Renilson Moraes-Ferreira

Introduction: We sought to evaluate the effects of a 12-week pulmonary rehabilitation (PR) program on lung function, mechanics, as well as pulmonary and systemic inflammation in a cohort of 33 individuals with moderate to severe post-COVID-19. Material and Methods: The pulmonary rehabilitation (PR) program employed a combination of aerobic and resistance exercises. Thirty minutes of treadmill training at 75% of the maximum heart rate, combined with 30 min resistance training consisting of 75% of one maximum repetition, three times a week throughout 12 weeks. Results: PR improved the lung function, FVC (p < 0.02), FEV1 (p < 0.02), FEV1/FVC (p < 0.01), MEF25% (p < 0.006), MEF50% (p < 0.03), and MEF75% (p < 0.02). PR also positively influenced lung mechanics, reducing respiratory impedance (Z5Hz, p < 0.03), respiratory reactance (X5Hz, p < 0.01), resistance of the entire respiratory system (R5Hz, p < 0.03), central airway resistance (RCentral, p < 0.03), and peripheral airway resistance (RPeripheral, p < 0.02). Moreover, muscle strength gains were evident, with significant improvements observed in hand grip strength for both the right (p < 0.02) and left (p < 0.01) hands, as well as maximal inspiratory (p < 0.02) and expiratory (p < 0.03) pressures. Additionally, PR exhibited anti-inflammatory effects by reducing the pro-inflammatory cytokines IL-1β (p < 0.0001) and IL-6 (p < 0.0001) and increasing the anti-inflammatory IL-1RA (p < 0.0004) and IL-10 (p < 0.003) and anti-viral IFN-γ (p < 0.0002) and IFN-β (p < 0.008) cytokines in breath condensate and serum samples. Conclusions: Collectively, these findings highlight the effectiveness of PR in ameliorating COVID-19 sequel across respiratory system, skeletal muscle, and immune responses. This highlights its promising potential as a therapeutic intervention for individuals recovering from COVID-19.

Beyond the common comorbidities related to obesity, such as type 2 diabetes and cardiovascular diseases, impaired lung function is already known, but whether the fat distribution (sub-cutaneous, visceral) affects the lung function and pulmonary immune response are poorly known. Few evidence has shown that visceral fat is associated with insulin resistance, low-grade inflammation, and reduced lung function. In the present study, the body composition and fat distribution were evaluated by multi-frequency octopolar bioimpedance. This study demonstrated a possible association of increased visceral fat with impaired lung function in obesity grade I (n = 28; 45.46 ± 10.38 years old) women that was not observed in normal weight (n = 20; 43.20 ± 10.78 years old) and in overweight women (n = 30; 47.27 ± 10.25 years old). We also identified a negative correlation in FVC% (R² = 0.9129; p < 0.0236), FEV1% (R² = 0.1079; p < 0.0134), PEF% (R² = 0.1673; p < 0.0018), and VC IN% (R² = 0.1330; p < 0.0057) in the obesity grade I group, clearly demonstrating that higher levels of visceral fat correlate with reduced lung function, but not with sub-cutaneous fat. In addition, for the first time, a negative correlation among anti-fibrotic protein klotho (R² = 0.09298; p < 0.0897) and anti-inflammatory IL-10 (R² = 0.1653; p < 0.0487) in plasma was observed, in contrast to increased visceral fat. On the contrary, in breath condensate, a positive correlation for adiponectin (R² = 0.5665; p < 0.0120), IL1-Ra (R² = 0.2121; p < 0.0544), and IL1-Beta (R² = 0.3270; p < 0.0084) was found. Thus, increased visceral fat directly influences the impairment of lung function and the systemic and pulmonary immune response of women with obesity grade I.

Aim: Physical activity attenuates hypertension in older adults, but its impact on pulmonary function and mechanics in hypertensive older adults is unknown. The study seeks to understand whether a physically active lifestyle can improve respiratory capacity, the mechanical efficiency of the lungs, and, consequently, the quality of life of these individuals, comparing data between groups of active and sedentary hypertensive older adults. Methods: This is a cross-sectional study. We evaluated 731 older adults, stratified into two initial groups: hypertensive older adults (HE; n = 445) and non-hypertensive older adults (NHE; n = 286). For a secondary analysis, we used the International Physical Activity Questionnaire to sub-stratify HE and NHE into four groups: physically inactive hypertensive (PIH; n = 182), active hypertensive (AH; n = 110), physically inactive non-hypertensive (PINH; n = 104), and active non-hypertensive (ANH; n = 65). Lung function was measured by spirometry, and lung mechanics were assessed by impulse oscillometry. Results: Hypertensive older adults presented reduced lung function compared to non-hypertensive older adults, and physical inactivity accentuated this decline. Regarding pulmonary mechanics, hypertensive older adults had higher resistance of the entire respiratory system (R5 Hz), the central airways (R20 Hz), and peripheral airways (R5–20 Hz), which may trigger bronchoconstriction. Conclusions: Hypertension is associated with impaired lung function and mechanics in older adults, and a physically active lifestyle attenuates these dysfunctions.

