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Habitual food intake and physical activity can affect chronic low-grade inflammation, which is common in the elderly, because of changes in the immune system and body composition. Thus, the present study proposes an evaluation of the influence of past eating habits on the effects of an intervention of resistance training plus dietary advice on the inflammatory profile of the elderly. We conducted an intervention study with 40 elderly people. The Revised Diet Quality Index (HEI-R) and the dietary total antioxidant capacity (dTAC) were calculated before the intervention based on a food frequency questionnaire validated to the elderly population. Participants were categorized according to the median of HEI-R and dTAC to assess the influence of the habitual diet quality on anthropometry and inflammatory markers (CRP, IL-8, CCL-2, and leptin) before and after the intervention. The 19-week intervention provided a long-term progressive resistance training associated with dietary advice focused on foods rich in compounds with anti-inflammatory and antioxidant properties. There was a greater reduction in weight, body mass index (BMI), and body fat (%) in the group with the lowest HEI-R and a greater reduction in the body fat (%) in the group with the lowest dTAC, indicating that the group that had a worse diet quality before the intervention responded better to it. The index HEI-R correlated negatively with Δ weight and Δ BMI. dTAC correlated positively with Δ monocyte 1 chemotactic protein (CCL-2) and Δ C-reactive protein (CRP). In this scenario, elderly persons with bad habits can benefit from interventions to lifestyle change, while the better diet quality including dietary antioxidant sources can be useful to control weight and inflammatory biomarkers in this population.

New finding What is the central question of this study? Eccentric contraction exercises cause damage to muscle fibers, induce inflammatory responses; the exacerbation of this process can induce deposition of fibrous connective tissue, leading to decreased muscle function. The aim of this study is to examine the role of Angiotensin-(1-7) in this context. What is the main finding and its importance? Our results show that oral treatment with Angiotensin-(1-7) decreases muscle damage induced by eccentric exercise, reducing inflammation and fibrosis in the gastrocnemius and soleus muscle. This study shows potential effect of Ang-(1-7) for the prevention of muscle injuries induced by physical exercise. Abstract Eccentric contraction exercises cause damage to the muscle fibers and induce inflammatory reaction. The protective effect of Angiotensin-(1-7) [Ang-(1-7)] in skeletal muscle has led us to examine the role that this peptide plays in modifying processes associated with inflammation and fibrogenesis induced by eccentric exercise. In this study, we sought to investigate the effects of the oral administration of Ang-(1-7) included in hydroxypropyl β-cyclodextrin (HPβ-CD) in preventing and treating muscle damage following downhill running. Male Wistar rats were divided into three groups: control (untreated and not exercised) (n = 10), treated/exercised HPβ-CD Ang-(1-7) (n = 40), and treated/exercised HPβ-CD (n = 40). Exercised groups were subjected to a single eccentric contraction exercise session on a treadmill inclined to -13° and a constant speed of 20 m.min-1, for 60 min. Oral administration with HPβ-CD Ang-(1-7) and HPβ-CD was performed three hours before the exercise protocol and daily as a single dose, until day of euthanasia. Samples were collected at 04/12/24/48 and 72 hours after the exercise session. The animals treated with the Ang-(1-7) showed lower levels of CK, lower levels of TNF-α in soleus muscle and increased levels of IL-10 cytokines. The inflammatory cells and deposition of fibrous connective tissue were lower in the group treated with Ang-(1-7) in soleus and gastrocnemius muscles. The results of this study show that treatment with an oral formulation of Ang-(1-7) plays a fundamental role in the process of muscle injury repair induced by eccentric exercise. This article is protected by copyright. All rights reserved.

