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J Exerc Rehabil > Volume 22(2);2026 > Article
Jo and Jee: Differential hemodynamic adaptations to identical body conditioning program across blood pressure categories: a quasi-experimental study

Abstract

This study examined whether identical body conditioning program would differentially affect hemodynamic, body composition, and physical fitness parameters across blood pressure (BP) categories, and explored the potential role of autonomic modulation in mediating exercise-induced adaptations. In this quasi-experimental study, 85 participants completed a structured 15-week exercise program. All participants were categorized into four groups as follows: normal BP (n=21), elevated BP (n=20), stage 1 hypertension (n=22), and stage 2 hypertension (n=22). Because muscle mass and basal metabolic rate (BMR) differed among the groups at baseline, a repeated-measures analysis of covariance was conducted using these variables as covariates to assess the effects of time and group. Significant interactions were observed for systolic BP with pronounced reductions in the stage 1 hypertension and stage 2 hypertension groups, particularly in stage 2 hypertension. Diastolic BP and heart rate also demonstrated significant differential responses across groups. Cardiorespiratory fitness showed group-dependent responses, with significant group and time × group effects observed for maximal oxygen uptake. In contrast, no significant interactions were found for body weight, fat mass, body circumferences and grip strength. Importantly, the hemodynamic improvements occurred independently of changes in body composition and were robust after adjustment for baseline muscle mass and BMR. These findings are consistent with the possibility that exercise-induced autonomic modulation may contribute to early BP improvements; however, direct autonomic indices were not measured.

INTRODUCTION

Hypertension is one of the most prevalent and modifiable risk factors for cardiovascular morbidity and mortality worldwide (Mills et al., 2020). Elevated blood pressure (BP) substantially increases the risk of stroke, myocardial infarction, heart failure, and premature death (Whelton et al., 2018). Although pharmacological treatment is effective, structured exercise training is widely recommended as a first-line nonpharmacological strategy for BP management (Almutairi et al., 2024; Whelton et al., 2018). Meta-analyses consistently demonstrate that regular aerobic exercise reduces resting systolic and diastolic BP, even in the absence of substantial weight loss (Cornelissen and Fagard, 2005; Cornelissen and Smart, 2013), suggesting that mechanisms beyond structural body composition changes may contribute to antihypertensive adaptations.
Hypertension is characterized by chronic sympathetic overactivity, impaired baroreflex sensitivity, and increased peripheral vascular resistance (Grassi et al., 2009; Mancia and Grassi, 2014). Exercise training has been shown to improve autonomic balance and vascular function, potentially attenuating excessive sympathetic vasoconstrictor drive (Green et al., 2004; Laterza et al., 2007). These regulatory adaptations may occur independently of measurable changes in body mass or fat distribution, indicating that early BP improvements may reflect functional rather than structural mechanisms. Importantly, such neural and vascular regulatory changes may occur prior to, or independently of, measurable alterations in body composition or structural physique or physical fitness (Bassuk and Manson, 2005).
Previous evidence has suggested that individuals with elevated baseline sympathetic tone might exhibit greater responsiveness to exercise-induced autonomic modulation (Cornelissen and Smart, 2013). This implies that identical exercise stimuli may produce heterogeneous hemodynamic responses depending on baseline BP status. Nevertheless, most prior investigations have examined clinically prescribed aerobic or resistance training programs specifically designed for hypertensive patients, often within narrowly defined BP categories. Few studies have directly compared exercise-induced responses across multiple BP classifications within a single standardized intervention, particularly while statistically adjusting for body composition–related confounders such as body weight and skeletal muscle mass. Moreover, although aerobic exercise is widely recognized as an effective strategy for BP reduction (Hamer et al., 2006; Whelton et al., 2002), real-world exercise settings—such as university body conditioning courses or community fitness programs—typically emphasize posture correction, weight control, or general fitness rather than targeted antihypertensive prescriptions. While various physiological benefits of such programs have been reported (Blumenthal et al., 2000; Elmer et al., 2006), it remains unclear whether BP improvements observed in such settings reflect secondary effects of weight loss or stress reduction, or whether they represent regulatory adaptations of the autonomic nervous system independent of structural changes in body composition.
Most previous trials have focused on clinically prescribed exercise protocols specifically targeting hypertensive patients, without directly comparing differential adaptations across baseline BP categories under identical exercise exposure. In addressing this gap, the study employed a quasi-experimental repeated-measures design implemented within a real-world educational setting. Conducting a randomized controlled trial within an academic body conditioning curriculum was not feasible due to institutional and ethical constraints, as all enrolled students were required to participate in the same educational program. Rather than imposing artificial allocation or withholding exercise exposure, the present design sought to examine naturally occurring adaptive responses within a real-world setting. Although quasi-experimental designs limit strict causal inference, they allow evaluation of differential physiological adaptations under ecologically valid conditions that reflect typical exercise participation among young adults. Therefore, the present study was initiated to investigate the effects of a combined theory-and-practice educational course—conducted within a general “body conditioning” curriculum rather than a program specifically designed to lower BP—on changes in hemodynamic variables, body composition, body circumference, and physical fitness parameters in young adults.

