Jaenisch RB, Hentschke VS, Quagliotto E, Cavinato PR, Schmeing LA, Xavier LL, Dal Lago P. Respiratory muscle training improves hemodynamics, autonomic function, baroreceptor sensitivity, and respiratory mechanics in rats with heart failure. J Appl Physiol 111: 1664 -1670, 2011. First published September 8, 2011 doi:10.1152/japplphysiol.01245.2010.-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 ϭ 8), trained sham (n ϭ 8), sedentary HF (n ϭ 8), or trained HF (n ϭ 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 Ͻ 0.01), increased LV systolic pressure (P Ͻ 0.01), and reduced right ventricular hypertrophy (P Ͻ 0.01) and pulmonary (P Ͻ 0.001) and hepatic (P Ͻ 0.001) congestion. It also decreased resting heart rate (HR; P Ͻ 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 Ͻ 0.05). The respiratory system resistance was reduced (P Ͻ 0.001), which was associated with the reduction in tissue resistance after RMT (P Ͻ 0.01). The respiratory system and tissue elastance (Est) were also reduced by RMT (P Ͻ 0.01 and P Ͻ 0.05, respectively). Additionally, the quasistatic Est was reduced after RMT (P Ͻ 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. myocardial infarction; cardiovascular control; diaphragm; cardiopulmonary interaction THE HALLMARK SYMPTOMS OF heart failure (HF) subsequent to myocardial infarction (MI) are dyspnea and early fatigue, leading to reduced exercise tolerance and functional capacity (1). Furthermore, after MI, the neurohumoral excitation, which initially helps to preserve the cardiac output of patients who have systolic dysfunction, becomes deleterious with the persistence of cardiac dysfunction (12). In HF, the neurohumoral excitation is characterized by sympathetic hyperactivity and the attenuation of parasympathetic activity (12), which is associated with blunted baroreflex sensitivity (BRS) (30). In this context, impaired short-term control of arterial pressure (AP) and decreased heart-rate variability (HRV) (30) have been associated with an increased risk of sudden death of cardiac origin (45) and postinfarct mortality, regardless of the ejection fraction or ventricular arrhythmias (30).Together with the cardiovascular alterations, changes in the r...

Following heart failure (HF), immune activation leads to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions. However, the effect of LLLT on the skeletal muscle of rats with HF remains unclear. The present report aimed to evaluate the influence of LLLT on the inflammatory profile of rats with HF. The left coronary artery was ligated to induce HF and a sham operation was performed in the control groups. Male Wistar rats (n=49) were assigned to one of six groups: placebo sham rats (P-Sham; n=8), LLLT at a dose of 3 J/cm(2) sham rats (3 J/cm(2)-Sham; n=8), LLLT at a dose of 21 J/cm(2) sham rats (21 J/cm(2)-Sham; n=8), placebo HF rats (P-HF; n=9), LLLT at a dose of 3 J/cm(2) HF rats (3 J/cm(2)-HF; n=8), and LLLT at a dose of 21 J/cm(2) HF rats (21 J/cm(2)-HF; n=8). Four weeks after myocardial infarction or sham surgery, rats were subjected to LLLT (InGaAlP 660 nm, spot size 0.035 cm(2), output power 20 mW, power density 0.571 W/cm(2), energy density 3 or 21 J/cm(2), exposure time 5.25 s and 36.75 s) on the right gastrocnemius for 10 consecutive days. LLLT reduced plasma IL-6 levels (61.3 %; P<0.01), TNF-α/IL-10 (61.0 %; P<0.01) and IL-6/IL-10 ratios (77.3 %; P<0.001) and increased IL-10 levels (103 %; P<0.05) in the 21 J/cm(2)-HF group. Moreover, LLLT reduced the TNF-α (20.1 % and 21.3 %; both P<0.05) and IL-6 levels (54.3 % and 37.8 %; P<0.01 and P<0.05, respectively) and the IL-6/IL-10 ratio (59.7 % and 42.2 %; P<0.001 and P<0.05, respectively) and increased IL-10 levels (81.0 % and 85.1 %; both P<0.05) and the IL-10/TNF-α ratio (171.5 % and 119.8 %; P<0.001 and P<0.05, respectively) in the gastrocnemius in the 3 J/cm(2)-HF and 21 J/cm(2)-HF groups. LLLT showed systemic and skeletal muscle anti-inflammatory effects in rats with HF.

Endothelial dysfunction plays as an important role on mismatch responses that occur during exercise in patients with congestive heart failure (CHF). However, cardiac rehabilitation, a core component of management of CHF patients, can improve endothelial function, contributing to reduce the morbidity and mortality of these patients. The primary aims of this review were to describe the importance of flow-mediated dilatation (FMD) as a non-invasive validation tool to assess endothelial dysfunction and to highlight the relevance of scientific studies that evaluated the effects of exercise interventions on peripheral vascular endothelial function as measured by FMD in patients with CHF with both preserved and reduced ejection fraction.

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