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This longitudinal and observational study investigated the consequences of the coronavirus disease 2019 lockdown on health-related physical fitness and biochemical responses in 16 overweight or obese male adolescents (aged 12.6±1.8 years). The anthropometry, body composition, physical fitness tests, and measures of blood biomarkers (fasting blood glucose, total cholesterol [TC], lowdensity lipoprotein cholesterol [LDL-c], triglycerides [TG], aspartate aminotransferase [AST], and alanine aminotransferase [ALT]) were evaluated before and after 8 months of lockdown. The results showed increased body weight, fat-free mass, and waist and hip circumference (p<0.05) after 8 months. Maximum isometric handgrip strength and flexibility increased, while muscle endurance decreased (p<0.05). Fasting blood glucose, TC, LDL-c, TG, TG/glucose, AST, ALT, TG/HDL-c, CT/HDL-c, and LDL/HDL increased (p<0.05), while the HDL-c levels decreased significantly (p<0.05). Therefore, eight months of social isolation promoted harmful effects on adolescents' morphological parameters and physical fitness. However, the small sample size prevents the generalization of these findings. [ABSTRACT FROM AUTHOR]

The medial amygdaloid nucleus (MeA) is a limbic structure that has been demonstrated to be part of the central circuitry regulating baroreflex function. However, the local neurochemical mechanisms involved in baroreflex control by this forebrain structure is poorly understood. Thus, in the present study, we investigated the specific role of AT1, AT2, and MAS angiotensinergic receptors within the MeA in baroreflex responses in unanesthetized rats. For this, the baroreflex function was assessed using both the pharmacological approach via intravenous infusion of vasoactive agents and the sequence analysis technique. Using the pharmacological approach, we observed that bilateral microinjection of the selective AT2 receptor antagonist PD123319 into the MeA increased the tachycardia evoked by blood pressure decrease, but without affecting the reflex bradycardia caused by blood pressure increase. Besides, bilateral microinjection of the selective MAS receptor antagonist A-779 decreased both tachycardic and bradycardic responses of the baroreflex. The sequence analysis technique indicated that PD123319 into the MeA increased baroreflex effectiveness index while A-779 had an opposite effect. Treatment of the MeA with the selective AT1 receptor antagonist losartan did not affect baroreflex function assessed by either the pharmacological approach or sequence analysis technique. Overall, these findings provide evidence that MAS receptor within the MeA plays a facilitatory role in baroreflex function, whereas local AT2 receptor inhibits cardiac baroreflex responses. Results also indicate that AT1 receptor within the MeA is not involved in the control of baroreflex function. [ABSTRACT FROM AUTHOR]

Background: Alcohol abuse is a health concern worldwide. Studies have associated alcohol abuse with cardiovascular impairments. In this study, we investigated differences in the effects of chronic alcohol vapor exposure on cardiovascular function between male and female rats by using the alcohol vapor chamber method to induce alcohol addiction‐like behaviors in rats. Methods: We exposed male and female Long‐Evans rats to alcohol vapor for 14 hours, followed by ethanol withdrawal for 10 hours, for 30 consecutive days or room air (control groups). The animals underwent preparation for the surgical implantation of cannulas into femoral vessels, for allowing the assessment of the basal arterial pressure and heart rate values, baroreflex function, and autonomic activity. Results: Female control rats showed higher basal heart rate compared to male control rats. Chronic alcohol vapor inhalation reduced basal heart rate in females, but not in males; this effect was followed by an increase in the parasympathetic tone of the heart. Further, female rats subjected to alcohol vapor showed an increase in the baroreflex activity. Conclusions: These findings suggest that females are more sensitive to chronic alcohol vapor exposure than males because they had a reduction in basal heart rate and changes in the baroreflex activity. [ABSTRACT FROM AUTHOR]