MATERIALS AND METHODS

Study design

This study was designed as a prospective, quasi-experimental, longitudinal intervention study. Participants were not stratified according to their baseline physiological characteristics prior to the intervention. Instead, individuals who voluntarily enrolled in the body conditioning program were assessed before and after completion of the educational course. Participants were classified into BP categories based on resting systolic BP (SBP) and diastolic BP (DBP) values obtained prior to the intervention, according to the 2017 American College of Cardiology/American Heart Association criteria, and physiological variables were subsequently analyzed according to these postintervention BP classifications. Although a nonexercise control group was not included, the within-subject repeated-measures design inherently accounts for stable individual characteristics, and baseline homogeneity across BP categories further minimizes the likelihood that the observed interaction effects were driven by pre-existing group differences. While the absence of a nonexercise control condition limits the strength of causal inference, the consistent direction of BP changes within the hypertensive categories supports a training-related effect rather than random temporal variation. The research protocol was reviewed and approved by the institutional review board of Hanseo University in Seosan, Korea (HS26-0209-01), and all participants provided informed consent prior to study enrollment in accordance with the Declaration of Helsinki.

Participants

Participants were university students aged 19–26 years who voluntarily enrolled in a standardized 15-week supervised exercise class. All participants completed the same exercise protocol under identical training conditions. Enrollment was based on participation in the academic exercise class rather than clinical recruitment, and participants generally considered themselves healthy at the time of study entry. A total of 95 students were initially enrolled in the program. Of these, 10 were excluded from the final analysis due to baseline SBP/DBP values not meeting the predefined classification criteria (n=8) and measurement errors (n=2). All remaining participants (n=85) completed both baseline and postintervention assessments, with no additional attrition during the intervention period. They were informed of the purpose and direction of the class and the outcomes measured in this study before and after class during the pre-class orientation. The appropriate sample size for this study design was 72, assuming a medium effect size (f=0.25), α=0.05, power (1−β)=0.80, 4 groups, and 2 repeated measurements using G*Power (v.3.1.9.4; Heinrich Heine University, Germany) (Faul et al., 2007). Eligibility criteria included no history of treatment or medication use affecting BP or body composition. Only students who had not engaged in a structured exercise program for at least 6 months were included. None of the participants were aware of their hemodynamic status prior to enrollment; therefore, BP, heart rate (HR), and other hemodynamic parameters were assessed during a pre-participation physical examination. Individuals with any diagnosed psychological disorder or major organ dysfunction were excluded. The longitudinal structure, with repeated measurements obtained before and after the 15-week program, enabled the assessment of within-subject changes over time and between-group differences in adaptive responses. At baseline (week 2, prior to the initiation of structured training), participants were categorized into groups based on standard SBP/DBP criteria (normal BP, <120/80 mmHg; elevated BP, 120–129/<80 mmHg; stage 1 hypertension, 130–139/80–89 mmHg; stage 2 hypertension, ≥140/≥90 mmHg) (Whelton et al., 2018).