Background The aim was to evaluate the distribution of ACE-I/D polymorphisms on Brazilian football players performance in aerobic capacity, strength, and speed tests. Methods The participants in this study were 212 Brazilian first division male football players genotyped in DD, ID. or II. Genotyping of DNA from leucocytes was performed using polymerase chain reaction and restriction fragment length polymorphism methods. We evaluated speed using a 30-m sprint test with speed measured at 10 m (V10), 20 m (V20), and 30 m (V30); muscular strength using counter-movement-jump and squat jump tests; and aerobic endurance using the Yo-Yo endurance test. The athletes were ranked in ascending order according to their performance in each test and divided into quartiles: first quartile (0-25%, Weak), second (25-50%, Normal), third (50-75%, Good), and fourth (75-100%, Excellent); these were clustered according to genotype frequency. Results We identified significant differences in the V20 test values and in the aerobic capacity test. Higher frequencies of the ACE-DD genotype were observed in the Excellent performance group in the V20. In the aerobic capacity test, higher frequencies of the ACE-II genotype were observed in Excellent and Good performance groups. Conclusions Players with higher performance in anaerobic and aerobic tests are ACE-DD and ACE-II genotypes, respectively.

New findings What is the central question of this study? How does swimming exercise training impact hydro-electrolytic balance, renal function, sympathetic contribution to resting blood pressure and cerebrospinal fluid (CSF) [Na+ ] in rats fed a high-sodium diet from weaning? What is the main finding and its importance? An exercise-dependent reduction in blood pressure was associated with decreased CSF [Na+ ], sympathetically driven vasomotor tonus and renal fibrosis indicating that the anti-hypertensive effects of swimming training in rats fed a high-sodium diet might involve neurogenic mechanisms regulated by sodium levels in the CSF rather than changes in blood volume. Abstract High sodium intake is an important factor associated with hypertension. High-sodium intake with exercise training can modify homeostatic hydro-electrolytic balance, but the effects of this association are mostly unknown. In this study, we sought to investigate the effects of swimming training (ST) on cerebrospinal fluid (CSF) Na+ concentration, sympathetic drive, blood pressure (BP) and renal function of rats fed a 0.9% Na+ (equivalent to 2% NaCl) diet with free access to water for 22 weeks after weaning. Male Wistar rats were assigned to two cohorts: (1) fed standard diet (SD) and (2) fed high-sodium (HS) diet. Each cohort was further divided into trained and sedentary groups. ST normalised BP levels of HS rats as well as the higher sympathetically related pressor activity assessed by pharmacological blockade of ganglionic transmission (hexamethonium). ST preserved the renal function and attenuated the glomerular shrinkage elicited by HS. No change in blood volume was found among the groups. CSF [Na+ ] levels were higher in sedentary HS rats but were reduced by ST. Our findings showed that ST effectively normalised BP of HS rats, independent of its effects on hydro-electrolytic balance, which might involve neurogenic mechanisms regulated by Na+ levels in the CSF as well as renal protection.

Aging is a biological process during which chronic low-grade inflammation is present due to changes in the immune system of the elderly. The main objective of this study is to evaluate the effects of resistance training associated with dietary advice on chronic inflammation in the elderly. We conducted a prospective intervention study in which we evaluated anthropometric parameters and inflammatory biomarkers (CRP, IL-8, CCL-2, and leptin) in 40 elderly people before and after long-term progressive resistance training (19 weeks) associated with dietary advice. The participants trained twice a week on nonconsecutive days, and the training lasted one hour with an intensity of 60-85% of 1-MR. Dietary advice was explained in person and individually focusing on foods rich in compounds with anti-inflammatory and antioxidant properties. Participants were instructed at the beginning of the training program, and dietary advice was reinforced verbally weekly. There was an improvement in body composition evidenced by a reduction in waist circumference and body fat percentage and by the increase in arm circumference, calf circumference, and corrected arm muscle area. In addition, there was a reduction in the inflammatory biomarkers CCL-2 (p=0.01) and leptin (p<0.01). Resistance training associated with dietary guidance can contribute to a healthy aging due to observed improvements in body composition and in the inflammatory profile of the elderly.

