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Background SGLT2 inhibitors reduce the risk of heart failure (HF) mortality and morbidity, regardless of the presence or absence of diabetes, but the mechanisms underlying this benefit remain unclear. Experiments with nondiabetic HF rats tested the hypothesis that the SGLT2 inhibitor empagliflozin (EMPA) inhibits proximal tubule (PT) NHE3 activity and improves renal salt and water handling. Methods Male Wistar rats were subjected to myocardial infarction or sham operation. After 4 weeks, rats that developed HF and sham rats were treated with EMPA or untreated for an additional 4 weeks. Immunoblotting and quantitative RT-PCR evaluated SGLT2 and NHE3 expression. Stationary in vivo microperfusion measured PT NHE3 activity. Results EMPA-treated HF rats displayed lower serum B-type natriuretic peptide levels and lower right ventricle and lung weight to tibia length than untreated HF rats. Upon saline challenge, the diuretic and natriuretic responses of EMPA-treated HF rats were similar to those of sham rats and were higher than those of untreated HF rats. Additionally, EMPA treatment prevented GFR decline and renal atrophy in HF rats. PT NHE3 activity was higher in HF rats than in sham rats, whereas treatment with EMPA markedly reduced NHE3 activity. Unexpectedly, SGLT2 protein and mRNA abundance were upregulated in the PT of HF rats. Conclusions Prevention of HF progression by EMPA is associated with reduced PT NHE3 activity, restoration of euvolemia, and preservation of renal mass. Moreover, dysregulation of PT SGLT2 may be involved in the pathophysiology of nondiabetic HF.

This study evaluated the effect of photobiomodulation therapy (PBMt) before or after a high-intensity resistance exercise (RE) session on muscle oxidative stress. Female Wistar rats were assigned to one of the following groups: Sham (non-exercised, undergoing placebo-PBMt); NLRE (exercised, undergoing placebo-PBMt); PBMt + RE (pre-exercise PBMt); RE + PBMt (post-exercise PBMt). The RE comprised four climbs bearing the maximum load with a 2 min rest between each climb. An 830-nm aluminum gallium arsenide diode laser (100 mW; 0.028 cm2; 3.57 mW/cm2; 142.8 J/cm2; 4 J; Photon Laser III, DMC, Sao Paulo, Brazil) was applied 60 s before or after RE in gastrocnemius muscles. Analyses were performed at 24 h after RE: lipoperoxidation using malondialdehyde (MDA) and protein oxidation (OP) on Western blot. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity were spectrophotometrically assessed. Nitric oxide (NO) level was determined by the Griess reaction. The MDA and OP levels were significantly higher in the NLRE group. Increased OP was prevented in all PBMt groups; however, increased MDA was prevented only in the RE + PBMT group. The RE + PBMt group had higher SOD activity compared to all other groups. A higher GPx activity was observed only in the PBMT + RE compared to Sham group, and CAT activity was reduced by RE, without PBMt effect. NO levels were unchanged with RE or PBMt. Therefore, PBMt application after a RE section has a more potent antioxidant effect than previous PBMt. Rats submitted to post-RE PBMt illustrated prevention of increased lipoperoxidation and protein oxidation as well as increased SOD activity. The photobiomodulation can attenuate oxidative stress induced by resistance exercise. A more evident benefit shows to be obtained with the application after exercise, in which it has increased the activity of superoxide dismustase.

This study evaluated the effects of light-emitting diode (LED) on mesenchymal stem cells (MSCs). An electronic search was conducted in PubMed/MEDLINE, Scopus, and Web of Science database for articles published from 1980 to February 2020. Ten articles met the search criteria and were included in this review. The risk of bias was evaluated to report quality, safety, and environmental standards. MSCs were derived from adipose tissue, bone marrow, dental pulp, gingiva, and umbilical cord. Protocols for cellular irradiation used red and blue light spectrum with variations of the parameters. The LED has been shown to induce greater cellular viability, proliferation, differentiation, and secretion of growth factors. The set of information available leads to proposing a complex signaling cascade for the action of photobiomodulation, including angiogenic factors, singlet oxygen, mitogen-activated protein kinase/extracellular signal-regulated protein kinase, Janus kinase/signal transducer, and reactive oxygen species. In conclusion, although our results suggest that LED can boost MSCs, a nonuniformity in the experimental protocol, bias, and the limited number of studies reduces the power of systematic review. Further research is essential to find the optimal LED irradiation parameters to boost MSCs function and evaluate its impact in the clinical setting.

