Diego Figueroa

Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats

BackgroundThe aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO2) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats.MethodsMale Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO2 were assessed 60 days after diabetes induction (STZ, 50 mg/Kg).ResultsVO2 maximum was reduced in STZ-diabetic rats (72.5 ± 1 mL/Kg/min-1) compared to CG rats (81.1 ± 1 mL/Kg/min-1). There were positive correlations between ET speed and VO2 (r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO2 reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO2 and VO2 predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO2 = 1.54 * ET speed + 52.34) and DG (VO2 = 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO2 reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO2 maximum for both groups (CG: r = 0.7 and DG: r = 0.7).ConclusionThese results suggest that: a) VO2 and VO2 reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats.

Effects of exercise training on autonomic dysfunction management in an experimental model of menopause and myocardial infarction.

Objective:The aim of this study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction in ovariectomized rats submitted to myocardial infarction. Methods:Female Wistar rats were divided into the following ovariectomized groups: sedentary ovariectomized (SO), trained ovariectomized (TO), sedentary ovariectomized infarcted (SOI), and trained ovariectomized infarcted (TOI). Trained groups were submitted to an exercise training protocol on a treadmill (8 wk). Arterial baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes, and cardiopulmonary baroreflex sensitivity was tested by bradycardic and hypotension responses to serotonin injection. Vagal and sympathetic effects were calculated by pharmacological blockade. Results:Arterial pressure was reduced in the TO in comparison with the SO group and increased in the TOI in relation to the SOI group. Exercise training improved the baroreflex sensitivity in both the TO and TOI groups. The TOI group displayed improvement in cardiopulmonary reflex sensitivity compared with the SOI group at the 16 &mgr;g/kg serotonin dose. Exercise training enhanced the vagal effect in both the TO (45%) and TOI (46%) animals compared with the SO and SOI animals and reduced the sympathetic effect in the TOI (38%) in comparison with the SOI animals. Significant correlations were obtained between bradycardic baroreflex responses and vagal (r = −0.7, P < 0.005) and sympathetic (r = 0.7, P < 0.001) effects. Conclusions:These results indicate that exercise training in ovariectomized rats submitted to myocardial infarction improves resting hemodynamic status and reflex control of the circulation, which may be due to an increase in the vagal component. This suggests a homeostatic role for exercise training in reducing the autonomic impairment of myocardial infarction in postmenopausal women.

Role of Training and Detraining on Inflammatory and Metabolic Profile in Infarcted Rats: Influences of Cardiovascular Autonomic Nervous System

The aim of this study was to evaluate the effects of exercise training (ET, 50–70% of VO2 max, 5 days/week) and detraining (DT) on inflammatory and metabolic profile after myocardial infarction (MI) in rats. Male Wistar rats were divided into control (C, n = 8), sedentary infarcted (SI, n = 9), trained infarcted (TI, n = 10; 3 months of ET), and detrained infarcted (DI, n = 11; 2 months of ET + 1 month of DT). After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis), and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI.

Resistance Training After Myocardial Infarction in Rats: Its Role on Cardiac and Autonomic Function

Background Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. Objective To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Methods Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. Results The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Conclusion Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats.

Aerobic exercise training promotes additional cardiac benefits better than resistance exercise training in postmenopausal rats with diabetes.

ObjectiveThe aim of this study was to evaluate the effects of aerobic exercise training or resistance exercise training on cardiac morphometric, functional, and oxidative stress parameters in rats with ovarian hormone deprivation and diabetes. MethodsFemale Wistar rats (200-220 g) were divided into a sham-operated group (euglycemic sham-operated sedentary [ES]; n = 8) and three ovariectomized (bilateral removal of ovaries) and diabetic (streptozotocin 50 mg/kg IV) groups as follows: diabetic ovariectomized sedentary (DOS; n = 8), diabetic ovariectomized undergoing aerobic exercise training (DOTA; n = 8), and diabetic ovariectomized undergoing resistance exercise training (DOTR; n = 8). After 8 weeks of resistance (ladder) or aerobic (treadmill) exercise training, left ventricle function and morphometry were evaluated by echocardiography, whereas oxidative stress was evaluated at the left ventricle. ResultsThe DOS group presented with increased left ventricle cavity in diastole and relative wall thickness (RWT), and these changes were attenuated in both DOTA and DOTR groups. Systolic and diastolic function was impaired in the DOS group compared with the ES group, and only the DOTA group was able to reverse this dysfunction. Lipoperoxidation and glutathione redox balance were improved in both trained groups compared with the DOS group. Glutathione peroxidase and superoxide dismutase were higher in the DOTA group than in the other studied groups. Correlations were observed between lipoperoxidation and left ventricle cavity in diastole (r = 0.55), between redox balance and RWT (r = 0.62), and between lipoperoxidation and RWT (r = −0.60). ConclusionsAerobic exercise training and resistance exercise training promote attenuation of cardiac morphometric dysfunction associated with a reduction in oxidative stress in an experimental model of diabetes and menopause. However, only dynamic aerobic exercise training is able to attenuate systolic and diastolic dysfunction under this condition.

