## 4 Discussion  
The main findings of the current study are as follows: (1) Bicep curl resistance exercise at a higher intensity (80%1 RM) contributes to a more significant reduction in muscle strain rate (greater muscle stiffness) after exercise than that of lower intensity (40%1 RM); (2) an acute bout of arm resistance exercise increases the carotid _uf_PWV parameters regardless of exercise intensity; (3) arm muscle stiffness was associated with ultrafast ultrasound-derived carotid local pulse wave velocity, but not central and systemic arterial stiffness indices. Our findings on muscle strain elastography changes after exercise are consistent with the previous studies [26, 27, 28, 29], showing that muscle stiffness increases after acute bouts of resistance exercise. Our data further suggest that a greater resistance exercise intensity results in lower mechanical deformation on muscle tissue. However, the average reduction in strain rate (40 vs. 80% = \(-\)0.1 vs. \(-\)0.3 in 1/s) and AUC (40 vs. 80% = \(-\)20 vs. \(-\)118) from our preliminary data did not clearly show a linear dose-response relationship between exercise intensity and induced muscle stiffness. This finding agrees with the finding of the previous in vivo study, demonstrating that the relationship between the applied strain to the developed strain in soft tissue elasticity imaging is nonlinear [30]. The underlying mechanism by which muscle stiffness increases following exercise could be primarily attributed to exercise-induced muscle alternations and their associated connective tissues. Indeed, resting intracellular calcium level might still be high immediately after exercise. Furthermore, the cross-bridge interactions [31] and engerged muscle bundles resulting from muscle recruitment and stretch reflex [32] are associated with augmented muscle stiffness. Therefore, higher neural activation and consequent structural alterations following higher exercise intensity might explain our finding on strain rate difference between 40 and 80%1 RM. Moreover, we cannot exclude the possibility that muscle fiber swelling resulting from exercise also plays a role, although intramuscular swelling is not closely linked with the initial increased muscle stiffness following eccentric exercise [7, 8]. We should be aware that the concentric exercise model was adopted in the present study and the extent to which exercise-induced muscle damage and inflammation are less pronounced than the eccentric. Interestingly, the nonlinear relationship between applied and developed strain in soft tissue is also inflammation dependent [30]. In this regard, the obtained muscle strain rate might also vary with exercise intensity and induced inflammatory status nonlinearly when applying strain elastography in an exercise setting. Future study needs to include more exercise intensities and different muscle contraction models (i.e., concentric vs. eccentric) to elucidate such relationship. In the present study, we chose to report strain rate changes as the passive muscle stiffness, instead of strain ratio that takes subcutaneous tissue stiffness as the reference [22], since our participants were all resistance-trained and some of them had a skinny subcutaneous fat layer, which makes it challenging to quantitate reference strain in this population. However, the results from our pilot work showed that data expressed as strain and strain ratio were consistent in other participants of the same population. Furthermore, \begin{table}
\begin{tabular}{c c} \hline \hline  & \(\Delta\) cPP \\ \hline \(\Delta\) muscle strain rate. 1/s & R\({}^{2}\) = 0.04 \\ \(\Delta\)_uf_PWV-sys, m/s & R\({}^{2}\) = 0.30 * (\(p\) = 0.003) \\ \(\Delta\)_uf_PWV-dia, m/s & R\({}^{2}\) = 0.04 \\ \(\Delta\) baPWV, cm/s & R\({}^{2}\) = 0.09 \\ \hline \hline \end{tabular} \({}^{\pi}\) = significant, \(p\) < 0.05  
\end{table} 
Table 4: Simple linear regression analysis of increased cPP in response to bicep curl resistance exercise (two exercise sessions combined).