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High‐intensity interval training (HIIT) has shown significant results in addressing adiposity and risk factors associated with obesity. However, there are no studies that investigate the effects of HIIT on contractility and intracellular Ca2+ handling. The purpose of this study was to explore the impact of HIIT on cardiomyocyte contractile function and intracellular Ca2+ handling in rats in which obesity was induced by a saturated high‐fat diet (HFD). Male Wistar rats were initially randomized into a standard diet and a HFD group. The experimental protocol spanned 23 weeks, comprising the induction and maintenance of obesity (15 weeks) followed by HIIT treatment (8 weeks). Performance was assessed using the maximum oxygen consumption test (V̇O2max${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}{\mathrm{max}}}}$). Evaluation encompassed cardiac, adipose and skeletal muscle histology, as well as contractility and intracellular Ca2+ handling. HIIT resulted in a reduction in visceral area, an increase in V̇O2max${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}{\mathrm{max}}}}$, and an augmentation of gastrocnemius fibre diameter in obese subjects. Additionally, HIIT led to a decrease in collagen fraction, an increase in percentage shortening, and a reduction in systolic Ca2+/percentage shortening and systolic Ca2+/maximum shortening rates. HIIT induces physiological cardiac remodelling, enhancing the contractile function of cardiomyocytes and improving myofilament sensitivity to Ca2+ in the context of obesity. This approach not only enhances cardiorespiratory and physical performance but also reduces visceral area and prevents interstitial fibrosis. What is the central question of this study?Does high‐intensity interval training (HIIT) enhance myocardial contractility in models of obesity induced by a saturated high‐fat diet, and does it promote an improvement in intracellular Ca2+ handling (Ca2+ influx and reuptake)?What is the main finding and its importance?HIIT, as a non‐pharmacological tool of short duration but high intensity, improves cardiovascular function and the sensitivity of myofilaments to intracellular Ca2+ handling, as well as promoting a reduction in visceral fat area. Thus, the obesity‐induced impairment of the heart's contractile properties was partially prevented by an 8‐week HIIT programme. [ABSTRACT FROM AUTHOR]

Background/Objectives: Capsinoids are potential antioxidant agents capable of reducing oxidative damage and the resulting complications triggered by obesity. Thus, this study aimed to investigate the effects of capsinoids on adiposity and biomarkers of cardiac oxidative stress in obese rats induced by a high-fat diet. Methods: Male Wistar rats were exposed to a high-fat diet for 27 consecutive weeks. After the characterization of obesity (week 19), some of the obese animals began to receive capsinoids (10 mg/kg/day) by orogastric gavage. Adiposity and comorbidities were assessed. In the heart, remodeling, injury, and biomarkers of oxidative stress were determined. Results: The treatment did not reduce obesity-induced adiposity but was efficient in reducing cholesterol levels. Capsinoid treatment did not cause a difference in heart and LV mass, despite having reduced troponin I concentrations. Furthermore, capsinoids did not reduce the increase in the advanced oxidation of protein products and carbonylated proteins caused by obesity in cardiac tissue. In addition, obese rats treated with capsinoids presented high levels of malondialdehyde and greater antioxidant enzyme activity compared to untreated obese rats. Conclusions: In conclusion, treatment with capsinoids increases antioxidative enzyme activity and prevents obesity-induced cardiac injury without positively modulating body fat accumulation and cardiac oxidative biomarkers. [ABSTRACT FROM AUTHOR]

