Exercise training is worldwide considered pivotal for maintaining and restoring general population health. Its potential beneficial effects touch several domains: metabolic, haemodynamic, psychological, and social. The European guidelines for hypertension recommend physical activity among the nonpharmacological interventions to manage ‘all patients with hypertension’ , and the harder effort is advocated in order to fight against sedentary living. In the domain of the exercise training, there are nonetheless many features to be considered. Indeed, haemodynamic modifications linked to exercise strictly depend on the type and the duration of the effort as well as the background of the individual who is going to be trained (i.e. age, sex, hypertensive or not, previously trained, or sedentary …). In literature, since several years, many attempts have been made to investigate the haemodynamic response to different exercise-training programs, with not always coherent conclusions. In 1987, Douglas et al.  reported on the effect of prolonged and high-intensity exercise (triathlon) on left ventricular function and found that immediately after the competition, the athletes presented reduced fractional shortening, driven by altered contractility and preload. These alterations recovered 1 day after the exercise, suggesting cardiac ‘fatigue.’ Similarly, 20 years later, Aslani et al.  demonstrated that the Ranger training program (consisting in 8 weeks of exhaustive exercise) was associated with impaired left ventricular function. As such, from the available data, it appears that high-intensity exercise is acutely and chronically associated with impaired haemodynamics. In addition, even aerobic exercise, when extremely vigorous like the marathon, is chronically associated with increased arterial stiffness .
Concerning aerobic exercise, there are no univocal data about its final effect on haemodynamics, also because of a very disparate methodology of the studies. Whenever considering a setting of healthy population, there is general agreement that aerobic exercise of either short or long duration is associated with an improvement of arterial compliance [5–8], even if the compliance variations are not always adjusted for blood pressure variations. Indeed, arterial stiffness depends strictly on the distending pressure of the vessels, represented by mean arterial pressure , and remarkably is directly correlated with SBP. Therefore, the interpretation of the results of studies investigating haemodynamic modifications after exercise should take into account blood pressure variations . Interestingly, Cameron et al. published a comprehensive analysis of the effect of 4-week exercise training on systemic arterial compliance in sedentary young men. They showed that exercise training increased arterial compliance independently of blood pressure changes, and that the compliance variations were related to improvement of the physical performance. From the data presented so far, it seems that the arterial haemodynamic modifications following exercise training could be considered as a marker of the beneficial effect of the training itself. Anyway, it has been shown that arterial stiffness is not only a marker but it can drive different cardiac responses to exercise. In particular, Cote et al.  have investigated the ventricular–arterial coupling following a bout of high-intensity exercise. They found that in both trained and nontrained individuals, there was an inverse correlation between baseline arterial stiffness and left ventricular twist augmentation after exercise. This experiment allowed to stress the arterial response to exercise and test the cardiac response. Indeed, during high-intensity exercise both arterial distending pressure and sympathetic activity rise, resulting in acute increase of arterial stiffness, which would be enhanced in the presence of baseline stiffer arterial tree. The exaggerated acute increase of arterial stiffness could drive modifications of the cardiac afterload that are both direct and mediated by an increase in wave reflection speed, and a greater impedance mismatch [12,13]. This finally leads to impaired ventricular response to stress.
Conversely, in the setting of hypertensive population, the effect of aerobic training has not been established. Most of the studies consistently found no benefit of aerobic training on arterial compliance. In particular, the study from Ferrier et al. showed that 8-week exercise training improved oxygen consumption and work capacity in 20 hypertensive patients without modifying arterial stiffness . These results are confirmed by a review of the literature by Montero et al.  that indicates that the improvement of arterial stiffness after training in hypertensive patients is observed only in association with great blood pressure changes and long training duration.
