovery times at 15 and 20°C compared with the 5 and 10°C groups; however, cortisol levels remained elevated at temperatures ≥20°C after 24 h. Oxygen consumption in fish acclimated to 23°C recovered quickest after exposure to acute stress. Standard MR was highest and factorial aerobic scope was lowest for fish held at temperatures ≥20°C. Our findings demonstrate how molecular and physiological responses predict acclimation limits in a freshwater fish as the brook trout in the present study had a limited ability to acclimate to temperatures beyond 20°C.

Effects Of PHB1 Changes In Different Exercise Models On Brain Mitochondrial Function And Energy Metabolism In Rats

PURPOSE: ATP synthesis plays the most important role. ATP synthesis is closely related to the structural and functional integrity of mitochondria. To investigate the effects of PHB1 expression changes on brain mitochondrial function in rats of different exercise modes. METHODS: 160 healthy male SD rats were randomly divided into four groups: normal control(NC),moderate intensity exercise(MIE),excessive fatigue exercise(EFE), and acute exhaustive exercise(AEE) groups.NC and AEE:routinely raised.MIE: 10 minutes per day at 10 m/min for the first week and increased for 10 minutes every day until the end of the second week.From the third week, rats run at 15 m/min for 60 min every day until the end of the 8th week. Slope:10%. EFE: From the first week of training, the speed of the running platform is 15 m/min, increased by 5 m/min per week to 30 m/min.Training time is 30 minutes and increased by 20 minutes per week until 110 minutes. Slope: increase by 5% per week until 15%. The EFE and AEE groups were trained for 6 days per week for 8 weeks. AEE:The rats were subjected to acute exhaustive exercise after 8 weeks. They were killed after 48 h of the last experiment. Mitochondrial respiratory control rate (RCR), ATP content, ROS level, complex V activity and PHB1 expression were measured. RESULTS: Compared with NC, in MIE group , RCR (+87%,P < 0.001), ATP content (+56%,P < 0.05), complex V activity (+81%,P < 0.05), PHB1 expression (+42%,P < 0.01) were increased, and ROS level (-67%,P < 0.001)was reduced; In EFE group , RCR (-43%,P < 0.01), ATP content (+53%,P < 0.05), complex V activity (+89%, P < 0.001), PHB1 expression (+28%,P < 0.01) and ROS level (+62%, P < 0.001) were increased; In AEE group ,the RCR (-78%, P < 0.05), ATP content (-75%,P < 0.05), complex V activity (-83%,P < 0.001), PHB1 expression (-35%,P < 0.01)decreased, and ROS (+96%,P < 0.05)level increased. Correlation analysis showed that PHB1 expression was positively correlated with ATP content in three groups. CONCLUSIONS: Changes in PHB1 expression brain tissue were consistent with changes in mitochondrial function under different motion modes.It is suggested that there may be interaction between PHB1 and ATP synthase. PHB1 participates in the stabilization of brain mitochondrial structure, changes mitochondrial function and affects the body's ability to exercise.

Acute Exhaustive Exercise under Normoxic and Normobaric Hypoxic Conditions Differentially Regulates Angiogenic Biomarkers in Humans.

Background and Objectives: Angiogenesis describes the outgrowth of new capillaries from already existing ones. Different biomarkers regulate this process. Physical exercise and hypoxia are key stimuli for the activation of different angiogenic molecules, such as the vascular endothelial growth factor (VEGF). matrix metalloproteases (MMPs)-2 and -9 or the extracellular matrix cleavage fragment endostatin. The present study aimed to investigate influences of short-term, intensive cycling exercise under both normoxic and normobaric hypoxic conditions on the mentioned parameters. Materials and Methods: Twelve male subjects (age: 23.3 ± 2.0 years) participated in the study. All subjects conducted four intensive cycling tests until individual exhaustion in a randomized order under the following conditions: normoxia, 2000 m, 3000 m and 4000 m above sea level. Blood samples were taken before (pre) and 10 min, 30 min, 60 min and 240 min post exercise and were analyzed by ELISA. Results: VEGF showed a significantly reduced concentration compared to the pre-value solely under 4000 m at 10 min post exercise. MMP-2 showed significantly reduced concentrations at 240 min post exercise under 4000 m. MMP-9 increased at 240 min post exercise under both 2000 m and 4000 m conditions. Endostatin was significantly increased at 10 min post exercise independently of the applied stimulus. Conclusions: The presented data show that intensive short-term exercise bouts facilitate the bioavailability of angiogenic, ECM (extracellular matrix)-related biomarkers. This finding is interesting for both health- and performance-related research as it demonstrates the positive effects of intensive short exercise interventions.

