Progressive strength training can reverse sarcopenia stage in middle-aged and older adults regardless of their genetic profile.

The aim of this study was to verify the association of the ACTN3-R577X polymorphism with sarcopenia stage, according to the Revised European Consensus on the Definition and Diagnosis of Sarcopenia, in middle-aged and older adults, pre- and post- ST. In the 12-week longitudinal study, 71 middle-aged and older adults were evaluated; the participants were assigned to either control or intervention group. The intervention group underwent progressive ST three times a week. All participants underwent blood collection, DNA extraction, genotyping of the ACTN3-R577X polymorphism, anthropometric evaluations, and diagnostic tests for sarcopenia. The last two tests were repeated after 12 weeks. No association of the ACTN3-R577X polymorphism with sarcopenia stage was observed before and after 12 weeks. However, the intervention group remained non-sarcopenic (n = 25, p <0.05) or achieved changes in sarcopenia stage (from sarcopenic to non-sarcopenic) (n = 13, p <0.05). Our study demonstrates that progressive ST performed regularly can reverse or prevent sarcopenia regardless of genotype for the ACTN3-R577X polymorphism.

Polymorphism of the angiotensin converting enzyme gene (ACE-I/D) differentiates the aerobic and speed performance of football players.

BACKGROUND: The aim of this study 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-meter sprint test with speed measured at 10 meters (V10), 20 meters (V20), and 30 meters (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.

Aerobic exercise training prevents impairment in renal parameters and in body composition of rats fed a high sucrose diet.

OBJECTIVE: This study aimed to evaluate the effect of swimming training (T) on the renal system and body composition parameters in young animals treated with a high sucrose diet (SUD) during 12 weeks. RESULTS: The SUD impaired the physical performance, increased the body adiposity index (BAI), Lee index (LI) and retroperitoneal adipose tissue (RAT) weight, plasma creatinine and number renal cells nuclei, decreased urinary volume and urinary creatinine excretion besides creatinine clearance. The T reversed the increased the BAI, LI, RAT weight, plasma and urinary creatinine, creatinine clearance and number renal cells nuclei in addition to promoting decrease in urinary protein excretion. This study found that eight weeks of swimming physical training protected renal function and restored normal glomerular filtration rate (GFR) values. Swimming training also contributed to prevention of the onset of a renal inflammatory process and caused a decrease in the risk of development of obesity promoted by SUD decreasing the body composition parameters (BAI, LI, and RAT weight).

The effects of aquatic and land exercise on resting blood pressure and post-exercise hypotension response in elderly hypertensives.

OBJECTIVE: This study compared resting blood pressure (BP) using ambulatory BP monitoring (ABPM) responses in two groups of subjects trained in land exercise (LE) and aquatic exercise (AE), and assessed post-exercise hypotension (PEH) using ABPM, after land- and aquatic-based exercises. METHODS: ABPM (24 hours) was used to measure the baseline BP in elderly hypertensive women trained in LE and AE and the PEH induced by exercise. For this, 40 subjects were evaluated at rest and after a land- or aquatic-based exercise session (aerobic: 75% of reserve heart rate combined with resistance exercise). RESULTS: The daytime BP was lower for AE [systolic BP (SBP) 124 ± 1.0 mmHg, diastolic BP (DBP) 70 ± 1.5 mmHg] than for LE (SBP 134 ± 0.9 mmHg, DBP 76 ± 0.9 mmHg), but there were no differences at night-time. The aquatic exercise-induced PEH in the second hour was maintained at the 24th hour post-exercise. For land exercise-induced PEH, it was maintained at the 12th hour post-exercise. The SBP and DBP were lower at the 24th hour for AE than for LE. CONCLUSIONS: Elderly hypertensive people trained in AE had lower baseline BP during the daytime. SBP and DBP values were lower for individuals trained in AE, and their PEH was more rapid and longer lasting after AE.

The effects of aquatic and land exercise on resting blood pressure and post-exercise hypotension response in elderly hypertensives

Objective: This study compared resting blood pressure (BP) using ambulatory BP monitoring (ABPM) responses in two groups of subjects trained in land exercise (LE) and aquatic exercise (AE), and assessed post-exercise hypotension (PEH) using ABPM, after land- and aquatic-based exercises.Methods: ABPM (24 hours) was used to measure the baseline BP in elderly hypertensive women trained in LE and AE and the PEH induced by exercise. For this, 40 subjects were evaluated at rest and after a land- or aquatic-based exercise session (aerobic: 75% of reserve heart rate combined with resistance exercise).Results: The daytime BP was lower for AE [systolic BP (SBP) 124 ± 1.0 mmHg, diastolic BP (DBP) 70 ± 1.5 mmHg] than for LE (SBP 134 ± 0.9 mmHg, DBP 76 ± 0.9 mmHg), but there were no differences at night-time. The aquatic exercise-induced PEH in the second hour was maintained at the 24th hour post-exercise. For land exercise-induced PEH, it was maintained at the 12th hour post-exercise. The SBP and DBP were lower at the 24th hour for AE than for LE.Conclusion: Elderly hypertensive people trained in AE had lower baseline BP during the daytime. SBP and DBP values were lower for individuals trained in AE, and their PEH was more rapid and longer lasting after AE

Alpha-Actinin-3 R577X Polymorphism Influences Muscle Damage and Hormonal Responses After a Soccer Game.