Body conditioning intervention

The theory-and-practice educational class was conducted over 15 weeks, with each session lasting 2 hr and consisting of 40 min of theoretical instruction followed by 80 min of practical training. All sessions began with standardized stretching and warm-up routines, which were consistently applied throughout the study. In week 1, participants attended an orientation session covering the basic principles of exercise. A demographic survey was conducted, followed by supervised flexibility exercises (stretching from the ankle to the cervical region) and aerobic warm-up activities ranging from brisk walking to light jogging. In week 2, baseline assessments were performed prior to the intervention. Measurements included body composition, BP, HR, respiratory rate, body circumferences (upper arm, forearm, abdomen, hip, thigh, and calf), grip strength, and maximum oxygen uptake (VO2max) estimated using the Harvard step test. During weeks 3–4, theoretical lectures addressed diet, weight control, energy metabolism, and the neuroendocrine system. Practical sessions included calisthenics (push-ups, squats, pull-ups, and lunges) and core stabilization exercises (front, back, and side planks). In week 5, following instruction on the musculoskeletal system, low-intensity machine-based resistance exercises were introduced in addition to core training. In week 6, principles of exercise training were taught, and participants performed calisthenics combined with machine-based resistance exercises at mild to moderate intensity. One-repetition maximum testing was conducted to determine appropriate training loads for advanced resistance training. During weeks 7–8, exercise intensity was progressively increased according to the principle of progressive overload, with greater repetitions and sets in machine-based exercises progressing from moderate to vigorous intensity. From weeks 9–12, a split-training routine was implemented targeting specific muscle groups: abdominal (week 9), back (week 10), shoulder (week 11), and chest (week 12). Training included machine-based exercises and free-weight exercises using dumbbells and barbells, with intensity gradually progressing from moderate to vigorous levels. In weeks 13–14, lower- and upper-limb resistance training sessions were conducted using free weights at mild to moderate intensity. In week 15, postintervention assessments identical to those conducted at baseline (week 2) were performed. Participants also completed an individualized self-training evaluation with peer assistance.

Demographic measures

Demographic variables comprised age and sex, along with medical history, family history, smoking status, and levels of physical activity. Daily sleep duration was determined from self-reported bedtime and wake-up time, including the point at which participants resumed their usual morning activities, and was operationally defined as total sleep time. Habitual physical activity was measured with the International Physical Activity Questionnaire (IPAQ)–Short Form, a validated instrument for assessing adult physical activity (Chun, 2012). Overall physical activity was expressed as metabolic equivalent hours per week based on established scoring guidelines.

Hemodynamic measures

BP and HR were measured using an automated oscillometric sphygmomanometer (BioZ, Cardio Dynamics, USA). Prior to measurement, participants rested for approximately 3 min in a seated position. All measurements were conducted in a quiet, temperature-controlled laboratory environment (22°C–24°C) to minimize external influences. Participants were instructed to refrain from caffeine, alcohol, smoking, and vigorous physical activity for at least 12 hr prior to testing. Upon arrival, participants rested in a seated position for a minimum of 10 min before measurement. During this period, they were instructed to remain relaxed, avoid talking, and maintain normal breathing. BP was measured with the participant seated comfortably in a chair with back support, feet flat on the floor, and legs uncrossed. The arm was supported at heart level on a table. An appropriately sized cuff (selected based on mid-upper arm circumference) was placed snugly on the nondominant arm, with the lower edge of the cuff positioned approximately 2–3 cm above the antecubital fossa. Three consecutive measurements were obtained at 1- to 2-min intervals. If the difference between SBP and DBP readings exceeded 5 mmHg, an additional measurement was performed (Landgraf et al., 2010). The average of the two closest readings was used for statistical analysis. BP classification was stratified into four levels according to resting measurements as follows: normal BP (NBP, systolic <120 mmHg and diastolic <80 mmHg), elevated BP (EBP, systolic 120–129 mmHg and diastolic <80 mmHg), stage 1 hypertension (S1HTN, systolic 130–139 mmHg or diastolic 80–89 mmHg), and stage 2 hypertension (S2HTN, systolic ≥140 mmHg or diastolic ≥90 mmHg) (Whelton et al., 2018). Meanwhile, HR was automatically recorded simultaneously by the BP monitor during each measurement. The mean value of the valid BP measurements was used as the resting HR for analysis. All measurements were conducted at the same time of day before and after the intervention to control for diurnal variation.

