Journal of Cachexia, Sarcopenia and Muscle最新文献

As we all know, it has been proven that tobacco smoking is associated with many diseases, including sarcopenia.¹ However, tobacco smoking as a lifestyle always affects our bodies for a quite long time, which is a great challenge for researchers to conduct a randomized controlled trial to identify the causal roles of tobacco smoking in diseases. We therefore read the recent paper by Park et al. This is a well-designed Mendelian randomization (MR) study, using genome-wide association studies (GWASs), which may prove the evidence of causal associations of tobacco smoking with telomere attrition and sarcopenia. These findings suggested that ever being a regular smoker in life (smoking initiation) was causally associated with shorter leucocyte telomere length (LTL), lower appendicular lean mass index (ALM), slower walking pace, and lower time spent on moderate-to-vigorous physical activity (MVPA).²

However, in this study, the high sample overlapping rate in the two-sample mendelian randomization raised concern about the conclusion: the data sources in the study were from UK Biobank (N = 337 138, for aging and sarcopenia) and a GWAS meta-analysis study named GSCAN (N = 1.2 million, for tobacco smoking).³ We carefully read the raw study of the GSCAN, and unfortunately, in the 1.2 million samples, 383 613 were from UK Biobank. According to the calculation methods for the maximum estimated value for sample overlapping rate, the cohort of aging and sarcopenia (337 138 samples) may be fully overlapped with samples for smoking (383 613 samples), which means the maximum estimated sample overlapping rate might be 100%. It was the violation of the essential assumptions of two-sample MR. The bias caused by sample overlapping should not be ignored.⁴

Interestingly, the raw data provided by GSCAN contains a dataset without UK Biobank cohorts (https://conservancy.umn.edu/handle/11299/201564). Therefore, using the GSCAN data without UK Biobank, we tried to re-perform the MR study by Park et al. Briefly, the data including 848 460 individuals for exposure (tobacco smoking) were from the GSCAN data without UK Biobank individuals. For outcomes, similar to Park's study, we used the summary GWAS data of the UK Biobank from the IEU database.⁵ Except for handgrip strength, the phenotypes of other outcomes were as same as the previous study: including LTL (N = 472 174, datasets ID: ieu-b-4879), adjusted appendicular lean mass (N = 450 243, datasets ID: GCST90000025), walking pace (N = 459 915, datasets ID: ukb-b-4711), moderate to vigorous physical activity (N = 377 234, datasets ID: GCST006097). In the study by Park et al., handgrip strength was defined as the average value of two hands. Because we did not have access to the detailed UK Biobank data, our study's phenotypes of handgrip strength were d

As individuals age, skeletal muscle mass and function, including lean body mass and grip strength, and respiratory muscle mass and strength, tend to decline.^{1, 2} The term ‘respiratory sarcopenia’ emerged during a discussion on sarcopenia. Respiratory sarcopenia should encompass respiratory muscle mass and strength or function to adhere to the original sarcopenia definition, which considers whole-body muscle mass, grip strength, and gait speed. However, the decreasing respiratory muscle mass associated with aging has not been adequately discussed. The concept may appear simple; however, defining respiratory sarcopenia has not been extensively explored.

Inspiratory and expiratory maximal mouth pressure measurement as direct evidence of respiratory muscle strength is simple; however, access to relevant measuring equipment is limited. Moreover, evaluating respiratory muscle mass is challenging, and the respiratory sarcopenia using low respiratory muscle mass cannot be virtually established. Therefore, we proposed defining respiratory sarcopenia using the peak expiratory flow rate (PEFR) as an alternative to directly measuring respiratory muscle strength.³ Subsequently, the Japanese Working Group of Respiratory Sarcopenia of the Japanese Association of Rehabilitation Nutrition (JARN) published criteria for respiratory sarcopenia, which was defined based on a decline in the maximal mouth pressure and respiratory muscle mass and the presence of whole-body-sarcopenia, as measured using skeletal muscle mass, strength, and physical performance.⁴ However, this definition has not been established due to a lack of consensus. Moreover, to the best of our knowledge, the future health-related outcomes of respiratory sarcopenia have never been evaluated. Therefore, this survey confirmed whether respiratory sarcopenia, defined using PEFR and the JARN criteria, is associated with future mortality among community-dwelling older adults.

We assessed respiratory sarcopenia-related mortality after a 5-year follow-up of 470 participants (185 men aged 75.2 ± 5.5 years and 285 women aged 74.2 ± 5.4 years) who participated in a comprehensive health checkup program called ‘The Otassha Study’ conducted in the Tokyo Metropolitan Institute for Geriatrics and Gerontology in 2015. Participants who underwent spirometry and sarcopenia assessment were included; however, patients with chronic obstructive pulmonary disease (COPD) were excluded.

An electronic spirometer (Autospiro AS-507, Minato, Osaka, Japan) was used to measure pulmonary function. The PEFR as a percentage of the predicted value (%PEFR), vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), VC as a percentage of the predicted value (%VC), FVC as a percentage of the predicted value (%FVC), lower limit of normal FVC (FVC_LLN), and FEV₁/FVC were assessed.

A