Background/Aims: Obesity resistance is associated with the complex interaction of stringent and environmental factors that confer the ability to resist mass gain and body fat deposition, even when eating high-calorie diets. Considering that there are numerous gaps in the literature on the metabolic processes that explain Obesity resistance, specifically in relation to oxidative stress, the purpose of the study was to investigate whether obesity-resistant (OR) rats develop elevated reactive oxygen species in cardiac tissue. Methods: Wistar rats were initially randomized into two groups: a standard diet (SD) and a high-fat diet (HFD) group. The SD and HFD groups were further divided into control (C), OR, and obese prone (OP) subgroups based on body weight. This criterion consisted of organizing the animals in each group in ascending order according to body weight (BW), and the cutoff point was identified in the animals by terciles: 1) lower BW; 2) intermediate BW; and 3) higher BW. Rats were sacrificed on the 14th week, and serum and organs were collected. Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Results: BW showed a significant difference between the standard diet and highfat diet groups in the 4th week of the experimental protocol, characterizing obesity. In the 4th week, after the characterization of Obesity resistance, there was a significant difference in BW between groups C, OP, and OR. The OP and OR groups showed a significant increase in caloric intake in relation to the C group. The OP group showed a significant increase in final BW, retroperitoneal fat pad mass, sum of corporal fat deposits and reactive oxygen species, in relation to groups C and OR. The area under the glycemic curve, insulin resistance index and basal glucose were elevated in the OP group in relation to the C. OP also promoted an increase in HOMA-IR when compared with C. OR rats showed a non-significant increase in insulin and HOMA-IR in OR vs. C (p = ~0.1), but no significant differences were observed between OP vs. OR for these parameters, suggesting that both groups suffered from decreased metabolic health. Total cardiac mass, left ventricular cross-sectional area, and cholesterol levels were significantly elevated in the OP and OR groups compared with the C group. Conclusion: A high-fat diet induces cardiac damage in obesity-resistant rodents with reduction in metabolic health. [ABSTRACT FROM AUTHOR]

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Previous studies have shown that food restriction promotes myocardial dysfunction in rats. However, the molecular mechanisms that are responsible are unclear. We investigated the role of sarcoplasmic reticulum [Ca.sup.2+]-ATPase (SERCA2) on myocardial performance in food-restricted rats. Male Wistar-Kyoto rats, 60 days old, were fed a control or restricted diet (daily energy intake reduced to 50% of the control) for 90 days. Expression of Serca2a, phospholamban (PLB), [NA.sup.2+]/[Ca.sup.2+] exchanger (NCX), and thyroid hormone receptor (TRα1, TRβ1) mRNA was determined by quantitative PCR. SERCA2 activity was measured by using 20 µmol/L cyclopiazonic acid (CPA) in a left ventricular papillary muscle preparation during isometric contraction in basal conditions and during post-rest contraction. Serum concentrations of thyroxine ([T.sub.4]) and thyrotropin (TSH) were also determined. The 50%-restricted diet reduced body and ventricular weight and serum [T.sub.4] and TSH levels. The interaction of CPA and food restriction reduced peak developed tension and maximum rate of tension decline (-dT/dt), but increased the resting tension intensity response during post-rest contraction. PLB and NCX mRNA were upregulated and TRα1 mRNA was downregulated by food restriction. These results suggest that food restriction promotes myocardial dysfunction related to impairment of sarcoplasmic reticulum [Ca.sup.2+] uptake as a result of a hypothyroid state. Key words: SERCA2, cyclopiazonic acid, calcium handling, food restriction, rats, myocardial function, thyroid hormone. Des etudes arterieures revelent que la restriction alimentaire suscite des dysfonctions myocardiques chez le rat. Cependant, on n'en connait pas bien les mecanismes moleculaires. On a analyse le role de la SERCA2 sur la performance myocardique de rats soumis a une restriction alimentaire. Des rats Wistar-Kyoto males ages de 60 jours sont diviseesen deux groupes, l'un de controle et l'autre, soumis a une restriction alimentaire consistant a ingeerer 50 % de l'apport du groupe de controle, et ce, durant 90 jours. On determine l'expression de la SERCA2,de la PLB, de l'eechangeur [NA.sup.2+]/[Ca.sup.2+] (NCX), de l'ARNm des recepteurs des hormones thyroidiennes (TRα1, TRβ1) par la quantification de la PCR. On mesure l'activite de la SERCA2 au moyen de 20 µmol/L d'acide cyclopiazonique (CPA) dans une preparation de muscle papillaire du ventricule gauche (LV) au cours d'une contraction isomeetrique dans des conditions de repos et a la suite d'une contraction post-repos. On evalue aussi les concentrations de [T.sub.4] et de TSH. Le regime avec restriction a 50 % suscite une diminution de la masse corporelle et de la masse du ventricule; les concentrations seriques de [T.sub.4] et de TSH diminuent. L'interaction du CPA et de la restriction alimentaire diminue DT et -dT/dt, mais augmente l'intensite de la reponse RT au cours de la contraction post-repos. La restriction alimentaire suscite une regulation a la hausse de l'ARNm de NCX et de la PLB, mais une regulation a la baisse de l'ARNm de TRα1. D'apres ces observations, la restriction alimentaire favorise la dysfonction du myocarde associeea la deterioration dans le reticulum sarcoplasmique de la captation du [Ca.sup.2+] causeee par l'etat hypothyroidien. Mots-cles: SERCA2, acide cyclopiazonique, prise en charge du calcium, restriction alimentaire, rats, fonction myocardique, hormone thyroidienne. [Traduit par la Redaction], Introduction Food restriction increases the maximum life span of rats (Berner and Stern 2004; Keenan et al. 1996) and slows or prevents a broad spectrum of age-related pathophysiological changes, such [...]

