## 4 Discussion
we quantitated muscle strain rate by using ultrafast imaging that allows us to measure transient displacement changes with the time with higher sensitivity than conventional techniques [18]; the identical external force (the probe tied with a sandbag) was carefully applied and lifted during the experiment to minimize possible variations by the same independent researcher (intraobserver coefficient of variation is about 7%). Therefore, the muscle strain rate obtained in this study was still valid as the indicator for muscle stiffness despite its strengths and limitations that have been addressed elsewhere [9]. To our knowledge, this is the first study characterizing _uf_PWV parameter changes in resistance exercise. The use of pulse wave imaging in assessing local carotid arterial stiffness has been studied in healthy and disease populations [19; 20; 24; 33; 34; 35]. Although we did not include a healthy sedentary control group in our study design, compared to the previous study also using ultrafast ultrasound imaging [20], our average _uf_PWV-dia (6.3 m/s) is higher than those reported in healthy age-matched counterparts (5.3 m/s). Nevertheless, the changes of _uf_PWV during a cardiac cycle were relatively more minor but within a reasonable range (0.5 vs. 0.8 m/s). Such discrepancy might be attributed to exercise training and age. Indeed, habitual high-intensity resistance exercise training has been demonstrated to reduce central arterial compliance [2; 36; 3] compared with the sedentary control; the higher _uf_PWV-dia in the present study indicates greater diastolic arterial stiffness in this population, which supports these previous findings. Moreover, age is the powerful determinant of carotid local arterial stiffness [35], and the gapping between systolic and diastolic _uf_PWV has also been reported to increase with aging [20]. Therefore, it may not be surprising that the change of arterial stiffness over the cardiac cycle was small since our participants were relatively young. Nevertheless, our results showed that our measures on _uf_PWV were within the normal range. To maximize the exercise-induced responses, we used a bicep curl exercise as the exercise model in the present study since upper limb exercise training was demonstrated to increase arterial stiffness compared with the lower limb [37; 38]. Previous studies indicate the induced arterial stiffening by resistance exercise is intensity dependent; acute low-intensity resistance exercise favors arterial compliance [39], whereas high-intensity resistance exercise increases arterial stiffness [4]. Our results indicate that upper arm exercise may result in systemic arterial stiffening (increased baPWV) even at lower exercise intensity. Similar stiffening effects were observed on the carotid artery as we found both _uf_PWV-sys and _uf_PWV-dia increase regardless of intensity; the increase in stiffness during systolic phase (_uf_PWV-sys), but not during the diastolic phase, contributed significantly (~30%) to the increase in cPP following exercise, which was in line with the literature [17; 35]. Our findings further support the notion that upper limb-biased resistance exercise may not favor vascular function. Another novel finding of this study is that passive muscle stiffness correlates with conventional local carotid function measures and _uf_PWV parameters in the habitual high-intensity resistance-trained population. Moreover, passive muscle stiffness correlated with carotid _uf_PWV, but not baPWV or cfPWV. Currently, the exact underlying mechanisms remain to be determined, and it might be associated with greater chronic motor activation [40] that has been proposed as the result of high-intensity resistance exercise. From a molecular perspective, accumulating evidence showed that the extracellular matrix is vital in determining skeletal [41] and carotid stiffness [42].