Giuseppe Potrick Stefani

Resistance Training Improves Hemodynamic Function, Collagen Deposition and Inflammatory Profiles: Experimental Model of Heart Failure

The role of resistance training on collagen deposition, the inflammatory profile and muscle weakness in heart failure remains unclear. Therefore, this study evaluated the influence of a resistance training program on hemodynamic function, maximum strength gain, collagen deposition and inflammatory profile in chronic heart failure rats. Thirty-two male Wistar rats submitted to myocardial infarction by coronary artery ligation or sham surgery were assigned into four groups: sedentary sham (S-Sham, n = 8); trained sham (T-Sham, n = 8); sedentary chronic heart failure (S-CHF, n = 8) and trained chronic heart failure (T-CHF, n = 8). The maximum strength capacity was evaluated by the one maximum repetition test. Trained groups were submitted to an 8-week resistance training program (4 days/week, 4 sets of 10–12 repetitions/session, at 65% to 75% of one maximum repetition). After 8 weeks of the resistance training program, the T-CHF group showed lower left ventricular end diastolic pressure (P<0.001), higher left ventricular systolic pressure (P<0.05), higher systolic blood pressure (P<0.05), an improvement in the maximal positive derivative of ventricular pressure (P<0.05) and maximal negative derivative of ventricular pressure (P<0.05) when compared to the S-CHF group; no differences were observed when compared to Sham groups. In addition, resistance training was able to reduce myocardial hypertrophy (P<0.05), left ventricular total collagen volume fraction (P<0.01), IL-6 (P<0.05), and TNF-α/IL-10 ratio (P<0.05), as well as increasing IL-10 (P<0.05) in chronic heart failure rats when compared to the S-CHF group. Eight weeks of resistance training promotes an improvement of cardiac function, strength gain, collagen deposition and inflammatory profile in chronic heart failure rats.

Interval and continuous exercise enhances aerobic capacity and hemodynamic function in CHF rats

OBJECTIVE: The aim of the present study was to compare the effects of continuous versus interval aerobic exercise training on hemodynamic parameters, cardiac remodeling, and maximal exercise capacity (MEC) in chronic heart failure (CHF) rats. METHOD: Twenty-four male Wistar rats were subjected to myocardial infarction (MI) surgery. Five weeks post MI, the animals were assigned to one of three groups: sedentary group (CHF-Sed, n=8), aerobic continuous training group (CHF-ACT, n=8), and aerobic interval training group (CHF-AIT, n=8). Treadmill training was performed five times a week for 8 weeks (ACT: 50 min/day at 15 m/min and AIT: 40 min/day with 8 min of warm-up at 10 m/min and exercise at 15 m/min 4×4 min interspersed with 4×4 min at 23 m/min). MEC was evaluated pre and post exercise program. RESULTS: Left ventricular end-diastolic pressure (LVEDP), left ventricular mass/body mass ratio (LVM:BM), and total collagen volume fraction were lower in the trained groups compared with the sedentary group, but no difference was found between the trained groups. Systolic ventricular pressure (SVP) and maximum positive derivative of LV pressure (+dP/dtmax) were higher in the trained groups, but CHF-ACT showed higher +dP/dtmax compared to CHF-AIT. Both training regimens were able to increase MEC. However, the aerobic interval training was superior for improving MEC. CONCLUSION: Aerobic training is an important intervention to improve cardiac function and remodeling and physical capacity in CHF rats. Interval training is a potential strategy to maximize the results, but exercise type and intensity are still topics to be explored.

Functional capacity in a rat model of heart failure: impact of myocardial infarct size

What is the central question of this study? To the best of our knowledge, no studies have evaluated oxygen uptake, carbon dioxide production and exercise tolerance in rats that have undergone myocardial infarction classified by myocardial infarct (MI) size. What is the main finding and its importance? Oxygen uptake and exercise intolerance are MI size dependent, and classification based on MI size can distinguish rats with functional capacity impairment. Rats with a large MI (>40% of the left ventricle) might provide a good model for the testing of new therapies that have the potential to modify the variables of functional capacity.

Resistance training and L-arginine supplementation are determinant in genomic stability, cardiac contractility and muscle mass development in rats

L-arginine supplementation has been related to increased maximum strength and improvement of hemodynamic parameters in several diseases. The aim of our study was to evaluate the effect of L-arginine supplementation and resistance training on muscle mass, hemodynamic function and DNA damage in healthy rats subjected to a low-arginine concentration diet. Twenty three Wistar rats (290-320g) were divided into 4 groups: Sedentary (SED-Arg, n = 6), Sedentary+Arg (SED+Arg, n = 6), Resistance Training (RT-Arg, n = 5), Resistance Training+Arg (RT+Arg, n = 6). Trained animals performed resistance training protocol in a squat apparatus adapted for rats (4 sets of 10–12 repetitions, 90s of interval, 4x/week, 65–75% of One Maximum Repetition, for 8 weeks). Comet assay was performed to measure DNA damage in leukocytes. The resistance training induced higher muscle mass in trained groups. The L-arginine supplementation increased both gastrocnemius and left ventricle to body mass ratio and increased left ventricle contractility without changing hemodynamic variables. The SED+Arg group showed higher concentration of extracellular heat shock protein 72 (eHSP72) and total testosterone, as well as lower uric acid concentration in blood versus SED-Arg group. The administration of isolated L-arginine supplementation and its association with resistance training promoted less damage in leukocytes DNA. In conclusion, the L-arginine supplementation showed synergistic effect with resistance training regarding leukocyte genomic stability in a low-L-arginine diet scenario.

Respiratory muscle training decreases diaphragm DNA damage in rats with heart failure

Respiratory muscle training (RMT) promotes beneficial effects on respiratory mechanics, heart and lung morphological changes, and hemodynamic variables in rats with heart failure (HF). However, the relation between RMT effects and diaphragm oxidative stress remains unclear. Therefore, the aim of this study was to evaluate the RMT effects on diaphragm DNA damage in HF rats. Wistar rats were allocated into 4 groups: sedentary sham (Sed-Sham, n = 8), trained sham (RMT-Sham, n = 8), sedentary HF (Sed-HF, n = 8), and trained HF (RMT-HF, n = 8). The animals underwent a RMT protocol (30 min/day, 5 days/week for 6 weeks), whereas sedentary animals did not exercise. Groups were compared by a two-way ANOVA and Tukeys post hoc tests. In rats with HF, RMT promoted reduction in pulmonary congestion (p < 0.0001) and left ventricular end diastolic pressure (p < 0.0001). Moreover, RMT produced a decrease in the diaphragm DNA damage in HF rats. This was demonstrated through the reduction in the percentage of tail DNA (p < 0.0001), tail moment (p < 0.01), and Olive tail moment (p < 0.001). These findings showed that a 6-week RMT protocol in rats with HF promoted an improvement in hemodynamic function and reduces diaphragm DNA damage.