Effects of Different Protocols of Moderate-Intensity Intermittent Hypoxic Training on Mental Health and Quality of Life in Brazilian Adults Recovered from COVID-19: The AEROBICOVID Double-Blind Randomized Controlled Study.

The aim of this study was to investigate the effects of different protocols of moderate-intensity intermittent hypoxic training in patients who had recovered from COVID-19 on quality of life (QoL) and mental health. The sample of this clinical trial-controlled double-blind study consisted of 67 participants aged 30-69 years, who were organized randomly according to Normoxia, Hypoxia, Hypoxia Recovery or Control Group. Eight weeks of cycle ergometer training were performed with a frequency of three training sessions per week in normoxic or hypoxic conditions (with or without hypoxic recovery). Health-related QoL and Mental Health Status were evaluated by 12-Item Short Form Survey and Depression Anxiety and Stress Scale instruments, respectively. All training groups improved the QoL's physical dimensions (Baseline-Post: Normoxia Group 42.1 (11.0)-48.7 (7.0), Hypoxia Group 46.9 (11.8)-53.5 (6.6) and Hypoxia Recovery Group 45.8 (9.2)-51.1 (5.3)) and mental dimensions (Baseline-Post: Normoxia Group 48.8 (7.9)-54.6 (4.6), Hypoxia Group 45.2 (7.7)-53.2 (3.8) and Hypoxia Recovery Group 46.5 (9.7)-52.0 (9.9)). Regarding mental health outcomes, all training groups decreased depressive symptoms (66.7% Normoxia, 31.2% Hypoxia Recovery and 31% Hypoxia groups), anxiety symptoms (46.5% Normoxia, 45.9% Hypoxia Recovery and 39.5% in the Hypoxia groups) and stress symptoms (40.6% Normoxia, 36.3% Hypoxia Recovery and 22.1% Hypoxia groups). Significant statistical difference was not found between groups. Normoxic and hypoxic training showed a similar effect on QoL and the mental health of Brazilian adults who had recovered from COVID-19.

A pilot study on the effects of far-infrared-emitting fabric on neuromuscular performance of knee extensor and male fertility.

The aim of this study was to evaluate the time course of the effects of far-infrared emitting fabric (FIR) on neuromuscular performance of knee extensor over 120 h and to investigate whether the use of FIR affects semen. This is a crossover, randomized, double-blind, and placebo-controlled trial split into neuromuscular and fertility assessments. Four (28.8 ± 4.7 years old) and six (29 ± 3.9 years old) healthy, resistance-trained males completed all neuromuscular and fertility assessments, respectively. In neuromuscular assessments, for five consecutive days, the participants underwent neuromuscular tests in an isokinetic dynamometer (maximal isometric voluntary contraction (MVC) and fatigue test) every 24 h in both conditions (FIR and Placebo). In fertility assessments, participants performed three semen collections: Baseline, FIR, and Placebo. FIR and Placebo collections were performed after five consecutive days of use of the pants. Conventional parameters and sperm DNA fragmentation were evaluated. In the FIR condition, the participants showed significant differences in total work at 96 h (p < 0.001; Cohen's d = 3.73), 120 h (p = 0.01; Cohen's d = 2.65), and pre-MVC at 120 h (p = 0.02; Cohen's d = 2.15) when compared to Placebo. FIR did not significantly (p > 0.05) affect the conventional semen parameters or sperm DNA fragmentation compared to Baseline or Placebo. FIR improved the knee extensor neuromuscular performance of healthy resistance-trained individuals, with 112.4 ± 7.8 h accumulated, and did not affect their seminal parameters (conventional or sperm DNA fragmentation), with 113.1 ± 10.2 h accumulated.

Impact of Intermittent Fasting Combined With High-Intensity Interval Training on Body Composition, Metabolic Biomarkers, and Physical Fitness in Women With Obesity.

