Rodrigo B. Jaenisch

Respiratory muscle training improves hemodynamics, autonomic function, baroreceptor sensitivity, and respiratory mechanics in rats with heart failure

Respiratory muscle training (RMT) improves functional capacity in chronic heart-failure (HF) patients, but the basis for this improvement remains unclear. We evaluate the effects of RMT on the hemodynamic and autonomic function, arterial baroreflex sensitivity (BRS), and respiratory mechanics in rats with HF. Rats were assigned to one of four groups: sedentary sham (n = 8), trained sham (n = 8), sedentary HF (n = 8), or trained HF (n = 8). Trained animals underwent a RMT protocol (30 min/day, 5 day/wk, 6 wk of breathing through a resistor), whereas sedentary animals did not. In HF rats, RMT had significant effects on several parameters. It reduced left ventricular (LV) end-diastolic pressure (P < 0.01), increased LV systolic pressure (P < 0.01), and reduced right ventricular hypertrophy (P < 0.01) and pulmonary (P < 0.001) and hepatic (P < 0.001) congestion. It also decreased resting heart rate (HR; P < 0.05), indicating a decrease in the sympathetic and an increase in the vagal modulation of HR. There was also an increase in baroreflex gain (P < 0.05). The respiratory system resistance was reduced (P < 0.001), which was associated with the reduction in tissue resistance after RMT (P < 0.01). The respiratory system and tissue elastance (Est) were also reduced by RMT (P < 0.01 and P < 0.05, respectively). Additionally, the quasistatic Est was reduced after RMT (P < 0.01). These findings show that a 6-wk RMT protocol in HF rats promotes an improvement in hemodynamic function, sympathetic and vagal heart modulation, arterial BRS, and respiratory mechanics, all of which are benefits associated with improvements in cardiopulmonary interaction.

Skeletal muscle electrical stimulation improves baroreflex sensitivity and heart rate variability in heart failure rats

The goal of the current study was to evaluate the effects of electrical stimulation (ES) on the arterial baroreflex sensitivity (BRS) and cardiovascular autonomic control in rats with chronic heart failure (CHF). Male Wistar rats were designated to one of four groups: placebo sham (P-Sham, n=9), ES sham (ES-Sham, n=9), placebo CHF (P-CHF, n=9) or ES CHF (ES-CHF, n=9). The ES was adjusted at a low frequency (30 Hz), duration of 250 μs, with hold and rest time of 8s (4 weeks, 30 min/day, 5 times/week). It was applied on the gastrocnemius muscle with intensity to produce a visible muscle contraction. The rats assigned to the placebo groups performed the same procedures with the equipment turned off. The two-way ANOVA and the post hoc Student-Newman-Keuls tests (P<0.05) were used to data comparison. The BRS was higher in ES-Sham group compared to the P-Sham group and the ES-CHF group compared to the P-CHF group. ES was able to decrease heart rate sympatho-vagal modulation and peripheral sympathetic modulation in ES-CHF compared to P-CHF group. Interestingly, heart rate sympatho-vagal modulation was similar between ES-CHF and P-Sham groups. Thus, ES enhances heart rate parasympathetic modulation on heart failure (ES-CHF) compared to placebo (P-CHF), with consequent decrease of sympatho-vagal balance in the ES-CHF group compared to the P-CHF. The results show that a 4 week ES protocol in CHF rats enhances arterial BRS and cardiovascular autonomic control.

Effects of l-arginine supplementation associated with continuous or interval aerobic training on chronic heart failure rats

OBJECTIVE Chronic heart failure (CHF) is related with exercise intolerance and impaired nitric oxide (NO) production, which can lead to several functional capacity alterations. Considering the possible superiority of aerobic interval training compared to continuous training and the capacity of l-arginine to restore the NO pathway, the aim of the present study was to investigate whether these treatments are beneficial to exercise capacity, muscle mass preservation and hemodynamic, inflammatory and oxidative stress parameters in CHF rats. METHODS Thirty-eight male Wistar rats post 6weeks of myocardial infarction (MI) surgery were randomly assigned into 6 CHF groups: sedentary (SED, n=6); SED+Arg (n=7); ACT (n=8); ACT+Arg (n=5); AIT (n=7); AIT+Arg (n=5). Exercise test capacity (ETC) was performed pre and post 8weeks of intervention. Supplemented rats received Arg (1g/kg) by oral gavage (7×/week). Exercise training was performed on a rat treadmill (5×/week). Hemodynamic variables, tissue collection, congestion, inflammatory cytokines, and oxidative parameters were evaluated at the end of protocols. RESULTS All trained groups showed a superior exercise capacity compared to SED groups on the post-intervention test (p<0.0001). Pulmonary congestion was attenuated in AIT and AIT+Arg compared with the SED group (p<0.05). Left ventricular end-diastolic pressure (LVEDP) was lower in ACT+Arg, AIT, and AIT+Arg groups than SED group (p<0.05). Association of AIT with Arg supplementation was able to improve hemodynamic responses (left ventricular systolic pressure (LVSP), systolic blood pressure (SBP), +dP/dtmax, and -dP/dtmax (p<0.05), likewise, decrease muscular and renal lipid peroxidation and tumor necrosis factor (TNF)-α, and increase interleukin (IL)-10/TNF-α plasmatic levels (p<0.01). Groups that associated aerobic exercise with Arg supplementation (ACT+Arg and AIT+Arg) revealed higher gastrocnemius mass compared to the SED group (p<0.01). CONCLUSIONS Both aerobic training protocols were capable to improve aerobic capacity, and the association with Arg supplementation was important to attenuate muscle loss. Moreover, interval training associated with Arg supplementation elicits greater improvements in hemodynamic parameters, contributing to reduction in pulmonary congestion, and demonstrated particular responses in the inflammatory profile and in the antioxidant status.

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.