There is strong evidence linking NWO and increased CVD and all-cause mortality, and women with NWO were 2.2 times more likely to die from CVD compared with those with low BF[10]. Female university students are the high incidence but underdiagnosed and understudied group of NWO. In this study, we used the bioelectrical impedance analyzer InBody-770 to measure and estimate the body composition and found, if left untreated, some significantly progressive adverse changes in NWO female university students, such as increased Body weight, BMI, BF%, BFM, BFM of left arm, and obesity degree, which will may aggravate the potential cardiovascular health hazard. Early numerous studies have validated that elevated BF% and BFM are associated with disturbances in lipids metabolism and cardiometabolic[29], which could impair cardiovascular function. Herein, if left untreated, we also found NWO females had obviously lifted resting HR, SBP, DBP, TG, and LDL over time. The normal range of SBP and DBP is respectively less than 120 and 80, however, both SBP and DBP were excessive in NWO females, implying the risk of hypertension. There was a study pointed out that the NWO subjects demonstrated left ventricle systolic and diastolic dysfunction, increased fibrosis intensity[30], so we recommend both systolic and diastolic BP should be evaluated to better define the metabolic and vascular profile of NWO females.
Previous evidence has shown that higher BMI, BP, TG, and LDL may cause persistent endothelial damage, which will lead to endothelial dysfunction and AS increase, and this is considered the first step in the progression of atherosclerosis[31]. Elevated HR is an important determinant of the mechanical properties of the vascular atherosclerotic lesions, which is related to the development and progression of vasculopathy[32, 33]. Two key points of HR elevation contribute to atherosclerosis: firstly, the elevated HR increases the oscillatory shear stress to lower the arterial distensibility. Secondly, it intensifies the pulsatile motion of the heart to hinder the local hemodynamics[34]. BP has been reported to be mediated by AS[35]. For example, elevated SBP is significantly associated with higher central arterial stiffness in healthy, normotensive men and women[36].
Blood-based biomarkers such as TC, TG, LDL, and HDL are well-established indicators of cardiovascular function risk. In this study, before the intervention, we found that the values of TC (suitable range < 5.20 mmol/L, edge elevated 5.20–6.20 mmol/L), TG (suitable range < 1.70 mmol/L, edge elevated 1.70–2.30 mmol/L), and LDL (suitable range 2.60–3.40 mmol/L, edge elevated 3.40–4.10 mmol/L) were within the edge elevated range, and HDL (suitable range ≥ 1.00 mmol/L, abnormal range < 1.00 mmol/L) were within the abnormal range in NWO females. Similarly, if left untreated, these indicators were further elevated or were abnormal. The characteristic of atherosclerosis is visible atherosclerotic lesions in the artery walls, especially in the coronary artery and aorta. These lesions primarily occur due to excessive lipid deposition[37]. Therefore, atherosclerosis originates from the passive diffusion of circulating LDL through endothelial junctions into the vessel intima[38]. One of the most representative is the elevated levels of TC and LDL[37]. The reduction of LDL can further lower cardiovascular mortality. TG is the major component of triglyceride-rich lipoproteins (TRLs), which needs to combine with associated proteins into lipoprotein particles[39]. Recently, some studies report that TG and TC content within TRLs may contribute to the development of atherosclerotic cardiovascular disease[40, 41]. In addition, HDL enhancing foam cell cholesterol efflux is considered as the first step of reversing TC transport, which is a promising antiatherogenic strategy[42]. The sensitivity of TC/HDL value is higher than the pure TC or HDL, which is used to independently predict the severity of fatty liver caused by obesity, atherosclerotic, and coronary heart disease[43].
AS is considered one of the earliest detectable measures of vascular damage. However, it’s very difficult to directly measure AS. In the last decade, a variety of non-invasive methods and devices such as CAVI, baPWV, cfPWV, IMT, and aortic augmentation index (aAI) has been used to evaluate atherosclerosis by assessing AS or impaired endothelial function. But currently available devices and methods are unsuitable for the patient screening or risk stratification in routine clinical practice owing to factors such as the postural requirements, variability among investigators, and time-consuming manual procedures. Recently, AVI and API, two novel non-invasive vascular indexes for evaluating systemic and peripheral AS, respectively, have been gaining attention. They are convenient, quick (about 1 min), and comfortable for systemic endothelial function and AS assessment using cuff oscillometry technologies and suprasystolic cuff oscillometric wave measurement (PASESA AVE-2000 PLUS, Japan) in the clinical setting. The AVI mainly reflects the AS from the aorta to the muscular artery and peripheral resistance, which is significantly associated with BMI, abdominal circumference, and TG[44]. While API mainly reflects the stiffness of the brachial artery, which is affected by coronary stenosis, arterial compliance and more sensitive to arterial SBP[45]. Meanwhile, they are both not only associated with baPWV, preclinical carotid arterial compliance, as well as AS in general populations[16, 44], but also with the number of cardiovascular risk factors, the Framingham risk score[46], and CAD[47]. These two new indexes are therefore expected to be useful clinically for predicting and evaluating the future risk of atherosclerotic diseases and cardiovascular events. However, data on subjects with NWO females remain scant, not even available in China.