Food restriction (FR) has been shown to impair myocardial performance. However, the mechanisms behind these changes in myocardial function due to FR remain unknown. Since myocardial L-type [Ca.sup.2+] channels may contribute to the cardiac dysfunction, we examined the influence of FR on L-type [Ca.sup.2+] channels. Male 60-day-old Wistar rats were fed a control or a restricted diet (daily intake reduced to 50% of the amount of food consumed by the control group) for 90 days. Myocardial performance was evaluated in isolated left ventricular papillary muscles. The function of myocardial L-type [Ca.sup.2+] channels was determined by using a pharmacological [Ca.sup.2+] channel blocker, and changes in the number of channels were evaluated by mRNA and protein expression. FR decreased final body weights, as well as weights of the left and right ventricles. The [Ca.sup.2+] channel blocker diltiazem promoted a higher blockade on developed tension in FR groups than in controls. The protein content of L-type [Ca.sup.2+] channels was significantly diminished in FR rats, whereas the mRNA expression was similar between groups. These results suggest that the myocardial dysfunction observed in previous studies with FR animals could be caused by downregulation of L-type [Ca.sup.2+] channels. Key words: food restriction, papillary muscle, L-type calcium channels function, L-type calcium mRNA, L-type calcium protein, diltiazem, rats. Des etudes ont demontre que la restriction calorique (RC) altere le fonctionnement du myocarde. Toutefois, les mecanismes a l'origine des modifications causees par la RC sont inconnus. Etant donne que les canaux [Ca.sup.2+] de type l'pourraient jouer un role dans la dysfonction du myocarde, nous avons examine l'influence de la RC sur ces canaux. Nous avons soumis des rats Wistar males de 60 jours a une diete temoin (T) ou a une diete restreinte en calories (apport quotidien reduit a 50 % de la quantite de nourriture consommee par le groupe T) pendant 90 jours. Nous avons evalue le fonctionnement du myocarde dans les muscles papillaires isoles du ventricule gauche. Nous avons determine la fonction des canaux de type L myocardiques au moyen d'un bloqueur pharmacologique des canaux [Ca.sup.2+], et evalue les modifications dans le nombre de canaux en examinant l'expression des ARNm et des proteines. La RC a diminue les poids corporels finaux ainsi que les poids des ventricules gauche et droit. Le bloqueur de canaux [Ca.sup.2+], diltiazem, a induit un blocage plus prononce de la tension developpee chez les groupes soumis a une RC que chez les temoins. La teneur en proteines des canaux [Ca.sup.2+] de type L a significativement diminue chez les rats soumis a une RC, alors que l'expression des ARNm a ete similaire chez les deux groupes. Ces resultats laissent supposer que la dysfonction du myocarde observee dans les etudes anterieures sur les animaux soumis a un RC pourrait etre liee a la diminution du nombre de canaux [Ca.sup.2+] de type L. Mots-cles : restriction calorique, muscle, fonction des canaux calciques de type L, ARNm du calcium de type L, proteine du calcium de type L, diltiazem, rats. [Traduit par la Redaction], Introduction Food restriction (FR) increases the maximum life span of rats (Berner and Stern 2004; Keenan et al. 1996) and retards or prevents a broad spectrum of age-related pathophysiological changes [...]

