Bout Of Exhaustive Exercise Research Articles

Protective effects of tea polyphenols on exhaustive exercise-induced fatigue, inflammation and tissue damage

ABSTRACTBackground: The beneficial properties of tea polyphenols have been extensively studied; however, less attention has been paid to their effects, especially anti-inflammatory effect during exhaustive exercise.Objective: The present study assessed the potential protective effects of tea polyphenols against the fatigue, inflammation and tissue injury caused by an exhaustive exercise bout in rats.Design: Twenty-four healthy male rats were divided into three groups. Group C was a sedentary control group, Groups E+TP and Group E performed a single exhaustive swimming test; all groups had normal diets, but Group E+TP was supplemented with tea polyphenols. All rats were immediately euthanized after exhaustive exercise, and biochemical and inflammatory parameters, including lactic acid (LA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), lactic dehydrogenase (LDH), and creatine kinase (CK) activity levels, were measured. Reverse transcription (RT) and Real-Time PCR was employed to evaluate the mRNA expression of IL-1β in the liver.Results: The results showed a decrease in serum LA levels (22%, p < 0.05) in rats that consumed dietary tea polyphenols. Interestingly, dietary tea polyphenols decreased the serum levels of pro-inflammatory factors (TNF-α: 13%, p < 0.05; IL-1β: 10%, p < 0.05; and IL-6: 48%, p < 0.05) and shifted the serum IL-10/TNF-α ratio to a predominantly anti-inflammatory milieu (0.52 ± 0.07 vs. 0.67 ± 0.10, p < 0.01). Furthermore, the polyphenols effectively inhibited the release of tissue damage markers (CK: 24%, p < 0.05 and LDH: 28%, p < 0.05) in the serum and decreased IL-1β mRNA expression in the liver.Conclusions: This study indicated that tea polyphenols could significantly protect rats from the fatigue, inflammation and tissue damage induced by acute exhaustive exercise.

Immunometabolic Responses after Short and Moderate Rest Intervals to Strength Exercise with and without Similar Total Volume.

This study investigated the influence of short and moderate intervals of recovery with and without equated volume during an acute bout exhaustive strength exercise on metabolic, hormonal and inflammatory responses in healthy adults. Eight physically active men (23.5 ± 3.1) performed three randomized sequences: Short (70% of 1 RM with 30 s of rest); Moderate (70% of 1 RM with 90 s of rest); and Volume-Equated Short (70% of 1 RM with 30 s of rest between sets with a repetition volume equal to that performed in Moderate). All sequences of exercises were performed until movement failure in the squat, bench press and T-bar row exercises, respectively. Glucose, lactate, testosterone, IL-6, IL-10, IL-1ra, and MCP-1 levels were assessed at rest, immediate post-exercise, and 1 h post. There was a main effect of time for testosterone (p < 0.001). The post hoc indicated differences between post-exercise and rest and post-1 h and post-exercise (p < 0.001). Lactate increased post-exercise when compared to pre and post-1 h (p < 0.001) and maintained higher post-1 h in relation to rest. IL-6 was greater post-exercise than rest (p = 0.045) and post-1 h and rest (p = 0.020). IL-10 was greater post-exercise (p = 0.007) and post-1 h (p = 0.002) than rest. IL-1ra increased post-exercise in relation to rest (p = 0.003) and MCP-1 was greater post-exercise than rest (p < 0.001) and post-1 h (p = 0.043). There were no significant differences between conditions or interaction. Thus, both short and moderate intervals of recovery induced greater metabolic, hormonal and inflammatory responses after acute bout of exhaustive strength exercise in healthy adult.

Impact of Short and Moderate Rest Intervals on the Acute Immunometabolic Response to Exhaustive Strength Exercise: Part I.

