Acute and chronic effects of physical exercise on IgA and IgG levels and susceptibility to upper respiratory tract infections: a systematic review and meta-analysis.

This systematic review and meta-analysis aimed at evaluating acute and chronic effects of physical exercise on IgA and IgG levels, as well as its relationship with the susceptibility to develop upper respiratory tract infections (URTI). This systematic review and meta-analysis was conducted and reported in accordance with PRISMA statement. A systematic search of PubMed, Web of Science, and EMBASE was performed in July 2020. This systematic review and meta-analysis included studies in which participants performed acute exercise or chronic physical training and were subjected to analyses of URTI incidence and concentrations of IgA and IgG. The selected studies for systematic review were divided into the following three groups: (I) trials that evaluated the effects of acute exercise in sedentary subjects, (II) trials that evaluated the effects of acute exercise in athletes/trained individuals, and (III) trials that evaluated the effects of chronic physical training on the incidence of URTI, as well as on the levels of IgA and IgG. Acute exercise increases the IgA levels in trained subjects but does not affect its levels in untrained subjects. Such increase in IgA levels induced by acute exercise is greater in trained individual that performed ultramarathon. On the other hand, chronic physical training reduces IgA levels in both trained and untrained subjects, does not change IgA levels in non-military subjects, besides from not affecting IgG levels. The present systematic review and meta-analysis indicates that acute exercise positively influences IgA levels in trained individuals, being this effect pronounced when a strenuous exercise such as ultramarathon is executed. Chronic physical training, in turn, does not affect IgG levels.

Exercise-based cardiac rehabilitation after myocardial revascularization: a systematic review and meta-analysis.

BACKGROUND: The present study aimed to analyze the effects of exercise-based cardiac rehabilitation (CR) on physical performance after myocardial revascularization. In addition, we compared the type and duration of exercise-based CR protocols to determine which ones produced the best performance improvements. METHODS: This systematic review and meta-analysis was conducted and reported in accordance with PRISMA statement. A systematic search of PubMed, Web of Science, SPORTDiscus and ProQuest, was performed in July 2020. Studies that met the following criteria were included: (i) participants submitted to myocardial revascularization (i.e., coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI)), (ii) participants submitted to exercise-based CR, and (iii) participants submitted to protocols for assessing physical performance before and after the exercise-based CR. RESULTS: Thirteen and eleven studies evaluating the effects of exercise-based CR after myocardial revascularization were included in the systematic review and meta-analysis, respectively. Exercise-based CR increased physical performance after myocardial revascularization (mean effect size (ES) 0.75; 95% confidence interval (CI) 0.62, 0.88), particularly when aerobic (ES 0.85; 95% CI 0.68, 1.01) and combined training (ES 1.04; 95% CI 0.70, 1.38) lasting 8-12 weeks (ES 1.20; 95% CI 0.87, 1.53) was prescribed. CONCLUSIONS: The present systematic review and meta-analysis indicates that exercise-based CR increases physical performance after myocardial revascularization. The prescription of physical training for these patients should emphasize aerobic and combined training lasting at least 8-12 weeks, which is more effective in improving physical performance. IMPACT: Our findings demonstrate the effectiveness of physical training in improving physical performance after myocardial revascularization.

Effects of Increased Central Cholinergic Activity on the Metabolic Challenge Induced by Submaximal Exercise in Rats: Adrenomedullary Secretion Influences.

AIM: The aim of this study was to assess the influence of adrenomedullary secretion on the plasma glucose, lactate, and free fatty acids (FFAs) during running exercise in rats submitted to intracerebroventricular (i.c.v.) injection of physostigmine (PHY). PHY i.c.v. was used to activate the central cholinergic system. METHODS: Wistar rats were divided into sham-saline (sham-SAL), sham-PHY, adrenal medullectomy-SAL, and ADM-PHY groups. The plasma concentrations of glucose, lactate, and FFAs were determined immediately before and after i.c.v. injection of 20 µL of SAL or PHY at rest and during running exercise on a treadmill. RESULTS: The i.c.v. injection of PHY at rest increased plasma glucose in the sham group, but not in the ADM group. An increase in plasma glucose, lactate, and FFAs mobilization from adipose tissue was observed during physical exercise in the sham-SAL group; however, the increase in plasma glucose was greater with i.c.v. PHY. Moreover, the hyperglycemia induced by exercise and PHY in the ADM group were blunted by ADM, whereas FFA mobilization was unaffected. CONCLUSION: These results indicate that there is a dual metabolic control by which activation of the central cholinergic pathway increases plasma glucose but not FFA during rest and exercise, and that this hyperglycemic response is dependent on adrenomedullary secretion.

