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This study investigated the association between nocturnal oxygen desaturation, muscle quality, and functional performance in individuals with Chronic Obstructive Pulmonary Disease (COPD), with and without coexisting Obstructive Sleep Apnea (OSAS). Forty-four participants (COPD: n  = 22; COPD-OSAS: n  = 22) underwent a standardized three-day evaluation protocol comprising: (1) clinical assessment, body composition analysis, and pulmonary function testing; (2) cardiac function evaluation and home sleep monitoring; and (3) handgrip strength (HGS) and six-minute walk test (6MWT). Muscle quality was operationalized as the ratio between appendicular skeletal muscle mass and isometric strength. Sleep parameters, including the apnea–hypopnea index (AHI) and oxygen desaturation index (ODI), were obtained via home polysomnography. Patients with COPD-OSAS showed significantly reduced 6MWT distance and HGS values compared with those with isolated COPD ( p  < 0.05). Indices of sleep-disordered breathing exhibited significant inverse associations with functional performance and muscle quality. In multivariable regression, sex, AHI, and ODI were identified as independent predictors of muscle quality, with ODI representing the strongest contributor after adjustment. These findings indicate that individuals with COPD-OSAS present greater impairments in muscle quality and physical performance, and that hypoxic burden is closely related to these outcomes. Further studies with larger cohorts and longitudinal designs are needed to elucidate underlying mechanisms and to determine the long-term clinical implications of these associations.

Purpose. To evaluate the influence of previous levels of physical activity on hemodynamic, vascular, ventilatory, and functional outcomes after coronavirus disease 2019 (COVID-19) hospitalization. Methods. Sixty-three individuals with COVID-19 had their clinical status and previous levels (12 month) of physical activity (Baecke Questionnaire of Habitual Physical Activity) assessed at hospital admission. Individuals were then allocated to lower levels of physical activity (ACTLOWER; N=22), intermediate levels of physical activity (ACTINTERMEDIATE; N=22), or higher levels of physical activity (ACTHIGHER; N=19) groups, according to tertiles of physical activity. Resting hemodynamic (heart rate and brachial/central blood pressures) and vascular (carotid-femoral pulse wave velocity, augmentation index, and brachial artery flow-mediated dilation) variables, pulmonary function (spirometry), respiratory muscle strength (maximal respiratory pressures), and functional capacity (handgrip strength, five-time sit-to-stand, timed-up and go, and six-minute walking tests) were measured at 30 to 45 days after hospital discharge. Results. ACTLOWER showed lower levels (P<0.05) of forced vital capacity, forced expiratory volume in the first second, maximal voluntary ventilation, and maximal expiratory pressure than ACTHIGHER. ACTLOWER also had lower (P=0.023) walking distance (~21%,) and lower percentage of predicted walking distance (~20%) at six-minute walking test during follow-up than ACTINTERMEDIATE. However, hemodynamic and vascular variables, handgrip strength, five-time sit-to-stand, and timed-up and go were not different among groups. Conclusion. ACTLOWER showed impaired ventilatory parameters and walking performance when compared with ACTHIGHER and ACTINTERMEDIATE, respectively. These results suggest that previous levels of physical activity may impact ventilatory and exercise capacity outcomes 30 to 45 days after COVID-19 hospitalization discharge.

The impact of COVID‐19 on cardiorespiratory fitness (CRF) is negative, increasing the likelihood of exertional symptoms such as fatigue and shortness of breath, and adversely affecting vascular function, impairing cardiovascular health. This study investigated endothelial function and its relationship with CRF in patients who have recovered COVID‐19. Patients were evaluated 1 month after infection, including clinical assessment, pulmonary function, endothelial function (measured by flow‐mediated dilation), and cardiopulmonary exercise testing. COVID‐19 survivors exhibited reduced exercise capacity, with poor values of peak V̇O2peak and FMD (%) according to disease severity. However, endothelial function was worse in COVID‐19 patients, regardless of severity, compared to the control group. Significant associations were observed between poorer FMD (%) and peak V̇O2, workload, circulatory power, and V̇O2peak/WR. Endothelial function was significantly associated with CRF in COVID‐19 patients according to disease severity. Strategies to improve CRF and reduce the negative impacts of endothelial function damage should be further investigated.