The purpose of this study was to verify the influence of the short and moderate intervals of recovery in response to an acute bout of exhaustive strength exercise on performance, inflammatory, and metabolic responses in healthy adults. Eight healthy subjects (age = 24.6 ± 4.1 years) performed 2 randomized sequences: short = 70% of 1 repetition maximum (1RM) with 30 seconds of rest between sets; moderate = 70% of 1RM with 90 seconds of rest between sets. All sequences of exercises were performed over 4 sets until movement failure in the squat and bench press exercises, respectively. The total number of repetitions performed was recorded for each set of each exercise for all sequences. The percentages of fat mass and fat-free mass were estimated by dual-energy x-ray absorptiometry. Glucose, tumor necrosis factor-α, interleukin (IL)-6, IL-10, and nonester fatty acid were assessed, at baseline, immediately after exercise, after 15 and 30 minutes. When compared with the maximum number of repetitions and the total weight lifted, there was a statistically significant decrease after both intervals. The only statistically significant decreases over time occurred at the post-15 minutes assessment of the IL-6 and glucose when a moderate interval of recovery was performed. When comparing the alterations between the pools (the mean of the cluster of all periods in each variable), there was a statistically significant increase on the IL-6 and IL-10 when a moderate interval of recovery was performed again, however, not considering a statistical difference on the IL-10. Thus, we concluded that different interval of recovery in response to exhaustive strength exercise decreases performance but in only moderate intervals, it is associated with inflammatory and metabolic response.

Comparing the impact of an acute exercise bout on plasma amino acid composition, intraerythrocytic Ca2+ handling, and red cell function in athletes and untrained subjects

The N-methyl d-aspartate receptors (NMDARs) mediating Ca2+ uptake upon stimulation with glutamate and glycine were recently discovered in red blood cells (RBC) of healthy humans. Activation of these receptors with agonists triggered transient Ca2+-dependent decrease in hemoglobin oxygen affinity in RBC suspension. The aim of this study was to assess the potential physiological relevance of this phenomenon. Two groups formed by either healthy untrained volunteers or endurance athletes were subjected to a stepwise incremental cycling test to exhaustion. Plasma glutamate levels, activity of the NMDARs, and hemoglobin O2 affinity were measured in blood samples obtained before and after the exercise in both groups. Increase in plasma glutamate levels following exercise was observed in both groups. Transient Ca2+ accumulation in response to the NMDAR stimulation with NMDA and glycine was followed by facilitated Ca2+ extrusion from the RBC and compensatory decrease in cytosolic Ca2+ levels. Short-term activation of the receptors triggered a transient decrease in O2 affinity of hemoglobin in both groups. These exercise-induced responses were more pronounced in athletes compared to the untrained subjects. Athletes were initially presented with lower basal intracellular Ca2+ levels and hemoglobin oxygen affinity compared to non-trained controls. High basal plasma glutamate levels were associated with induction of hemolysis and formation of echinocytes upon stimulation with the receptor agonists. These findings suggest that glutamate release occurring during exhaustive exercise bouts may acutely facilitate O2 liberation from hemoglobin and improve oxygen delivery to the exercising muscle.

The effect of AQP3 deficiency on fuel selection during a single bout of exhausting exercise.

Aquaporin-3 (AQP3) is an integral membrane protein that facilitates the transport of water and glycerol across cell membranes. However, the precise localization and function of AQP3 in skeletal muscles is currently unknown. In this study, we investigated the capacity of AQP3 knockout mice to perform a single bout of exhausting exercise and analyzed the parameters related to skeletal muscle energy metabolism during exhausting exercise. Mice were exposed to a single bout of treadmill running at a speed of 12m/min with 10° inclination until exhaustion, and sacrificed immediately, 24 h and 48h after exercise. Both immunohistochemistry and double immunofluorescence staining revealed that AQP3 is expressed at the cell surface with no evidence of colocalization with either AQP1 or AQP4 in hamstring skeletal muscles. When exposed to a single bout of exhaustive exercise, AQP3 knockout mice fatigued more easily with the average time to exhaustion shorter than the wild-type mice. After exhausting exercise, plasma glucose, muscle glycogen, muscle triglyceride, and muscle free fatty acid levels decreased compared with the values before exercise in both AQP3 knockout and wild-type mice. However, muscle glycerol concentration after exercise decreased in the wild-type mice, but rather increased in AQP3 knockout mice. These findings suggest that decreased glycerol efflux from the skeletal muscles in AQP3 knockout mice may result in low exercise capacity, presumably due to the limitations in the constant energy supply through hepatic gluconeogenesis from glycerol during the prolonged endurance exercise.