To evaluate whether Porphyromonas gingivalis (P. gingivalis) inoculation could induce cardiac remodelling in rats.The study was conducted on 33 Wistar rats, which were distributed in the following experimental groups: not inoculated; inoculated with 1 × 10Impact of the bacteria was more evident in rats that received higher P. gingivalis concentration. Thus, 3 × 10P. gingivalis bacteraemia is significantly associated with adverse cardiac remodelling and may play a biological role in the genesis of heart failure.

BACKGROUND Acute and chronic stresses have become a health problem in the contemporary society, and prolonged exposure to stressful events is related to the pathogenesis of cardiovascular diseases. Physical exercise is a well recognized effective nonpharmacological therapy for cardiovascular diseases and stress-induced injuries. Thus, this study evaluated the effect of exercise on the cardiac remodelling of chronically stressed rats. METHODS AND RESULTS Wistar adult rats were used (n = 10 each group) and chronic stress protocol consisted of restricting movement in individual rodent restrainers (60 min, 5 days/week, 12 weeks); and exercise consisted of swimming session in a pool (60 min, 5 days/week, 12 weeks). During protocol, blood pressure was measured in conscious rats, and at the end cardiac morphology/function was assessed. Animals exposed to stress exhibited continuous rise in blood pressure from the sixth week, but exercise attenuated it. Similarly, restrained rats increased serum corticosterone compared with nonstressed rats, but exercise also prevented it. No changes were found in cardiac mass, but chronic stress not only impaired the steady state contractions of the cardiac muscle, but also reduced inotropic responses to stretching, increasing calcium and beta-adrenergic receptor stimulation. Despite this, exercise was unable to prevent these functional impairments induced by stress, and instead, the association of stress and physical exercise worsened myocardial compliance. CONCLUSION Despite the known benefits to the cardiovascular system, our results indicate that aerobic swimming exercise for 12 weeks reduced blood pressure but did not impede the chronic stress-induced myocardial damages in rats.

Background and method This study evaluated the effects of a linear block strength training programme on the parameters of cardiac remodelling in spontaneously hypertensive rats. Thirty-nine rats were equally distributed in four groups: normotensive sedentary, normotensive trained, hypertensive sedentary and hypertensive trained. The strength training protocol was organized in three mesocycles of 4 weeks, with an increase in the training load organized in a linear fashion for each block, considering the weight established in the maximum loaded load test. The following parameters were evaluated: ventricular function assessed by echocardiogram, caudal blood pressure, ventricular haemodynamics and cardiac masses. Two-way analysis of variance was used to determine the differences between the group and time. Results After 12 weeks of training, the hypertensive trained group presented the following results: increased muscle strength, reduced blood pressure, reduced heart rate, isovolumetric relaxation time and total collagen content, with increased cardiac function, without promoting changes in the mass and nuclear volume of cardiomyocytes. Also, blood pressure reduction seems to be associated with both muscle strength adjustments and total load progress. Conclusion The findings of this study showed that the training programme carried out attenuated systemic arterial pressure and preserved the ventricular function of spontaneously hypertensive rats without cardiac mass change.

We previously showed that digitoxin prolongs the survival of rats with heart failure due to myocardial infarction (MI). In this study, we evaluated the effect of digitoxin on myocardial structure, ventricular function, and proteins involved in calcium kinetics. Seventy-two rats with MI >35% of the left ventricle were randomly assigned to 4 treatment groups: sham (n = 15), digitoxin (n = 11), infarction (n = 20), and infarction + digitoxin (n = 26). The rats were assessed 120 days after surgery by echocardiogram, hemodynamics, papillary muscle mechanics, collagen content, cardiomyocyte nuclear volume, and Western blot analysis of proteins involved in calcium kinetics. Digitoxin was administered via the rat chow. Two-way analysis of variance was used for comparisons. Myocardial infarction caused inotropic impairment, pulmonary congestion, increase of nuclear volume, myocardial collagen, and Na+/Ca2+ exchanger levels, and decreased SERCA2 and phosphorylated phospholamban levels. Treatment with digitoxin showed improvements in cardiac remodeling, inotropism, ventricular performance, pulmonary congestion, collagen accumulation, nuclear volume, and proteins involved in calcium kinetics. In rats with heart failure due to MI, long-term treatment with digitoxin attenuates congestive heart failure, mitigates myocardial remodeling and contractile impairment, and preserves myocardial levels of proteins involved in calcium kinetics.

