According to reports from different countries in Asia, the prevalence of sarcopenia varies from 7.8%-35.3% depending on different diagnostic instruments, different age and living conditions of the study participants in each study17. In our study, the mean age is 62.4 (SD ± 8.3) and the prevalence of sarcopenia is 19.31%, which was similar to a cohort study in Taiwan using the AWGS diagnostic criteria that the prevalence of sarcopenia was 21% in participants aged 75 years and older18. Another cohort study in northern Taiwan included 302 individuals (157 men and 145 women) aged 65 years and older, and the prevalence of sarcopenia in that study was 18.6% in elderly women and 23.6% in elderly men using BIA analysis11. A previous study in Chengdu found approximately 10% community-dwelling elderly have sarcopenia in a number of 947 residents aged ≥ 60 years old which is also estimated by the BIA analysis19. And the prevalence of sarcopenia was 12.3% in Chinese men and 7.6% in Chinese women aged 70 years and older in Hongkong estimated by dual-energy X-ray absorptiometry20. This study found a higher prevalence than Chengdu and Hongkong. The reason might be that most participants were living in the village that were poorer and have lower education level even through the mean age of our study is lower than the previous studies. This shows sarcopenia are happening younger in rural areas. And the difference may also be derived from the geographical and diagnostic criteria for sarcopenia and the difference in cognitive function diagnostic criteria. Besides, our study also found that advanced age with a dose response effect associated with sarcopenia and this is compatible with many other studies20 − 22. Moreover, our study found that the prevalence of sarcopenia in male is higher than in the female. This is not consistent with other previous studies which showed Chinese women may be more vulnerable to severe sarcopenia in old age than men23. The reason might be that the mean age of male is older than the female in our study.
Our findings revealed that sarcopenia was significantly associated with cognition impairment in the multi-ethnic western Chinese population, independent of age, gender, ethnics, marriage status, lifestyle factors, indoor or outdoor housework, sleep quality, chronic diseases comorbidities and depression status. The cognitive impairment might be an independent risk factor of sarcopenia and has a dosage effect. This is compatible with several other studies that shows a positive relationship between cognitive impairment and sarcopenia24 − 26. While in the EPIDOS cohort study, sarcopenia was not shown to be associated with cognitive impairment in elderly women27. Several possible mechanisms in many studies could explain this association. Firstly, cognitive impairment leads to reduced physical activity and dietary intake, which could trigger excessive muscle loss in older adults, accelerating sarcopenia28. Secondly, low-grade inflammation is considered to be associated with both sarcopenia and cognitive impairment. Interleukin-6 (IL-6) and tumor necrosis factor‐α (TNF-α) have also been reported as inflammatory parameters, which are the important factors to lead to sarcopenia29 and the development of cognitive impairment30. Third, excessive oxidative stress related to chronic diseases also play important roles in age-related muscle atrophy, interfering with the balance between protein synthesis and breakdown, causing mitochondrial dysfunction, inducing apoptosis, and lead to sarcopenia31. While products of oxidative and nitrosative stress accumulate with aging, which is also the main risk factor for cognition impairment32. In the end, cognitive impairment reinforces and emphasizes the neuronal changes in the central nervous system leading to changes in the levels and activity of neurotransmitters, which together with the inadequate distribution of oxygen to the brain, lead to a reduction in motor units and in the ability to maintain muscle activation, which might be related to sarcopenia33. Thus, there exists a close relationship between sarcopenia and cognitive impairment which share some common mechanisms.
Besides, our study found that the association between sarcopenia with moderate/severe cognitive impairment in male has a higher odds ratio than female which might be related to hormone regulation. And moderate/severe cognitive impairment is positively related to sarcopenia in women and men, while the mild cognitive impairment seems not be related to sarcopenia in male. And a recent study indicated significant associations of sarcopenia and physical frailty with cognitive decline was could be more easier to be found in females34. One study explained this sex differences may be partly due to systemic inflammation35. A larger sample prospective cohort studies are required to illustrate gender differences.
Moreover, our study analyzed the association between cognitive impairment and the three elements in the fully regression model and it shows significant association in grip strength, gait speed and ASMI with a dosage effect separately. And this is consistent with recent studies. A study had shown that handgrip strength could be a means of monitoring progression of cognitive decline36. And some longitudinal studies found that those with slower walking speeds and a greater decline in speed over time were at greater risk of developing dementia and could predict transitioning from mild to severe cognitive impairment37,38. However, for the element of ASMI, recent study found that Lower-extremity functioning, rather than ASMI, is closely related to multiple cognitive domains39. While low muscle mass was found to be predictors of long-term mortality in nonagenarian and centenarian women40. Whether ASMI could be used as a predictor of cognitive impairment required more studies.
This is a large study to assess sarcopenia defined by the AWGS criteria and its association with cognitive impairment in multi-ethnic western China, adjusting the analysis for relevant confounders, such as sociodemographic characteristics, marriage status, lifestyle factors, and chronic diseases comorbidities. Nonetheless, this study presents some limitations. It is derived from a cross-sectional study, in such a way that it is not possible to conclude the existence of a causal association between sarcopenia in the participants and the associated factors mentioned here, which is feasible in longitudinal designs. Although regression models were adjusted for many variables, residual confounding is still possible. In addition, chronic disease information, cognition, and depression adjustment come from self-reported questionnaires, and in spite that all the data in the questionnaires have been previously validated, this information should be treated with caution. In the end, we conducted a centralized investigation, not a household survey in which most of the participants who can come by themselves are relatively healthy people. As a result of it, there exists offset in the result of prevalence. However, despite these limitations, this study has enough samples for adjustment of the regression models to major confusion factors of clinical interests. Moreover, it presented similar results to those found in studies with a more robust methodology.