Primary ciliary dyskinesia (PCD) is a rare, hereditary disorder characterized by impaired motile ciliary function, resulting in abnormal mucociliary clearance (MCC). This leads to persistent infection and inflammation, progressive airway damage, and bronchiectasis. Physiotherapy, particularly airway clearance therapy (ACT), is considered a cornerstone of PCD management to compensate for the mechanical MCC deficit, aiming to reduce infection risk, prevent disease progression, and improve quality of life (QOL). However, evidence supporting specific physiotherapy regimens in PCD remains limited. Current practice varies widely across centers and countries, with no standardized guidelines. Common ACT methods include positive expiratory pressure (PEP) with or without oscillation, autogenic and postural drainage, active cycle of breathing technique (ACBT), intrapulmonary percussive ventilation (IPV), and high-frequency chest wall oscillation (HFCWO). Comparative studies show no clear superiority among techniques. Evidence for mucolytic therapy, such as hypertonic saline or rhDNAse, is weak or controversial. Scarce data demonstrate potential benefits of exercise interventions in improving ventilatory capacity and QOL. Age-specific considerations are crucial: ACT should be started early, be adapted to developmental stages, and be combined with strategies to enhance adherence. Despite physiotherapy being standard care, randomized controlled trials are challenging due to ethical constraints, potentially reducing a therapy that is already believed to be helpful. Future priorities include developing international guidelines and conducting high-quality studies to optimize treatment strategies. In conclusion, physiotherapy plays a crucial role in PCD management, but current recommendations rely largely on expert opinion and extrapolation from related conditions like cystic fibrosis (CF) and non-CF bronchiectasis (BRECT), underscoring the need for robust evidence.

Bioimpedance is increasingly growing in clinical utility for within-session monitoring; however, many studies neglect to report the test-retest reliability of their devices. The purpose of this study was to examine the within-session test-retest reliability of whole-body bioelectrical variables measured by four common bioimpedance devices among adults. Ninety-six adults (age = 46.1 ± 21.7yrs, female = 63.5%, BMI = 26.4 ± 5.2 kg/m2) were tested in the morning-time on each device after providing a urine sample to confirm euhydration in addition to 10 minutes of passive rest in each device's respective testing position (standing or supine). Each device assessed whole-body impedance, resistance, reactance, and phase angle in duplicate with approximately 10 seconds between trials; bioelectrical variables were extracted at 5, 50, 250, 500, and 1000 kHz as available from each device. Reliability was assessed using intraclass correlation coefficients (ICC2,1) and coefficients of variation (CV). At 5, 50, and 250 kHz, reliability across devices and measures was excellent (ICC2,1 > 0.90, CV = 0.78 ± 0.55%). Precision at 500 kHz for PhA (CV = 5.41%) and Xc (CV = 4.9%) was low and approaching low, respectively. Measures of Xc and PhA at higher frequencies (500 and 1000 kHz) may be less precise, but further research is needed to confirm, particularly with 1000 kHz where negative Xc values may limit the interpretability of CVs. Clinicians, researchers, and practitioners using these devices for within-session monitoring of raw bioelectrical variables should ideally test the reliability of their own devices but may use the data within this manuscript as a point of reference.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous pulmonary disorder characterized by airway or alveolar abnormalities. Beyond pulmonary impairment, COPD frequently leads to skeletal muscle dysfunction, manifesting as muscle atrophy, myofibrillar type switching, and reduced muscle strength and endurance, which severely impair exercise capacity and quality of life. Mitochondrial dysfunction, including reduced mitochondrial density, altered respiratory function, and increased oxidative stress, is recognized as a key contributor to skeletal muscle impairment in COPD. Resistance exercise (RE), an effective exercise therapy, has been shown to improve lower-limb muscle function and quality in COPD patients, and it appears feasible even for those with severe airflow obstruction and significant dyspnea. Mechanistically, RE may enhance mitochondrial respiratory capacity and promote mitochondrial biogenesis, and might also counteract mitochondrial dysfunction induced by secondhand smoke. In this narrative review, we analyze the effects of RE on skeletal muscle dysfunction in COPD and summarize the underlying mitochondrial mechanisms.

Aerobic exercise is associated with reduced depressive symptoms, but the neurobiological processes supporting this effect remain incompletely understood. We investigated whether short-term aerobic exercise reduces depressive symptoms in healthy young adults and whether such reduction is related to cortical structural change and neurotransmitter-receptor organization. Forty-eight participants completed a two-week aerobic running intervention and a two-week control period, with depressive symptoms and structural MRI assessed at baseline, week 2 and week 4. Aerobic exercise significantly reduced depressive symptoms relative to the control period. Across individuals, greater symptom reduction was associated with larger increases in anterior cingulate cortical thickness, an association observed only during the active intervention. The cortical map of this symptom-thickness association showed selective spatial correspondence with normative distributions of serotonergic 5-HT1A, 5-HT1B, 5-HT2A and 5-HT4 receptors, and the glutamatergic mGluR5 receptor, and this correspondence was observed only during the exercise period. These results indicate that short-term aerobic exercise is associated with changes in depressive symptoms and anterior cingulate structure. They also provide a neurobiologically informed context for understanding these exercise-related changes.