Background: Intermittent fasting (IF) is a dietary approach that is widely popular due to its effects on weight and body fat loss, but it does not appear to ensure muscle mass preservation. Incorporating high-intensity interval training (HIIT) into an individual's routine could be an attractive and viable therapeutic option for improving body composition, lifestyle and health promotion. Problematizing the emerging situation of fighting obesity, led us to clarify gaps about IF and hypothesize that IF and HIIT in conjunction may protect against muscle mass decline without impairing nitrogen balance (NB), in addition to improving the physical fitness of women with obesity. Objectives: To evaluate the effects of IF alone and combined with HIIT on body composition, NB and strength and physical fitness in women with obesity. Methods: Thirty-six women (BMI 34.0 ± 3.2; 32.2 ± 4.4 years) participated and were randomly distributed into three groups: (1) Intermittent fasting combined with exercise group (IF + EX); (2) Exercise group (EX); and (3) Intermittent fasting group (IF). The interventions took place over 8 weeks and all evaluations were performed pre and post-intervention. The HIIT circuit was performed 3x/week, for 25 mins/session, at 70-85% of the maximum heart rate. The intermittent fasting protocol was a 5:2 diet with two meals within 6 h on fasting days, being 25% of total energy intake, plus 18 h of complete fasting. The protocol was performed 2x/week and 5 days of ad libitum ingestion. Resting metabolic rate (RMR) was measured by indirect calorimetry, body composition by BodPod®, NB from urinary nitrogen, food consumption by food records and physical and strength performance were measured by physical tests. ANOVA two-way repeated measures mixed model was performed followed by Sidak post hoc (p < 0.05). This project was registered in ClinicalTrials.gov, NCT05237154. Results: There were a reduction in body weight (P = 0.012) and BMI (P = 0.031) only in the IF + EX group. There was body fat loss in the IF + EX group (-4%, P < 0.001) and in the EX group (-2.3%, P = 0.043), an increase in fat-free mass in the IF + EX group (+3.3%, P < 0.001) and also in the EX group (+2%, P = 0.043), without differences between groups and the IF group showed no changes. The NB was equilibrium in all groups. All parameters of aerobic capacity and strength improved. Conclusion: Combining IF with HIIT can promote increments in fat-free mass, NB equilibrium and improve physical fitness and strength.

Chronic rapamycin treatment decreases hepatic IL-6 protein, but increases autophagy markers as a protective effect against the overtraining-induced tissue damage.

Regular endurance exercise is a non-pharmacological strategy to protect the liver against diseases. Conversely, exercise may be harmful when excessive, the so-called overtraining. As expected, mice who underwent an overtraining protocol presented higher levels of proinflammatory cytokines in the serum and liver. Based on the relationship among overtraining, inflammation and mammalian target of rapamycin complex 1 (mTORC1) upregulation, the present study verified if animals submitted to an overtraining protocol, but with inhibition of the mTOR pathway via rapamycin injections could mitigate the liver and serum inflammation. Once autophagy can be linked to the improvement of hepatic dysfunction, we also investigated if the inhibition of mTORC1 by rapamycin can improve hepatic autophagy. The animals were randomized into four groups: control (CT; sedentary mice), overtraining by downhill running (OT; mice submitted to the downhill running-based overtraining protocol), overtraining by downhill running with chronic administration of rapamycin (OT/Rapa; mice submitted to the downhill running-based overtraining protocol with intraperitoneal injections of rapamycin) and aerobic (AER; submitted to aerobic training protocol). The serum and liver of the animals were used for biochemical analysis, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunoblotting. The main results are (a) OT and OT/Rapa protocols decreased the performance; (b) the protein levels of interleukin 6 (IL-6) were higher for the OT group; the OT/Rapa group reduced the autophagic genes, increased the microtubule-associated protein light chain 3 II/I (LC3II/LC3I) protein ratio and decreased the sequestosome 1 (SQSTM1) protein. In conclusion, rapamycin appears efficiently to increase the autophagy proteins and decrease IL-6 protein in the liver of overtraining mice.

Autonomic Disbalance During Systemic Inflammation is Associated with Oxidative Stress Changes in Sepsis Survivor Rats.

Sepsis affects 31.5 million people worldwide. It is characterized by an intense drop in blood pressure driving to cardiovascular morbidity and mortality. Modern supportive care has increased survival in patients; however, after experiencing sepsis, several complications are observed, which may be potentiated by new inflammatory events. Nevertheless, the interplay between sepsis survivors and a new immune challenge in cardiovascular regulation has not been previously defined. We hypothesized that cecal ligation and puncture (CLP) cause persistent cardiovascular dysfunctions in rats as well as changes in autonomic-induced cardiovascular responses to lipopolysaccharide (LPS). Male Wistar rats had mean arterial pressure (MAP) and heart rate (HR) recorded before and after LPS or saline administration to control or CLP survivor rats. CLP survivor rats had similar baseline MAP and HR when compared to control. LPS caused a drop in MAP accompanied by tachycardia in control, while CLP survivor rats had a noteworthy enhanced MAP and a blunted tachycardia. LPS-induced hemodynamic changes were related to an autonomic disbalance to the heart and resistance vessels that were expressed as an increased low- and high-frequency power of pulse interval in CLP survivors after saline and enhancement in the low-frequency power of systolic arterial pressure in control rats after LPS. LPS-induced plasma interferon γ, but not interleukin-10 surges, was blunted in CLP survivor rats. To further access whether or not LPS-induced autonomic disbalance in CLP survivor rats was associated with oxidative stress dysregulation, superoxide dismutase (SOD) activity and thiobarbituric acid reactive substances (TBARS) plasma levels changes were measured. LPS-induced oxidative stress was higher in CLP survivor rats. These findings indicate that key changes in hemodynamic regulation of CLP survivors rats take place in response to LPS that are associated with oxidative stress changes, i.e., reduced SOD activity and increased TBARS levels.