Exercise-stimulated FGF23 promotes exercise performance via controlling the excess reactive oxygen species production and enhancing mitochondrial function in skeletal muscle

ObjectivePhysical exercise induces many adaptive changes in skeletal muscle and the whole body and improves metabolic characteristics. Fibroblast growth-factor 23 (FGF23) is a unique member of the FGF family that acts as a hormone regulating phosphate metabolism, calcitriol concentration, and kidney functions. The role of FGF23 in exercise and skeletal muscle is largely unknown yet. Materials and methodsC57BL/6J mice were exercised on a motor treadmill. Mice serum FGF23 levels; FGF23 mRNA expression in various organs including the liver, heart, skeletal muscle tissue, and thyroid; and FGF23 receptor Klotho mRNA expression were examined using enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and immunoblotting, respectively, after a single bout of acute exercise (60min), exhaustive exercise, and chronic prolonged exercise (60min every day for one week). C57BL/6J mice were injected with recombinant FGF23 (100mg/kg, twice per day, i.p.) or vehicle control (saline) for 3days, and then the exercise performance, reactive oxygen species (ROS), H2O2 production, and mitochondrial functional biomarkers in muscle (gene expression of sirtuin 1, PPAR-δ, PGC-1α and mitochondrial transcription factor A [TFAM], and citrate synthase activity) were assayed. ResultsThree forms of exercise, acute exercise, exhaustive exercise, and chronic exercise, increased serum FGF23 levels. However, only chronic exercise upregulated FGF23 mRNA and protein expression in skeletal muscle. FGF23 mRNA expression in the heart, liver, and thyroid was not affected. FGF23 protein was mainly located in the cytoplasm in skeletal muscle tissue and the localization of FGF23 was not altered by exercise. Exogenous FGF23 treatment significantly extended the time to exhaustion and reduced the exercise-induced ROS and H2O2 production. FGF23 treatment increased the mRNA level of PPAR-δ and citrate synthase activity, but did not influence the mRNA expression of sirtuin 1, PGC-1α, and TFAM in skeletal muscle. ConclusionThese results demonstrate that exercise-stimulated FGF23 promotes exercise performance via controlling the excess ROS production and enhancing mitochondrial function in skeletal muscle, which reveals an entirely novel role of FGF23 in skeletal muscle.

Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes.

Experimental study. Exercise improves functional capacity in spinal cord injury (SCI). However, exhaustive exercise, especially when sporadic, is linked to the production of reactive oxygen species that may have a detrimental effect on SCI. We aimed to study the effect of a single bout of exhaustive exercise on systemic oxidative stress parameters and on the expression of antioxidant enzymes in individuals with paraplegia. The study was conducted in the Physical Therapy department and the Physical Education and Sports department of the University of Valencia. Sixteen paraplegic subjects were submitted to a graded exercise test (GET) until volitional exhaustion. They were divided into active or non-active groups. Blood samples were drawn immediately, 1 and 2 h after the GET. We determined plasma malondialdehyde (MDA) and protein carbonylation as markers of oxidative damage. Antioxidant gene expression (catalase and glutathione peroxidase-GPx) was determined in peripheral blood mononuclear cells. We found a significant increase in plasma MDA and protein carbonyls immediately after the GET (P<0.05). This increment correlated significantly with the lactate levels. Active paraplegics showed lower levels of exercise-induced oxidative damage (P<0.05) and higher exercise-induced catalase (P<0.01) and GPx (P<0.05) gene expression after the GET. These results suggest that exercise training may be useful in SCI patients to develop systemic antioxidant defenses that may protect them against exercise-induced oxidative damage.

Melatonin Has An Ergogenic Effect But Does Not Prevent Inflammation and Damage In Exhaustive Exercise.