AVI and API have emerged as surrogate markers of cardiovascular disease in obesity and a predictor for CVD events in adulthood. According to the manufacturer’s instructions, the normal range of AVI is 11 to 15 (age 18–23), and the API is 15 to 22 (age 15–22). In the current study, we found both AVI and API exceeded the normal range in NWO female university students. Even worse, the API further increased in the Control group due to they did not get effective intervention. Combined with the abnormal body composition, BP, and lipids metabolism, these results strongly suggested that the NWO females have an increased risk of arteriosclerosis and CVD. Early detection of the degree of arteriosclerosis in the NWO population and timely intervention are of great significance for preventing and treating cardiovascular and cerebrovascular diseases. The previous study has revealed that the enhanced AVI represents increased workload on the heart with elevated central BP and is highly correlated with the augmentation index. API is a useful predictor of future cardiovascular disease, which is independently associated with both the Framingham Cardiovascular Risk Score and the Suita Score[46]. Fujiwara et al. found that AVI and API were higher in patients with coronary artery disease and positively correlated with the severity of coronary artery stenosis[14]. Therefore, the higher values of AVI and API represent the higher propensity for AS and assess the potential risk of CVD in the NWO population. The mechanisms of NOW increasing AS and impairing the vascular function ascribe to chronic high fat accumulation, which stimulates multiple pro-inflammatory cytokines and elevates NOX-mediated ROS production, induces oxidative stress, provokes vascular endothelial cells functional disorder, and disturbs the secretion of vascularizing factors (nitric oxide synthase and nitric oxide) and vasoconstrictor factor (Ang-Ⅱ and endothelin, vasoconstrictor)[48, 49]. Moreover, perivascular adipose tissue also seems to promote local inflammation and reduce capillary density and microvascular nitric oxide (NO, vasodilator) bioavailability to resulting in impaired endothelial function and vasodilatation, which will eventually accelerate the atherosclerotic process at an early stage[50].
Prescribing physical activity to people with obesity is no longer a rarity and in fact has become recognized as a necessity. In recent years,HIIT is among the most highly recommended measures for obesity because it is well tolerated and favorably affects cardiometabolic risk factors. Our study showed that 4-week HIIT effectively reduced the Body weight, BMI, BF%, BFM, LBFM, and obesity degree while increased SMM, protein content, BMC, FFM, LFFM, TBW, LTBW, BCM, and Inbody score in the HIIT group, only LMC had no difference. Interestingly, after HIIT intervention, most of the results of the between-group comparisons were in line with the within-group of the HIIT group except for no difference of body weight, BMC, LFFM, and LTBW. The main reason may be possibly due to the difference in sample size between the two groups (HIIT n = 17 vs. Control n = 13), it’s also possible that the statistic method of repeated measures ANOVA may be overly strict. Nevertheless, based on these results, we were still able to demonstrate that short-term HIIT could be a potent stimulus for effectively improving the body composition in NWO females. Previous evidence allows us to speculate that these positive improvements in body composition after HIIT training were likely the result of an upregulation of bioenergetic oxidation (especially fat oxidation) and energy expenditure due to excess postexercise oxygen consumption (EPOC)[51, 52]. HIIT consumes large amounts of glycogen during exercise, so more fat will be oxidized during the recovery period to resynthesize glycogen. And, HIIT training may mobilize quite a bit of skeletal muscles, which also may activate the skeletal muscles’ catabolism signaling mechanisms (especially lipodieresis) and increase muscle protein synthesis[53, 54]. Besides these, HIIT could promote the secretion of catecholamines, epinephrine, norepinephrine, and growth hormone, which will accelerate fat decomposition to achieve effective fat and body weight loss[26].
Previous studies elucidated that HIIT could decrease BMI, BF, and BFM in overweight and obesity[22, 55], and HIIT elicited superior benefits than MICT in weight control, fat loss (especially abdominal and visceral fat), FFM, and SMM in both healthy and chronic illness populations [56–58]. Excessive amounts of cardiac adipose tissue are reported to be associated with CVD. HIIT has been shown to even reduce epicardial adipose tissue mass and cardiovascular risk in physically inactive participants with abdominal obesity[59]. The results imply that HIIT is a sustainable and training strategy for improving weight management. Furthermore, although generating a similar magnitude of improving BFM and waist circumference modest as the MICT does in overweight and obese individuals, HIIT can save nearly 40% time commitment each week[60]. Therefore, HIIT is considered as a time-efficient and effective exercise strategy for managing overweight and obesity.