The article by Lefferts et al.  in the present issue of the Journal provides data about the effect of a single aerobic exercise bout on arterial stiffness and cerebrovascular pulsatility, comparing 30 hypertensive and 30 nonhypertensive patients. After excluding patients with previous cardiovascular events and other significant comorbidities (including dementia), the cohort was deeply examined by an initial health test with standard anthropometric and biochemical analysis; home blood pressure monitoring during 7 days; physical activity monitoring (by accelerometer and questionnaire); and cardiopulmonary test. The exercise test consisted of 30 min of moderate-intensity cycling and was preceded and followed by measure of pulse wave velocity (by applanation tonometry) as a marker of arterial stiffness. Furthermore, carotid arterial stiffness, and carotid and middle cerebral artery pulsatility were measured. Wave intensity analysis was performed in order to obtain wave separation and to analyze the contribution of the forward and reflected waves. The two groups of patients differed mainly concerning physical performance (oxygen consumption, physical activity indicators), which was superior in nonhypertensive participants; and blood pressure levels (higher but well controlled in hypertensive patients). The analysis found no substantial differences in terms of blood pressure (both brachial and central) pre/post exercise and between the two groups, with no significant time/group interaction. The contribution of the reflected waves decreased in both groups after the exercise, while heart rate increased. The carotid artery haemodynamics showed a trend for reduction in mean diameter (statistically significant, but clinically negligible), an increase in the forward wave intensity and in the negative area (corresponding to the contribution of the reflected waves); carotid pulsatility index was increased by exercise in both groups. Concerning middle cerebral artery haemodynamics, no significant change was found, but the pulsatility index was slightly increased by exercise in both groups. Importantly, arterial stiffness was found to increase slightly after the exercise in both groups. A path analysis showed an intercorrelation between changes in carotid diameter, forward wave intensity, and carotid pulsatility, the latter being correlated with cerebral pulsatility. The acute aerobic exercise bout was thus associated with modest haemodynamic modifications, which were similar in hypertensive and nonhypertensive patients. It is plausible that the increase in cardiac output during exercise resulted in increased carotid pulsatility index, mainly driven by the forward energy component, and was associated with slight diameter compensatory reduction. Given the small intensity of the exercise, it is not striking that no differences were found between nonhypertensive and hypertensive patients. Interestingly, the increase of carotid pulsatility index did not translate into relevant increase in middle cerebral artery pulsatility, which could indicate a compensatory mechanism to protect cerebral vessel haemodynamics. Notably, arterial stiffness was modestly increased by exercise in both groups, with clinically nonsignificant differences of 0.2 m/s (nonhypertensive individuals) and 0.5 m/s (hypertensive patients) that lose statistical significance whenever adjusting for heart rate changes. Interestingly, these results confirms the findings from the article from Tordi et al.  who addressed the different haemodynamic effects of intermittent versus constant aerobic training in young healthy men. Firstly, the individual underwent the intermittent aerobic training following the SWEET protocol, which consist of 30 min of exercise characterized by alternating phases of base (4 min at 65% of the predicted maximal heart rate) and peak (1 min at 85% of predicted maximal heart rate). After 48 h, the participants underwent the constant exercise test: 30 min of exercise at constant heart rate (the average heart rate obtained from intermittent test). Measures of arterial stiffness were collected every 2 min after the 30-min test, for the subsequent 30 min after the exercise. The carotid-pedis stiffness (mainly attributed to aortic stiffness) was reduced for the intermittent test and unmodified for the constant test. This behaviour persisted from the very first minutes after the exercise (4–5 min) to the end of the follow-up (30 min after the exercise).
The cardiovascular response to exercise training is a complex phenomenon implicating left ventricular function, arterial system haemodynamics, ventricular–arterial coupling, and peripheral vessel acute and chronic modifications. Also the sympathetic/parasympathetic balance and the type and duration of the exercise play a pivotal role [18,19]. Unfortunately, many of the published studies differ in term of exercise protocol, population setting, and haemodynamic parameters so that it is difficult to compare the results and drive conclusions.
Conflicts of interest
There are no conflicts of interest.
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