Aim To evaluate physical fitness and cardiovascular effects in rats with renovascular hypertension, two kidneys, one clip (2K1C) submitted to voluntary exercise (ExV). Main methods 24 h after surgery (SHAM and 2K1C) rats were submitted to ExV for one week (adaptation). ExV adherent rats were separated into exercise (2K1C-EX and SHAM-EX) or sedentary (2K1C-SED and SHAM-SED) groups. After 4 weeks, exhaustion test, plasma lactate, cardiovascular parameters were evaluated and gastrocnemius muscle was removed for evaluation of gene expression of muscle metabolism markers (PGC1α; AMPK, SIRT-1, UCP-3; MCP-1; LDH) and of the redox process. Key findings ExV decreased blood lactate concentration and increased SOD and CAT activity and a SIRT-1 and UCP-3 gene expression in the gastrocnemius muscle of 2K1C-ExV rats compared to 2K1C-SED rats. Gene expressions of PGC1α, UCP-3, MCT-1, AMPK were higher in 2K1C-ExV rats compared to SHAM-SED rats. Blood pressure in 2K1C-ExV was lower compared to 2K1C-SED and higher in SHAM-SED rats. Reflex bradycardia in 2K1C-EX rats increased compared to 2K1C-SED and was similar to SHAM-SED. The variation in mean blood pressure induced by ganglion blocker hexamethonium and Ang II AT1 receptor antagonist, losartan in the 2K1C-ExV rats was smaller compared to the 2K1C-SED rats and it was similar to the SHAM-SED rats. Significance O ExV induced adaptive responses in 2K1C-ExV rats by decreasing sympathetic and Ang II activities and stimulating intracellular signaling that favors redox balance and reduced blood lactate concentration. These adaptive responses, then, contribute to reduced arterial pressure, improved baroreflex sensitivity and physical fitness of 2K1C rats.

Experimental studies in animal models have described the benefits of physical exercise (PE) to kidney diseases associated with hypertension. Land- and water-based exercises induce different responses in renal function. Our aim was to evaluate the renal alterations induced by different environments of PE in spontaneously hypertensive rats (SHRs). The SHRs were divided into sedentary (S), swimming exercise (SE), and running exercise (RE) groups, and were trained for 8 weeks under similar intensities (60 min/day). Arterial pressure (AP) and heart rate (HR) were recorded. The renal function was evaluated through urinary volume at each week of training; sodium and potassium excretions, plasma and urinary osmolarities, glomerular filtration rate (GFR), levels of proteinuria, and renal damage were determined. SE and RE rats presented reduced mean AP, systolic blood pressure, and HR in comparison with S group. SE and RE rats showed higher urine osmolarity compared with S. SE rats showed higher free water clearance (P P P P

The aim was to investigate a possible role of the ACTN3 R577X polymorphism in a Brazilian football player’s career progression. 2 questions were formulated: 1. Does ACTN3 polymorphism affect the probability of an individual being a professional football player? 2. Does this polymorphism affect the progression of the athlete throughout his career? The study included 353 players from first division Brazilian football clubs in the following categories: under-14 (U-14), U-15, U-17, U-20, and professional (PRO). The control group (CON) was composed of 100 healthy non-athletes. The chi-squared test was used to assess differences between the allele and genotype frequencies. Comparing football categories, the XX genotype was less frequent among professional players than in the U-20 (p

The development of new strategies to attenuate exercise-induced muscle damage may be helpful for training regimens. The aim of this study was to determine whether a oral formulation of angiotensin Ang-(1-7)[HPβCD/Ang-(1-7)] is effective to reduce pain, and muscle damage markers after eccentric-overload exercise. HPβCD (Placebo) and HPβCD/Ang-(1-7) (Ang-(1-7) group were treated for 7 days (one capsule/day). The pain was measured by visual analogue scale, maximal strength (MS) using force platform. Blood samples were collected for cytokines and creatine kinase (CK) analysis. The Ang-(1-7)-treated group reported less pain immediately (3.46±0.64 vs. placebo 3.80±0.77 cm) and 24 h after exercise (3.07±0.71 vs. 3.73±0.58 cm placebo) and higher MS at 24 h (24±12 N) and 48 h (30±15 N) vs. placebo (-8±9 N and -10±9 N). The CK for Ang-(1-7) (0.5±0.1 and 0.9±0.2 U/L) were lower at 48 and 72 h vs. placebo (fold changes of 1.7±0.5 and 1.5±0.3 U/L). The TNF-α level was lower in the treated group post-exercise (38±2.5 pg/ml) vs. placebo (45±2.9 pg/ml) but no significant changes were observed for IL-6 and IL-10. Our data indicate that treatment with Ang-(1-7) may attenuate pain, some of the muscle damage markers and improves performance following eccentric exercise.