Temporomandibular joint arterial variability.

The study aimed to investigate temporomandibular joint (TMJ) arterial variability. In this prospective study, the vasculature variability was studied using a 3D volume rendering CT angiography including random patients at two hospitals. A 16-quadrant (A1-D4) evaluation grid was developed using the Frankfurt plan as main reference. For each quadrant, the number of arterial ramus or branches was scored as clearly visible (2), partially visible (1), or not visible (0). A total of 50 patients were enrolled (mean age of 62.9 ± 16.0); 21 (42%) were men, and 29 (58%) were women. The authors observed bilaterally higher arterial density in the posterior aspect of the ascending ramus of the mandible (p < 0.0001), corresponding to quadrants B2 (5.92 ± 2.27 and 6.14 ± 2.56), B3 (9.76 ± 2.97 and 11.18 ± 2.86) and B4 (7.38 ± 2.78 and 8.10 ± 2.42). A strong correlation was found between the number of vessels and the variability of the region (r = 0.87, p = 0.00001). No differences were observed between men and women. Within the limitations of the study, arterial variability was observed in the TMJ territory. The posterior zone of the condyle and ramus is the most vascularized area, with great variability, representing an increased risk for surgical bleeding. Therefore, this knowledge seems to be particularly relevant for surgeons dedicated to TMJ and other facial surgery or facial/cerebral radiologic interventions. The authors encourage future studies to include larger samples and to identify thoroughly the arterial branches in this area.

Recent Advances in Molecular Hydrogen Research Reducing Exercise-Induced Oxidative Stress and Inflammation.

Physical exercise-induced oxidative stress and inflammation may be beneficial when exercise is a regular activity, but it is rather harmful when exercise is exhaustive and performed by unaccustomed organisms. Molecular hydrogen (H2) has recently appeared as a potent antioxidant and anti-inflammatory molecule in numerous pathological conditions. However, its role is relatively unknown under physiological conditions such as physical exercise. Therefore, this review summarizes the current knowledge of the H2, reducing oxidative stress and inflammation in physical exercise, reporting data from both animal and human studies.

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-1ß, 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.

Comparação da aptidão física de mulheres adultas e idosas de acordo com o histórico de quedas e a prática regular de diferentes modalidades de exercícios físicos / Comparison of the physical fitness of older adult women according to the history of falls and the regular practice of different physical exercises

RESUMO: Objetivos:Comparar a aptidão física de mulheres de acordo com o histórico de quedas e a prática regular de diferentes modalidades de exercícios físicos (treinamento combinado: musculação e resistência aeróbia; treinamento funcional: multicomponente; e treinamento multimodal: duas ou mais modalidades). Métodos: Estudo transversalcom 44 mulheres (idade entre 50 e 80 anos). Foram coletados dados sociodemográficos e sobre o histórico de quedas no último ano, além da avaliação antropométrica e testes motores (flexibilidade, força de membros superiores e inferiores, capacidade aeróbia e agilidade e equilíbrio dinâmico) para avaliar a aptidão física. Na análise estatística, foram realizados o Teste t para amostras independentes e a ANCOVA utilizando idade, índice de massa corporal e tempo de exercício físico como covariáveis. Resultados: As participantes que tiveram ocorrência de quedas no último ano apresentaram piores resultados nos testes de flexibilidade (sentar e alcançar e mãos nas costas), força de membros superiores (flexão de cotovelo) e de membros inferiores (sentar e levantar), bem como capacidade aeróbia (teste de caminhada de seis minutos). Em relação às diferentes modalidades de exercícios físicos, não foi possível observar diferença estatística para nenhuma das variáveis estudadas. Entretanto, resultados satisfatórios de acordo com os valores normativos foram observados nos três grupos. Conclusões: O grupo com histórico de quedas apresentou piores resultados na aptidão física. Em relação às diferentes modalidades de treinamento, não houve diferença entre os grupos para nenhuma variável analisada. Entretanto, observa-se que estas modalidades são importantes para a manutenção de bons níveis de aptidão física no contexto do envelhecimento