The post-myocardial infarction heart failure (HF) still carries a huge burden since current therapy is unsuccessful to abrogate poor prognosis. Thus, new approaches are needed, and photobiomodulation therapy (PBMt) may be a way. However, it is not known whether PBMt added to a standard HF therapy provides additional improvement in cardiac remodeling in infarcted rats. This study sought to determine the combined carvedilol-drug and PBMt with low-level laser therapy value in HF. Rats with large infarcts were treated for 30 days. The functional fitness was evaluated using a motorized treadmill. Echocardiography and hemodynamic measurements were used for functional evaluations of left ventricular (LV). ELISA, Western blot and biochemical assays were used to evaluate inflammation and oxidative stress in the myocardium. Carvedilol and PBMt had a similar action in normalizing pulmonary congestion and LV end-diastolic pressure, attenuating LV dilation, and improving LV systolic function. Moreover, the application of PBMt to carvedilol-treated rats inhibited myocardial hypertrophy and improved +dP/dt of LV. PBMt alone prevented inflammation with a superior effect than carvedilol. Carvedilol and PBMt normalized 4-hydroxynonenal (a lipoperoxidation marker) levels in the myocardium. However, importantly, the addition of PBMt to carvedilol attenuated oxidized protein content and triggered a high activity of the anti-oxidant catalase enzyme. In conclusion, these data show that the use of PBMt plus carvedilol therapy results in a significant additional improvement in HF in a rat model of myocardial infarction. These beneficial effects were observed to be due, at least in part, to decreased myocardial inflammation and oxidative stress.

BACKGROUND: Occupations might influence the employees’ psychophysical conditions and an important issue is the human activity mechanization, which favors a hypokinetic work status and leads to several chronic diseases. One of the most hypokinetic occupations is the supermarket cashier, in which the individual may spend many hours a day in the same body position. OBJECTIVE: The goal of this study was to evaluate the association between cardiovascular risk, quality of life and physical activity level in supermarket cashiers. METHODS: This is a cross-sectional study which included 200 supermarket cashiers aged 20 to 41 years from São Paulo, Brazil. The following cardiovascular risk factors were evaluated: overweight, obesity, hypertension, diabetes mellitus, and tobacco smoking. Physical activity level and quality of life were assessed with the short-form of the International Physical Activity Questionnaire (IPAq) and World Health Organization Quality of Life (WHOQOL), respectively. Student t test and Chi-square were carried out to evaluate mean gender comparations and frequency, respectively. Logistic regression models were applied to determine the association between cardiovascular risk factors and physical activity level. RESULTS: The prevalence for all cardiovascular risk factors was significantly high in the cashiers with a low physical activity level. However, there was a significant reduction in several risk factors in the groups with moderate and high physical activity levels. The odds ratio values were significantly reduced for the association between the cardiovascular risk factors and the moderate and high physical activity levels. The cashiers with moderate and high physical activity levels showed significantly higher quality of life scores for the social and environmental domain. CONCLUSIONS: A high physical activity level is positively related to quality of life in supermarket cashiers.

