Physical inactivity and sedentary behavior are key lifestyle-related risk factors for developing cardiovascular diseases (CVD) and are associated with an increased risk of all-cause mortality and morbidity (Lavie et al., 2019). The cardiac autonomic function is a variable affected by a sedentary lifestyle, and the impairment of its function is a predictable marker for CVD (Lavie et al., 2019; Niemelä et al., 2019). Heart rate variability (HRV) is a noninvasive method for evaluating the cardiac autonomic control of heart rate (HR), which represents electrical cardiac variation by the time interval between R-R intervals (Thayer et al., 2010). HRV is tightly controlled by the autonomic nervous system (ANS) through parasympathetic modulations (Thayer et al., 2010). Previous studies indicate that the decrease in HRV (i.e., reduced vagal modulations) is associated with an increased risk of CVD, sudden cardiac death, and all-cause mortality (Thayer et al., 2010; Sessa et al., 2018). Recently, HRV has been suggested as a method to monitor the influence of sedentary behavior on the cardiac autonomic control of HR (Niemelä et al., 2019).

Arterial stiffness (AS) is typically measured by pulse wave velocity (PWV) and is a marker of vascular function as well as an independent risk factor for cardiovascular events and overall mortality (Mattace-Raso et al., 2006; Mitchell, 2009). The specific role that the ANS plays with respect to AS is somewhat contentious (Mäki-Petäjä et al., 2016). However, the ANS has a regulatory role in HR and vascular tone and therefore might augment AS (Mäki-Petäjä et al., 2016; Sheng and Zhu, 2018). A sedentary lifestyle may be accompanied by a dysfunction of the ANS (i.e., decrease in HRV) and impairment of vascular function (i.e., increase in PWV), thus leading to an increased risk of CVD (Thayer et al., 2010; Ahmadi-Abhari et al., 2017).

Regular exercise training could be an effective way to counteract the above-mentioned sedentary lifestyle consequences on cardiovascular function (Ahmadi-Abhari et al., 2017). Exercise training accompanied by improved cardiorespiratory fitness increases vagal modulations, which plays an important role in improving HRV (Locateli et al., 2018; Singh et al., 2018; Veijalainen et al., 2019). Furthermore, exercise training improves vascular function and decreases AS by promoting shear stress and nitric oxide (NO) bioavailability, thereby reducing oxidative stress and inflammation (Birk et al., 2013; Cocks et al., 2016; Lessiani et al., 2016). Although the effects of exercise training on either HRV or AS have been determined, it remains unclear that which exercise training variables, intensity or volume, are associated with greater adaptations (Dos Santos et al., 2019). Previous studies have demonstrated that similar positive improvements of HRV and vascular function follow both moderate-intensity and high-volume exercise training in comparison to high-intensity exercise training (Bhati et al., 2017; Rodrigues et al., 2020). In contrast, other studies show greater improvements in HRV and AS following high-intensity training (Bahmanbeglou et al., 2019; Ramírez-Vélez et al., 2020). These contradictory results may be due to differences between the exercise mode and workloads, as well as the differences in the training duration, sex, age, and nutritional status of participants, and training status (sedentary vs. trained) (Medeiros et al., 2021). Moreover, the workloads of most of the previous studies were not equated internally (caloric expenditure) (Kilpatrick et al., 2009; Alansare et al., 2018) or externally (Km per week) (Alansare et al., 2018; Ramírez-Vélez et al., 2020), which make it challenging to compare protocols with different intensities and volumes. In addition, previous studies have not reported adherence to their protocols, which could have an important clinical impact on designing exercise protocols for sedentary people (Alansare et al., 2018; Ramírez-Vélez et al., 2020).

Therefore, the purpose of this study was to investigate the effects of high-volume moderate-intensity (HVMIT) and low-volume high-intensity training (LVHIT) with equated caloric expenditure and workloads (Km/per week) on HRV and AS in sedentary young men. We hypothesized that LVHIT would improve HRV and decrease AS when compared to HVMIT.

In all study groups (i.e., control, HVMIT, and LVHIT), no significant differences (p > 0.05) were observed for age, weight, BMI, BF%, FFM, SBP, DBP, and VO₂max (Table 1). Moreover, there were no significant differences (p > 0.05) between the groups for HRV variables and PWV at baseline (Table 3).