Low angiotensin-(1-7) (Ang-(1-7)) concentration is observed in some cardiovascular diseases and exercise training seems to restore its concentration in the heart. Recently, a novel formulation of an orally active Ang-(1-7) included in hydroxy-propyl-beta-cyclodextrin (HPB-CD) was developed and chronically administered in experimental models of cardiovascular diseases. The present study examined whether chronic administration of HPB-CD/Ang-(1-7) produces beneficial cardiovascular effects in spontaneously hypertensive rats (SHR), as well as to compare the results obtained with those produced by exercise training. Male SHR (15-week old) were divided in control (tap water) or treated with HPB-CD/Ang-(1-7) (corresponding to 30μgkg(-1)day(-1) of Ang-(1-7)) by gavage, concomitantly or not to exercise training (treadmill, 10 weeks). After chronic treatment, hemodynamic, morphometric and molecular analysis in the heart were performed. Chronic HPB-CD/Ang-(1-7) decreased arterial blood pressure (BP) and heart rate in SHR. The inclusion compound significantly improved left ventricular (LV) end-diastolic pressure, restored the maximum and minimum derivatives (dP/dT) and decreased cardiac hypertrophy index in SHR. Chronic treatment improved autonomic control by attenuating sympathetic modulation on heart and vessels and the SAP variability, as well as increasing parasympathetic modulation and HR variability. Overall results were similar to those obtained with exercise training. These results show that chronic treatment with the HPB-CD/Ang-(1-7) inclusion compound produced beneficial effects in SHR resembling the ones produced by exercise training. This observation reinforces the potential cardiovascular therapeutic effect of this novel peptide formulation.

The G protein-coupled receptor Mas was recently described as an angiotensin-(1–7) [Ang-(1–7)] receptor. In the present study, we demonstrate an antinociceptive effect of Ang-(1–7) for the first time. Additionally, we evaluated the anatomical localization of Mas in the dorsal root ganglia using immunofluorescence. This is the first evidence indicating that this receptor is present in sensitive neurons. The antinociceptive effect was demonstrated using the rat paw pressure test. For this test, sensitivity is increased by intraplantar injection of prostaglandin E2. Ang-(1–7) administered locally into the right hind paw elicited a dose-dependent antinociceptive effect. Because the higher dose of Ang-(1–7) did not produce an effect when injected into the contralateral paw, this effect was considered local. The specific antagonist for the Mas receptor, A-779, inhibited the peripheral antinociception induced by exposure to 4 µg/paw Ang-(1–7) in a dose-dependent manner. The highest dose completely reversed the antinociceptive effect induced by Ang-(1–7), suggesting that the Mas receptor is an obligatory component in this process and that other angiotensin receptors may not be involved. When injected alone, the antagonist was unable to induce hyperalgesia or antinociception. Alternatively, naloxone was unable to inhibit the antinociceptive effect induced by Ang-(1–7), suggesting that endogenous opioid peptides may not be involved in this response. These data provide the first anatomical basis for the physiological role of Ang-(1–7) in the modulation of pain perception via Mas receptor activation in an opioid-independent pathway. Taken together, these results provide new perspectives for the development of a new class of analgesic drugs.