It is well documented that exhaustive physical exercise leads to inflammation and skeletal muscle tissue damage. With this in mind, melatonin has been acutely administered before physical exercise; nevertheless, the use of melatonin as an ergogenic agent to prevent tissue inflammation and damage remains uncertain. We evaluated the effects of melatonin on swimming performance, muscle inflammation and damage and several physiological parameters after exhaustive exercise at anaerobic threshold intensity (iLAn) performed during light or dark circadian periods. The iLAn was individually determined and two days later, the animals performed an exhaustive exercise bout at iLAn 30 minutes after melatonin administration. The exercise promoted muscle inflammation and damage, mainly during the dark period, and the exogenous melatonin promoted a high ergogenic effect. The expressive ergogenic effect of melatonin leads to longer periods of muscle contraction, which superimposes a possible melatonin protective effect on the tissue damage and inflammation.

Predicting time to exhaustion during high-intensity exercise using rating of perceived exertion

Summary Objectives This study aimed to predict the time to exhaustion (Tlim) at different high-intensity exercises using a linear regression between 14–17 points of Borg scale and their respective time, verify the agreement and compare them to the real Tlim. Methods Nineteen healthy male subjects undertook four constant-load exhaustive exercise bouts on cycle ergometer. These tests were performed on different days and with four different intensities. The power output imposed in each test was determined based on familiarization trials in order to induce a subjects’ exhaustion between 2 and 15 min. They were also asked to report the rating of perceived exertion (RPE) during these constant-load exercise bouts. The first value was freely chosen as soon as the subject felt able to accurately report RPE levels, the number corresponding to the verbal anchor on the Borg scale, within of first minute of exercise. Thereafter, whenever they felt that the RPE was increased, the value was recorded. A linear regression was fitted plotting the 14–17 RPE range as a function of time of each test. The Tlim was estimated by extrapolation of the linear relationship to the RPE 19 (Tlim19) and 20 (Tlim20). Results The measured Tlim values were significantly higher at the Tlim19 at 230 ± 33 W, 256 ± 33 W and 289 ± 36 W ( P P > 0.05). Furthermore, the intraclass correlation coefficients were all strong (ICC = 0.79–0.87). The RPE at same percentages of Tlim (25, 50, 75 and 100%) during the four constant-load exercise bouts were not different ( P > 0.05). Conclusion Tlim during high-intensity exercises can be accurately predicted by the use of RPE values in the 14–17 range assuming that exhaustion occurs at RPE = 20.

Transcriptional modulation of mitochondria biogenesis pathway at and above critical speed in mice.

High- or moderate-intensity endurance training leads to mitochondrial biogenesis via the peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α)/mitochondrial transcription factor A (Tfam) signaling pathway. Although this pathway is stimulated during acute exercise, the relationship between its activity and the intensity of the exercise has not been characterized. In animal studies, individualized running speeds have not previously been assessed. Here, we sought to determine whether this pathway was modulated after a bout of exhaustive exercise at different relative intensities (at and over critical speed (CS)). Our starting hypotheses were that (i) exercise-induced overexpression of PGC-1α in skeletal muscle falls at intensities above CS, and (ii) transcriptional activity of the mitochondrial biogenesis signaling cascade is intensity-sensitive at and above CS. To test these hypothesis, male Friend Virus B-Type mice were divided into a control group and three exercise groups (exercising at CS, peak velocity (vPeak) and 150 % CS, respectively). mRNA expression levels for genes involved in mitochondrial biogenesis signaling were analyzed in the quadriceps muscle. PGC-1α was overexpressed at all exercise intensities. We also identified that, PGC-1α mRNA expression was negatively correlated with exercise intensity and blood lactate levels but not with maximal oxygen uptake, vPeak, or CS. Expression of the PGC-1α co-activator peroxisome proliferator-activated receptor β was negatively correlated with the exercise intensity. In contrast, expression levels of Tfam were dissociated from exercise intensity. Our data indicate that at the intensities used in endurance training, the expression of mitochondrial biogenesis genes is finely modulated by the relative intensity of exhaustive exercise.