Impaired thermoregulation in spontaneously hypertensive rats during physical exercise is related to reduced hypothalamic neuronal activation.

This study aimed to evaluate the physical exercise-induced neuronal activation in brain nuclei controlling thermoregulatory responses in hypertensive and normotensive rats. Sixteen-week-old male normotensive Wistar rats (NWRs) and spontaneously hypertensive rats (SHRs) were implanted with an abdominal temperature sensor. After recovery, the animals were subjected to a constant-speed treadmill running (at 60% of the maximum aerobic speed) for 30 min at 25 °C. Core (Tcore) and tail-skin (Tskin) temperatures were measured every minute during exercise. Ninety minutes after the exercise, the rats were euthanized, and their brains were collected to determine the c-Fos protein expression in the following areas that modulate thermoregulatory responses: medial preoptic area (mPOA), paraventricular hypothalamic nucleus (PVN), and supraoptic nucleus (SON). During treadmill running, the SHR group exhibited a greater increase in Tcore and an augmented threshold for cutaneous heat loss relative to the NWR group. In addition, the SHRs showed reduced neuronal activation in the mPOA (< 49.7%) and PVN (< 44.2%), but not in the SON. The lower exercise-induced activation in the mPOA and PVN in hypertensive rats was strongly related to the delayed onset of cutaneous heat loss. We conclude that the enhanced exercise-induced hyperthermia in hypertensive rats can be partially explained by a delayed cutaneous heat loss, which is, in turn, associated with reduced activation of brain areas modulating thermoregulatory responses.

The magnitude of physical exercise-induced hyperthermia is associated with changes in the intestinal permeability and expression of tight junction genes in rats.

We investigated whether the magnitude of exercise-induced hyperthermia influences intestinal permeability and tight junction gene expression. Twenty-nine male Wistar rats were divided into four groups: rest at 24 °C and exercise at 13 °C, 24 °C or 31 °C. The exercise consisted of a 90-min treadmill run at 15 m/min, and different ambient temperatures were used to produce distinct levels of exercise-induced hyperthermia. Before the experimental trials, the rats were treated by gavage with diethylenetriaminepentaacetic acid labeled with technetium-99 metastable as a radioactive probe. The rats' core body temperature (TCORE) was measured by telemetry. Immediately after the trials, the rats were euthanized, and the intestinal permeability was assessed by measuring the radioactivity of blood samples. The mRNA levels of occludin and zonula occludens-1 (ZO-1) genes were determined in duodenum samples. Exercise at 24 °C increased TCORE to values close to 39 °C, without changing permeability compared with the resting trial at the same environment. Meanwhile, rats' TCORE exceeded 40 °C during exercise at 31 °C, leading to greater permeability relative to those observed after exercise in the other ambient temperatures (e.g., 0.0037%/g at 31 °C vs. 0.0005%/g at 13 °C; data expressed as medians; p < 0.05). Likewise, the rats exercised at 31 °C exhibited higher mRNA levels of ZO-1 and occludin genes than the rats exercised at 24 °C or 13 °C. The changes in permeability and gene expression were positively and significantly associated with the magnitude of hyperthermia. We conclude that marked hyperthermia caused by exercise in the warmer environment increases intestinal permeability and mRNA levels of tight junction genes.

Infrared photobiomodulation (PBM) therapy improves glucose metabolism and intracellular insulin pathway in adipose tissue of high-fat fed mice.

