Regiane Albertini

Background: Aging is associated with sarcopenia, chronic low-grade inflammation, impaired functional capacity, and reduced respiratory muscle strength. Resistance training is recognized as an effective intervention to attenuate these age-related alterations; however, its effects on respiratory function and anti-aging biomarkers such as Klotho remain incompletely understood. Methods: In this randomized controlled trial, 60 community-dwelling older adults (60–75 years) were randomly allocated to a control group (n = 30) or a resistance training group (n = 30). Participants in the intervention group completed a supervised 12-week resistance training program (three sessions/week). Assessments performed before and after the intervention included anthropometry, body composition, respiratory muscle strength (maximal inspiratory and expiratory pressures), handgrip strength, 1 min sit-to-stand test, oxygen saturation, plasma levels of IL-6, IL-10, TNF-α, Klotho, and hematological parameters. Results: The resistance training group presented significantly increased maximal inspiratory and expiratory pressures, handgrip strength, and 1 min sit-to-stand performance while attenuating exercise-induced oxygen desaturation. The intervention also reduced plasma IL-6 concentrations and markedly increased circulating IL-10 and Klotho levels, indicating a favorable anti-inflammatory and anti-aging response. No significant changes were observed in systemic hematological parameters, whereas anthropometric adaptations were modest. Conclusions: Twelve weeks of resistance training significantly improved respiratory muscle strength and systemic inflammatory status in older adults. The concomitant increase in circulating Klotho suggests that resistance training may promote biological mechanisms associated with healthy aging, supporting its implementation as a non-pharmacological strategy to preserve functional independence and respiratory health in the elderly.

Age‐related declines in pulmonary function and immune regulation increase morbidity and mortality in older adults. Physical activity mitigates these effects, but the isolated impact of resistance training (RT) on lung function and immune responses remains unclear. Sixty‐nine older adults without participation for at least one year in structured exercise programs (aged 60–85 years) were recruited from a community extension program at a Brazilian university and randomized into an RT group ( n = 31) or a control group ( n = 38). This randomized controlled trial evaluated the effects of a 12‐week supervised RT program performed three times per week. Primary outcomes included spirometry parameters (FVC, FEV ₁ , FEV ₁ /FVC, PEF, and FEF ₂₅ – ₇₅ %), respiratory muscle strength (MIP and MEP), and inflammatory biomarkers (IL‐6, IL‐10, TNF‐α, and Klotho) in plasma and exhaled breath condensate. Secondary outcomes included handgrip strength, sit‐to‐stand performance, oxygen saturation, and body composition. Normally distributed outcomes were analyzed using repeated‐measures ANOVA, whereas non‐normally distributed longitudinal outcomes were analyzed using the Brunner–Langer approach for factorial longitudinal data. Between‐group differences in pre‐to‐post changes were additionally estimated using bootstrap 95% confidence intervals. No significant Group × Time interactions were observed for spirometric parameters. Significant Group × Time interactions were observed for MIP and MEP; however, significant pre‐to‐post changes were observed in the control group but not in the RT group. A significant Group × Time interaction was also observed for sit‐to‐stand performance, with improvement in the control group but not in the RT group. No significant Group × Time interactions were observed for handgrip strength or oxygen saturation. Significant Group × Time interactions were observed for plasma IL‐6, IL‐10, and Klotho (all p < 0.001), as well as exhaled breath condensate IL‐6 ( p = 0.006) and Klotho ( p = 0.003). In contrast, no significant interactions were observed for plasma TNF‐α, exhaled breath condensate IL‐10, or exhaled breath condensate TNF‐α. Twelve weeks of supervised RT were associated with differential changes in respiratory muscle strength, functional capacity, and selected systemic and airway biomarkers in older adults. Significant Group × Time interactions were observed for MIP, MEP, the 1‐min sit‐to‐stand test, and selected inflammatory and aging‐related biomarkers, but not for pulmonary function. These findings indicate that the effects of RT varied across outcomes, rather than demonstrating consistent improvement across all assessed measures. Trial Registration: ClinicalTrials.gov identifier: NCT06682221

The incidence of metabolic syndrome (MetS) is rising rapidly, particularly among older adults, and is associated with comorbidities that impair respiratory and immune functions. Physical exercise has proven effective in mitigating the adverse effects of both aging and MetS. However, evidence on the impact of high-intensity resistance training (HIRT) on the respiratory and immune systems in older adults with MetS remains limited. This study aimed to evaluate the effects of HIRT on respiratory function, skeletal muscle strength, and immune modulation in older adults with MetS, highlighting its potential as a complementary therapeutic approach. A total of 43 older adults with MetS were enrolled and divided into two groups: a HIRT intervention group (n = 23; mean age 66.71 ± 4.98 years) and a non-exercising control group (n = 20; mean age 66.91 ± 5.26 years). The HIRT protocol involved twice-weekly sessions (10 total) over 5 weeks, performed at 80–90% of one-repetition maximum. Results showed that HIRT significantly improved lung mechanics (R5Hz, R20Hz, Z5Hz, X5Hz), peripheral muscle strength, and both maximal expiratory and inspiratory pressures. Furthermore, HIRT increased anti-inflammatory and anti-fibrotic cytokines in sputum (klotho, IL-10, adiponectin) and serum (klotho, relaxin-1, relaxin-3, IL-10), while reducing pro-inflammatory cytokines in sputum (IL-6, TNF-α) and serum (IL-1ra, IL-6, TNF-α, leptin). A decrease in total leukocyte, neutrophil, lymphocyte, and monocyte counts was also observed. In conclusion, HIRT effectively mitigates the effects of MetS on respiratory, muscular, and immune functions in older adults and may be recommended as a complementary strategy for managing MetS in this population.