BackgroundSodium-glucose cotransporter type 2 (SGLT2) inhibitors reduce the risk of heart failure (HF) mortality and morbidity, regardless of the presence or absence of diabetes, but the mechanisms underlying this benefit remain unclear. We tested the hypothesis that the SGLT2 inhibitor empagliflozin inhibits proximal tubule (PT) Na+/H+ exchanger isoform 3 (NHE3) activity and improves renal salt and water handling in nondiabetic rats with HF.Methods and ResultsMale Wistar rats were subjected to myocardial infarction or sham operation. After four weeks, rats that developed HF and sham rats were treated with empagliflozin (EMPA) or untreated for an additional four weeks. EMPA-treated HF rats displayed lower levels of serum brain natriuretic peptide (BNP) and lower right ventricle and lung weight to tibia length than untreated HF rats. Upon saline challenge, the diuretic and natriuretic responses of EMPA-treated HF rats were similar to those of sham rats and were higher than those of untreated HF rats. Additionally, EMPA treatment normalized the glomerular filtration rate and proteinuria in HF rats. PT NHE3 activity was higher in HF rats than in sham rats, whereas treatment with EMPA markedly reduced NHE3 activity. Unexpectedly, SGLT2 function and protein and mRNA abundance were upregulated in the PT of HF rats.ConclusionCollectively, our data show that the prevention of HF progression by empagliflozin is associated with inhibition of PT NHE3 activity and restoration of euvolemia. Moreover, we propose that the dysregulation of PT SGLT2 may be involved in the pathophysiology of nondiabetic HF.SIGNIFICANCE STATEMENTSGLT2 inhibitors represent a class of drugs that were originally developed for improving glycemic control. Cardiovascular outcome trials that were designed to evaluate cardiovascular safety yielded unexpected and unprecedented evidence of the cardiorenal benefits of SGLT2 inhibitor. Many hypotheses have been proposed to explain the mechanisms underlying these effects. Our study demonstrates that SGLT2 inhibition restores extracellular volume homeostasis in nondiabetic heart failure (HF) rats by preserving GFR and inhibiting proximal tubule NHE3-mediated sodium reabsorption. The attenuation of kidney dysfunction may constitute an essential mechanism by which SGLT2 inhibitors attenuate HF development and progression either in the presence or absence of diabetes.

Despite the strong evidence on the cardiac and renal damages after chronic exposure to cigarette smoke, there is a paucity of data on its short-term effects. The study evaluated the short-term effects of cigarette smoking on left ventricular (LV) remodeling, in vitro myocardial and renal function. Female Wistar rats were randomized to control (C) and cigarette smoking rats for eight weeks. Physical capacity was assessed using an adapted model of exhaustive swim; left ventricle (LV) morphology and function were also evaluated. Renal function was assessed by creatinine clearance and urine protein. The in vitro myocardial performance was analyzed in isolated papillary muscles. Rats exhibited reduced physical capacity after short-term cigarette smoking. Although there was no change on LV function, reduced chamber diameter was found in the smoking group associated with an increased LV wall thickness. There was augmented cardiac mass compared to C that was confirmed by increased cardiomyocyte nucleus volume, but in vitro myocardial performance and renal function were unchanged. A short-term cigarette smoking induces cardiac remodeling without abnormalities in function. The smoking group still preserved renal function and in vitro myocardial performance. However, the reduced physical capacity may suggest an impairment of the cardiac reserve.

Stem cell (SC) therapy is a promising approach to improve post-myocardial infarction (MI) cardiac remodeling, but the proinflammatory microenvironment may lead to SC loss and, therefore, may have a negative impact on therapy. It appears that exercise training (ET) improves myocardial microenvironment for SC transplantation. Therefore, we tested the effect of ET on post-infarction retention of adipose-derived SCs (ADSCs) and its combined effects on the inflammatory microenvironment. Fischer-344 female rats were randomized to one of the following groups: Sham; sedentary coronary occlusion who did not receive ADSCs (sMI); sedentary coronary occlusion who received ADSCs; exercise coronary occlusion who received ADSCs. Rats were trained nine weeks prior to MI, followed by ADSCs transplantation. The MI led to left ventricle (LV) dilation and dysfunction, myocardial hypertrophy and fibrosis, and increased proinflammatory profile compared to Sham rats. Conversely, ADSCs transplanted rats exhibited, better morphological and functional LV parameters; inhibition of myocardial hypertrophy and fibrosis; and attenuation of proinflammatory cytokines (interleukins 1β and 10, tumor necrosis factor α, and transforming growth factor β) in the myocardium compared to sMI rats. Interestingly, ET enhanced the effect of ADSCs on interleukin 10 expression. There was a correlation between cytokine expression and myocardial ADSCs retention. The. ET enhanced the beneficial effects of ADSCs in infarcted myocardium, which was associated with higher ADSCs retention. These findings highlight the importance of ET in myocardial retention of ADSCs and attenuation of cardiac remodeling post-infarction. Cytokine analysis suggests improvement in ET-linked myocardial microenvironment based on its anti-inflammatory action.