Obesity represents a continuously growing global epidemic and is associated with the development of type 2 diabetes mellitus. The etiology of type 2 diabetes is related to the resistance of insulin-sensitive tissues to its action leading to impaired blood glucose regulation. Photobiomodulation (PBM) therapy might be a non-pharmacological, non-invasive strategy to improve insulin resistance. It has been reported that PBM therapy in combination with physical exercise reduces insulin resistance. Therefore, the aim of this study was to investigate the effects of PBM therapy on insulin resistance in obese mice. Male Swiss albino mice received low-fat control diet (n = 16, LFC) or high-fat diet (n = 18, HFD) for 12 weeks. From 9th to 12th week, the mice received PBM therapy (LASER) or Sham (light off) treatment and were allocated into four groups: LFC Sham (n = 8), LFC PBM (n = 8), HFD Sham (n = 9), and HFD PBM (n = 9). The PBM therapy was applied in five locations: to the left and right quadriceps muscle, upper limbs and center of the abdomen, during 40 s at each point, once a day, 5 days a week, for 4 weeks (780 nm, 250 mW/cm2, 10 J/cm2, 0.4 J per site; 2 J total dose per day). Insulin signaling pathway was evaluated in the epididymal adipose tissue. PBM therapy improved glucose tolerance and phosphorylation of Akt (Ser473) and reversed the HFD-induced reduction of GLUT4 content and phosphorylation of AS160 (Ser588). Also, PBM therapy reversed the increased area of epididymal and mesenteric adipocytes. The results showed that chronic PBM therapy improved parameters related to obesity and insulin resistance in HFD-induced obesity in mice.

Central cholinergic activation induces greater thermoregulatory and cardiovascular responses in spontaneously hypertensive than in normotensive rats.

There is evidence that central cholinergic stimulation increases heat dissipation in normotensive rats besides causing changes on the cardiovascular system via modulation of baroreceptors activity. However, the contribution of the central cholinergic system on thermoregulatory responses and its relationship with cardiovascular adjustments in spontaneously hypertensive rats (SHRs), an animal model of reduced baroreceptor sensitivity and thermoregulatory deficit, has not been completely clarified. Therefore, the aim of this study was to verify the involvement of the central cholinergic system in cardiovascular and thermoregulatory adjustments in SHRs. Male Wistar rats (n = 17) and SHRs (n = 17) were implanted with an intracerebroventricular cannula for injections of 2 µL of physostigmine (phy) or saline solution. Tail temperature (Ttail), internal body temperature (Tint), systolic arterial pressure (SAP), heart rate (HR) and metabolic rate were registered during 60 min while the animals remained at rest after randomly receiving the injections. The variability of the SAP and the HR was estimated by the fast Fourier transform. Phy treatment began a succession of cardiovascular and thermoregulatory responses that resulted in increased SAP, reduced HR and increased Ttail in both Wistar and SHRs groups. The magnitude of these effects seems to be more intense in SHRs, since the improvement of heat dissipation reflected in Tint. Taken together, these results provide evidence that hypertensive rats present greater cardiovascular and thermoregulatory responses than normotensive rats after central cholinergic stimulation.

Movement Patterns of a U-20 National Women's Soccer Team during Competitive Matches: Influence of Playing Position and Performance in the First Half.

The aim of this study was to determine the match locomotor characteristics of a sample of U-20 Brazilian female soccer players. Seven international matches were analyzed during the 2015 U-20 South American Championship, using global positioning technology. During a typical match, fullbacks and forwards covered greater distances in high-intensity running and sprinting than central defenders and midfielders (effect size [ES]=1.42-3.69). In the final 15 min of a game, total and high-intensity running distance and player load were ≈20 to 35% (ES=0.41-3.86) lower than in the first 15 min period for midfielders, fullbacks, forwards, and central defenders. Sprinting, and high-intensity running distances, and the frequency of accelerations >2 m.s-2 immediately after the most intense 5-min period declined in forwards (ES=1.78-2.67), fullbacks (ES=1.96-5.25), midfielders (ES=1.66-3.77), and central defenders (ES=1.50-4.22). Maintaining 'high' levels of activity in the first half resulted in ≈19% reductions in the second half for sprinting distance and frequency of accelerations >2 m.s-2 (ES=0.43 and 0.88), while increases in these locomotor activities were observed in situations with 'low' levels of activity (ES=0.64 and 1.12, for sprinting and accelerations >2 m.s-2, respectively) (within-subject analysis). The data demonstrate that high-intensity efforts are reduced during various phases of international matches and overall activity patterns vary among playing positions. This information could be useful in the development and prescription of sex- and age-specific training regimes.

Increased brain L-arginine availability facilitates cutaneous heat loss induced by running exercise.

