Arterial stiffness (AS) is a strong predictor of future cardiovascular events and all-cause mortality [1]. Although aging and hypertension are the main factors influencing the stiffening process, obesity is also considered an independent predictor of AS [2]. There is consistent evidence that aerobic training (AT) reduces AS [3]. However, the role of AT intensity in reducing AS is still unclear [3]. In obese individuals, it appears that moderate-to-high intensity AT does not improve AS [4]. In fact, Clark et al. [5] recently did not find a reduction in AS after 6 weeks of high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT) in overweight/obese men, despite a significant decrease in central blood pressure (BP). Nevertheless, little is known about the effects of HIIT and MICT on AS and central BP in obese women. In a previous study, we found that a single bout of HIIT or MICT did not change AS, wherein only HIIT reduced the augmentation index (AIx) and central systolic BP (SBP) in young obese women [6]. Thus, the aim of this study was to investigate the effects of 8 weeks of HIIT and MICT on AS and central BP in young obese women.

Twenty-five young obese women (18–35 years; BMI = 30–39.9 kg/m2), with no history of chronic diseases or continuous medication use, participated in this parallel experimental design study (Supplementary Table 1). They were randomly assigned to HIIT (4 × 4 min at 85–95% of HRmax, interspersed with 3-min periods of active recovery at 65–75% of HRmax) or MICT (41 min at 65–75% of HRmax) (Supplementary Fig. 1). The exercise protocols were performed on a running track and standardized to maintain similar energy expenditure [6]. Central BP, carotid–femoral pulse wave velocity (cfPWV) and AIx were measured by SphygmoCor® (AtCor Medical, Sydney, Australia) [7] before and after 8 weeks. This study was approved by the local ethics committee (CAAE-08935419.5.0000.0104) and registered on the Brazilian Clinical Trials Registry (RBR-3v3dqf).

Training attendance was 81 ± 5% for HIIT and 85 ± 5% for MICT. The average distance covered per training session was 3.3 ± 0.3 and 4.1 ± 0.2 km, and the relative intensity reached per session was 81 ± 13% of HRmax and 71 ± 1% of HRmax for HIIT and MICT, respectively. There were no significant group × time interactions for any measure of AS (Fig. 1) or BP (Table 1). Both HIIT and MICT significantly reduced cfPWV (Δ = −0.37 ± 0.2, p < 0.001, ES = −0.44 and Δ = −0.35 ± 0.3, p < 0.001, ES = −0.45, respectively). In addition, there was a reduction in augmentation pressure (AP) (Δ = −3.0 ± 5.1, p = 0.033, ES = −0.69) and a tendency toward a reduction in AIx (Δ = −6.4 ± 14.8, p = 0.092, ES = −0.56) and augmentation index adjusted for 75 beats per minute (AIx@75) (Δ = −7.6 ± 15.1, p = 0.053, ES = −0.68) after HIIT. Significant reductions in brachial SBP (Δ = −6.3 ± 5.7, p = 0.033) and central SBP (Δ = −6.6 ± 6.8, p = 0.010) were observed after HIIT, and significant reductions in brachial diastolic BP (DBP) (Δ = −3.7 ± 4.6, p = 0.018) and central DBP (Δ = −3.6 ± 5.0, p = 0.026) were observed after MICT.

Fig. 1
figure 1

Carotid–femoral pulse wave velocity (cfPWV), augmentation pressure (AP), augmentation index (AIx), and augmentation index adjusted for 75 beats per minute (AIx@75) measures before and after 8 weeks of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT). Asterisk denotes Differences in relation to baseline values. Comparisons between groups and time were analyzed via ANOVA for repeated measures followed by Bonferroni correction. d, effect size (Cohen’s d)

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Table 1 Brachial, and central blood pressure, and heart rate measures before and after 8 weeks of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT)
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The novelty of this study is that both HIIT and MICT reduced cfPWV after 8 weeks in young obese women. These findings corroborate a previous meta-analysis that showed a reduction of 0.37 m/s in cfPWV after AT [3]. However, our results disagree with recent findings in overweight/obese men, which did not observe any changes in AS after HIIT or MICT [5]. The discrepancies in these results could be attributed to differences in cfPWV at baseline or length of the training protocols, which are considered factors associated with cfPWV changes following AT [3]. The mechanisms by which AT reduces cfPWV could be directly related to the reduction in elastin breakdown and collagen deposition on arterial layers or indirectly related to improvements in oxidative stress and inflammation, as well as reductions in sympathetic nervous activity (SNA) [4].

Another important finding of the present study is that HIIT significantly reduced brachial and central SBP. These findings are in line with Clark et al. [5], who found a reduction in central SBP (~4.5 mmHg, p = 0.039) and a tendency toward a reduction in brachial SBP (~5.0 mmHg, p = 0.055) after HIIT in overweight/obese men. The reduction of ~6.0 mmHg in brachial and central SBP observed in our study is considered clinically relevant, since minimal reductions in central BP could decrease myocardial work and aortic wall stress during the ejection phase, thereby decreasing the risk of ventricular hypertrophy and cardiac remodeling [8]. In addition, this reduction in brachial BP is close to those achieved by first-line antihypertensive medications [9] and is related to a reduction in CVD risk by 20–30% [10]. In addition, we found a significant decrease in AP and a tendency toward a reduction in AIx and AIx@75 after HIIT. In contrast, Clark et al. [5] did not find changes in AIx after HIIT or MICT in overweight/obese men, which may be explained by sex differences in AP responses to exercise. Yan et al. [11] found a significant effect of sex on changes in AIx, wherein women had a two times greater reduction in AIx than men. This might occur because women have greater β-adrenergic receptor sensitivity, which offsets α-adrenergic vasoconstriction, resulting in less vasoconstriction for a given amount of SNA [7]. In addition, it may be related to the direct effects of estrogen enhancing β-adrenergic receptor sensitivity or indirectly by increasing NO availability, which may increase β-adrenergic-mediated vasodilation in the peripheral vasculature [7]. AP is the measure of the impact that the reflected wave (RW) exerts on SBP and obtained by measuring the RW coming from the arterial embranchments to the heart [7]. AS causes a faster and earlier return of the RW, which arrives in systole rather than in diastole, and increases SBP and decreases DBP. Consequently, there is an increase in left ventricular afterload and impaired coronary perfusion [8].

The mechanisms by which HIIT could reduce AP and AIx are still uncertain. Nevertheless, HIIT is superior to MICT in improving endothelial function [12] by increasing NO bioavailability on the peripheral vessels, which may attenuate the impedance mismatches between the central arteries and peripheral vessels, decreasing the RW to the aorta, which could, eventually, reduce AP and AIx [6].

Although a relatively high dropout rate was observed for the HIIT protocol (50%), a similar dropout rate was verified for MICT (~40%). High dropout rates were also observed in studies with cardiovascular disease patients, in which the range of dropout rates was 0–50% for HIIT and 0–47% for MICT [13]. Nevertheless, robust evidence has also reported a dropout rate of ~50% for antihypertensive drug treatments [14].

In conclusion, both HIIT and MICT reduced AS in obese young women. However, only HIIT was able to reduce central and brachial BP and AP in this population, showing salutary benefits as an antihypertensive nondrug therapy.