1. IntroductionAsthma, a heterogeneous disease, is characterized by chronic airway inflammation, leading to variable airflow limitation and resulting in respiratory symptoms like wheezing, shortnes...

This study investigated the influence of the marathon on lung function, mechanics, and pulmonary inflammation. Twenty-eight male amateur marathon runners (42.1±6.2 years) were evaluated before and immediately after marathon. Pulmonary function and mechanics were assessed using spirometry and impulse oscillometry, respectively, whereas fatigue of the respiratory muscles by manovacuometry and lung inflammation by fractional exhaled nitric oxide (FeNO). Marathon induced a significant reduction in the lung function as compared to baseline values: FVC (4.81±0.72 vs 4.67±0.62, p=0.0095), VC IN (4.81±0.72 vs 4.67±0.62, p=0.009), FEV1 (3.83±0.62 vs 3.72±0.59, p=0.0232), and FEV6 (4.87±0.68 vs 4.57±0.63, p=0.0006), as well as an impairment in the lung mechanics in comparison to baseline values: reduced pulmonary impedance (Z5Hz; 2.96±1.36 vs 2.67±1.11; p=0.0305), reduced resistance of the whole respiratory system (R5Hz; 2.76±1.27 vs 2.5±1.08; p=0.0388) and pulmonary reactance (X5Hz; -1.05±0.55 vs -0.91±0.36; p=0.0101) and of resistance of proximal airways (R5Hz; 1.26±0.73 vs 1.06±0.86; p= 0.0377). In addition, maximal inspiratory (MIP; 94.14±41.88 vs 72.52±25.50; p=0.0023) and expiratory (MEP; 99.31±31.84 vs 91.29±19.94; p=0.0454) pressures, as well as FeNO levels were lower after the marathon than values pre-marathon (p=0.0359). Marathon running causes an acute disturbance in lung function and mechanics and compromises respiratory muscle strength.

Several benefits of aerobic training for asthmatic patients have been demonstrated. However, its effects on systemic inflammation and on airway remodeling mediators and lung mechanics are unknown. This prospective study included 21 intermittent and mild asthma patients, and as primary outcomes, the evaluation of pro‐ and anti‐inflammatory and pro‐ and antifibrotic mediators in exhaled breath condensate (EBC) and blood were performed, beyond the cell counting in blood and in induced sputum. Aerobic training was performed for 3 months, 3 times per week. Aerobic training increased the levels of anti‐inflammatory cytokines and of antifibrotic mediators in the breath condensate: IL‐1ra (p = 0.0488), IL‐10 (p = 0.0048), relaxin‐3 (p = 0.0019), and klotho (p < 0.0043), respectively. Similarly, in plasma, increased levels of IL‐1ra (p = 0.0147), IL‐10 (p < 0.0001), relaxin‐3 (p = 0.004), and klotho (p = 0.0023) were found. On contrary, reduced levels of proinflammatory cytokines in the breath condensate, IL‐1β (p = 0.0008), IL‐4 (p = 0.0481), IL‐5 (p < 0.0001), IL‐6 (p = 0.0032), IL‐13 (p = 0.0013), and TNF‐α (p = 0.0001) and profibrotic markers VEGF (p = 0.0017) and TSLP (p = 0.0056) were found. Similarly, in plasma, aerobic training significantly reduced the levels of proinflammatory cytokines IL‐1β (p = 0.0008), IL‐4 (p = 0.0104), IL‐5 (p = 0.0001), IL‐6 (p = 0.006), IL‐13 (p = 0.0341), and TNF‐α (p = 0.0003) and of profibrotic markers VEGF (p = 0.0009) and TSLP (p < 0.0076). Fractional exhaled nitric oxide (FeNO) was reduced after the intervention (p = 0.0313). Regarding inflammatory cells in sputum, there was a reduction in total cells (p = 0.008), eosinophils (p = 0.009), and macrophages (p = 0.020), as well as of blood eosinophils (p = 0.0203) and lymphocytes (p = 0.0198). Aerobic training positively modulates chronic airway inflammation and remodeling mediators, beyond to improve systemic inflammation in intermittent and mild asthmatic patients.