Coelho, DB, Pimenta, EM, Rosse, IC, Veneroso, C, Pussieldi, GDA, Becker, LK, De Oliveira, EC, Carvalho, MRS, and Silami-Garcia, E. Alpha-actinin-3 R577X polymorphism influences muscle damage and hormonal responses after a soccer game. J Strength Cond Res 33(10): 2655-2664, 2019-The purpose of this study was to evaluate indicators of muscle damage and hormonal responses after soccer matches and its relation to alpha-actinin-3 (ACTN3) gene expression (XX vs. RR/RX), considering that the R allele produces alpha-actinin-3 and provides greater muscle strength and power. Thirty players (10 XX and 20 RR/RX) younger than 16 years were evaluated in this study. Blood samples were collected immediately before, after, 2, and 4 hours after the games to assess muscle damage (creatine kinase [CK] and alpha-actin) and hormonal responses (interleukin-6 [IL-6], cortisol, and testosterone). Postgame CK was higher as compared to the pregame values in both groups and it was also higher in the RR/RX (p < 0.05) than in the XX. The concentrations of alpha-actin and IL-6 were similar for both groups and did not change over time. Testosterone was increased after the game only in the RR/RX group (p < 0.05). Cortisol concentrations in group RR/RX were higher immediately after the game than before the game, and 2 and 4 hours after the game the concentration decreased (p < 0.05). The RR and RX individuals presented higher markers of muscle microtrauma and hormonal stress, probably because they performed more speed and power actions during the game, which is a self-regulated activity. From the different responses presented by RR/RX and XX genotypes, we conclude that the genotypic profile should be taken into account when planning training workloads and recovery of athletes.

The alpha-actinin-3 r577x polymorphism and physical performance in soccer players.

BACKGROUND: The aim of this study was to investigate the association between ACTN3 genotype (RR, RX, and XX) and physical performance of 138 adult, professional, U-20 and U-17 years Brazilian first-division soccer players. METHODS: The following three parameters were investigated: first, speed, using a 30-meter sprint test with speed measured at 10 meters, 20 meters, and 30 meters; second, muscular strength, using counter-movement-jump and squat jump tests; and third, aerobic endurance using the Yo-Yo endurance test. The athletes were ranked in ascending order according to their performance in each test. After which they were divided into quartiles and clustered according to genotype and allele frequency. The χ2 was used to compare the genotype frequencies (RR, RX and RR) and allele frequencies (R and X) within and between the different quartiles of performance rating. RESULTS: No significant differences were observed in genotypic or allelic frequencies between different performance ratings. The ACTN3 genotype was not associated to any of the physical performance parameters. CONCLUSIONS: Our study provides no ervidence for an assocviation between alpha-actinin-3 R577x genotypes and differences in physical performance in adult, professional, U-20 and U-17 years Brazilian first-division soccer players.

Angiotensin-(1-7) induces peripheral antinociception through mas receptor activation in an opioid-independent pathway.

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 E(2). 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.

Swimming training improves the vasodilator effect of angiotensin-(1-7) in the aorta of spontaneously hypertensive rat.

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-Pro(7)-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.

Brain-selective overexpression of human Angiotensin-converting enzyme type 2 attenuates neurogenic hypertension.

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.

Selective increase of angiotensin(1-7) and its receptor in hearts of spontaneously hypertensive rats subjected to physical training.

In the present study we investigated the effects of physical training on plasma and cardiac angiotensin(1-7) [Ang(1-7)] levels. In addition, possible changes in expression of the Ang(1-7) Mas receptor in the heart were also evaluated. Normotensive Wistar rats and spontaneously hypertensive rats (SHR) were subjected to an 8 week period of 5% overload swimming training. Blood pressure was determined by a tail-cuff system. Heart and left ventricle weights and cardiomyocyte diameter were analysed to evaluate cardiac hypertrophy. Radioimmunoassay was used to measure angiotensin levels. Expression of Mas was determined by semi-quantitative polymerase chain reaction, immunofluorescence and Western blotting. Physical training induced cardiac hypertrophy in Wistar rats and SHR. A significant decrease of plasma angiotensin II (Ang II) levels in both strains was also observed. Strikingly, trained SHR, but not trained Wistar rats, showed a twofold increase in left ventricular Ang(1-7) levels. No significant changes were observed in plasma Ang(1-7) and left ventricular Ang II concentrations in either strain. Furthermore, Mas mRNA and protein expression in left ventricle were substantially increased in trained SHR. The physical training protocol used did not change blood pressure in either strain. These results suggest that the beneficial effects induced by swimming training in hypertensive rats might include an augmentation of Ang(1-7) and its receptor in the heart.

Immunofluorescence localization of the receptor Mas in cardiovascular-related areas of the rat brain.

The G protein-coupled receptor Mas was recently described as an angiotensin-(1-7) [ANG-(1-7)] receptor. In the present study we evaluated the anatomical localization of Mas using immunofluorescence in the central nervous system of adult male Wistar rats. An abundant labeling was found in the hippocampus, amigdala, anterodorsal thalamic nucleus, cortex, and hypoglossal nucleus. More importantly, a dense ANG-(1-7) receptor Mas immunoreactivity was observed in cardiovascular-related areas of the medulla and forebrain, shown in several previous studies as sites for the action of ANG-(1-7) in the brain. A strong staining was found in the nucleus of the solitary tract, caudal and rostral ventrolateral medulla, inferior olive, parvo and magnocellular portions of the paraventricular hypothalamic nucleus, supraoptic nucleus, and lateral preoptic area. Furthermore, Mas staining was predominantly present in neurons. At the medullary sites, a specific and high-intensity binding for rhodamine-ANG-(1-7) was also shown. The specific ANG-(1-7) binding was completely displaced by the anti-Mas antibody or by the ANG-(1-7) antagonist, A-779. The data presented provide the first anatomical basis for the physiological role of ANG-(1-7)/Mas axis in the modulation of different cardiovascular functions and give new insights for clarifying the role of ANG-(1-7) in the central nervous system.

Cardiovascular effects of angiotensin II and angiotensin-(1-7) at the RVLM of trained normotensive rats.

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.