The primary goal of our study was to evaluate whether the baseline aPWV, a surrogate index of the aortic stiffness and CAS, increases to a greater degree post-race than pre-race in response to the same external task capable of activating the sympathetic nervous system. Therefore, it was investigated whether the effects of the half-marathon race change the physiological effects induced by the same external stimulus on the aPWV. We employed a novel technique to measure the aPWV by processing the finger photoplethysmographic signal as previously indicated . This algorithm provides the aortic pulse transit time from the left ventricle to the aortic bifurcation. The aPWV is then calculated as pulse transit distance divided by pulse transit time. This technique displays high repeatability as shown by the small bias of 0.022 m/s we found in our test-retest analysis. Our data show that 2 min of SYMP did not affect the pre-race baseline aPWV but significantly augmented the post-race one. Therefore, the same external stimulus appeared to increase the stiffness of the central arterial segments post-race but not pre-race. The baseline aPWV measured 7 to 8 min after the half-marathon conclusion was statistically similar (p = 0.09) when compared to pre-race resting values. According to the BORG CR100 scale, the overall score of about 88 AU displays a race effort between very and extremely strong.
Pre-exercise resting aPWV
Previous research has questioned whether increased CAS at rest may be a health risk factor [9,10,11,12]. Therefore, cut-off values of pulse wave velocity to score the cardiovascular risk have been proposed . A previous meta-analysis suggested an increase in the relative risk for cardiovascular disease events and mortality by 12% and 9%, respectively, for a chronic increase in cf-PWV of 1 m/s . Chronic endurance training induces anatomical vascular remodeling and changes in neurovascular regulation [28, 29]. It increases the artery diameter, decreases the artery thickness, and changes the artery viscoelastic properties by changing the gene expression of structural proteins [28, 29]. Positive effects of chronic endurance training on vascular health have been shown by increasing artery flow-mediated vasodilation, an important index of coronary artery disease . Regular endurance exercise at low or moderate intensity has also been shown to decrease central arterial stiffness as evidenced by a decrease in cf-PWV . CAS diminishes in individuals who undergo recreational endurance training sessions at low or moderate intensity compared to sedentary individuals, but it can increase again in competitive long-distance athletes due to the higher endurance exercise level . Indeed, strong elevations in systolic arterial pressure (SAP) during physical exercise have been suggested to overload the viscoelastic tissue of the arterial walls and to modify the arterial structure if repeated chronically . Such a condition is also typical of resistance exercise. Indeed, a study found a decreased carotid arterial compliance after chronic resistance training at high intensity, but not at low intensity, which was associated with the acute change in SAP during exercise sessions . The chronic repetition of strenuous endurance exercise sessions has also been shown to contribute to endothelial dysfunction and vascular inflammation, inducing an oxidative vascular environment as a large production of reactive oxygen species overpowers the nitric oxide production [34, 35]. Whether the chronic repetition of strenuous training and races might negatively affect the CAS in competitive endurance athletes has thus been questioned. The pre-race aPWV by about 7.5 m/s we found in our runners is within the limits (6–10 m/s) suggested for healthy individuals between 24 and 62 years old . This suggests that the repetition of strenuous exercises competitive half-marathon runners undergo do not result in out-of-limit augmented CAS. It is relevant to mention that any possible augmented aPWV in competitive endurance runners compared to other populations may not necessarily be linked to increased cardiovascular risk. Competitive runners might present increased resting aPWV values compared to other populations, but be totally healthy. Such a condition could, however, categorize them as individuals at higher cardiovascular risk after preliminary aPWV screening tests.
Effect of a strenuous half-marathon on the aPWV
Our data show that the post-race baseline aPWV assessed 7 to 8 min after the half-marathon was similar to that pre-race. This finding is in agreement with previous studies suggesting CAS be at or below resting values > 5 min after the conclusion of submaximal aerobic exercises . Conversely, resistance exercise has been shown to induce long-lasting CAS increases after the exercise conclusion [8, 13, 33, 36]. Interestingly, our finding reveals an exercise intensity-independent effect on the post-exercise aPWV. This might be due to the similar post- and pre-race MAPs. Indeed, any MAP increase would stretch arterial vessels and increase their stiffness, and vice versa, due to the blood pressure dependence of the stress-strain relationship . In accordance with these findings, previous studies showed that post-exercise decrements of aPWV were associated with lower MAP during the recovery .