The effects of increased brain availability of L-arginine (L-arg), a precursor for nitric oxide synthesis, on core body temperature (Tcore ) and cutaneous heat loss were evaluated in running rats. One week prior to the experiments, adult male Wistar rats received the following implants: a chronic guide cannula in the lateral cerebral ventricle and a temperature sensor in the abdominal cavity. On the day of the experiments, the rats were assigned to receive a 2-µL intracerebroventricular injection of either NaCl (0.15 mol/L) or L-arg solution (0.825, 1.65 or 3.30 mol/L); Tcore and tail skin temperature were measured while the rats ran at a speed of 18 m/min until they were fatigued. L-arginine induced a dose-dependent reduction in the threshold Tcore required for cutaneous heat loss (38.09 ± 0.20°C for 3.30-mol/L L-arg vs 38.61 ± 0.10°C for saline; P < 0.05), which attenuated the exercise-induced hyperthermia. Although the rats treated with L-arg presented a lower Tcore at the end of exercise (~0.7°C lower after treatment with the highest dose), no changes in the time to fatigue were observed relative to the control trial. These results suggest that brain L-arg controls heat loss during exercise, most likely by modulating the sympathetic vasoconstrictor tonus to skin vessels. Furthermore, despite facilitating cutaneous heat loss mechanisms, increased brain L-arg availability did not enhance physical performance.

L-arginine supplementation prevents increases in intestinal permeability and bacterial translocation in male Swiss mice subjected to physical exercise under environmental heat stress.

Dietary supplementation with l-arginine has been shown to improve the intestinal barrier in many experimental models. This study investigated the effects of arginine supplementation on the intestinal permeability and bacterial translocation (BT) induced by prolonged physical exercise under heat stress. Under anesthesia, male Swiss mice (5-wk-old) were implanted with an abdominal sensor to record their core body temperature (T(core)). After recovering from surgery, the mice were divided into 3 groups: a non-supplemented group that was fed the standard diet formulated by the American Institute of Nutrition (AIN-93G; control), a non-supplemented group that was fed the AIN-93G diet and subjected to exertional hyperthermia (H-NS), and a group supplemented with l-arginine at 2% and subjected to exertional hyperthermia (H-Arg). After 7 d of treatment, the H-NS and H-Arg mice were forced to run on a treadmill (60 min, 8 m/min) in a warm environment (34°C). The control mice remained at 24°C. Thirty min before the exercise or control trials, the mice received a diethylenetriamine pentaacetic acid (DTPA) solution labeled with technetium-99m ((99m)Tc-DTPA) or (99m)Tc-Escherichia coli by gavage to assess intestinal permeability and BT, respectively. The H-NS mice terminated the exercise with T(core) values of ∼40°C, and, 4 h later, presented a 12-fold increase in the blood uptake of (99m)Tc-DTPA and higher bacterial contents in the blood and liver than the control mice. Although supplementation with arginine did not change the exercise-induced increase in T(core), it prevented the increases in intestinal permeability and BT caused by exertional hyperthermia. Our results indicate that dietary l-arginine supplementation preserves the integrity of the intestinal epithelium during exercise under heat stress, acting through mechanisms that are independent of T(core) regulation.

Resveratrol increases brown adipose tissue thermogenesis markers by increasing SIRT1 and energy expenditure and decreasing fat accumulation in adipose tissue of mice fed a standard diet.

PURPOSE: Adipose tissue is central to the regulation of energy balance. Two functionally different fat pads are present in mammals: white adipose tissue, the primary site of triglyceride storage, and brown adipose tissue (BAT), which is specialized in heat production. In this context, new strategies capable of modulating the development and function of white and BAT become relevant. In the present study, we analyzed the influence of resveratrol (sirtuin activator) on energy balance and the expression of thermogenesis markers. METHODS: Mice were divided into two groups: standard diet (ST) and standard diet plus resveratrol (ST + RSV). RESULTS: After 2 months of treatment, ST + RSV mice presented significantly decreased fat accumulation in adipose tissue, with diminished total cholesterol and glucose plasma levels. Additionally, increased oxygen consumption was observed in ST + RSV group. Analyses of mRNA of thermogenesis-related genes showed significant increase in UCP1, SIRT1, PTEN and BMP-7 expression in BAT. CONCLUSION: Our data suggest that improved metabolism produced by oral administration of resveratrol is, at least in part, associated with increased thermogenesis followed by high expression of UCP1 and SIRT1, which can mediate higher energy expenditure and decreased fat accumulation in adipose tissue.