Asthma is a chronic inflammatory disease of the airways, resulting in worse quality of life. There are evidences that physical activity improves quality of life and lung function of asthmatic patients, but some aspects, such as lung mechanics, has never been evaluated. Thus, we investigated the impact of physical inactivity on pulmonary function and mechanics of asthmatic patients. Twenty asthmatic (persistent moderate) individuals were classified according to GINA criteria and included in the study and then, stratified into active or inactive, according to the International Physical Activity Questionnaire: Ten physically active (38.22±14.64 years old) and 10 physically inactive (31.83±8.45 years old). Lung function was assessed by spirometry and lung mechanics by impulse oscillometry, both using MasterScreen (Jaeger, Germany) and exhaled nitric oxide by NoBreath monitor (Bedfont Scientific, UK). The results showed no difference in lung function FVC, FEV%, FEV1, FEV1% and FEV1/FVC (p>0.05). However, inactive asthmatics showed higher impedance of the respiratory system (Z5Hz, p<0.01), increased resistance of the whole respiratory system (R5Hz, p<0.01), resistance of proximal airways (R20Hz, p<0.01) and of distal airways (R5-R20Hz, p<0.01). In addition, the reactance of the lung tissue (X5Hz, p<0.01) was lower in physically inactive asthmatic patients. Furthermore, exhaled nitric oxide levels were higher in inactive asthmatic compared to active asthmatic (27,44±16,91 x 19±2,12 ppb; p<0.04). So, we conclude that physical inactivity accentuates the impairment of pulmonary mechanics in asthmatic patients, presenting an involvement of nitric oxide.

Airway remodeling is a hallmark of asthma driven by non-resolved chronic inflammatory response, beyond exacerbated release of pro-fibrotic mediators. Aerobic exercise (AE) improves asthma management and airway inflammation, but its effects on pulmonary and systemic cellular and humoral immune response are unknown. Treadmill aerobic exercise (AE) (12 weeks, 3x/week, 40min/session, 60-80%MaxHR) was applied to 17 persistent moderate asthmatic patients (42.11±19.13). Body mass index (BMI), lung function, induced sputum, breath condensate, whole blood analysis and CD4+ cells proliferation, 6MWT, exhaled nitric oxide, was evaluated. AE improved VEF3 (L) (p<0.03) and PEF (L/min) (p<0.005) and PEF (%) (p<0.004), reduced the number of total leukocytes, eosinophils, neutrophils, lymphocytes and macrophages (p<0.01), as well as the levels of IL-1beta, IL-4, IL-5, IL-6, IL-8, IL-13, IL-17, IL-23 (p<0.01) in induced sputum. AE also reduced the levels of IL-1beta, IL-5, IL-6, IL-13, VEGF (p<0.01), while increased the levels of anti-inflammatory IL-1ra and IL-10 (p<0.01) and anti-fibrotic Relaxin 3 (p<0.01) in breath condensate. Systemically, AE reduced the number of eosinophils, neutrophils and lymphocytes (p<0.01), as well as the levels of IL-1beta, IL-5, IL-6, IL-13, VEGF (p<0.01), while increased anti-inflammatory IL-1ra, IL-10 (p<0.01) and anti-fibrotic Relaxin 3 (p<0.01) in plasma. AE improved 6MWT (p<0.01) and reduced exhaled nitric oxide (p<0.01) and CD4+ cells proliferation (p<0.01). AE improves airway and systemic inflammation reducing pro-inflammatory cytokines, while increased anti-inflammatory and anti-fibrotic mediators systemically and into the lungs.

Evidence concerning the prescription of isolated resistance training (RT) to hypertensive individuals is limited. Guidelines are divergent concerning RT inclusion for prehypertensive and hypertensive persons. A meta-analysis investigating data with larger sample sizes provides more robust effect size estimates and allows for inferences on clinical choices concerning the effectiveness of RT alone. In this context, the aim of this meta-analysis was to assess the effects of RT alone on the systolic (SBP) and diastolic (DBP) blood pressures in prehypertensive and hypertensive individuals. Data from 13 studies involving 417 participants (207 assigned to RT and 210 controls) were obtained. The results indicate significant reductions in SBP (−6.16 mmHg CI −8.27 to −4.04; I²: 31.0% P value for heterogeneity = 0.136 and effect size = −0.59) and DBP (−3.70 mmHg CI −5.19 to −2.21; I²: 18.3% P value for heterogeneity = 0.106 and effect size = −0.55) when compared to control groups. In conclusion, RT alone is able to reduce SBP and DBP in prehypertensive and hypertensive subjects, especially in elderly individuals.