Cardioprotection afforded by exercise training prior to myocardial infarction is associated with autonomic function improvement

BackgroundIt has been suggested that exercise training (ET) protects against the pathological remodeling and ventricular dysfunction induced by myocardial infarction (MI). However, it remains unclear whether the positive adjustments on baroreflex and cardiac autonomic modulations promoted by ET may afford a cardioprotective mechanism. The aim of this study was to evaluate the effects of aerobic ET, prior to MI, on cardiac remodeling and function, as well as on baroreflex sensitivity and autonomic modulation in rats.MethodsMale Wistar rats were divided into 4 groups: sedentary rats submitted to Sham surgery (C); trained rats submitted to Sham surgery (TC); sedentary rats submitted to MI (I), trained rats submitted to MI (TI). Sham and MI were performed after ET period. After surgeries, echocardiographic, hemodynamic and autonomic (baroreflex sensitivity, cardiovascular autonomic modulation) evaluations were conducted.ResultsPrior ET prevented an additional decline in exercise capacity in TI group in comparison with I. MI area was not modified by previous ET. ET was able to increase the survival and prevent additional left ventricle dysfunction in TI rats. Although changes in hemodynamic evaluations were not observed, ET prevented the decrease of baroreflex sensitivity, and autonomic dysfunction in TI animals when compared with I animals. Importantly, cardiac improvement was associated with the prevention of cardiac autonomic impairment in studied groups.ConclusionsPrior ET was effective in changing aerobic capacity, left ventricular morphology and function in rats undergoing MI. Furthermore, these cardioprotective effects were associated with attenuated cardiac autonomic dysfunction observed in trained rats. Although these cause-effect relationships can only be inferred, rather than confirmed, our study suggests that positive adaptations of autonomic function by ET can play a vital role in preventing changes associated with cardiovascular disease, particularly in relation to MI.

Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents

OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23±3%) when compared with the myocardial infarction (42±7%, p<0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32±3; diabetes + myocardial infarction: 35±0.7; control-sham: 12±2; myocardial infarction: 16±0.1 pmol min-1 mg-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). CONCLUSIONS: These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.

Effect of fasting and refeeding on the consequences of myocardial infarction in rats