Acute Exercise‐Induced Mitophagy is Mediated in Part by PGC‐1α

Chronic exercise results in systemic metabolic benefits in the major metabolic centers of the body. Skeletal muscle is a pillar of whole body metabolism and this tissue undergoes metabolic remodelling with repeated bouts of contractile activity. This is accomplished by increased mitochondrial turnover with a concurrent increase in both organelle biogenesis and removal. While biogenesis is largely orchestrated by the transcriptional co-activator PGC-1α, the regulation of mitochondrial degradation (i.e mitophagy) is less well established. Coincidentally, both mitochondrial biogenesis and autophagy are activated by an acute bout of exercise. However, the induction of mitophagy following exercise, and the interplay between autophagy and PGC-1α following acute exercise, have not been thoroughly examined. To address this, we subjected wild type (WT) and PGC-1α knockout animals (KO) to an acute bout of exhaustive exercise. Lack of PGC-1α resulted in a 40% drop in mitochondrial content and a 25% decline in running performance. KO mice also depicted a greater increase and a slower recovery of blood lactate following exercise, indicating metabolic distress. Indeed, exercise-induced activation of AMPK and p38 was greater in KO as compared to WT animals. Exercise also induced a 2-3-fold increase in gene transcripts of various mitochondrial (e.g COXIV, Tfam) and autophagy-related genes (e.g. p62, LC3) in WT animals only. Moreover, both autophagy and mitophagy flux were induced by exercise, but this increase was attenuated in KO animals. These results suggest that an acute bout of exercise is sufficient to induce mitochondrial turnover through increased biogenesis and degradation. Moreover, these two processes appear to be, at least in part, regulated by PGC-1α.

Effects of tadalafil administration on plasma markers of exercise-induced muscle damage, IL6 and antioxidant status capacity.

Physical exercise is associated with enhanced production of reactive oxygen species, which if uncontrolled can result in tissue injury. Phosphodiesterase type 5 inhibitors (PDE5i) exhibit protective effect against oxidative stress, both in animals and healthy/unhealthy humans. However, the effect of a chronic administration of PDE5i, particularly combined with physical exercise, has never been investigated. The present study was designed to evaluate the effect of the long-acting PDE5i tadalafil on oxidative status and muscle damage after exhaustive exercise in healthy males included in a double-blind crossover trial. Tadalafil, having a putative antioxidant activity, may reduce oxidative damage after strenuous exercise. Each volunteer randomly received two tablets of placebo or tadalafil (20 mg/day) with 36 h of interval before performing exhaustive exercise. After 2 weeks of washout, the volunteers were crossed over. Blood samples were collected immediately before exercise, immediately after, and during recovery (15, 30, 60 min). Plasma total antioxidant status, glutathione homeostasis (GSH/GSSG), malondialdehyde (MDA), protein carbonyls, creatine kinase (CK), lactate dehydrogenase (LDH) and the inflammatory cytokine interleukin 6 were assessed. Tadalafil administration per se affected redox homeostasis (GSH/GSSG -36%; p < 0.05), cellular (CK +75% and LDH +36%; p < 0.05) and oxidative damage (MDA +41% and protein carbonyls +50%; p < 0.05) markers. The exhaustive exercise increased all the above-reported biochemical parameters, with subjects from the tadalafil group showing significantly higher values with respect to the placebo group. A prolonged exposure to tadalafil decreases antioxidant capacity at resting condition, therefore making subjects more susceptible to the oxidative stress induced by an exhaustive bout of exercise.