Soluble TNF receptors are produced at sites of inflammation and are inversely associated with self-reported symptoms (WOMAC) in knee osteoarthritis.

The aim of the study was to analyze the concentrations of sTNFR1 and sTNFR2 in both plasma and synovial fluid of patients with primary knee osteoarthritis (OA) and to determine their relationship to self-reported pain, stiffness and physical function. Twenty-seven patients with knee OA and 19 healthy subjects were enrolled in the study. The Western Ontario and McMaster University Osteoarthritis Index questionnaire was used to evaluate self-reported physical function, pain and stiffness. The sTNFR1 and sTNFR2 levels in the plasma and synovial fluid were measured by enzyme-linked immunosorbent assay. The sTNFR1 levels in synovial fluid of OA patients (2,587 ± 66.12 pg/mL) were 2.5-fold higher than in corresponding blood samples and were 1.5-fold higher than in the plasma of healthy controls. The plasma sTNFR2 levels in the patients with knee OA were lower than in healthy controls (2,249 ± 126.3 vs. 2,700 ± 126.3 pg/mL, p < 0.05), and sTNFR2 levels in synovial fluid of knee OA patients (2,021 ± 107.0 pg/mL) were lower than in the plasma of healthy controls. Synovial fluid sTNFR1 levels were negatively correlated with pain and physical function self-reported (r s - 0.6785, p < 0.0001 and r s - 0.4194, p = 0.03, respectively). Synovial fluid sTNFR2 levels were negatively correlated with pain and joint stiffness (r s - 0.5433, p = 0.01 and r s - 0.4249, p = 0.02, respectively). The findings of this study demonstrated the presence of soluble receptors for TNF-alpha, particularly sTNFR1, in the synovial fluid of patients with primary knee OA and the relationship of these receptors with clinical parameters.

Involvement of BDNF in knee osteoarthritis: the relationship with inflammation and clinical parameters.

The aim of this study was to analyze the levels of brain-derived neurotrophic factor (BDNF) in both the plasma and synovial fluid of patients with primary knee osteoarthritis compared with control individuals and to investigate the relationship between BDNF levels and self-reported pain. Twenty-seven patients with knee osteoarthritis (OA) and 19 healthy subjects were enrolled in the study. Anteroposterior knee radiographs were taken to determine the disease severity of the affected knee. Radiographic grading of OA in the knee was performed using the Kellgren-Lawrence criteria. The BDNF levels in the plasma and synovial fluid were measured by enzyme-linked immunosorbent assay. The mean plasma BDNF levels of the knee OA patients were significantly higher than that of the healthy controls (2,378 ± 1,067.2 vs. 1,756 ± 804.3 pg/mL, p < 0.05). BDNF levels in the synovial fluid of OA patients (358.9 ± 178.4 pg/mL) were sixfold lower than in corresponding blood samples (p < 0.0001) and fourfold lower than in the plasma of healthy controls (p < 0.0001). Subsequent analyses showed that the plasma BDNF levels significantly correlated with self-reported pain (Western Ontario and McMaster Universities Osteoarthritis Index) (r s = 0.39, p = 0.04). Furthermore, no correlation was found between the plasma and synovial fluid BDNF concentrations and knee OA severity. The findings of this study suggest that systemic BDNF levels are most likely associated with the mechanism of joint pain in knee OA in the acute stage of joint inflammatory process. Further studies are necessary to address the functional role of BDNF in the modulation of pain to establish new therapeutic implications.

Physical exercise-induced changes in the core body temperature of mice depend more on ambient temperature than on exercise protocol or intensity.

The mechanisms underlying physical exercise-induced hyperthermia may be species specific. Therefore, the present study aimed to investigate the effects of exercise intensity and ambient temperature on the core body temperature (T core) of running mice, which provide an important experimental model for advancing the understanding of thermal physiology. We evaluated the influence of different protocols (constant- or incremental-speed exercises), treadmill speeds and ambient temperatures (T a) on the magnitude of exercise-induced hyperthermia. To measure T core, a telemetric sensor was implanted in the abdominal cavity of male adult Swiss mice under anesthesia. After recovering from the surgery, the animals were familiarized to running on a treadmill and then subjected to the different running protocols and speeds at two T a: 24 °C or 34 °C. All of the experimental trials resulted in marked increases in T core. As expected, the higher-temperature environment increased the magnitude of running-induced hyperthermia. For example, during incremental exercise at 34 °C, the maximal T core achieved was increased by 1.2 °C relative to the value reached at 24 °C. However, at the same T a, neither treadmill speed nor exercise protocol altered the magnitude of exercise-induced hyperthermia. We conclude that T core of running mice is influenced greatly by T a, but not by the exercise protocols or intensities examined in the present report. These findings suggest that the magnitude of hyperthermia in running mice may be regulated centrally, independently of exercise intensity.