This study compared maximum oxygen consumption (VO2max) on a 20-meter multistage shuttle run test (20-Srt) with a cardiopulmonary exercise test (CPET) to determine a VO2max prediction equation for a 20-Srt in children aged 6–10 years. Eighty healthy children performed the CPET on a treadmill, while the 20-Srt took place on a sports court. Heart rate (HR) was measured and the expired gases were continuously measured breath-by-breath using a portable gas analyzer. The VO2max was lower (p

This study aimed to determine whether photobiomodulation therapy (PBMT) in diabetic rats subjected to high-intensity exercise interferes with the expression of the oxidative stress marker in the gastrocnemius muscle. Twenty-four male Wistar rats were included in this study comprising 16 diabetic and eight control rats. The animals were allocated into three groups-control, diabetic fatigue, and diabetic PBMT fatigue groups. Diabetes was induced via the intraperitoneal administration of streptozotocin (50 mg/kg). We subsequently assessed blood lactate levels and PBMT. The animals of the diabetic fatigue group PBMT were irradiated before the beginning of the exercises, with dose of 4 J and 808 nm, were submitted to treadmill running with speed and gradual slope until exhaustion, as observed by the maximum volume of oxygen and lactate level. The animals were euthanized and muscle tissue was removed for analysis of SOD markers, including catalase (CAT), glutathione peroxidase (GPx), and 2-thiobarbituric acid (TBARS) reactive substances. CAT, SOD, and GPx activities were significantly higher in the diabetic PBMT fatigue group (p 0.05) than in the diabetic fatigue group. Outcomes for the diabetic PBMT fatigue group were similar to those of the control group (p 0.05), while their antioxidant enzymes were significantly higher than those of the diabetic fatigue group. PBMT mitigated the TBARS concentration (p 0.05). PBMT may reduce oxidative stress and be an alternative method of maintaining physical fitness when subjects are unable to perform exercise. However, this finding requires further testing in clinical studies.

Exercise training effects on the contractility of aged myocardium have been investigated for more than 20 years, but the data are still unclear. This study evaluated the hypothesis that a swimming training (ST) may improve myocardial inotropism in older rats. Male Wistar rats aged 4 (young)-and 21 (old)-months-old were divided into young untrained (YNT), old untrained (ONT), and old trained (OTR; 6 weeks of ST) groups. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function. Myocardial mechanics was evaluated on papillary muscles. Histological and immunoblotting were carried out to evaluate fibrosis and proteins that modulate the myocardial function and calcium handling. We found that older rats did not show cardiac dysfunction, but ONT group showed lower physical performance during a swimming test (YNT: 5 ± 2; ONT: -16 ± 0.4; OTR: 51 ± 3; Δ%, sec). Moreover, ONT group showed worse myocardial inotropism, in which it was reversed by ST (Peak developed tension: YNT: 6.2 ± 0.7; ONT: 3.9 ± 0.3; OTR: 6.9 ± 0.9; g/mm2). The ST was associated with preserved collagen content (YNT: 0.38 ± 0.05; ONT: 0.78 ± 0.12; OTR: 0.34 ± 0.09; %). Exercise partially mitigated the effects of aging on intracellular Ca2+-regulating protein (eg, L-Ca2+ channel and phospholamban) and β-isoform of myosin. Thus, we propose that these molecular alterations together with inhibition of collagen increase contribute to improved myocardial performance in older rats.

