Noninvasive Ventilation as an Important Adjunct to an Exercise Training Program in Subjects With Moderate to Severe COPD.

BACKGROUND: The primary objective of this study was to investigate whether noninvasive ventilation (NIV) can positively affect exercise capacity, maximum oxygen uptake (V̇O2 ), and symptoms after a 6-week physical training program for subjects with moderate to very severe COPD. METHODS: 47 subjects with COPD who were enrolled in a physical training program were randomized to either physical training alone or NIV + physical training (NIV-Physical training). Physical training consisted of dynamic aerobic exercises on a treadmill 3 times/week for 6 weeks, for a total of 18 sessions. NIV was titrated according to the subject's tolerance at rest and during exercise. Assessments included physiological responses and symptoms at the incremental cardiopulmonary exercise test peak and during submaximal exercise on a treadmill, 6-min walk distance, maximum inspiratory (PImax) and expiratory pressure (PEmax), BODE index, and health-related quality of life. RESULTS: 43 subjects completed the 6-week physical training program. Both groups improved 6-min walk distance, PImax, BODE index, and quality of life, and no differences were found between groups. However, significant improvements were observed for subjects in the NIV-Physical training group with regard to PEmax, maximum V̇O2 , maximum metabolic equivalents, circulatory power, and maximum SpO2 . CONCLUSIONS: A 6-week physical training program alone can improve tolerance for exercise and quality of life, in addition to reducing the risk of mortality. However, NIV associated with a physical training program was shown to have an additive beneficial effect on powerful prognostic markers (maximum V̇O2 and circulatory power) and to reduce symptoms and improve oxygen saturation in subjects with moderate to very severe COPD.

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 Tukey's 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.

Respiratory Muscle Training Improves Chemoreflex Response, Heart Rate Variability, and Respiratory Mechanics in Rats With Heart Failure.

BACKGROUND: The aim of the present report was to evaluate respiratory muscle training (RMT) effects on hemodynamic function, chemoreflex response, heart rate variability, and respiratory mechanics in rats with heart failure (HF rats). METHODS: Wistar rats were divided into 4 groups: sedentary-sham (Sed-Sham, n = 8), respiratory muscle trained-sham (RMT-Sham, n = 8), sedentary-HF (Sed-HF, n = 8) and respiratory muscle trained-HF (RMT-HF, n = 8). Animals were submitted to an RMT protocol performed 30 minutes per day, 5 days per week for 6 weeks, whereas the sedentary animals did not exercise. RESULTS: In HF rats, RMT promoted the reduction of left ventricular end-diastolic pressure, right ventricular hypertrophy, and pulmonary edema. Moreover, RMT produced a reduction in pressure response during chemoreflex activation, sympathetic modulation, and sympathetic vagal balance in addition to an increase in parasympathetic modulation. Also after RMT, HF rats demonstrated a reduction in respiratory system resistance, tissue resistance, Newtonian resistance, respiratory system compliance, and quasistatic compliance. CONCLUSIONS: These findings suggested that 6 weeks of RMT in HF rats promoted beneficial adaptations in hemodynamics, autonomic function, and respiratory mechanics and attenuated pressure response evoked by chemoreflex activation in HF rats.

Experimental lung injury promotes alterations in energy metabolism and respiratory mechanics in the lungs of rats: prevention by exercise.

In the present study we investigated the effects of lung injury on energy metabolism (succinate dehydrogenase, complex II, cytochrome c oxidase, and ATP levels), respiratory mechanics (dynamic and static compliance, elastance and respiratory system resistance) in the lungs of rats, as well as on phospholipids in bronchoalveolar lavage fluid. The protective effect of physical exercise on the alterations caused by lung injury, including lung edema was also evaluated. Wistar rats were submitted to 2 months of physical exercise. After this period the lung injury was induced by intratracheal instillation of lipopolysaccharide. Adult Wistar rats were submitted to 2 months of physical exercise and after this period the lung injury was induced by intratracheal instillation of lipopolysaccharide in dose 100 µg/100 g body weight. The sham group received isotonic saline instillation. Twelve hours after the injury was performed the respiratory mechanical and after the rats were decapitated and samples were collected. The rats subjected to lung injury presented a decrease in activities of the enzymes of the electron transport chain and ATP levels in lung, as well as the formation of pulmonary edema. A decreased lung dynamic and static compliance, as well as an increase in respiratory system resistance, and a decrease in phospholipids content were observed. Physical exercise was able to totally prevent the decrease in succinate dehydrogenase and complex II activities and the formation of pulmonary edema. It also partially prevented the increase in respiratory system resistance, but did not prevent the decrease in dynamic and static compliance, as well as in phospholipids content. These findings suggest that the mitochondrial dysfunction may be one of the important contributors to lung damage and that physical exercise may be beneficial in this pathology, although it did not prevent all changes present in lung injury.

Low-level laser therapy improves the inflammatory profile of rats with heart failure.

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.

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.