Exploring mechanisms of fatigue during repeated exercise and the dose dependent effects of carbohydrate and protein ingestion: study protocol for a randomised controlled trial

BackgroundMuscle glycogen has been well established as the primary metabolic energy substrate during physical exercise of moderate- to high-intensity and has accordingly been implicated as a limiting factor when such activity is sustained for a prolonged duration. However, the role of this substrate during repeated exercise after limited recovery is less clear, with ongoing debate regarding how recovery processes can best be supported via nutritional intervention. The aim of this project is to examine the causes of fatigue during repeated exercise bouts via manipulation of glycogen availability through nutritional intervention, thus simultaneously informing aspects of the optimal feeding strategy for recovery from prolonged exercise.Methods/DesignThe project involves two phases with each involving two treatment arms administered in a repeated measures design. For each treatment, participants will be required to exercise to the point of volitional exhaustion on a motorised treadmill at 70% of previously determined maximal oxygen uptake, before a four hour recovery period in which participants will be prescribed solutions providing 1.2 grams of sucrose per kilogram of body mass per hour of recovery (g.kg-1.h-1) relative to either a lower rate of sucrose ingestion (that is, 0.3 g.kg-1. h-1; Phase I) or a moderate dose (that is, 0.8 g.kg-1.h-1) rendered isocaloric via the addition of 0.4 g.kg-1.h-1 whey protein hydrolysate (Phase II); the latter administered in a double blind manner as part of a randomised and counterbalanced design. Muscle biopsies will be sampled at the beginning and end of recovery for determination of muscle glycogen resynthesis rates, with further biopsies taken following a second bout of exhaustive exercise to determine differences in substrate availability relative to the initial sample taken following the first exercise bout.DiscussionPhase I will inform whether a dose–response relationship exists between carbohydrate ingestion rate and muscle glycogen availability and/or the subsequent capacity for physical exercise. Phase II will determine whether such effects are dependent on glycogen availability per se or energy intake, potentially via protein mediated mechanisms.Trial registrationISRCTN87937960.

Influence of Affective Changes on Behavioral and Cognitive Performances After Acute Bout of Exhaustive Exercise

The present study was conducted to evaluate the influence of acute, exhaustive, exercise on affective responses (affective valence and activation) and behavioral and cognitive performances in medical students using circumplex model, reaction time (RT), and P300, respectively. Twelve healthy, untrained, male medical students participated in self-controlled, counterbalanced trial conducted over two sessions: baseline and exercise. In the baseline session, recordings of auditory reaction time (ART), visual RT (VRT), and P300 latency and amplitude (using acoustic “oddball” paradigm) were taken at the end of 15 min seated rest. Exercise session comprised of continuous maximal graded incremental exercise until volitional exhaustion, on a computer-based motorized treadmill and recordings done after heart rate returned to within +10% of pre-exercise values. Perceived exertion, affective valence, and activation were assessed pre-exercise, during (30 s before the end of each stage), and post-exercise (immediately, 5 and 10 min after) by Borg’s scale, feeling scale (FS), and felt-arousal scale (FAS), respectively. There was marked variability in individual affective responses to a single bout of exhaustive exercise with few subjects showing activated pleasure (Energetic Arousal) and others showing activated displeasure (Tense arousal). The results further indicated an overall improvement in behavioral (as evidenced by the decrease in ART and VRT) and cognitive performances (as evidenced by increase in the P300 amplitude and decrease in the P300 latency) in medical students in the exercise session relative to the baseline session despite bidirectional shifts in valence suggesting that interdependent neural systems might mediate these effects.

A Role of AQP3 in Skeletal Muscle Contraction and Energy Metabolism during a Single Bout of Exhaustive Exercise

A Role of AQP3 in Skeletal Muscle Contraction and Energy Metabolism during a Single Bout of Exhaustive Exercise

Aerobic and Anaerobic Performances in Tethered Swimming

The purpose of this study was to investigate whether the critical force (CritF) and anaerobic impulse capacity (AIC) - estimated by tethered swimming - reflect the aerobic and anaerobic performance of swimmers. 12 swimmers performed incremental test in tethered swimming to determine lactate anaerobic threshold (AnTLAC), maximal oxygen uptake ( ˙VO2MAX) and force associated with the ˙VO2MAX (i ˙VO2MAX). The swimmers performed 4 exhaustive (tlim) exercise bouts (100, 110, 120 and 130% i ˙VO2MAX) to compute the CritF and AIC (F vs. 1/tlim model); a 30-s all-out tethered swimming bout to determine their anaerobic fitness (ANF); 100, 200, and 400-m time-trials to determine the swimming performance. CritF (57.09±11.77 N) did not differ from AnTLAC (53.96±11.52 N, (P>0.05) but was significantly lower than i ˙VO2MAX (71.02±8.36 N). In addition, CritF presented significant correlation with AnTLAC (r=0.76; P<0.05) and i ˙VO2MAX (r=0.74; P<0.05). On the other hand, AIC (286.19±54.91 N.s) and ANF (116.10±13.66 N) were significantly correlated (r=0.81, p<0.05). In addition, CritF and AIC presented significant correlations with all time-trials. In summary, this study demonstrates that CritF and AIC can be used to evaluate AnTLAC and ANF and to predict 100, 200, and 400-m free swimming.

