Our study demonstrates for the first time that not only brachial BP but also ankle BP exhibit a sustained elevation after acute MS.
In this study, the increased brachial BP induced by acute MS persisted for 30 min post-stress, which is congruent with previous reports demonstrating long-lasting arm BP elevations after acute MS [1–4]. On the other hand, other studies have reported the absence of a sustained pressor response post-stress [5, 6]. The reason for the inconsistency among the studies may be due to the differences in the participant characteristics, task types or durations, or BP measurement method.
In addition to the above brachial pressor response, we found an increase in ankle BP after acute MS, which was sustained for 30 min. Acute MS is known to substantially increases the circulating levels of catecholamines [15, 16], which would affect various tissues via blood circulation. In addition, robust elevation in muscle sympathetic nerve activity (MSNA) has been observed after acute MS [14, 17], which can be observed in both upper and lower limbs [17], suggesting the presence of a systemic effect. Both norepinephrine infusion and elevated MSNA increase vascular resistance of vessels in the limbs [18–20]. Moreover, it has recently been suggested that delayed BP recovery after acute MS occurs, in part, via a neurogenic vascular mechanism mediated by α1-adrenergic receptors [21]. Considered together, we speculate that the observed brachial and ankle pressor response after acute MS is likely to be attributed to the increased sympathetic vasoconstrictor tone at a systemic level. Direct evidence supporting our assertion is not available, and further investigations, therefore, are warranted. On the other hand, we observed an increase in ankle DBP at 30 min after the task in the CON group. Such vascular response seems to be caused by the basal vascular tone to maintain the peripheral blood flow, and the observed increase in ankle DBP in the MS group might also be partially due to the same mechanism.
It has been reported that a marked arm pressor response to acute MS is linked to CVD [8]. In this study, we provide the first evidence demonstrating that acute MS results in a long-lasting elevation in ankle BP. Therefore, repeated exposure to increased ankle BP due to stressful exposures during daily life activities may cause a chronic elevation of ankle BP, which is identified as an independent predictor of CVD [10, 11]. Although this aspect is largely speculative at this time, we consider that the measurement of ankle BP in addition to arm BP can be used as an important assessment of stress response, and this would further expand our understanding of the association between human cardiovascular response to acute MS and CVD.
In conclusion, the present study demonstrates that acute MS results in a sustained elevation in BP in both upper (i.e., the brachium) and lower (i.e., the ankle) limbs vessels in young, healthy men, suggesting a stress-induced systemic pressor response.