Introduction: Although the rapid weight loss process is undertaken by combat sports athletes very often, the impact of this practice on cardiovascular health is not fully understood. Objective: To verify the effects of the rapid weight loss process undertaken by combat sports athletes on hemodynamic parameters, cardiovascular autonomic modulation and mood state. Methods: Eight male fighters (21.62±1.49 years, 71.25±3.54 kg, 1.74±0.03 cm) were assessed in the city of São Paulo. The subjects had 5.37±0.77 years of practice and were training 5.75±0.45 days per week, for 3.05±0.69 hours per day. The athletes were assessed on 2 occasions: 14 days before and 1 day before official weigh-in. Weight, height and bioimpedance were used for body composition analysis. Mood state was assessed using the Brums Mood Scale. Blood pressure was measured at rest with a digital meter. Cardiovascular autonomic modulation was obtained through an analysis of heart rate variability recorded for 25 minutes at rest. The Student's t-test for dependent samples was used for comparison between time points. Values of p<0.05 were considered significant. Results: No differences in body composition were observed between the time points evaluated. After the weight loss strategy, increases in mood state parameters related to anger, vigor and fatigue categories were observed. Blood pressure did not change between the time points evaluated. However, an increase in heart rate associated with greater sympathetic modulation was observed after the weight loss strategy. There were no differences in autonomic modulation parameters representing parasympathetic activity. Conclusions: The study provided evidence of a higher cardiovascular risk in athletes as a result of this rapid weight loss practice, which is very concerning since combat sports athletes repeat this process several times during their lives. Level of Evidence IV; Study type: Case series.
Despite consensus on the benefits of food readjustment and/or moderate‐intensity continuous exercise in the treatment of cardiometabolic risk factors, there is little evidence of the association between these two cardiovascular risk management strategies after menopause. Thus, the objective of this study was to evaluate the effects of food readjustment and/or exercise training on metabolic, hemodynamic, autonomic, and inflammatory parameters in a model of loss of ovarian function with diet‐induced obesity. Forty C57BL/6J ovariectomized mice were divided into the following groups: high‐fat diet‐fed ‐ 60% lipids throughout the protocol (HF), food readjustment ‐ 60% lipids for 5 weeks, readjusted to 10% for the next 5 weeks (FR), high‐fat diet‐fed undergoing moderate‐intensity exercise training (HFT), and food readjustment associated with moderate‐intensity exercise training (FRT). Blood glucose evaluations and oral glucose tolerance tests were performed. Blood pressure was assessed by direct intra‐arterial measurement. Baroreflex sensitivity was tested using heart rate phenylephrine and sodium nitroprusside induced blood pressure changes. Cardiovascular autonomic modulation was evaluated in time and frequency domains. Inflammatory profile was evaluated by IL‐6, IL‐10 cytokines, and TNF‐alpha measurements. Only the exercise training associated with food readjustment strategy induced improved functional capacity, body composition, metabolic parameters, inflammatory profile, and resting bradycardia, while positively changing cardiovascular autonomic modulation and increasing baroreflex sensitivity. Our findings demonstrate that the association of these strategies seems to be effective in the management of cardiometabolic risk in a model of loss of ovarian function with diet‐induced obesity.