Background and Purpose: Endocannabinoid signalling has been reported as an important neurochemical mechanism involved in responses to stress. Previous studies provided evidence of endocannabinoid release in the bed nucleus of the stria terminalis (BNST) during aversive stimuli. Nevertheless, a possible involvement of this neurochemical mechanism in stress responses has never been evaluated. Therefore, in the present study we investigated the involvement of BNST endocannabinoid neurotransmission, acting via local CB1 receptors, in the cardiovascular responses to acute restraint stress in rats.Experimental Approach: The selective CB1 receptor antagonist AM251 (1, 30 and 100 pmol 100 nL(-1) ) and/or the fatty acid amide hydrolase (FAAH) enzyme inhibitor URB597 (30 pmol 100 nL(-1) ) or the monoacylglycerol lipase (MAGL) enzyme inhibitor JZL184 (30 pmol 100 nL(-1) ) was microinjected into the BNST before the acute restraint stress.Key Results: Microinjection of AM251 into the BNST enhanced the tachycardia caused by restraint stress, without affecting the increase in arterial pressure and the sympathetic-mediated cutaneous vasoconstrictor response. Conversely, the increased endogenous levels of AEA in the BNST evoked by local treatment with the FAAH enzyme inhibitor URB597 decreased restraint-evoked tachycardia. Inhibition of the hydrolysis of 2-arachidonoylglycerol (2-AG) in the BNST by local microinjection of the MAGL enzyme inhibitor JZL184 also decreased the HR response. These effects of URB597 and JZL184 were abolished by BNST pretreatment with AM251.Conclusions and Implications: These findings indicate an involvement of BNST endocannabinoid neurotransmission, acting via CB1 receptors, in cardiovascular adjustments during emotional stress, which may be mediated by the local release of either AEA or 2-AG. [ABSTRACT FROM AUTHOR]

Consistent evidence has shown an important role of emotional stress in pathogenesis of cardiovascular diseases. Additionally, studies in animal models have demonstrated that daily exposure to different stressor (heterotypic stressor) evokes more severe changes than those resulting from repeated exposure to the same aversive stimulus (homotypic stressor), possibly due to the habituation process upon repeated exposure to the same stressor. Despite these pieces of evidence, the mechanisms involved in the stress- evoked cardiovascular dysfunction are poorly understood. Therefore, the present study investigated the involvement of angiotensin II (Ang II) acting on the type 1 Ang II receptor (AT1) in the cardiovascular dysfunctions evoked by both homotypic and heterotypic chronic emotional stresses in rats. For this purpose, we compared the effect of the chronic treatment with the AT1 receptor antagonist losartan (30 mg/kg/day, p.o.) on the cardiovascular and autonomic changes evoked by the heterotypic stressor chronic variable stress (CVS) and the homotypic stressor repeated restraint stress (RRS). RRS increased the sympathetic tone to the heart and decreased the cardiac parasympathetic activity, whereas CVS decreased the cardiac parasympathetic activity. Additionally, both stressors impaired the baroreflex function. Alterations in the autonomic activity and the baroreflex impairment were inhibited by losartan treatment. Additionally, CVS reduced the body weight and increased the circulating corticosterone; however, these effects were not affected by losartan. In conclusion, these findings indicate the involvement of angiotensin II/AT1 receptors in the autonomic changes evoked by both homotypic and heterotypic chronic stressors. Moreover, the present results provide evidence that the increase in the circulating corticosterone and body weight reduction evoked by heterotypic stressors are independent of AT1 receptors. [ABSTRACT FROM AUTHOR]

Previous evidence indicates that body fat can distinguish Brazilian jiu-jitsu (BJJ) athletes according to the competitive level. However, propositions of cut-off points for establishing classifications of body fat percentage for combat sports athletes and, specifically, for BJJ athletes are still incipient in the literature. In this sense, the main aim of the present study was to establish a normative table for the classification of body fat percentage in BJJ athletes. As a secondary aim, athletes were compared according to competitive level. Ninety male BJJ athletes (aged: 29.0 ± 8.2 years; practice time: 6.0 ± 2.1 years; body mass: 82.1 ± 12.7 kg; height: 175.9 ± 6.5 cm; fat mass: 16.0 ± 8.9 kg; bone mineral content: 3.7 ± 0.6 kg; muscle mass: 37.9 ± 5.4 kg; body fat percentage: 17.3 ± 6.8 %; basal metabolic rate: 1811.4 ± 193.4 kcal) from different competitive levels: state (n= 42), national (n= 26) and international (n= 22) took part in this study. All athletes had their body composition measured via tetrapolar bioelectrical impedance. Percentiles p10, p25, p50, p75, and p90 were used to establish the classification. As a result, the following classification was obtained: <7.7 % (very low); -7.7-11.5 % (low); 11.6-17.0 % (medium); 17.1-24.0 % (high) and -24.1 % (very high). State-level athletes had a higher fat percentage than national and international-level athletes (p<0.05). The proposed cut-off points can help professionals responsible for sports training and nutritional prescription in monitoring the body fat of BJJ athletes. [ABSTRACT FROM AUTHOR]