Among the mechanisms of action of hyperbaric oxygenation (HBO), the chance of reducing injury by interfering with the mechanisms of redox homeostasis in the heart leads to the possibility of extending the period of viability of the myocardium at risk. This would benefit late interventions for reperfusion to the ischemic area. The objective of the present study was to investigate the changes in the redox system associated with HBO therapy maintained during the first hour after coronary occlusion in an acute myocardial infarction (MI) rat model. Surviving male rats (n=105) were randomly assigned to one of three groups: Sham (SH=26), myocardial infarction (MI=45) and infarction+hyperbaric therapy (HBO=34, 1 h at 2.5 atm). After 90 min of coronary occlusion, a sample of the heart was collected for western blot analysis of total protein levels of superoxide dismutase, catalase, peroxiredoxin and 3‑nitrotyrosine. Glutathione was measured by enzyme‑linked immunosorbent assay (ELISA). The detection of the superoxide radical anion was carried out by oxidation of dihydroethidium analyzed with confocal microscopy. The mortality rate of the MI group was significantly higher than that of the HBO group. No difference was noted in the myocardial infarction size. The oxidized/reduced glutathione ratio and peroxiredoxin were significantly higher in the SH and MI when compared to the HBO group. Superoxide dismutase enzymes and catalase were significantly higher in the HBO group compared to the MI and SH groups. 3‑Nitrotyrosine and the superoxide radical were significantly lower in the HBO group compared to these in the MI and SH groups. These data demonstrated that hyperbaric oxygenation therapy decreased mortality by improving redox control in the hearts of rats in the acute phase of myocardial infarction.

The relationship between disturbances in glucose homeostasis and heart failure (HF) progression is bidirectional. However, the mechanisms by which HF intrinsically impairs glucose homeostasis remain unknown. The present study tested the hypothesis that the bioavailability of intact glucagon-like peptide-1 (GLP-1) is affected in HF, possibly contributing to disturbed glucose homeostasis. Serum concentrations of total and intact GLP-1 and insulin were measured after an overnight fast and 15 min after the ingestion of a mixed breakfast meal in 49 non-diabetic patients with severe HF and 40 healthy control subjects. Similarly, fasting and postprandial serum concentrations of these hormones were determined in sham-operated rats, and rats with HF treated with an inhibitor of the GLP-1-degrading enzyme dipeptidyl peptidase-4 (DPP4), vildagliptin, or vehicle for 4 weeks. We found that HF patients displayed a much lower increase in postprandial intact and total GLP-1 levels than controls. The increase in postprandial intact GLP-1 in HF patients correlated negatively with serum brain natriuretic peptide levels and DPP4 activity and positively with the glomerular filtration rate. Likewise, the postprandial increases in both intact and total GLP-1 were blunted in HF rats and were restored by DPP4 inhibition. Additionally, vehicle-treated HF rats displayed glucose intolerance and hyperinsulinemia, whereas normal glucose homeostasis was observed in vildagliptin-treated HF rats. We conclude that the postprandial increase in GLP-1 is blunted in non-diabetic HF. Impaired GLP-1 bioavailability after meal intake correlates with poor prognostic factors and may contribute to the establishment of a vicious cycle between glucose disturbance and HF development and progression.

High-intensity resistance exercise (RE) increases oxidative stress leading to deleterious effects on muscle performance and recovery. The aim of this study was to assess the effect of applying low-level laser therapy (LLLT) prior to a RE session on muscle oxidative stress and to determine the possible influence of the dosimetric parameters. Female Wistar rats were assigned to non-LLLT (Ctr: non-exercised control; RNI: RE) or LLLT groups subjected to RE (radiant energy: 4 J, 8 J, and 12 J, respectively). RE consisted of four maximum load climbs. An 830-nm DMC Lase Photon III was used to irradiate three points in gastrocnemius muscles (two limbs) before exercise. Animals were euthanized after 60 min after the end of the exercise, and muscle tissue was removed for analysis of oxidative stress markers. All doses resulted in the prevention of increased lipoperoxidation; however, LLLT prevented protein oxidation only in rats that were pretreated with 8 J and 12 J of energy by LLLT. RE and LLLT did not change catalase activity. However, RE resulted in lower superoxide dismutase activity, and the opposite was observed in the LLLT group. These data indicate that LLLT prior to RE can prevent muscle oxidative stress. This study is the first to evaluate the impact of dosimetric LLLT parameters on the oxidative stress induced by RE, wherein both 8 J and 12 J of energy afforded significant protection.