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.

Main Goals: To analyze whether acupuncture and photobiomodulation have an effect on muscle fatigue. Secondary goals: identify which is more efficient in reducing fatigue effects; verify if after the protocols applying the individuals are able to perform the same workload, or improve it. Methods: It is a quantitative and experimental study; sample: [72 active subjects (42 males 32 females, 20 to 38 y, median: age 25.79 years, height 172.01 cm, weight 72.28 kg, body mass index 24.37)]. Fatigue assessed by BOSCO modified protocol in force plate, generated with 100 counter movement jump until failure, or at the request of the individual. Results: After the treatment protocols, the results show a significant difference after the intervention in groups A and D, as can be seen in chart 3, figures 3 and 4. Conclusion: We conclude that acupuncture and photobiomodulation are efficient in minimizing fatigue, indicating that these treatment intervention protocols can improve muscular performance with jump height gain.

Background: The aging process promotes changes in skeletal muscles that influence muscle strength and fatigue, however physical exercise has a direct effect on the aging process. Objective: The aim of this study was investigated the strength and strength fatigability and the muscle activities of the forearm of elderly women’s handgrip according physical level. Method: The patterns of rapid muscle strength, maximum strength and fatigability of 32 elderly women during handgrip task were evaluated in this cross-sectional study. Both hands were evaluated and the muscle activity of the carpal flexors and extensors was monitored with an electromyography simultaneously. Volunteers were grouped into two groups based on their level of physical activity: physically active and sedentary. Results were compared by group and time factors. Results: Rapid muscle strength and maximum isometric strength were substantially higher in the physically active. Loss of strength was verified in physically active while the fatigue by muscle activity was identified in sedentary group. Discussion: The volunteers' physical activity pattern was able to change their muscle contraction strategies. The active group mainly practices strength training or combined training that includes strength training with at least 3 sessions per week. This volume was also enough to promote gains in the strength and rapid strength. Conclusion: The physical activity profile of the elderly women in this study have influenced strength, fatigability, and muscle activity during handgrip strength.

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.

The present study was aimed to investigate the phototherapy effect with low-level laser on human bronchial epithelial cells activated by cigarette smoke extract (CSE). Phototherapy has been reported to actuate positively for controlling the generation/release of anti-inflammatory and pro-inflammatory mediators from different cellular type activated by distinct stimuli. It is not known whether the IL-8 and IL-10 release from CSE-stimulated human bronchial epithelium (BEAS) cells can be influenced by phototherapy. Human bronchial epithelial cell (BEAS) line was cultured in a medium with CSE and irradiated (660 nm) at 9 J. Apoptosis index was standardized with Annexin V and the cellular viability was evaluated by MTT. IL-8, IL-10, cAMP, and NF-κB were measured by ELISA as well as the Sp1, JNK, ERK1/2, and p38MAPK. Phototherapy effect was studied in the presence of mithramycin or the inhibitors of JNK or ERK. The IL-8, cAMP, NF-κB, JNK, p38, and ERK1/2 were downregulated by phototherapy. Both the JNK and the ERK inhibitors potentiated the phototherapy effect on IL-8 as well as on cAMP secretion from BEAS. On the contrary, IL-10 and Sp1 were upregulated by phototherapy. The mithramycin blocked the phototherapy effect on IL-10. The results suggest that phototherapy has a dual effect on BEAS cells because it downregulates the IL-8 secretion by interfering with CSE-mediated signaling pathways, and oppositely upregulates the IL-10 secretion through of Sp1 transcription factor. Graphical Abstract The manuscript provides evidence that the phototherapy can interfere with MAPK signaling via cAMP in order to attenuate the IL-8 secretion from CSE-stimulated BEAS. In addition, the present study showed that phototherapy effect is driven to downregulation of the both the IL-8 and the ROS secretion and at the same time the upregulation of IL-10 secretion. Besides it, the increase of Sp-1 transcription factor was crucial for laser effect in upregulating the IL-10 secretion. The dexamethasone corticoid produces a significant inhibitory effect on IL-8 as well as ROS secretion, but on the other hand, the corticoid blocked the IL-10 secretion. Taking it into consideration, it is reasonable to suggest that the beneficial effect of laser therapy on lung diseases involves its action on unbalance between pro-inflammatory and anti-inflammatory mediators secreted by human bronchial epithelial cells through different signaling pathway.