We investigated the effects of 48 hours (h)-fasting followed by permanent coronary artery occlusion and 48 h-refeeding on the infarct size; ejection fraction; plasma creatine kinase activity; and levels of IL1-β, CINC 2α/β and IL-6, triglycerides, glycogen and ATP in the left ventricle of adult rats. Permanent coronary artery occlusion was performed in ad libitum fed (fed/fed) and 2-days-fasted rats (fasted/re-fed). After infarction induction, both groups were re-fed for 48 h, and infarction area and ejection fraction were assessed using echocardiography. The levels of glycogen, triglyceride, ATP, and proinflammatory cytokines in the left ventricle, and the concentrations of glucose and free fatty acids in plasma were measured at the end of the 2-day fasting period. The infarct size was significantly smaller in the fasted/ re-fed group compared with the fed animals. This was accompanied by decreased plasma creatine kinase activity and improved ejection fraction. Fasting per se led to an increase in glycogen, ATP, CINC 2 α/β, interleukin (IL)-1β, and IL-6, and a decrease in triacylglycerol levels in the left ventricle; along with an increase in free fatty acid concentrations and a decrease in glucose levels in the plasma. This study indicates that 2-days-fasting followed by 48 h refeeding protected the heart from ischemia-induced injury, which may be related to the fasting-induced metabolic condition. Introduction Acute myocardial infarction (AMI) is a major cause of mortality and morbidity worldwide [1]. AMI is initiated by a lack of blood flow resulting in marked reduction in the supply of oxygen and nutrients to the cardiac muscle. This in turn leads to a decrease in ATP production and causes oxidative stress, loss of ion gradient across membrane, accumulation of toxic metabolites, and inflammation [2]. Fatty acid (FA) oxidation is the main source of ATP to the heart in aerobic conditions [3,4]; however, during ischemia, ATP production occurs through anaerobic glycolysis using glucose derived from glycogen [4]. Expression of pro-inflammatory cytokines, such as IL-1β, tumor necrosis factor (TNF)-α, and IL-6, usually absent in the normal heart, is increased in the hearts of animals and humans affected by AMI [5,6]. The influx of inflammatory cells and production of pro-inflammatory mediators contribute to myocardial injury. However, broad inhibition of inflammation has adverse effects on outcomes following an AMI [7,8]. Inflammation is not an injurious process per se, since it triggers the first steps for proper AMI healing [9,10]. Dietary restriction increases cardiac tolerance to ischemic injury [11,12]. Intermittent fasting increases capillary density [13], reduces the number of apoptotic cells, and decreases the inflammatory response in the ischemic heart [14]. A fasting period of one to three days protects from renal [15] and hepatic [16] ischemic/reperfusion injury in mice. Nevertheless, the impact of short-term fasting followed by shortterm re-feeding on cardiac tolerance to ischemic injury, dissociated from reperfusion damage, has not been examined yet. In the present study, the infarct size, ejection fraction (EF), left ventricle (LV) mass, and levels of ATP, triglycerides (TG), glycogen and proinflammatory cytokines in the LV of rats subjected to fasting for 2 days followed by permanent coronary artery occlusion and 48 h re-feeding were investigated. Materials and methods Animals and the experimental protocol Male Wistar rats weighing 260-280 g were obtained from the Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo. Animals were housed under a 12:12 h light-dark cycle at 23 ± 1°C. The rats were randomly assigned to two experimental groups: fed ad libitum (fed/fed) or 48 h fasting and 48 h refeeding (fasted/re-fed). Six animals were used from the fed and fasted groups to evaluate the metabolic/inflammatory conditions before infarction. Animals in the fasted/re-fed group did not have access to food for 48 h prior to infarct induction. The animals were fed a standard laboratory chow (NUVILAB CR-1, Nuvital, Curitiba, Brazil). All groups received water ad libitum. The ethical committee of the Institute of Biomedical Correspondence to: Alcione Lescano de Souza Junior, Faculty of Health Sciences, University of Mato-Grosso. Av. Tancredo Neves, 1095-Cavalhada II -78200-000-Cáceres-Mato GrossoPABX +55 (65) 3221-0000, Brazil; E-mail: lescanoalcione9@gmail.com

Interval and continuous aerobic exercise training similarly increase cardiac function and autonomic modulation in infarcted mice

The present study aimed to compare the effects of moderate-intensity continuous and high-intensity interval exercise training (ET) on exercise tolerance, cardiac morphometry and function, hemodynamic, and cardiac autonomic modulation in myocardial infarcted mice. Wild-type mice (WT) were divided into four groups: sedentary WT (S); WT myocardium infarction sedentary (IS); WT myocardium infarction underwent to moderate-intensity continuous ET (MICT), and WT myocardium infarction underwent to high-intensity interval ET (MIIT). After 60 days of descending coronary artery ligation, moderate-intensity continuous ET consisted of running at 60% of maximum, while the high-intensity interval training consisted of eight sprints of 4 min at 80% of maximum and a 4-min recovery at 40% of maximum. Both exercises were performed 1 hr a day, 5 days a week, during 8 weeks. Results demonstrated that IS showed elevated exercise tolerance, as well as decreased hemodynamic and heart function, and autonomic control. On the other hand, both programs of ET were equally effective to increase all parameters, without further differences between the groups. In conclusion, the results of the present study showed that myocardial infarction leads to damage in both investigated strains and the two types of physical exercise attenuated the major impairments provoked by myocardial infarction in exercise tolerance, cardiac structure, cardiac function, hemodynamic and cardiac autonomic modulation.

Influência dos hormônios sexuais no consumo de oxigênio de ratos

Introduction: Literature findings suggest that fluctuations of female sex hormones may change the maximum oxygen consumption (VO2max).Objective:To compare the VO2max among male rats (M, n = 8), female rats on ovulatory (OV, n=8) or non-ovulatory (NOV, n=8) phases of the estrous cycle and ovariectomized (OS, n=8).Methods:The evaluation of oxygen consumption was performed on a treadmill coupled with metabolic box.Results: At rest VO2 was similar among groups. The M group had a higher VO2max compared to the NOV group, however showed similar values when compared to OV group. The VO2max was lower in the ovariectomized group (OS: 62±3 ml.kg-1.min-1) compared to other groups (M: 92±2; NOV: 77 ± 4; OV: 87 ± 3 ml.kg-1.min-1).Conclusions: These findings suggest that hormonal variation resulting from different phases of the estrous cycle and ovarian hormone deprivation can induce changes in maximal oxygen uptake in rats.