While the majority of individuals with coronavirus disease 2019 (COVID-19) recover completely, a significant percentage experience persistent symptom, which has been characterized as Long COVID and may be associated with cardiac and autonomic dysfunction. We evaluated heart rate variability (HRV) at rest and during deep-breathing (M-RSA) in patients with Long COVID. Case–control design involved 21 patients with Long COVID and 20 controls; the HRV was evaluated (POLAR system) at rest in the supine position and during M-RSA and expressed in time domain and non-linear analysis. In the supine position we found a reduction HRV measures in Long COVID’ patients compared to controls for: Mean_iRR ( p  < 0.001), STD_iRR ( p  < 0.001); STD_HR ( p  < 0.001); SD1 ( p  < 0.001); SD2 ( p  < 0.001); alpha2 ( p  < 0.001). In the M-RSA we found reduction Mean_iRR ( p  < 0.001), STD_iRR ( p  < 0.001), STD_HR ( p  < 0.001), rMSSD ( p  < 0.001), RR_tri-index ( p  < 0.001) in Long COVID’ patients except for highest Mean_HR p  < 0.001. In conclusion, Long COVID reduced HRV at rest and during deep breathing. These findings may imply impairment of cardiac autonomic control when symptoms of COVID-19 persist following initial recovery.

Enhanced respiratory muscle strength in patients with heart failure positively alters the clinical trajectory of heart failure. In an experimental model, respiratory muscle training in rats with heart failure has been shown to improve cardiopulmonary function through mechanisms yet to be entirely elucidated. The present report aimed to evaluate the respiratory muscle training effects in diaphragm citrate synthase activity and hemodynamic function in rats with heart failure. Wistar rats were divided into four experimental groups: sedentary sham (Sed-Sham, n=8), trained sham (RMT-Sham, n=8), sedentary heart failure (Sed-HF, n=7) and trained heart failure (RMT-HF, n=7). The animals were submitted to a RMT protocol performed 30 minutes a day, 5 days/week, for 6 weeks. In rats with heart failure, respiratory muscle training decreased pulmonary congestion and right ventricular hypertrophy. Deleterious alterations in left ventricular pressures, as well as left ventricular contractility and relaxation, were assuaged by respiratory muscle training in heart failure rats. Citrate synthase activity, which was significantly reduced in heart failure rats, was preserved by respiratory muscle training. Additionally, a negative correlation was found between citrate synthase and left ventricular end diastolic pressure and positive correlation was found between citrate synthase and left ventricular systolic pressure. Respiratory muscle training produces beneficial adaptations in the diaphragmatic musculature, which is linked to improvements in left ventricular hemodynamics and blood pressure in heart failure rats. The RMT-induced improvements in cardiac architecture and the oxidative capacity of the diaphragm may improve the clinical trajectory of patients with heart failure.

The aim of this study is to characterize the presence of exercise oscillatory ventilation (EOV) and to relate it with other cardiopulmonary exercise test (CET) responses and clinical variables. Forty-six male patients (age: 53.1±13.6 years old; left ventricular ejection fraction [LVEF]: 30±8%) with heart failure were recruited to perform a maximal CET and to correlate the CET responses with clinical variables. The EOV was obtained according to Leite et al. criteria and VE/VCO2 > 34 and peak VO2 < 14 ml/kg/min were used to assess patients' severity. The EOV was observed in 16 of 24 patients who performed the CET, as well as VE/VCO2 > 34 and peak VO2 < 14 ml/kg/min in 14 and 10 patients, respectively. There was no difference in clinical and CET variables of the patients who presented EOV in CET when compared to non-EOV patients. Also, there was no difference in CET and clinical variables when comparing patients who presented EOV and had a VE/VCO2 slope > 34 to patients who just had one of these responses either. The present study showed that there was an incidence of patients with EOV and lower peak VO2 and higher VE/VCO2 slope values, but they showed no difference on other prognostic variables. As well, there was no influence of the presence of EOV on other parameters of CET in this population, suggesting that this variable may be an independent marker of worst prognosis in HF patients.