Effects of concurrent eight-week aerobic trainings and Rosa canina L. fruit hydroalcoholic extract on liver enzymes and malondialdehyde of liver in male rats following an acute aerobic exercise until exhaustion

Background: Rosa canina L. has high levels of carotenoids, flavonoids and, vitamin C antioxidant compounds that can withstand the destructive effects of exhaustive exercise-induced oxidative stress. The present study aims to investigate the effects of concurrent eight-week aerobic training and Rosa canina L. fruit hydroalcoholic extract on some liver enzymes and malondialdehyde of liver in male rats following an acute aerobic exercise until exhaustion. Methods: The present research was an experimental study. Forty male Wistar rats were randomly divided into four groups (N=10): placebo (without exercise + distilled water 2 ml supplement), supplement (without exercise + Rosa canina L extract, 100 mg/kg), exercise (8 weeks exercise + distilled water 2 ml), combined (8 weeks exercise + Rosa canina L extract, 100 mg/kg). At the end of the experiment, half of the rats were killed immediately before exhaustive exercise; while the other half were killed immediately after performing an acute exhaustive exercise on the treadmill. Serum enzymes AST, ALT, and hepatic malondialdehyde levels were measured by ELISA and thiobarbituric acid methods, respectively. Results: The results show that in all groups except the combined group serum AST, ALT, and malondialdehyde of the liver were significantly increased following an acute exhaustive exercise compared to the prior exhaustive exercise (P&lt;0.05). Conclusion: The use of Rosa canina L Fruit hydroalcoholic extract with aerobic exercise prevented the increase of hepatic malondialdehyde and serum enzymes AST, ALT levels following an acute exhausting exercise.

Molecular hydrogen downregulates acute exhaustive exercise-induced skeletal muscle damage.

Physical exercise-induced skeletal muscle damage may be characterized by increased oxidative stress, inflammation, and apoptosis which may be beneficial when exercise is regular, but it is rather harmful when exercise is exhaustive and performed acutely by unaccustomed individuals. Molecular hydrogen (H2) has emerged as a potent antioxidant, anti-inflammatory, and anti-apoptotic agent, but its action on the deleterious effects of acute exhaustive exercise in muscle damage remain unknown. Therefore, we tested the hypothesis that H2 decreases acute exhaustive exercise-induced skeletal muscle damage of sedentary rats. Rats ran to exhaustion on a sealed treadmill inhaling an H2-containing mixture or the control gas. We measured oxidative stress (SOD, GSH, and TBARS), inflammatory (TNF-α, IL-1β, IL-6, IL-10, and NF-κB phosphorylation), and apoptotic (expression of caspase-3, Bcl-2, and HSP70) markers. Exercise caused no changes in SOD activity but increased TBARS levels. H2 caused increases in exercise-induced SOD activity and blunted exercise-induced increased TBARS levels. We observed exercise-induced TNF-α and IL-6 surges as well as NF-κB phosphorylation, which were blunted by H2. Exercise increased cleaved caspase-3 expression, and H2 reduced this response. In conclusion, H2 effectively downregulates muscle damage, reducing oxidative stress, inflammation, and apoptosis after acute exhaustive exercise performed by an unaccustomed organism.

Effect Of Phb1 On F O F 1 -atpase And Mitochondrial Function In Energy Metabolism