Is melatonin as an ergogenic hormone a myth? a systematic review and meta-analysis.

PURPOSE: Melatonin supplementation has been disclosed as an ergogenic substance. However, the effectiveness of melatonin supplementation in healthy subjects has not been systematically investigated. The present study analyzed the effects of melatonin supplementation on physical performance and recovery. In addition, it was investigated whether exercise bout or training alter melatonin secretion in athletes and exercise practitioners. METHODS: This systematic review and meta-analysis were conducted and reported according to the guidelines outlined in the PRISMA statement. Based on the search and inclusion criteria, 21 studies were included in the systematic review, and 19 were included in the meta-analysis. RESULTS: Melatonin supplementation did not affect aerobic performance relative to time trial (-0.04; 95% CI: -0.51 to 0.44) and relative to VO2 (0.00; 95% CI: -0.57 to 0.57). Also, melatonin supplementation did not affect strength performance (0.19; 95% CI: -0.28 to 0.65). Only Glutathione Peroxidase (GPx) secretion increased after melatonin supplementation (1.40; 95% CI: 0.29 to 2.51). Post-exercise melatonin secretion was not changed immediately after an exercise session (0.56; 95% CI: -0.29 to 1.41) and 60 min after exercise (0.56; 95% CI: -0.29 to 1.41). CONCLUSION: The data indicate that melatonin is not an ergogenic hormone. In contrast, melatonin supplementation improves post-exercise recovery, even without altering its secretion.

The central administration of C75, a fatty acid synthase inhibitor, activates sympathetic outflow and thermogenesis in interscapular brown adipose tissue.

The present work investigated the participation of interscapular brown adipose tissue (IBAT), which is an important site for thermogenesis, in the anti-obesity effects of C75, a synthetic inhibitor of fatty acid synthase (FAS). We report that a single intracerebroventricular (i.c.v.) injection of C75 induced hypophagia and weight loss in fasted male Wistar rats. Furthermore, C75 induced a rapid increase in core body temperature and an increase in heat dissipation. In parallel, C75 stimulated IBAT thermogenesis, which was evidenced by a marked increase in the IBAT temperature that preceded the rise in the core body temperature and an increase in the mRNA levels of uncoupling protein-1. As with C75, an i.c.v. injection of cerulenin, a natural FAS inhibitor, increased the core body and IBAT temperatures. The sympathetic IBAT denervation attenuated all of the thermoregulatory effects of FAS inhibitors as well as the C75 effect on weight loss and hypophagia. C75 induced the expression of Fos in the paraventricular nucleus, preoptic area, dorsomedial nucleus, ventromedial nucleus, and raphé pallidus, all of which support a central role of FAS in regulating IBAT thermogenesis. These data indicate a role for IBAT in the increase in body temperature and hypophagia that is induced by FAS inhibitors and suggest new mechanisms explaining the weight loss induced by these compounds.

Differences between 48 and 72-hour intervals on match load and subsequent recovery: a report from the Brazilian under-20 national football team.

Purpose: To compare the external and internal load and subsequent recovery of football players after international tournament matches separated by 48 h vs. 72 h. Methods: A total of 14 male football players from the Brazilian National Team, competing in the 2019 South American Under-20 Championship, participated in the study. Match load was quantified using GPS variables and perceived exertion ratings (1). Additionally, before and 13-15 h after each match, players answered questions about the number of hours and quality of sleep, recovery status, and muscle soreness (0-10) and provided a blood sample for creatine kinase and reactive C-protein analysis. Values of all variables were compared between matches played with 48-h intervals (matches 1-4) and 72-h intervals (matches 5-8). Results: No significant differences in performance or perceptual parameters were observed between matches (p = 0.136-0.953). However, CK was higher in matches 1-4 compared to matches 5 and 6; and ΔPCR was higher in matches 2 and 3 compared to matches 5 and 6, and in match 4 compared to matches 5 and 8. Conclusions: After matches with a 48-h rest interval, players showed increased markers of inflammation and muscle damage compared to matches with a 72-h rest interval.