Rationale : Angiotensin converting enzyme type 2 (ACE2) is a new member of the brain renin-angiotensin system, that might be activated by an overactive renin-angiotensin system. Objective : To clarify the role of central ACE2 using a new transgenic mouse model with human (h)ACE2 under the control of a synapsin promoter, allowing neuron-targeted expression in the central nervous system. Methods and Results : Syn-hACE2 (SA) transgenic mice exhibit high hACE2 protein expression and activity throughout the brain. Baseline hemodynamic parameters (telemetry), autonomic function, and spontaneous baroreflex sensitivity (SBRS) were not significantly different between SA mice and nontransgenic littermates. Brain-targeted ACE2 overexpression attenuated the development of neurogenic hypertension (Ang II infusion: 600 ng/kg per minute for 14 days) and the associated reduction of both SBRS and parasympathetic tone. This prevention of hypertension by ACE2 overexpression was reversed by blockade of the Ang-(1-7) receptor ( d -Ala7-Ang-[1-7]; 600 ng/kg per minute). Brain angiotensin II type 2 (AT 2 )/AT 1 and Mas/AT 1 receptor ratios were significantly increased in SA mice. They remained higher following Ang II infusion but were dramatically reduced after Ang-(1-7) receptor blockade. ACE2 overexpression resulted in increased NOS and NO levels in the brain, and prevented the Ang II–mediated decrease in NOS expression in regions modulating blood pressure regulation. Conclusions : ACE2 overexpression attenuates the development of neurogenic hypertension partially by preventing the decrease in both SBRS and parasympathetic tone. These protective effects might be mediated by enhanced NO release in the brain resulting from Mas and AT 2 receptor upregulation. Taken together, our data highlight the compensatory role of central ACE2 and its potential benefits as a therapeutic target for neurogenic hypertension.

The renin-angiotensin system (RAS) is related to physiological adaptations induced by exercise. Angiotensin-converting enzyme (ACE) 2 is a major regulator of the RAS in tissues, as it metabolizes angiotensin (Ang) II to Ang-(1-7). The aim of this study was to determine the effects of ACE2 deficiency on physical performance and physiological adaptations induced by voluntary running. Physical performance, body composition and plasma angiotensin levels, as well as tissue morphology and gene expression of RAS components in the left ventricle (LV) and skeletal muscle (gastrocnemius), were evaluated in ACE2-deficient (ACE2(-/y)) and wild-type (ACE2(+/y)) mice after 6 weeks of voluntary wheel running. ACE2(-/y) mice run less than ACE2(+/y) mice (19±4.7 vs. 26±12.6 revolutions per day × 100, P

The cardiovascular effects of microinjection of the amino acids glutamate and glycine within the rostral ventrolateral medulla (RVLM) after swimming training (ST) in unrestrained awake rats were investigated. Unilateral microinjection of l -glutamate (5, 20 and 50 mM, in 100 nl) produced a dose dependent increase in mean arterial pressure (MAP) in control (C) (16 ± 5 mm Hg; 29 ± 6 mm Hg; 43 ± 6 mm Hg) and swim (SW) (1 ± 1 mm Hg; 16 ± 2 mm Hg; 25 ± 3 mm Hg) groups. However, the magnitude of this response was lower in the swim group. Prazosin injection produced hypotension and tachycardia in both groups (C = − 43 ± 3 mm Hg/98 ± 16 bpm; SW = − 61 ± 5 mm Hg/115 ± 32 bpm). In the SW group the hypotension caused by prazosin was greater compared to C group, but the tachycardia was not different between them. After prazosin, glutamate response in RVLM was blocked in both groups as well. When glycine (10 mM or 1 M, in 100 nl) were microinjected into the RVLM of C group we observed two different effects: decrease in MAP with the lower dose and an increase in MAP with the higher dose (10 mM = − 13 ± 2 mm Hg; 1 M = 47 ± 6 mm Hg). However, after ST the hypertensive response to glycine was blunted with no alterations in the hypotensive response (10 mM = − 14 ± 1 mm Hg; 1 M = 18 ± 4 mm Hg). These findings suggest that RVLM is involved in the modulation of the sympathetic outflow to the cardiovascular system during exercise training.