ABSTRACT: Objectives: Comparing women's physical fitness according to the history of falls and regular practice of different physical exercises (combined training: strength and aerobic training; functional training: multicomponent; and multimodal training: two or more styles). Methods: A cross-sectional study was conducted with 44 women (aged between 50 and 80 years old). Sociodemographic data and history of falls in the last year were collected, in addition to anthropometric assessment and motor tests (flexibility, upper and lower limb strength, aerobic capacityand agility, and dynamic balance) to assess physical fitness. In the statistical analysis, independent samples t-test and ANCOVA using age, body mass index, and time of physical exercise as covariates were performed. Results: The participants who had falls in the last year presented worse outcomes in the flexibility tests (sit and reach and hands-on-the back), strength tests of upper limbs (elbow flexion), and lower limbs (sit and stand up), as well as aerobic capacity (six-minute walking test). Regarding the different modalities of exercises, it was not possibleto observe statistical differences for any of the variables studied. However, satisfactory results according to the normative values were observed in the three groups. Conclusions: The group with a history of falls had worse outcomes in physical fitness. Regarding the different modalities of training, there was no difference between the groups for any variable analyzed. However, it seems that these modalities are essential to maintain satisfactorylevels of physical fitness in the context of aging.

Increased lipopolysaccharide-induced hypothermia in neurogenic hypertension is caused by reduced hypothalamic PGE2 production and increased heat loss.

KEY POINTS: The mechanisms involved in hypothermia and fever during systemic inflammation (SI) remain largely unknown. Our data support the contention that brain-mediated mechanisms are different in hypertension during SI. Considering that, clinically, it is not easy to assess all mechanisms involved in cardiovascular and thermoregulatory control during SI, the present study sheds light on these integrated mechanisms that may be triggered simultaneously in septic hypertensive patients. The result obtained demonstrate that, in lipopolysaccharide-induced SI, an increased hypothermia is observed in neurogenic hypertension, which is caused by reduced hypothalamic prostaglandin E2 production and increased heat loss in conscious rats. Therefore, the results of the present study provide useful insight for clinical trials evaluating the thermoregulatory outcomes of septic patients with hypertension. ABSTRACT: Hypertension is a prevalent disease characterized by autonomic-induced elevated and sustained blood pressure levels and abnormal body core temperature (Tb) regulation. The present study aimed to determine the brain-mediated mechanisms involved in the thermoregulatory changes observed during lipopolysaccharide (LPS)-induced systemic inflammation (SI; at a septic-like model) in spontaneously hypertensive rats (SHR). We combined Tb and skin temperature (Tsk) analysis, assessment of prostaglandin (PG) E2 levels (the proximal mediator of fever) in the anteroventral region of the hypothalamus (AVPO; an important site for Tb control), oxygen consumption analysis, cardiovascular recordings, assays of inflammatory markers, and evaluation of oxidative stress in the plasma and brain of male Wistar rats and SHR that had received LPS (1.5 mg kg-1 ) or saline. LPS induced hypothermia followed by fever in Wistar rats, whereas, in SHR, a maintained hypothermia without fever were observed. These thermoregulatory responses were associated with an increased heat loss in SHR compared to Wistar rats. We measured LPS-induced increased PGE2 levels in the AVPO in Wistar rats, but not in SHR. The LPS-induced drop in blood pressure was higher in SHR than in Wistar rats. Furthermore, LPS-induced plasma and brain [regions involved in autonomic control: nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM)] cytokine surges were blunted, whereas oxidative stress was higher in SHR. LPS-induced SI leads to blunted cytokine surges both systemically (plasma) and centrally (NTS and RVLM) and reduced hypothalamic PGE2 production, which are all associated with increased hypothermia mediated by increased heat loss, but not by heat production, in SHR.

Inhaled molecular hydrogen attenuates intense acute exercise-induced hippocampal inflammation in sedentary rats.

