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Objective: This study aimed to assess the changes in the frequency of physical activity (PA) counseling and in the predictors of primary care PA promotion in Québec primary care physicians (PCPs) between 2010 and 2020. Methods: In 2010, we conducted a survey among Québec PCPs. Questions included: frequency of promoting PA to patients, perceived barriers, needs to improve PA promotion practice, frequency of PCPs' PA practice, and sociodemographic information. In 2020, we took over the 2010 questionnaire to document the evolution of the PA promotion practice. Results: The proportion of PCPs discussing PA with their patients significantly increased (P <.05) in 2020 for the following health conditions: depression, low back pain, chronic obstructive pulmonary disease, and cancer; it declined (P <.05) for overweight patients, those with metabolic syndrome, and in primary prevention. Collaboration with PA professionals was the major need identified, and it increased in 2020. PCPs' own practice of PA was a predictor of PA promotion in 2010 (odds ratio = 6.679; P <.001) and in 2020 (odds ratio = 6.679; P <.001). In both 2010 and in 2020, older or more experienced PCPs were more likely to discuss PA with their patients without diagnosed diseases than younger ones or those with less experience. Conclusions: Over the last 10 years, there has been a significant increase in PCPs promoting PA in Québec; however, it has been mainly oriented toward secondary prevention. It is concerning that PA counseling in primary prevention has declined, notably among younger PCPs. The stronger claim for closer collaboration with kinesiologists suggests that PCPs are in favor of an interprofessional strategy, namely collaboration with PA specialists. [ABSTRACT FROM AUTHOR]

BackgroundSkeletal muscle dysfunction is a common extrapulmonary manifestation of chronic obstructive pulmonary disease (COPD). Alterations in skeletal muscle myosin heavy chain expression, with reduced type I and increased type II myosin heavy chain expression, are associated with COPD severity when studied in largely male cohorts. The objectives of this study were (1) to define an abnormal myofibre proportion phenotype in both males and females with COPD and (2) to identify transcripts and transcriptional networks associated with abnormal myofibre proportion in COPD.MethodsForty-six participants with COPD were assessed for body composition, strength, endurance and pulmonary function. Skeletal muscle biopsies from the vastus lateralis were assayed for fibre-type distribution and cross-sectional area via immunofluorescence microscopy and RNA-sequenced to generate transcriptome-wide gene expression data. Sex-stratified k-means clustering of type I and IIx/IIax fibre proportions was used to define abnormal myofibre proportion in participants with COPD and contrasted with previously defined criteria. Single transcripts and weighted co-expression network analysis modules were tested for correlation with the abnormal myofibre proportion phenotype.ResultsAbnormal myofibre proportion was defined in males with COPD (n = 29) as 22% type IIx/IIax fibres and in females with COPD (n = 17) as 12% type IIx/IIax fibres. Half of the participants with COPD were classified as having an abnormal myofibre proportion. Participants with COPD and an abnormal myofibre proportion had lower median handgrip strength (26.1 vs. 34.0 kg, P = 0.022), 6-min walk distance (300 vs. 353 m, P = 0.039) and forced expiratory volume in 1 s-to-forced vital capacity ratio (0.42 vs. 0.48, P = 0.041) compared with participants with COPD and normal myofibre proportions. Twenty-nine transcripts were associated with abnormal myofibre proportions in participants with COPD, with the upregulated NEB, TPM1 and TPM2 genes having the largest fold differences. Co-expression network analysis revealed that two transcript modules were significantly positively associated with the presence of abnormal myofibre proportions. One of these co-expression modules contained genes classically associated with muscle atrophy, as well as transcripts associated with both type I and type II myofibres, and was enriched for genetic loci associated with bone mineral density.ConclusionsOur findings indicate that there are significant transcriptional alterations associated with abnormal myofibre proportions in participants with COPD. Transcripts canonically associated with both type I and type IIa fibres were enriched in a co-expression network associated with abnormal myofibre proportion, suggesting altered transcriptional regulation across multiple fibre types.