The following results can be found in Table 3, unless otherwise stated. A significant interaction between group and time was observed for SDNN (F2,42 = 20.9 and p < 0.05), RMSSD (F2,42 = 124 and p < 0.05), LF (F2,42 = 403 and p < 0.05), HF (F2,42 = 263 and p < 0.05), LF-HF (F2,42 = 1,043 and p < 0.05), HR (F2,42 = 30.6 and p < 0.05), PWV (F2,42 = 286 and p < 0.05), SBP (F2,42 = 71.4 and p < 0.05), BF% (F2,42 = 69.3 and p < 0.05), VO₂max (F2,42 = 67.5 and p < 0.05), and Vmax (F2,42 = 38.4 and p < 0.05). SDNN and HF significantly increased in both training protocols (i.e., HVMIT and LVHIT), when compared with the control group (p < 0.05). However, these increases were significantly greater in LVHIT when compared with the HVMIT protocol (p < 0.05). Moreover, paired sample t-test indicated significant increases (p < 0.05) in SDNN and HF following 12 weeks when compared with baseline in both training protocols. Data analysis showed a significant decrease in LF-HF ratio in HVMIT and LVHIT protocols in comparison with the control group (p < 0.05). However, a more significant decrease was observed in LVHIT compared with the HVMIT protocol (p < 0.05). Both training protocols showed significant decreases (p < 0.05) in LF-HF ratio post 12 weeks when compared with the baseline. Furthermore, RMSSD (increased) and LF (decreased) showed significant changes only in the LVHIT protocol when compared with control group (p < 0.05). However, these changes in the HVMIT protocol were not significant (p > 0.05). The changes from baseline to 12 weeks in RMSSD and LF were significant (p < 0.05) in HVMIT and LVHIT protocols. HR showed no significant difference (p > 0.05) in either training protocols compared with the control group. But a significant reduction (p < 0.05) in both training protocols from baseline to 12 weeks was demonstrated. PWV (ES: 0.93), SBP (ES: 0.77), and BF% significantly decreased in LVHIT compared with the control group (p < 0.05) (Figures 2, 3 and Table 3). However, no significant changes were observed in the HVMIT protocol (Figures 2, 3 and Table 3).

There were significant correlations in both training conditions (i.e., LVHIT and HVMIT) (p < 0.05) between PWV with SDNN (r = −0.524), RMSSD (r = −0.358), HR (r = 0.276), LF (r = 0.442), HF (r = −0.481), and LF-HF (r = 0.559) as determined by the Pearson correlation analyses (Table 4).

Neither training protocol showed significant decreases from baseline to 12 weeks in PWV, SBP, and BF%. VO2max significantly increased only in the LVHIT protocol when compared with the control group (p < 0.05). However, both training protocols resulted in a significant increase (p < 0.05) in VO2max from baseline to 12 weeks. Vmax changes in both training protocols were not significant when compared with the control group. However, these changes in HVMIT and LVHIT were significant (p < 0.05) after 12 weeks when compared with baseline. No significant changes were observed in DBP, BMI, and FFM in both training protocols when compared with the control group (Figure 3 and Table 3).

This study examines the exercise effects of different volumes and intensities of endurance training on HRV variables, PWV, cardiorespiratory fitness, hemodynamic markers, and body composition in sedentary adult males. The main findings were that the LVHIT is more effective in improving HRV variables (i.e., SDNN, RMSSD, LF, HF, and LF-HF), PWV SBP, VO₂max, Vmax, and BF% when compared with an HVMIT protocol. Thus, a shorter protocol of higher intensity was more effective for improving cardiovascular health metrics in sedentary adult men.

Both training protocols improved the time domain (SDNN and HR) and frequency domain (HF and LF/HF) variables; however, this improvement was more significant in the LVHIT than the HVMIT protocol. Moreover, RMSSD and LF showed improvement by only following the LVHIT protocol. This improvement of HRV agrees with other studies, which show that exercise intensity plays a crucial role in modifying HRV variables (Heydari et al., 2013; Alansare et al., 2018). It is well established that cardiovascular adaptation resulting from exercise training can be affected by the ANS (Michelini and Stern, 2009; Fürholz et al., 2013). Exercise training can decrease sympathetic activity and increase parasympathetic activity, thus decreasing resting HR, which was observed to positively change early on during the 12 weeks of exercise (Rosenwinkel et al., 2001). Moreover, a greater increase in epinephrine and norepinephrine has been observed when exercise is performed with higher intensities, suggesting a higher sympathetic nervous system activity and greater physiological stress during exercise sessions (Jacob et al., 2004). This might lead to greater physiological and cardio-autonomic adaptations in the short term (Aubert et al., 2003; Jacob et al., 2004). Furthermore, an increase in catecholamine concentration could increase lipolysis in adipose tissues, which may be why there was a significant reduction in BF% following the LVHIT protocol (Zouhal et al., 2013). Exercise intensity is also known to increase shear stress and subsequently plays a critical role in releasing NO in the arteries (Cocks et al., 2016). NO could be responsible for modulating the cardio-autonomic system by decreasing sympathetic outflow and increasing parasympathetic influences (Schultz, 2009). Improvements in the variables associated with HRV in the LVHIT protocol might be explained by these physiological adaptations that occur following shorter duration and higher intensity endurance exercise training.