Physical exercise-induced inflammation may be beneficial when exercise is regular but it may be harmful when exercise is intense and performed by unaccustomed individuals/rats. Molecular hydrogen (H2) has recently emerged as a powerful anti-inflammatory, antioxidant and anti-apoptotic molecule in a number of pathological conditions, but little is known about its putative role under physiological conditions such as physical exercise. Therefore, we tested the hypothesis that H2 decreases intense acute exercise-induced inflammation in the hippocampus, since it is a brain region particularly susceptible to inflammation. Moreover, we also assessed hippocampus oxidative status. Rats ran on a sealed treadmill inhaling either the H2 (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and hippocampal samples were collected immediately or 3 h after exercise. We measured hippocampal levels of cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6 and IL-10] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. Exercise increased TNF-α, IL-6 and IL-10 immediately after the session, whereas no change in IL-1ß levels was observed. Conversely, exercise did not cause any change in SOD activity, TBARS and NOx levels. H2 inhibited the exercise-induced surges in TNF-α and IL-6, and potentiated the IL-10 surge, immediately after the exercise. Moreover, no change in IL1-ß levels of rats inhaling H2 was observed. Regarding the oxidative stress markers, H2 failed to cause any change in SOD activity, TBARS and NOx levels. No significant change was observed in any of the assessed parameters 3 h after the exercise bout. These data are consistent with the notion that H2 acts as a powerful anti-inflammatory agent not only down-modulating pro-inflammatory cytokines (TNF-α and IL-6) but also upregulating an anti-inflammatory cytokine (IL-10) production without affecting the local oxidative stress status. These data indicate that H2 effectively decreases exercise-induced inflammation in the hippocampus, despite the fact that this region is particularly prone to inflammatory insults.

Splenic anti-inflammatory reflex in immune tolerance.

The injection of repeated doses of lipopolysaccharide (LPS) results in attenuation of the immune response, which is an important mechanism to prevent deleterious long-term excessive inflammation. Brain-mediated mechanisms are involved in this endogenous anti-inflammatory effect, but nothing is known about the putative role of the splenic anti-inflammatory reflex (which has recently been described as a powerful mechanism involved in the suppression of immune response) during immune tolerance. Therefore, we tested the hypothesis that endotoxin tolerance is at least in part mediated by the splenic anti-inflammatory reflex. Body core temperature (Tb) was measured in rats previously submitted to splenectomy. Immune tolerance was induced by means of five consecutive LPS (100 µg/kg) intraperitoneal injections at 24-h intervals. In sham operated rats, we observed a significant reduction of the febrile response to repeated administration of LPS, which was not altered in rats submitted to splenectomy. Moreover, plasma pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6] and prostaglanding E2 (PGE2) surges besides preoptic PGE2 levels were observed after the first LPS administration but not in tolerant animals, and this pattern was kept the same in splenectomized rats. These data are consistent with the notion that the splenic anti-inflammatory reflex does not modulate immune tolerance in rats.

Molecular hydrogen potentiates hypothermia and prevents hypotension and fever in LPS-induced systemic inflammation.

Molecular hydrogen (H2) exerts anti-oxidative, anti-apoptotic, and anti-inflammatory effects. Here we tested the hypothesis that H2 modulates cardiovascular, inflammatory, and thermoregulatory changes in systemic inflammation (SI) induced by lipopolysaccharide (LPS) at different doses (0.1 or 1.5 mg/kg, intravenously, to induce mild or severe SI) in male Wistar rats (250-300 g). LPS or saline was injected immediately before the beginning of 360-minute inhalation of H2 (2% H2, 21% O2, balanced with nitrogen) or room air (21% O2, balanced with nitrogen). Deep body temperature (Tb) was measured by dataloggers pre-implanted in the peritoneal cavity. H2 caused no change in cardiovascular, inflammatory parameters, and Tb of control rats (treated with saline). During mild SI, H2 reduced plasma surges of proinflammatory cytokines (TNF-α and IL-6) while caused an increase in plasma IL-10 (anti-inflammatory cytokine) and prevented fever. During severe SI, H2 potentiated hypothermia, and prevented fever and hypotension, which coincided with reduced plasma nitric oxide (NO) production. Moreover, H2 caused a reduction in surges of proinflammatory cytokines (plasma TNF-α and IL-1ß) and prostaglandin E2 [(PGE2), in plasma and hypothalamus], and an increase in plasma IL-10. These data are consistent with the notion that H2 blunts fever in mild SI, and during severe SI potentiates hypothermia, prevents hypotension reducing plasma NO production, and exerts anti-inflammatory effects strong enough to prevent fever by altering febrigenic signaling and ultimately down-modulating hypothalamic PGE2 production.