The present study aimed to analyze the effects of reperfusion of a distant coronary artery on cardiac function, the ultrastructure, and the molecular environment of the remote myocardium immediately after the completion of myocardial regional necrosis: delayed reperfusion (DR). Additionally, the effects of prior exercise on the outcomes of DR were investigated. Female rats with permanent occlusion or delayed reperfusion were randomly assigned to an exercise (swimming, 1 h/day, 5 days/week for 8 weeks) or sedentary protocol. Thus, the study included the following four groups: sedentary permanent occlusion, exercise permanent occlusion, sedentary delayed reperfusion, and exercise delayed reperfusion. The descending coronary artery was occluded for 1 h. Reperfusion was confirmed by contrast echocardiography, and the rats were observed for 4 weeks. Permanent occlusion and DR caused similar myocardial infarction sizes among the four groups. Interestingly, exercise significantly decreased the mortality rate. Delayed reperfusion resulted in significant benefits, including enhanced hemodynamics and papillary muscle contraction, as well as reduced apoptosis and collagen content. Protein calcium kinetics did not change. Meanwhile, developed tension and the Frank-Starling mechanism were enhanced, suggesting that calcium sensitivity was intensified in myofilaments. Remarkable remote myocardial benefits occurred after distant DR, and prior exercise intensified cardiac recovery. Our findings provide valuable information about DR. Our data might explain the better clinical outcomes in recent studies showing that late reperfusion could improve heart failure in patients with myocardial infarction. In conclusion, DR has remote myocardial benefits, including inotropism enhancement, pulmonary congestion reduction, and collagen and apoptosis attenuation, which are enhanced by prior exercise.

Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling and right ventricle overload. Given that angiogenesis is a key factor involved in the reduction of vascular resistance to blood flow, we tested the hypothesis that aerobic exercise exerts a positive impact on hydrogen peroxide (H 2 O 2 ) and protein kinase B (Akt) levels in the lung parenchyma. To study the effects of aerobic exercise on lung angiogenesis signaling, Wistar rats were administered monocrotaline (MCT) (60 mg/kg i.p.) or the same volume of saline (0.9% NaCl i.p.). There was an increase in H 2 O 2 (43%) in PAH-trained animals (TM) compared to control animals (SM). H 2 O 2 showed a positive correlation (r = 0.77) with vascular endothelial growth factor (VEGF). VEGF was higher (4.7 fold) in TM animals compared to SM. VEGF and angiopoietin-1 (Ang-1) showed positive staining in the lung parenchyma of TM and SM. Glutathione peroxidase showed higher activity in the TM group (49%) compared to trained control (TC). Aerobic exercise increased the activity of peroxiredoxin (P 2 O 2 /VEGF/p-Akt signaling for pulmonary physiological angiogenesis. It is associated with an improvement in RV function, as evaluated by echocardiography.

OBJECTIVE: Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs) are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-α is involved in the beneficial effects of previous exercise on myocardial infarction (MI) and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome. METHODS AND RESULTS: Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1) or 4 weeks (EI4 or SI4) of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-α, TNF-α and NF-κB antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%), without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35%) and a higher apoptosis/area rate (3.97±0.61 vs 1.90±1.82) in infarcted areas (both p=0.001). Immunohistochemistry also revealed higher TNF-α levels in SI1 than in EI1 (9.59 vs 4.09, p

The aim of the present study was to determine whether low-level laser therapy (LLLT) in conjunction with aerobic training interferes with oxidative stress, thereby influencing the performance of old rats participating in swimming. Thirty Wistar rats (Norvegicus albinus) (24 aged and six young) were tested. The older animals were randomly divided into aged-control, aged-exercise, aged-LLLT, aged-LLLT/exercise, and young-control. Aerobic capacity (VO2max(0.75)) was analyzed before and after the training period. The exercise groups were trained for 6 weeks, and the LLLT was applied at 808 nm and 4 J energy. The rats were euthanized, and muscle tissue was collected to analyze the index of lipid peroxidation thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities. VO2 (0.75)max values in the aged-LLLT/exercise group were significantly higher from those in the baseline older group (p0.01) and the LLLT and exercise group (p0.05). The results indicate that the activities of CAT, SOD, and GPx were higher and statistically significant (p0.05) in the LLLT/exercise group than those in the LLLT and exercise groups. Young animals presented lesser and statistically significant activities of antioxidant enzymes compared to the aged group. The LLLT/exercise group and the LLLT and exercise group could also mitigate the concentration of TBARS (p 0.05). Laser therapy in conjunction with aerobic training may reduce oxidative stress, as well as increase VO2 (0.75)max, indicating that an aerobic exercise such as swimming increases speed and improves performance in aged animals treated with LLLT.