To evaluate heart rate variability during an inspiratory muscle endurance protocol at three different load levels [30%, 60% and 80% of maximal inspiratory pressure], in patients who had previously undergone coronary artery bypass grafting. Nineteen late postoperative myocardial revascularization patients participating in a cardiovascular rehabilitation program were studied. Maximal inspiratory pressure maneuvers were performed. An inspiratory muscle endurance protocol at 30%, 60% and 80% of maximal inspiratory pressure was applied for four minutes each, in random order. Heart rate and RR intervals were recorded and heart rate variability was analyzed by time (RMSSD-the mean of the standard deviations for all R-R intervals, and RMSM-root-mean square differences of successive R-R intervals) and frequency domains indices (high and low frequency) in normalized units. ANOVA for repeated measurements was used to compare heart rate variability indices and Student t-test was used to compare the maximal inspiratory pressure and maximal expiratory pressure values. Heart rate increased during performance of maximal respiratory pressures maneuvers, and the maximal inspiratory pressure and maximal expiratory pressure mean values were significantly lower than predicted values (P <0.05). RMSSD increased significantly at 80% in relation to rest and 30% of maximal inspiratory pressure and RMSM decreased at 30% and 60% of maximal inspiratory pressure in relation to rest (P <0.05). Additionally, there was significant and progressive decrease in low frequency and increase in high frequency at 30%, 60% and 80% of maximal inspiratory pressure in relation to the resting condition. These results suggest that respiratory muscle training at high intensities can promote greater parasympathetic activity and it may confer important benefits during a rehabilitation program in post-coronary artery bypass grafting.

Impaired lung function, respiratory muscle weakness and exercise intolerance are present in COPD and contribute to poor prognosis. However, the contribution of the combination of these manifestations to define prognosis in COPD is still unknown. This study aimed to define cut-off points for both inspiratory and expiratory muscle strength (MIP and MEP, respectively) for mortality prediction over 42-months in patients with COPD, and to investigate its combination with other noninvasive established prognostic measures (FEV 1 , V̇ O 2peak and 6MWD) to improve risk identification. Patients with COPD performed pulmonary function, respiratory muscle strength, six-minute walk and cardiopulmonary exercise tests, and were followed over 42 months to analyze all-cause mortality. A total of 79 patients were included. The sample was mostly (91.1%) comprised of severe ( n  = 37) and very severe ( n  = 34) COPD, and 43 (54%) patients died during the follow-up period. Cut-points of ≤ 55 and ≤ 80 cmH 2 O for MIP and MEP, respectively, were associated with increased risk of death (log-rank p  = 0.0001 for both MIP and MEP) in 42 months. Furthermore, MIP and MEP substantially improved the mortality risk assessment when combined with FEV 1 (log-ranks p  = 0.006 for MIP and p  < 0.001 for MEP), V̇ O 2peak (log-rank: p  < 0.001 for both MIP and MEP) and 6MWD (log-ranks: p  = 0.005 for MIP; p  = 0.015 for MEP). Thus, patients severely affected by COPD presenting MIP ≤ 55 and/or MEP ≤ 80 cmH2O are at increased risk of mortality. Furthermore, MIP and MEP substantially improve the mortality risk assessment when combined with FEV1, V̇O2peak and 6MWD in patients with COPD.

This study investigated the impact of mild COVID-19 on HRV in groups stratified by time after infection and to compare to a healthy group of the same age without previous virus infection and without need of hospitalization. This is a cross-sectional study. We divided the sample into four groups: control group (CG) ( n  = 31), group 1 (G1): ≤6 weeks ( n  = 34), group 2 (G2): 2–6 months ( n  = 30), group 3 (G3): 7–12 months ( n  = 35) after infection. For HRV analysis, we used the indices of linear (time and frequency domain) and non-linear analysis. For comparisons between groups, ANOVA one way test or Kruskal–Wallis was used according to the data distribution. The effect size was calculated based on Cohen’s d or η 2 . Simple and multiple linear regressions were performed to investigate the interaction between clinical outcomes and HRV parameters. A total of 130 individuals were included. Groups G1 and G2 showed less parasympathetic modulation when compared to CG ( p  < 0.05), while G3 showed an increase in parasympathetic modulation when compared to G1 ( p  < 0.05). Moderate to large effect sizes were found according to Cohen d or η 2 . The multiple linear regression models identified age and infection duration as significant predictors for RMSSD (adjusted R 2 = 0.227) and SD1 (adjusted R 2 = 0.242), while age was significant for SDNN (adjusted R 2 = 0.213). BMI, hypertension, and dyslipidemia were non-significant in all models. For HF (n.u.), infection duration was consistently significant, with stress emerging as a predictor in Model 2 (adjusted R 2 = 0.143). The recovery time since diagnosis and age influences recovery from HRV, suggesting a transient effect of the disease on the autonomic nervous system.