The PWV and SBP also decreased significantly after 12 weeks in the LVHIT but not in the HVMIT protocol. This is somewhat surprising given that previous studies have reported improvement in AS and SBP following high-intensity exercise training (Bahmanbeglou et al., 2019; Soltani et al., 2020). Previous studies have also observed that high-intensity exercise when compared with low or moderate exercise has greater effects on vascular function. This occurs through enhanced shear stress and plasma NO production, with a subsequent increase in vasorelaxation (Ramos et al., 2015; Cocks et al., 2016). We speculated that the LVHIT would have more significant effects than the HVMIT protocol on vascular function due to greater stimulation of the shear rate resulting in increasing NO bioavailability and as a result, improved PWV and SBP. Furthermore, improvement of the arterial baroreflex sensitivity following exercise training plays a significant role in modulating HR and vascular tone and therefore could be associated with reducing AS and increasing cardiac autonomic function (Heydari et al., 2013; Chaswal et al., 2015; Sheng and Zhu, 2018). In addition, other mechanisms, such as a decrease in inflammation and oxidative stress, may have a contributing role in reducing PWV (Munk et al., 2011; Bogdanis et al., 2013; Ismaeel et al., 2018).

The significant increase in VO₂max only in the LVHIT protocol is another interesting finding in our study and supports the results found by Ross et al. (2015). These authors reported a greater increase in VO₂max following continuous training at 75% relative to 50% of VO₂max (Ross et al., 2015). This increase was attributed to both central (i.e., cardiac output increase) and peripheral (i.e., mitochondrial density) adaptations (MacInnis and Gibala, 2017). The improvement in PWV may also be related to central adaptations following the LVHIT protocol (Boreham et al., 2004). Improvements in VO₂max, SBP, and PWV reinforce the importance of exercise intensity for inducing physiological adaptation, which leads to improvement in HRV variables. Röhling et al. (2017) suggested that it is possible that an increase in VO₂max would result in an improvement in cardiac autonomic function which would have a significant effect on parasympathetic modulations (Ueno et al., 2002). Furthermore, one novel finding in this study is the low-to-moderate correlations found between HRV parameters and PWV, which would suggest some interplay between central and peripheral cardiovascular mechanisms after training that warrants further research.

The limitation of this study is that we did not measure the NO or baroreceptor sensitivity, and the inclusion of these measurements may have increased our understanding of the mechanisms behind some of the findings. The reliability and validity of BIA have been confirmed with previous studies (Jackson et al., 1988; Ling et al., 2011). However, BIA can be considered a limitation because it underestimates BF% and overestimates FFM, particularly in individuals who are categorized as obese (Coppini et al., 2005). Additionally, HRV parameters mostly represent parasympathetic influences on HR, and therefore, we suggested that future studies evaluate the sympathetic activity with other techniques such as microneurography and systolic time intervals for better understanding the ANS activity and its relationship with AS. Moreover, in this study, we did not measure carotid-femoral stiffness, which is the gold standard and a more reliable method for measuring AS (Tanaka et al., 2009).

The strengths of this study included a randomized control design, with strictly controlled supervised exercise sessions and matched caloric expenditure for both training protocols. Our higher intensity protocol could be an attractive option given the time efficiency associated with the design and prescription of exercise training for adult men with sedentary behavior. However, more studies are needed to be specified in different populations (i.e., individuals with obesity and cardiovascular patients) to confirm the effectiveness and safety of the protocols of this study.

This study demonstrates that both HVMIT and LVHIT protocols improved some HRV variables. However, these improvements were significantly greater in the LVHIT protocol. Moreover, RMSSD, LF, PWV, SBP, VO₂max, and BF% improved only in the LVHIT protocol following 12 weeks of exercise. Based on these findings, exercise intensity was associated with higher benefits rather than exercise volume. Thus, the higher intensity of exercise training needs to be considered when planning an exercise intervention to improve the ANS activity, AS, cardiorespiratory fitness, and body composition of sedentary adult men. However, further studies are needed to confirm these findings in other populations and further elucidate the mechanisms involved in such adaptations, including the potential association between HRV parameters and PWV after training regimens.

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

The studies involving human participants were reviewed and approved by the Institutional Review Board of Islamic Azad University (Ethics code: IR-IAU1398-18). The patients/participants provided their written informed consent to participate in this study.

MS, MB, AS, DB, AD, and HZ contributed to the conception and design of the study. MS, AD, AS, HZ, KD, SM, and TV contributed to the acquisition, analysis, or interpretation of data. MS, PD-B, DB, BK, and TV drafted the manuscript. All authors critically revised the manuscript, and gave final approval and agreed to be accountable for all aspects of work ensuring integrity and accuracy.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.