PURPOSE: To investigate the mechanism of PHB1 on F0F1-ATPase and its effect on exercise capacity,and whether PHB1 can be used as a scientific basis for regulating energy metabolism. METHODS: An animal model of moderate-intensity exercise and exhaustive exercise and a complete C2C12 cell line culture system,PHB1 overexpression and RNA interference in adenovirus vectors were established.32 8-week-old healthy male SD rats were randomly divided into three groups: normal control(NC),moderate intensity exercise(MIE)and acute exhaustive exercise(AEE)groups.NC and AEE:routinely raised. MIE:Rats were run at 15m/min per day for 60min until the end of the 8th week.Slope:10%.AEE:The rats were subjected to acute exhaustive exercise after 8 weeks.They were sacrificed 48h after the last experiment.PHB1 expression,ATP content,FOF1-ATPase,oxidative stress (ROS),cellular oxygen consumption rate (OCR),and mitochondrial respiratory function(RCR)in skeletal muscle were measured by animal and cell experiments. RESULTS: Compared with NC,MIE group RCR(+73%,p<0.001),ATP content (+48%,p<0.05),FOF1-ATPase activity(+79%,p<0.05),PHB1 expression(+42%,p<0.01),ROS level(-75%,p<0.001)decreased;AEE group RCR(-58%,p<0.05),ATP content (-55%,p<0.05),FOF1-ATPase activity(-56%,p<0.001),PHB1 expression(-31%,p<0.01)decreased,and ROS(+79%,p<0.05)increased.In C2C12 cells,PHB1 overexpression group,ATP content(+86%,p<0.01),FOF1-ATPase mRNA level(+59%,p<0.05),FOF1-ATPase protein expression level(+69%,p<0.05),FOF1-ATPase activity(+226%, p<0.01),and OCR(+256%,p<0.01),ROS level(-74%,p<0.01),significant enhancement of cellular respiratory function.In the low expression group of PHB1,ATP content(-21%,p<0.01),FOF1-ATPase mRNA level(-64%, p<0.05),FOF1-ATPase protein expression level(-89%,p<0.05),FOF1-ATPase activity(-93%,p<0.01),and OCR(-190%,p<0.01),ROS production was significantly increased(+104%,p<0.01),and cellular respiratory function was significantly reduced. CONCLUSION: In energy metabolism,PHB1 may play a role in stabilizing the mitochondrial structure and positively regulating FOF1-ATPase activity,thereby enhance mitochondrial function and promoting energy metabolism.Supported by NSFC(No.31470061)

Total Dietary Antioxidant Intake Including Polyphenol Content: Is it Capable to Fight against Increased Oxidants within the Body of Ultra-Endurance Athletes?

The role of dietary antioxidants on exhaustive exercise-induced oxidative stress has been well investigated. However, the contribution of total dietary antioxidant capacity on exogenous antioxidant defense and exercise performance has commonly been disregarded. The aims of the present investigation were to examine (i) the effects of dietary total antioxidant intake on body antioxidant mechanisms, and (ii) an exhaustive exercise-induced oxidative damage in ultra-endurance athletes. The study included 24 ultra-marathon runners and long-distance triathletes (12 male and 12 female) who underwent an acute exhaustive exercise test (a cycle ergometer (45 min at 65% VO2max) immediately followed by a treadmill test (75% VO2max to exhaustion). Oxidative stress-related biomarkers (8-isoprostaglandin F2alpha (8-iso PGF2a), total oxidant status (TOS, total antioxidant status (TAS)) in plasma were collected before and after exercise. Oxidative stress index was calculated to assess the aspect of redox balance. Blood lactate concentrations and heart rate were measured at the 3rd and 6th min after exercise. Dietary antioxidant intake was calculated using the ferric reducing ability of plasma (FRAP) assay. Dietary total antioxidant intake of the subjects was negatively correlated with pre-exercise TOS concentrations (rs = −0.641 in male, and rs = −0.741 in females) and post- vs. pre- (∆) 8-iso PGF2a levels (rs = −0.702 in male; p = 0.016, and rs = −0.682 in females; p = 0.024), and positively correlated with ∆ TAS concentrations (rs = 0.893 in males; p = 0.001, and rs = 0.769 in females; p = 0.002) and post- exercise lactate concentrations (rs = 0.795 for males; p = 0.006, and rs = 0.642 for females; p = 0.024). A positive meaningful (p = 0.013) interaction was observed between time at exhaustion and dietary antioxidant intake (rs = 0.692) in males, but not in females. In conclusion, the determination of total dietary antioxidant intake in ultra-endurance athletes may be crucial for gaining a better perspective on body antioxidant defense against exhaustive exercise-induced oxidative stress. However, the effects of dietary antioxidant on exercise performance and recovery rate needs further investigation.

Effects of Acute Exhaustive Exercise on Oxidant and Antioxidant System Parameters in Rats with Streptozotocin Induced Diabetes Mellitus

Effects of Acute Exhaustive Exercise on Oxidant and Antioxidant System Parameters in Rats with Streptozotocin Induced Diabetes Mellitus