Molecular hydrogen reduces acute exercise-induced inflammatory and oxidative stress status.

Physical exercise induces inflammatory and oxidative markers production in the skeletal muscle and this process is under the control of both endogenous and exogenous modulators. Recently, molecular hydrogen (H2) has been described as a therapeutic gas able to reduced oxidative stress in a number of conditions. However, nothing is known about its putative role in the inflammatory and oxidative status during a session of acute physical exercise in sedentary rats. Therefore, we tested the hypothesis that H2 attenuates both inflammation and oxidative stress induced by acute physical exercise. Rats ran at 80% of their maximum running velocity on a closed treadmill inhaling either the H2 gas (2% H2, 21% O2, balanced with N2) or the control gas (0% H2, 21% O2, balanced with N2) and were euthanized immediately or 3 h after exercise. We assessed plasma levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6] and oxidative markers [superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. In addition, we evaluated the phosphorylation status of intracellular signaling proteins [glycogen synthase kinase type 3 (GSK3α/ß) and the cAMP responsive element binding protein (CREB)] that modulate several processes in the skeletal muscle during exercise, including changes in exercise-induced reactive oxygen species (ROS) production. As expected, physical exercise increased virtually all the analyzed parameters. In the running rats, H2 blunted exercise-induced plasma inflammatory cytokines (TNF-α and IL-6) surges. Regarding the oxidative stress markers, H2 caused further increases in exercise-induced SOD activity and attenuated the exercise-induced increases in TBARS 3 h after exercise. Moreover, GSK3α/ß phosphorylation was not affected by exercise or H2 inhalation. Otherwise, exercise caused an increased CREB phosphorylation which was attenuated by H2. These data are consistent with the notion that H2 plays a key role in decreasing exercise-induced inflammation, oxidative stress, and cellular stress.

Effect of Physical Exercise on the Febrigenic Signaling is Modulated by Preoptic Hydrogen Sulfide Production.

We tested the hypothesis that the neuromodulator hydrogen sulfide (H2S) in the preoptic area (POA) of the hypothalamus modulates the febrigenic signaling differently in sedentary and trained rats. Besides H2S production rate and protein expressions of H2S-related synthases cystathionine ß-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MPST) and cystathionine γ-lyase (CSE) in the POA, we also measured deep body temperature (Tb), circulating plasma levels of cytokines and corticosterone in an animal model of systemic inflammation. Rats run on a treadmill before receiving an intraperitoneal injection of lipopolysaccharide (LPS, 100 µg/kg) or saline. The magnitude of changes of Tb during the LPS-induced fever was found to be similar between sedentary and trained rats. In sedentary rats, H2S production was not affected by LPS. Conversely, in trained rats LPS caused a sharp increase in H2S production rate that was accompanied by an increased CBS expression profile, whereas 3-MPST and CSE expressions were kept relatively constant. Sedentary rats showed a significant LPS-induced release of cytokines (IL-1ß, IL-6, and TNF-α) which was virtually abolished in the trained animals. Correlation between POA H2S and IL-6 as well as TNF-α was observed. Corticosterone levels were augmented after LPS injection in both groups. We found correlations between H2S and corticosterone, and corticosterone and IL-1ß. These data are consistent with the notion that the responses to systemic inflammation are tightly regulated through adjustments in POA H2S production which may play an anti-inflammatory role downmodulating plasma cytokines levels and upregulating corticosterone release.

Bone repair: Effects of physical exercise and LPS systemic exposition.

Bone repair can be facilitated by grafting, biochemical and physical stimulation. Conversely, it may be delayed lipopolysaccharide (LPS). Physical exercise exerts beneficial effects on the bone, but its effect on bone repair is not known. We investigated the effect of exercise on the LPS action on bone healing through bone densitometry, quantitative histological analysis for bone formation rate and immunohistochemical markers in sedentary and exercised animals. Rats ran on the treadmill for four weeks. After training the rats were submitted to a surgical procedure (bone defect in the right tibia) and 24h after the surgery LPS was administered at a dose of 100µg/kg i.p., whereas the control rats received a saline injection (1ml/kg, i.p.). Right tibias were obtained for analysis after 10days during which rats were not submitted to physical training. Physical exercise had a positive effect on bone repair, increasing bone mineral density, bone mineral content, bone formation rate, type I collagen and osteocalcin expression. These parameters were not affected by systemic administration of LPS. Our data indicate that physical exercise has an important osteogenic effect, which is maintained during acute systemic inflammation induced by exposure to a single dose of LPS.