Identifying indicators that contribute to a favourable living condition becomes of great value for the diagnosis, as well as implementing preventive and health-promoting actions. The present work objective was to evaluate and compare the lifestyle, depressive symptoms and functional aptitude of elderly men and women attending a community centre. The sample consisted of 277 elderly people, 197 (71%) women and 80 (29%) men aged above 60 years. The elderly were evaluated using a questionnaire to assess lifestyle and depressive symptoms, and their functional fitness was assessed by functional autonomy tests. The differences between the parameters were analysed by the student's t-test and χ² whenever appropriate. Depressive symptoms were present in 35% of the elderly; however, the lifestyle analysis showed that 57.40% of the elderly had a very good classification, followed by 24.55% as good, 17.33% as excellent and 0.72% as regular. Regarding functional fitness, 19.39% of the elderly had a score related to a very good level, 15.97% good, 16.35% fair and 45.29% weak. The results found in this study suggest that the elderly attending the community centre presented low depressive symptoms with a lifestyle classification considered very good, however, with poor functional fitness with differences in some parameters between men and women. [ABSTRACT FROM AUTHOR]

Background/Aims: Oxidative stress is associated with cardiometabolic alterations, and the involvement of excess glucose and fatty acids has been demonstrated in this process. Thus, the aim of this study was to investigate the effects of different hypercaloric diets on cardiac oxidative stress. Methods: Wistar rats were randomized into four groups: control (C), high-sucrose (HS), high-fat (HF), and high-fat with sucrose (HFS). Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Cardiac oxidative stress was analyzed by malondialdehyde (MDA) and carbonylated proteins, and the cardiac protein expression levels of type 1 angiotensin receptor (AT-1), nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2), superoxide dismutase (SOD 1 e 2), glutathione peroxidase (GPX), and catalase (CAT) were determined by western blot. Results: The HF group showed an increase in adiposity; however, it did not present adipocyte hypertrophy and comorbidities. Cardiac MDA and carbonylated protein levels were higher in the HF and HFS compared with the C group. The levels of oxidant and antioxidant proteins showed no difference between the groups. Conclusion: HF and HFS dietary interventions promoted cardiac oxidative stress, in the presence and absence of obesity, respectively. However, this process was neither mediated by the pro-oxidants AT1 and Nox2, nor by the quantitative reduction of antioxidant enzymes. [ABSTRACT FROM AUTHOR]

Digoxin is a cardiotonic that increases the cardiac output without causing deleterious effects on heart, as well as improves the left ventricular performance during physical exercise. We tested whether the association between chronic digoxin administration and aerobic interval training (AIT) promotes beneficial cardiovascular adaptations by improving the myocardial contractility and calcium (Ca2+) handling. Male Wistar rats were randomly assigned to sedentary control (C), interval training (T), sedentary digoxin (DIGO) and T associated to digoxin (TDIGO). AIT was performed on a treadmill (1h/day, 5 days/week) for 60 days, consisting of successive 8-min periods at 80% and 20% of VO2 máx for 2 min. Digoxin was administered by orogastric gavage for 60 days. Left ventricle samples were collected to analysis of Ca2+ handling proteins; contractility and Ca2+ handling were performed on isolated cardiomyocytes. TDIGO group had a greater elevation in fractional shortening (44%) than DIGO, suggesting a cardiomyocyte contractile improvement. In addition, T or TDIGO groups showed no change in cardiomyocytes properties after Fura2-acetoxymethyl ester, as well as in sarcoplasmic reticulum Ca2+- ATPase (SERCA2a), phospholamban and calcineurin expressions. The main findings indicate that association of digoxin and aerobic interval training improved the cardiomyocyte contractile function, but these effects seem to be unrelated to Ca2+ handling. [ABSTRACT FROM AUTHOR]