IntroductionConsidering the increase in cardiometabolic risk after menopause, and that diet and exercise training (ET) are the pillars of prevention/treatment strategies, the objective of this study was to evaluate the metabolic, hemodynamic and autonomic effects of exercise training in an experimental model of menopausal undergoing a high‐fat diet followed by dietary adjustment. Twenty female C57BL/6J mice (8 weeks aged), all oophorectomized (bilateral ovarian removal) divided into 4 experimental groups (n = 5) were used: sedentary submitted to a high‐fat diet (OSD), sedentary submitted to 4 weeks of high‐fat diet and 4 weeks of control diet (OSRa), trained submitted to a high‐fat diet (OTD), trained submitted to 4 weeks of high‐fat diet and 4 weeks of control diet (OTRa). Oophorectomy was performed at the end of the 4th week of the protocol. Fasting glycemia and oral glucose tolerance were evaluated. ET had duration of 4 weeks (6th to 9th week of protocol, 5 days/week, 1 hour/day, intensity 50–70% of the maximum treadmill test). At the end of the protocol, the animals were cannulated for direct recording of arterial pressure (AP), after which baroreflex sensitivity and cardiovascular autonomic modulation were analyzed.RESULTSDietary adjustment promoted a reduction in glycemia and a better glucose tolerance, associated with reduction in cardiac sympathetic modulation (LF‐PI: OSD: 0.54±0.02; OSRa: 0.37±0.06; OTD: 3.0±0.02, OTRa: 0.19±0.02 ms2) and vascular (LF‐SAP: OSD: 11.3±1.7, OSRa: 3.6±0.9, OTD: 1.6±0.2; OTR:3.0±0.5mmHg2). ET, with or without dietary adjustment, increased physical capacity, reduced heart rate, improved baroreflex sensitivity, increased cardiac parasympathetic modulation (HF‐PI: OSD: 0.47±0.04, OSRa: 0,63±0.07, OTD: 0.86±0.02, OTRa: 0.75±0.07 ms2) and reduction of cardiac and vascular sympathetic modulation. However, only the association of ET with dietary adjustment was able to promote reduction in body weight, glycemia, improvement in glucose tolerance, reduction in blood pressure (mean AP: OSD: 123±2.1, OSRa: 114±0.8; OTD: 120±1.4; OTR: 110±4.0 mmHg), and further increase in parasympathetic modulation. Thus, the association of ET with dietary adjustment may be considered an important behavior for the management of cardiovascular risk in the association of obesity with ovarian deprivation.Support or Funding InformationCoordenação de Aperfeiçoamento de Pessoal de Nível Superior ‐ Brazil (CAPES) ‐ Funding Code: 001.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Ketamine hydrochloride is a drug widely used to treat depression, the most mentally disabling disease in the world. However, there is increasing evidence of cardiovascular damage resulting from the chronic use of ketamine. While regular practice of physical activity has been increasingly recommended as an adjunct in the treatment of depression, physical training promotes beneficial effects on the cardiovascular system. Therefore, the hypothesis of this study is that physical training can mitigate and/or prevent the harmful effects of ketamine on the cardiovascular system. Thus, the aim of this study was to evaluate the effects of aerobic physical training on cardiac morphometry and function, hemodynamic parameters and baroreflex sensitivity in Wistar rats treated with ketamine hydrochloride. For this, 24 Wistar rats were divided into 4 groups (n=6 in each): control (S), trained (T), sedentary treated with ketamine hydrochloride (SK) and trained treated with ketamine hydrochloride (TK). The treatment with ketamine hydrochloride was performed 3 times a week, for 6 weeks (ip, 10mg/kg). The physical training was aerobic on a treadmill (50‐70% of the maximum running capacity, 1 hour/day, 5 days/week, 6 weeks). At the end of the protocol, the animals were submitted to echocardiography analysis and cannulation for direct recording of the arterial pressure (AP) and then, baroreflex sensitivity was evaluated. The results demonstrate that chronic treatment with ketamine hydrochloride induces reduction in left ventricular shortening fraction (S: 35.4±1.7; T: 35.7±2.3; SK: 31.5±1.6; TK: 27.9±1.3), increase in systolic (S: 147±2.2; T: 153±2.5; SK: 161±2.8; TK: 155±2.8) and diastolic (S: 97±2.2; T: 103±0.8; SK: 107±3.6; TK: 103±1.5) arterial pressure, increased heart rate (S: 361±2.4; T: 365±8.1; SK: 401±18.1; TK: 354±10.0), and impaired baroreflex tachycardic response (S: 3.0±0.18; T: 3.1±0.18; SK: 2.3±0.06; TK: 3.1±0.10). On the other hand, aerobic physical training seems to be promising to prevent hemodynamic damage, since ketamine‐trained animals did not present such damages. In addition, TF promoted resting bradycardia (groups T and TK). These results demonstrate the protective role of physical training, preventing the onset of cardiovascular damage after chronic use of ketamine hydrochloride, suggesting that physical training should be recommended as an adjunct to the treatment of patients using this drug.
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