Respiratory rate measure

Respiratory rate was measured while the participant remained seated comfortably with the back supported, feet flat on the floor, and hands resting on the thighs. Participants were instructed to breathe normally and to refrain from talking during the assessment. To minimize voluntary control of breathing, participants were not informed that their respiration was being specifically monitored at the time of measurement. Respiratory movements were assessed by visually observing thoracic excursions. One complete respiratory cycle was defined as one inhalation and one exhalation. Respiratory rate was counted for 60 sec using a stopwatch. If breathing appeared irregular, measurement was repeated after an additional rest period. Two measurements were obtained, and the average value was used for statistical analysis. All measurements were performed at approximately the same time of day before and after the intervention to reduce the influence of circadian variation.

Body composition measure

Body composition was assessed using a bioelectrical impedance analysis device, the InBody 320 (Biospace Co., Korea), which provides measurements of body weight and skeletal muscle mass. Standing height was measured with a BMS330 stadiometer (Biospace Co.). The bioelectrical impedance analysis device evaluates segmental impedance by detecting voltage differences across both the upper and lower body. Prior to assessment, participants were instructed to remove all metal accessories and any items that could interfere with electrical conductivity. Each participant stood barefoot on the measurement platform, grasped the hand electrodes, and remained still for approximately 3 min while the assessment was conducted. To minimize measurement error, participants were asked to refrain from food intake for at least 4 hr, alcohol consumption for 48 hr, and any form of exercise for 10 hr prior to testing. Additionally, they were instructed to empty their bladder approximately 30 min before the assessment. In this study, the body composition variables assessed were body weight, muscle mass, fat mass, body mass index (BMI), fat percentage, waist-to-hip ratio (WHR), and basal metabolic rate (BMR).

Body circumference measure

All circumferences were measured using a nonelastic anthropometric tape to the nearest 0.1 cm. Measurements were taken on the dominant side of the body with participants in a standardized standing position of the upper arm, forearm, abdomen, hip, thigh, calf (Kalkışım et al., 2022). Each site was measured twice, and the average value was recorded. If the two measurements differed by more than 0.5 cm, a third measurement was obtained.

Grip strength measure and VO2max estimation

Handgrip strength, an indicator of muscular strength, was measured for both the left and right hands using a dynamometer (T.K.K 5401, Tachometer, Takei, Japan). Participants stood with their arms slightly abducted and exerted maximal force for 3–5 sec. Two trials were conducted for each hand, and the higher value was recorded (Lee et al., 2022). Meanwhile, VO2max was estimated using the HR ratio method described by Uth et al. (2004), according to the formula: VO2max=15.3×(HRmax/HRrest), expressed in mL/kg/min. HRrest was measured under standardized resting conditions prescribed above, and HRmax was predicted using age-based equations: HRmax=208–(0.7×age). All tests were conducted at approximately the same time of day before and after the intervention to control for diurnal variation.