Effect of SYMP on the aPWV
It was investigated whether the effects of the half-marathon race change the physiological effects on CAS induced by the same external task capable of activating the sympathetic nervous system. The handgrip exercise was shown to reliably increase the muscle sympathetic nerve activity and peripheral resistances as confirmed by the large availability of microneurography recordings [20,21,22]. Raising the exercising forearm above the heart augments the normal sympathetic activation in response to handgrip exercise compared to the same exercise performed at heart level . Consistent with previous investigations [20, 22], SYMP progressively increased MAP ad HR over time before physical exercise. Such responses were also noted after the half-marathon. SYMP did not affect the aPWV before the race. Whether the sympathetic outflow can modulate the stiffness of elastic large arteries at rest has not yet been well defined. Lower body negative pressure mediated SYMP did not alter the compliance of the distal abdominal aorta  or carotid artery . However, this result might be due to the central MAP drop needed to unload baroreceptors . In contrast to our results, another study using a similar handgrip exercise to induce SYMP increased the aPWV at rest . However, in that study, the stimulus was applied for twice the time than it had been in ours. This suggests that a similar sympathetic stimulant may increase the CAS at rest but the stressful situation must be longer lasting.
Two minutes of SYMP significantly augmented the post-race baseline aPWV, but did not affect the pre-race baseline aPWV. Therefore, the same external stimulus augmented the baseline stiffness of the central arterial segments post-exercise but not pre-exercise. We have previously shown that peripheral sympathetic vasoconstriction is augmented within 15 min after a half-marathon by specifically using the same handgrip exercise, modality, and timing of stimulus application we employed in the present study . Although defining the underlying mechanisms is beyond the scope of this project, previous studies showed the preeminent role for the sympathetic nervous system in constricting the vascular tissue immediately after endurance exercise than at rest through a mechanism mediated by α1‐adrenergic activity [40, 41]. Furthermore, there might be a synergistic effect of augmented circulating blood catecholamines  on the effects of handgrip exercise after a half-marathon. Moreover, the same handgrip workload may correspond to a higher percentage of MVC after the race compared to pre-race due to fatigue . However, the same handgrip exercise intensity was shown to induce less MSNA > 60 min after a prolonged endurance exercise compared to before exercise , but MSNA recordings immediately (< 15 min) after prolonged endurance exercise are not available due to methodological limits.
Specialists involved in sports medicine must carefully evaluate the effects of exercises before suggesting them to their athletes, particularly in at-risk individuals . We primarily sought to assess whether the effects of the same external task capable of activating the sympathetic nervous system on the stiffness of central artery segments are augmented after the conclusion on a half-marathon race compared to before the race. A wide variety of stressful stimuli can acutely activate the sympathetic nervous system, including mental stress and emotions . Our data show that the same stressful stimulus augments the baseline stiffness of the central arterial segments post-exercise but not pre-exercise. As mentioned in the introduction, an increase in CAS can augment cardiac work and oxygen consumption . Following the conclusion of physical exercise, this condition occurs in the presence of a reduced diastolic time that may impair coronary perfusion. Unfortunately, there is currently no information to adequately score the impact of a temporary CAS increment on the risk for acute cardiovascular events. However, this finding reveals the need for further investigations into the interaction effects between physical exercise and sympathetic activation on cardiovascular risk. Furthermore, it was unknown if and how CAS changes after a strenuous half-marathon race. This issue is relevant considering that the half-marathon has gained the most popularity out of all long-distance races in terms of number of participants . Our findings reveal that a half-marathon race affects the CAS similarly as aerobic exercises at lower intensities do.
The technique we employed to assess the aPWV was the most suitable method for the goals of our study, but not the gold-standard method. The gold-standard cf-PWV assessment requires two different measurements in the carotid and femoral arteries at two separate time points . This method would not allow an appropriate aPWV assessment during SYMP due to the progressive cardiovascular changes over time [22, 47]. Conversely, the method we employed allows the aPWV assessment beat-by-beat and with a single site measurement. Moreover, the method we employed shows high repeatability during test-retest measures compared to other techniques . This study has evaluated absolute values of aPWV reached in the presence of haemodynamics altered by sympathetic activation and physical exercise. The interest was investigating the stiffness of central arterial segments reached in the presence of such haemodynamic conditions. Our study was not intended to investigate how the arterial viscoelastic structure would be in the presence of similar resting haemodynamic conditions, as it is done for other purposes such as evaluating the chronic effects of exercise training or pharmacological therapy on arterial stiffness at rest. In the present study, we specifically used 2 min of handgrip exercise at 30% MVC as sympathetic stimulant. We employed the same methodology we used in our previous study that led to increased sympathetic vasoconstriction after a half-marathon race within 2 min from the stimulus application . The use of other sympathetic stimulants, modalities, or timing of stimulus application is possible but may not guarantee an increased post-race sympathetic vasoconstriction within 2 min from application and the same effects on the aPWV we found in this study . Previous research has shown sex differences in arterial stiffness following running exercise . In this regard, our sample size was not equally divided between males and females. Finally, race-related stress in the pre-race period could have occurred in runners and affected the aPWV. However, we scrupulously followed the aPWV measurement guidelines to obtain the measure in the most basal conditions possible avoiding external interferences.