Endurance exercise is a remarkable intervention for the treatment of many diseases. Mitochondrial changes on skeletal muscle are likely important for many of the benefits provided by exercise. In this study, we aimed to evaluate the effects that a regular physical activity (swimming without workload) has on mitochondrial morphological alterations and glucometabolic parameters induced by a high-sugar diet (HSD). Weaned male Wistar rats fed with a standard diet or a HSD (68% carbohydrate) were subjected to 60 minutes of regular physical activity by swimming (without workload) for four- (20 sessions) or eight-week (40 sessions) periods. After training, animals were euthanized and the sera, adipose tissues, and skeletal muscles were collected for further analysis. The HSD increased body weight after an 8- week period; it also increased the fat pads and the adipose index, resulting in glucose intolerance and insulin resistance (IR). Transmission electron microscopy showed an increase in alterations of mitochondrial ultrastructure in the gastrocnemius muscle, as well as a decrease in superoxide dismutase (SOD) activity, and an increase in protein carbonylation. Regular physical activity partially reverted these alterations in rats fed a HSD, preventing mitochondrial morphological alterations and IR. Moreover, we observed a decrease in Pgc1α expression (qPCR analysis) in STD-EXE group and a less pronounced reduction in HSD-EXE group after an 8-week period. Thus, regular physical activity (swimming without workload) in rats fed a HSD can prevent mitochondrial dysfunction and IR, highlighting the crucial role for physical activity on metabolic homeostasis.

Introduction: endothelial dysfunction plays a critical role in the pathogenesis of hypertension. It is well established that physical training has beneficial effects on the cardiovascular system. We recently reported that angiotensin-(1–7) [Ang-(1–7)] concentration and the Mas receptor expression is increased in the left ventricle of trained spontaneous hypertensive rats (SHR). The vascular effects of Ang-(1–7) in trained animals remain so far unknown. In the present study we investigated the effects of physical training on the vasodilator effect of Ang-(1–7) in the aorta of SHR. Methodology: normotensive Wistar rats and SHR were subjected to an 8-wk period of 5% overload of body weight swimming training. Changes in isometric tension were recorded on myograph. Western blot was used to investigate Ang-(1–7) receptors expression. Results: in aortas from normotensive rats Ang-(1–7) and ACh induced a concentration-dependent vasodilator effect, which was not modified by the physical training. Vessels from SHR had an impaired vasodilator response to Ang-(1–7) and ACh. The swimming training strongly potentiated the vasodilator effect induced by Ang-(1–7) in SHR, but did not modify the effect of ACh. Interestingly, Mas receptor protein expression was substantially increased by physical training in SHR. In trained SHR, the vasodilator effect of Ang-(1–7) was abrogated by removal of the endothelium and by the selective Ang-(1–7) receptor antagonists A-779 and d-Pro7-Ang-(1–7). l-NAME decreased Ang-(1–7) vasodilator response and indomethacin abolished the remaining dilatory response. Conclusion: physical training increased Mas receptors expression in SHR aortas, thereby improving the vasodilator effect of Ang-(1–7) through an endothelium-dependent mechanism involving nitric oxide and prostacyclin.

We evaluated the effect of physical training on the cardiovascular responses produced by angiotensin peptides at the rostroventrolateral medulla (RVLM) of non-anesthetized normotensive rats. The RVLM pressor effect induced by Ang II was significantly greater in trained rats, while, in contrast, the Ang-(1–7) pressor effect was significantly smaller in trained in comparison to sedentary rats. In addition, the RVLM microinjection of Losartan (AT1 Ang II receptor antagonist) or A-779 (Ang-(1–7) receptor antagonist) induced opposite effect in trained rats. These results show that exercise training induces a differential RVLM responsiveness to Ang peptides, which was corroborated by the selective antagonists, indicating that the RVLM is a site in the central nervous system involved in the adaptive mechanisms triggered during exercise training.