However, to the best of our knowledge, little is known regarding the effects of HIIT on CVD factors, namely BP, lipids metabolism, and AVI/API, in NWO female university students. Firstly, BP is closely correlated with cardiovascular health, and hypertension has led to high cardiovascular morbidity and mortality worldwide[61]. Some studies have shown that HIIT had a superior function of decreasing resting HR, SBP, and DBP[62–64], and was associated with greater improvements in dealing with hypertension when compared to MICT among the hypertensive patients and the overweight/obesity adolescent girls[65–67]. These results are concordant with our findings. Secondly, HIIT has been reported to have the function of redressing lipid metabolism disorders in obesity[68, 69] and may be a preferable therapy for atherosclerosis. Our results demonstrated that 4-week HIIT could significantly reduce TC, TG, LDL, and TC/HDL, and raise HDL in the HIIT group, and the changes of these indexes were consistent with that of when compared with the controls. More importantly, HIIT could adjust these indexes to the normal ranges, and our finding was consistent with Fisher et al in overweight and obese young men[70]. Gripp et al. reported that most of the positive effects of the HIIT were also found to be longer-lasting and maintained after the suspension for 4 weeks[71]. Accumulation of LDL inside the blood vessels serves as a major cause of arteriosclerosis, while HIIT can prevent LDL accumulation[26]. Moreover, HIIT also can affect HDL function, including the promotion of reverse cholesterol transport and lipid peroxide transport clearing[72]. Therefore, this pattern of short-term HIIT will benefit the NWO females from ameliorating lipid metabolism.
Thirdly, although the effects of aerobic exercise on reducing AS and CVD risk have been investigated before, the relationship between AVI/API and HIIT improved NOW females AS has not been studied fully. Here, we examined for the first time the effect of HIIT on the two new arterial indices on AS in Chinese NWO female university students. We verified that HIIT could significantly lower the values of AVI and API to the normal ranges, and the fully automatic and rapid measurement of AVI/API may enhance the practical value in a large population to identify subjects at high risk of atherosclerosis. AS is mainly influenced by vascular endothelial function, HIIT has well-established beneficial effects on endothelial function in overweight men/adolescents and obese young women[73, 74]. Adaptive changes in endothelial function have been shown to depending (to a large extent) on the activity of eNOS, which induces NO production to relax smooth muscle cells, capillaries, and small arterioles, subsequently dilates blood vessels and increases arterial compliance in the muscular arteries[75, 76]. HIIT has been reported to increase endothelial eNOS protein content and NO availability, and caused significant improvements in brachial artery endothelial-dependent dilatation and aortic stiffness in obese individuals with elevated CVD risk[77]. Additionally, a meta-analysis showed that HIIT was associated with up to a twofold increase in endothelial dilator function at the macrocirculatory level when compared with MICT in adults with metabolic and cardiovascular disease[78].
However, the mechanism of reducing the propensity for AS is still unclear in our study. There are many gaps in the literature on NWO unlike for overt obesity and further study should disclose the underlying relationship between the HIIT and the vascular adaptation in improving the AS in NWO female university students and explore the molecular mechanisms. It should be noted that the exercise risk assessment needs to be carried out before the formulation of HIIT prescription, and the adaptive training along with the increasing intensity and sufficient warm-up, relaxation, and cooling-down are essential for avoiding sports fatigue and sports injuries even the concurrently health risk. In this study, we did not observe any adverse exercise events (e.g., muscle injury, overfatigue, syncope, palpitation, angina, abnormal fluctuation of blood pressure, nausea, vomiting, dyspnea) during the HIIT intervention. Hence, HIIT utilization is safe for NWO females. Last but not least, large, multicenter, and prospective studies are required to establish the optimal HIIT protocols for NWO female university students.
Limitations
The study was designed as a prospective, randomized controlled trial (RCT) exercise intervention trial comparing the effects of a 4-week HIIT training program on NOW female university students. While, this study has some limitations that should be considered before interpreting the results. First, the sample size was relatively small and the control group had a higher attrition rate (35%), probably because they didn’t see the weight loss or benefit. In contrast, the HIIT group had high adherence. Even so, it did not prevent us from seeing clear differences between the two groups, and the magnitude of the beneficial effects of HIIT on NWO females’ AS was adequate. Second, although it has been reported that HIIT may result in suppressed appetite[79], participants were instructed to not alter their diet behaviors for the duration of the intervention, change in habitual energy intake was not monitored, which may affect the final results. Third, we did not examine the arterial compliance, reflected wave, vascular endothelial function, or female hormones, which could have important effects on AS.