Exercise-induced oxidative stress in elderly subjects: the effect of red orange supplementation on the biochemical and cellular response to a single bout of intense physical activity

Aging is characterized by an impaired capacity to maintain the redox balance both in physiological and pathological situations associated with an increased production of reactive oxygen species. Since the extent of this phenomenon may be influenced by an antioxidants-rich diet, we investigated the effect of supplementation with fresh red orange juice (ROJ) on biochemical and cellular biomarkers of oxidative stress in healthy, trained elderly women after a single bout of exhaustive exercise (EE). To this purpose, a sample of 22 females, 15 (69.0 ± 5.1 years) taking the ROJ supplementation and 7 (68.1 ± 2.7 years) as Control group, was constituted. Blood samples were collected immediately before, 30 minutes, and 24 hr after a single bout of EE, at baseline and after 4 weeks. Our results demonstrate that markers of DNA damage or apoptosis were not affected by EE both in Control and ROJ group, and by ROJ, whereas, exercise temporarily affected the redox balance in both groups. Controls didn't change their response to EE after the experimental period, but experimental group after ROJ supplementation had lower EE-induced MDA, consumed less ascorbic acid, and had less activation of the hypoxanthine/xanthine system, i.e., they seemed to be protected from hypoxia/reoxygenation mechanisms.

Relationship between a single bout of exhaustive exercise and endoplasmic reticulum stress in skeletal muscle

Relationship between a single bout of exhaustive exercise and endoplasmic reticulum stress in skeletal muscle

A single bout of exhaustive exercise in relation to endoplasmic reticulum stress in liver

A single bout of exhaustive exercise in relation to endoplasmic reticulum stress in liver

Effect of post-exercise hydrotherapy water temperature on subsequent exhaustive running performance in normothermic conditions

Despite the widespread use of cold water immersion (CWI) in normothermic conditions, little data is available on its effect on subsequent endurance performance. This study examined the effect of CWI as a recovery strategy on subsequent running performance in normothermic ambient conditions (∼22°C). Nine endurance-trained men completed two submaximal exhaustive running bouts on three separate occasions. The running bouts (Ex1 and Ex2) were separated by 15min of un-immersed seated rest (CON), hip-level CWI at 8°C (CWI-8) or hip-level CWI at 15°C (CWI-15). Intestinal temperature, blood lactate and heart rate were recorded throughout and V˙O2, running economy and exercise times were recorded during the running sessions. Running time to failure (min) during Ex2 was significantly (p<0.05, ES=0.7) longer following CWI-8 (27.7±6.3) than CON (23.3±5) but not different between CWI-15 (26.3±3.4) and CON (p=0.06, ES=0.7) or CWI-8 and CWI-15 (p=0.4, ES=0.2). Qualitative analyses showed a 95% and 89% likely beneficial effect of CWI-8 and CWI-15 during Ex2 compared with CON, respectively. Time to failure during Ex2 was significantly shorter than Ex1 only during the CON condition. Intestinal temperature and HR were significantly lower for most of Ex2 during CWI-8 and CWI-15 compared with CON but they were similar at failure for the three conditions. Blood lactate, running economy and V˙O2 were not altered by CWI. These data indicate that a 15min period of cold water immersion applied between repeated exhaustive exercise bouts significantly reduces intestinal temperature and enhances post-immersion running performance in normothermic conditions.