Dietary Soy Isoflavones Prevent Metabolic Disturbs Associated with a Deleterious Combination of Obesity and Menopause.

This study aimed to evaluate the effects of soy isoflavone supplementation (25 mg/kg) on insulin resistance and inflammation in adipose tissue in an experimental model of menopause-obesity. Twenty-four female Wistar rats were ovariectomized (O) and distributed among the groups: OSD-ovariectomized rats submitted to normocaloric standard diet (n = 6); OHF-ovariectomized rats submitted to high-fat diet (n = 9); and OHFI-ovariectomized rats submitted to high-fat diet with isoflavones (n = 9). Weight gain, body adiposity, food and caloric intake, blood pressure, and glucose tolerance were assessed. After 24 weeks, the rats were euthanized; the thoracic blood collected for serum insulin determination and the homeostatic model assessment-insulin resistance) (HOMA-IR) and homeostatic model assessment-ß cell (HOMA-ß) indices were calculated. Abdominal adipose tissues were removed, weighed, and fixed for immunohistochemical and morphometric studies. Isoflavones decreased weight gain and blood pressure without changing the food and caloric intake (P < .05). Isoflavones did not affect the weight of the abdominal adipose tissue depots (P < .05). Although they did not alter glucose tolerance, the isoflavones reduced HOMA-IR and HOMA-ß, serum insulin levels, in addition to reducing adipocytes' size (P < .05). The number of macrophages, lymphocytes, and crown-like structures in adipose tissue was lower in the group treated with isoflavones (P < .05). In conclusion, our data show that dietary soy isoflavones' supplementation prevents many of well-known deleterious combination of obesity and menopause on metabolism, such as body overweight, adipocyte hypertrophy, and hypertension, as well as insulin resistance and adipose tissue inflammation.

Fatigue and Recovery Time Course After Female Soccer Matches: A Systematic Review And Meta-analysis.

BACKGROUND: This study aimed to analyze the extent of fatigue responses after female soccer matches and the ensuing recovery time course of performance, physiological, and perceptual responses. METHODS: Three databases (PubMed, Web of Science, and SPORTDiscus) were searched in October 2020 and updated in November 2021. Studies were included when participants were female soccer players, regardless of their ability level. Further, the intervention was an official soccer match with performance, physiological, or perceptual parameters collected pre- and post-match (immediately, 12 h, 24 h, 48 h, or 72 h-post). RESULTS: A total of 26 studies (n = 465 players) were included for meta-analysis. Most performance parameters showed some immediate post-match reduction (effect size [ES] = - 0.72 to - 1.80), apart from countermovement jump (CMJ; ES = - 0.04). Reduced CMJ performance occurred at 12 h (ES = - 0.38) and 24 h (ES = - 0.42) and sprint at 48 h post-match (ES = - 0.75). Inflammatory and immunological parameters responded acutely with moderate-to-large increases (ES = 0.58-2.75) immediately post-match. Creatine kinase and lactate dehydrogenase alterations persisted at 72 h post-match (ES = 3.79 and 7.46, respectively). Small-to-moderate effects were observed for increased cortisol (ES = 0.75) and reduced testosterone/cortisol ratio (ES = -0.47) immediately post-match, while negligible to small effects existed for testosterone (ES = 0.14) and estradiol (ES = 0.34). Large effects were observed for perceptual variables, with increased fatigue (ES = 1.79) and reduced vigor (ES = - 0.97) at 12 h post-match, while muscle soreness was increased immediately post (ES = 1.63) and at 24 h post-match (ES = 1.00). CONCLUSIONS: Acute fatigue exists following female soccer matches, and the performance, physiological, and perceptual parameters showed distinctive recovery timelines. Importantly, physical performance was recovered at 72 h post-match, whereas muscle damage markers were still increased at this time point. These timelines should be considered when planning training and match schedules. However, some caution should be advised given the small number of studies available on this population. REGISTRATION: The protocol for this systematic review was pre-registered on the International Prospective Register of Systematic Reviews (PROSPERO, Registration Number: CRD42021237857).

Corrigendum: Modulation of leukocyte subsets mobilization in response to exercise by water immersion recovery.

[This corrects the article DOI: 10.3389/fphys.2022.867362.].