Statistical analysis

All statistical analyses were performed using IBM SPSS Statistics ver. 23.0 (IBM Co., USA). Graphical representations were generated using GraphPad Prism ver. 11, (GraphPad Software Inc., USA). Data are presented as mean±standard deviation. Normality of demographic, anthropometric, and clinical variables was assessed using the Kolmogorov–Smirnov test. Before conducting the primary analyses, baseline values were examined using the Kruskal–Wallis test to identify any initial group differences. Variable comparisons were performed using a repeated-measures (4×2) analysis of covariance (ANCOVA) with covariates, muscle mass and BMR. Because random allocation was not performed and no separate nonexercise control group was included, the study is classified as quasi-experimental. However, repeated measurements were conducted before and after the intervention, allowing within-subject comparisons over time and between-group comparisons of differential adaptations. This longitudinal repeated-measures structure enabled the evaluation of time effects, group effects, and time-by-group interactions while statistically adjusting for relevant baseline covariates. Effect sizes were calculated using Cohen d (η2), defined as the mean difference between groups divided by the pooled standard deviation (Cohen, 1992). For a more detailed evaluation, changes across time were expressed as delta (Δ) percentages. SBP and DBP were predefined as the primary outcomes of this study. Other physiological variables were considered secondary or exploratory outcomes. Bonferroni-adjusted post hoc comparisons were applied for significant interaction effects. Statistical significance was established at P≤0.05.

RESULTS

Demographic and anthropometric features

The final sample of 85 participants exceeded this requirement, indicating adequate statistical power to detect time-by-group interaction effects. There were no meaningful differences in age across groups (overall mean 22.14±1.96 years). As shown in Table 1, there were no significant differences among groups in age, sex distribution, disease status, family history, smoking status, physical activity level, IPAQ score, sleep duration, fat mass, BMI, body fat percentage, or WHR (all P>0.05). These findings indicate baseline homogeneity across the four BP categories (NBP, EBP, S1HTN, and S2HTN). However, significant between-group differences were observed for muscle mass and BMR, with moderate effect sizes.

Comparison results of hemodynamic variables

Pre- and postintervention changes in hemodynamic variables are presented in Table 2. After adjustment for baseline muscle mass and BMR, repeated-measures ANCOVA revealed significant time× group interactions for both SBP and DBP. For SBP, significant main effects of time and group were observed, along with a robust interaction effect (P=0.001, η2=0.684), indicating that training responses differed according to baseline BP status. As illustrated in Fig. 1A, reductions were most pronounced in the S2HTN group, followed by S1HTN, whereas normotensive groups showed minimal change. In within-group analyses, SBP decreased by 7.2 mmHg (95% confidence interval [CI], −11.2 to −3.2) in the S1HTN group and by 17.2 mmHg (95% CI, −21.1 to −13.3) in the S2HTN group, whereas changes in the NBP and EBP groups were not statistically significant. Significant time×muscle mass and time×BMR interactions suggest that baseline body composition partially moderated SBP responses. For DBP, although the main effect of time was not significant, a significant group effect and time×group interaction were detected (Fig. 1B), with the greatest reductions observed in S2HTN. Within-group analysis indicated that DBP decreased by 7.3 mmHg (95% CI, −12.9 to −1.7) in the S2HTN group, whereas changes in the NBP, EBP, and S1HTN groups were not statistically significant. No significant moderating effects of muscle mass or BMR were identified. HR showed no significant main effects but demonstrated a significant time×group interaction (Fig. 1C), reflecting heterogeneous adaptations across BP categories. In contrast, respiratory rate remained relatively stable, with no significant main or interaction effects (Fig. 1D).

Comparison results of body composition

Changes in body composition variables are presented in Table 3. Repeated-measures ANCOVA adjusted for baseline muscle mass and BMR revealed no significant main effects of time, no significant group effects, and no significant time×group interactions for body weight, fat mass, BMI, body fat percentage, or WHR (all P>0.05). Although small directional changes were observed—such as modest reductions in fat mass in the EBP and S2HTN groups and slight increases in body weight in some normotensive participants—these changes were minimal in magnitude and did not differ significantly across BP categories. Percentage changes across variables generally remained within a narrow range, indicating relative stability of structural body composition over the 15-week intervention period.

Comparison results of body circumference variables

As shown in Table 4, no significant main effects of time or group, nor significant time×group interactions, were detected for abdomen, hip, upper arm, forearm, thigh, or calf circumference (all P>0.05). Although minor directional changes were observed—such as slight increases in upper and forearm girth across several groups and small reductions in abdominal circumference in S2HTN —these changes were modest in magnitude and did not significantly differ between BP categories after covariate adjustment. Percentage changes were generally small and inconsistent across groups, indicating the absence of systematic structural remodeling over the 15-week intervention period.