Many of the studies, that have evaluated the role of photobiomodulation (PBM) in alleviating excessive oxidative stress induced by exercise, were carried out in the setting of aerobic activities. In line with this notion, the aim of this Research Highlights article was to summarize the new role of PBM in the oxidative stress resulting from anaerobic exercise. Thus, this Research Highlights article briefly summarizes the findings reported in a recent article published in Oxidative Medicine and Cellular Longevity (February 18, 2018; doi: 10.1155/2018/5763256) by de Oliveira et al., which reported that low-level laser therapy (LLLT) can protect skeletal muscles from oxidative stress induced by acute resistance exercise (RE). In fact, rats that underwent laser irradiation in the gastrocnemius muscle prior to RE bout showed a similar lipoperoxidation level to that of non-exercised rats. Animals in the LLLT group were also protected from attack by reactive oxygen species on their amino acids, as was revealed by the changes in the oxidized proteincontent. This study by de Oliveira et al. provides novel insights into the PBM process, which acts as a suppressor of the excessive oxidative stress evoked by RE.

We investigated whether low-level laser therapy (LLLT) prior to or post resistance exercise could attenuate muscle damage and inflammation. Female Wistar rats were assigned to non-LLLT or LLLT groups. An 830-nm DMC Laser Photon III was used to irradiate their hind legs with 2J, 4J, and 8J doses. Irradiations were performed prior to or post (4J) resistance exercise bouts. Resistance exercise consisted of four maximum load climbs. The load work during a resistance exercise bout was similar between Control (non-LLLT, 225 ± 10 g), 2J (215 ± 8 g), 4J (210 ± 9 g), and 8J (226 ± 9 g) groups. Prior LLLT did not induce climbing performance improvement, but exposure to 4J irradiation resulted in lower blood lactate levels post-exercise. The 4J dose decreased creatine kinase and lactic dehydrogenase levels post-exercise regardless of the time of application. Moreover, 4-J irradiation exposure significantly attenuated tumor necrosis factor alpha, interleukin-6, interleukin-1β, cytokine-induced neutrophil chemoattractant-1, and monocyte chemoattractant protein-1. There was minor macrophage muscle infiltration in 4J-exposed rats. These data indicate that LLLT prior to or post resistance exercise can reduce muscle damage and inflammation, resulting in muscle recovery improvement. We attempted to determine an ideal LLLT dose for suitable results, wherein 4J irradiation exposure showed a significant protective role.

The aim of this study was to determine whether oxidative stress markers are influenced by low-intensity laser therapy (LLLT) in rats subjected to a high-intensity resistive exercise session (RE). Female Wistar rats divided into three experimental groups (Ctr: control, 4J: LLLT, and RE) and subdivided based on the sampling times (instantly or 24 h postexercise) underwent irradiation with LLLT using three-point transcutaneous method on the hind legs, which was applied to the gastrocnemius muscle at the distal, medial, and proximal points. Laser (4J) or placebo (device off) were carried out 60 sec prior to RE that consisted of four climbs bearing the maximum load with a 2 min time interval between each climb. Lipoperoxidation levels and antioxidant capacity were obtained in muscle. Lipoperoxidation levels were increased (4-HNE and CL markers) instantly post-RE. LLLT prior to RE avoided the increase of the lipid peroxidation levels. Similar results were also notified for oxidation protein assays. The GPx and FRAP activities did not reduce instantly or 24 h after RE. SOD increased 24 h after RE, while CAT activity did not change with RE or LLLT. In conclusion, LLLT prior to RE reduced the oxidative stress markers, as well as, avoided reduction, and still increased the antioxidant capacity.