## 4 Discussion  
In this study, we identified eight determinants that were associated with sarcopenia in postmenopausal women who had undergone total thyroidectomy, of which GNRI was the only determinant to affect both muscle mass and physical function. Several thyroid blood markers were related to ASM/ht\({}^{2}\)\(\leq\) 5.4 in this study. First, low TSH, but not high free T4, was associated with low muscle mass. In contrast to these findings, a few studies have reported that high free T4 [19], high free T3 [20], or high free T3/free T4 ratio [20] were associated with sarcopenia, but low TSH was not [20]. However, these studies focused on older euthyroid subjects, and patients with subclinical or overt thyroid diseases were excluded. As mentioned previously, there is a clear relationship between overt thyroid dysfunction and sarcopenia. Although there is currently no clear conclusion as to whether or not subclinical thyroid dysfunction can affect muscle health, at least one study has reported no significant increased risk of low muscle mass in subclinical hypothyroidism older people [21]. In addition, another study reported that subclinicalhypertroidism was correlated with low muscle mass and strength [22]. Fewer studies [23; 24] have focused on muscle health in patients who receive levothyroxine supplements; however, they did not quantify the contribution of determinants with regression analysis as in the present study. We confirmed the negative impact of levothyroxine over-replacement on muscle mass, and also found that TSH was a good index. Second, thyroglobulin Ab was also positively associated with muscle mass, which has not previously been reported in patients without overt hypothyroidism. There are currently no recognized extra-thyroid targets of this specific autoantibody [25]; however, a study on hypothyroid myopathy found that these patients usually had higher thyroglobulin \begin{table}
\begin{tabular}{c c c} \hline \hline
**Gait Speed** & **Multivariate (Forward)** & \\ \hline \multicolumn{3}{c}{**Unstandardized Coefficient**} \\  & \(\mathbf{\beta}\) (95\% CD) & \(\mathbf{p}\) \\ \hline Age (per 1 year) & 0.043 (0.003, 0.084) & 0.036 \\ GNRI (per 1 score) & 0.062 (0.019, 0.105) & 0.006 \\ T3 (log per 1 ng/mL) & \(-3.541\) (\(-7.019\), \(-0.063\)) & 0.046 \\ \hline \hline \multicolumn{3}{c}{R\({}^{2}\) = 0.280, F change = 4.241, Durbin-Watson test = 1.292.} \\ \end{tabular}
\end{table} 
Table 4: Determinants of gait speed using multivariable stepwise linear regression analysis. Ab than microsomal Ab [26], which seems to be the reverse of our results. A previous study reported that this autoantibody declined after thyroidectomy in thyroid carcinoma patients [27], and as more than 60% of our study population had this cancer, the lower autoantibody level may imply a longer duration of levothyroxine replacement therapy or over-suppression, which would therefore further increase the risk of sarcopenia. Third, T3 was negatively associated with gait speed. This was peculiar but could still explain why T3 was correlated with gait speed but not with ASM/ht2 or handgrip strength. Muscle mass itself is not equal to muscle quality [28], which is defined as muscle strength divided by muscle area. Walking or performing other physical activities requires both muscle power and also good vision, neural function, and coordination. A previous study attributed this to cognitive decline before a decline in muscle mass in subclinical hyperhydroxism patients [29]. Furthermore, another study reported a positive association between T3 and lower limb muscle mass but not upper limb muscle mass in euthyroid young men [30]. Nevertheless, this does not apply to our study directly because serum T3 levels were not correlated with free T4, TSH, or even supplemental doses taken by the levothyroxine replacement patients according to previous studies [31; 32], so it appears to be an additional independent marker for physical performance in this specific population.