In the current study we investigated the association between sarcopenia and control groups on inflammatory markers like TNF-a, il-6, and hs-CRP. The findings showed that the levels of TNF-a and IL-6 between normal and abnormal groups of muscle mass and muscle performance were not significant. However, a significant difference in hs-CRP level between normal and abnormal muscle strength groups was observed. Several previous studies showed that inflammation plays a vital role in the development of sarcopenia. A longitudinal aging study in Amsterdam revealed a positive association between higher levels of IL-6 and CRP and elevated risk of muscle strength loss but not muscle mass 13.
Moreover, in another prospective cohort study, this author found that increased levels of inflammatory markers were significantly correlated with a more 5-year decrease in the thigh muscle area. Higher TNF-a and its soluble receptors investigated the most consistent relationship with lower grip strength and muscle mass 12. Zhao et al. In a cross-sectional study on middle-aged and older adults indicated a higher platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and systemic immune-inflammation index (SII), were associated with increased odds of sarcopenia 15. In support of these findings, a systematic review and meta-analysis that evaluated the association of markers of inflammation with muscle strength and muscle mass found a significant relationship between increased levels of circulating TNF-α, CRP, and IL-6 with a decline in muscle mass, handgrip and knee extension strength 16. On the other hand, a systematic review and meta-analysis of cross-sectional studies investigated that subjects with sarcopenia compared with controls have higher levels of serum hs-CRP. However, levels of IL-6 and TNF-α were not significantly different 17. TNF-α, CRP, and IL-6 are inflammatory markers that are suitable indicators to show the association of inflammatory status with sarcopenia and its components.
CRP is an indicator of acute and chronic phase inflammation and increases chronic diseases such as type 2 diabetes, cardiovascular disease, and sarcopenia. Muscle mass, muscle strength, and physical performance decline 17–19. Increased level of CRP influences muscle cell size by suppression of muscle protein synthesis pathway 20. High levels of CRP are associated with obesity and insulin resistance 21. It seems that there is a direct relation between the mechanical and metabolic performance of aged muscles. Increasing CRP levels can increase insulin resistance, which disturbs muscles' metabolic function, and as a result, mechanical function is also impaired 22. Although the reason is unknown, the mechanism of cellular and molecular changes in sarcopenia and insulin resistance are the same. In both cases, there is an accumulation of fat in muscle fibers which can affect the insulin pathway 23. Furthermore, disruption of a critical protein in muscles, such as myosin heavy chain, can be seen in insulin resistance and aging muscles 24,25. However, the exact effect of CRP on muscle atrophy is still unknown 16.
IL-6 is an Inflammatory cytokine secreted by immune cells in tissue damage or infection conditions 16. Also, IL-6 is known as a myokine, which is produced by skeletal muscle and regulates muscle contraction and metabolism 26,27. Some studies showed that temporal and low levels of IL-6 could be beneficial 28; however, it is well understood that chronic exposure to IL-6 may result in muscle atrophy and facilitate muscle catabolism 29. TNFα is a pro-inflammatory cytokine and has been associated with muscle pathology 30. Muscle catabolism in various inflammatory diseases, including congestive heart failure 31, cancer 32, and chronic obstructive pulmonary disease (COPD) 33, has been attributed to TNF-α. Studies investigate that TNF-α interferes with the muscle differentiation process and can elevate catabolism in mature cells. Also, TNF-α, through another pathway mediated by reactive oxygen species (ROS) and nuclear factor-kappa B, promotes muscle wasting 34. In the present study, we found no significant association between inflammatory markers and sarcopenia and its components, including muscle mass and muscle performance. We have just seen a significant association between normal and abnormal muscle strength groups evaluated based on handgrip strength. Our findings could be related to the limited number of participants in this study, and more longitudinal studies are needed to clarify our findings. Also, this inconsistency between our results and previous studies may be due to racial and age differences in the current study.
It may be because of the way that cytokines were measured. The measurement of plasma inflammatory cytokines may not suffice to determine the differences, and cellular cytokines must be measured. Inflammation statuses such as disability, neurodegenerative processes, and aging-related hormonal changes can be other causes of sarcopenia.35
Our study has some limitations that need to be considered: Insufficient budget, which affected the sample size, and this limited number of participants affects the validity of the results and should be considered to interpret our findings. The causality association between inflammatory markers and sarcopenia cannot be identified due to the study's cross-sectional design. Moreover, because of using FFQ for dietary assessment, recall bias and measurement error were inevitable. Finally, we conducted the present study on older adults, so generalization of these results to other age groups should be cautious.