Comparison results of physical fitness variables

Physical fitness outcomes are presented in Table 5. Repeated-measures ANCOVA adjusted for baseline skeletal muscle mass and BMR revealed no significant main effects of time or group, and no significant time×group interactions for left or right grip strength (all P>0.05). Although mean grip strength values demonstrated modest increases across most groups, with percentage improvements generally small and comparable between categories, these changes did not differ significantly according to baseline BP status. Furthermore, no significant time×muscle mass or time×BMR interactions were identified, indicating that baseline body composition did not meaningfully moderate strength adaptations. In contrast, VO2max demonstrated a significant group effect and a significant time×group interaction, indicating heterogeneous responses across BP classifications. As shown in Table 5, improvements were primarily observed in the NBP and S2HTN groups, whereas the S1HTN group exhibited a slight decline and the EBP group showed minimal change. Despite these differential patterns, no significant moderating effects of baseline muscle mass or BMR were detected.

DISCUSSION

The present findings indicate that when identical exercise stimuli were applied, hemodynamic improvements were disproportionately greater in hypertensive participants, whereas body composition and physical fitness variables remained largely unchanged. This pattern suggests that functional regulatory mechanisms may have contributed to BP reduction, although direct mechanistic pathways were not measured in the present study.
Hypertension is characterized by chronic sympathetic overactivity, reduced parasympathetic tone, and impaired arterial baroreflex sensitivity (Grassi et al., 2009; Mancia and Grassi, 2014). Elevated sympathetic vasoconstrictor drive increases peripheral vascular resistance and sustains higher SBP levels. Regular exercise training has been shown to attenuate central sympathetic outflow through adaptations at multiple regulatory levels, including reduced activity of the rostral ventrolateral medulla and improved afferent baroreceptor signaling (Laterza et al., 2007). Restoration of baroreflex sensitivity enhances short-term BP buffering capacity and contributes to sustained reductions in resting SBP. Specifically, the marked reduction in SBP observed in the S2HTN group of this study may reflect a greater “autonomic reserve” for adaptation. Individuals with higher baseline sympathetic tone appear to exhibit amplified responsiveness to exercise-induced sympathoinhibition (Cornelissen and Smart, 2013). This phenomenon aligns with the concept of normalization rather than universal enhancement—exercise preferentially reduces elevated physiological stress states rather than lowering already optimal parameters. The absence of substantial SBP reductions in normotensive participants further supports this selective autonomic recalibration hypothesis.
Beyond neural mechanisms, exercise-induced improvements in endothelial function likely contributed to the observed hemodynamic changes. Chronic sympathetic overactivity in hypertension impairs nitric oxide bioavailability and increases arterial stiffness. Exercise enhances endothelial nitric oxide synthase activity and reduces oxidative stress, thereby decreasing total peripheral resistance (Green et al., 2004). The resulting reduction in afterload may occur independently of changes in body mass or fat distribution, explaining why significant BP improvements were detected without parallel alterations in BMI or fat mass. Post-exercise hypotension and chronic training adaptations are also linked to decreased muscle sympathetic nerve activity and improved vascular conductance (Halliwill et al., 2013). These neural-vascular interactions occur relatively rapidly and do not require substantial changes in muscle hypertrophy or fat loss. In the present study, the lack of significant alterations in muscle mass, BMI, or circumference measures suggests that structural remodeling was minimal, further reinforcing the likelihood that neural regulatory mechanisms predominated. Additionally, exercise training enhances cardiovagal modulation and reduces resting HR variability imbalance, even when maximal aerobic capacity changes are modest (Carter et al., 2003). Although direct indices of autonomic function were not measured in this study, the selective improvement in SBP and partial changes in HR patterns are physiologically consistent with improved sympathovagal balance. Collectively, the present findings suggest improvements in autonomic regulation and vascular function. Although the observed reductions in BP are consistent with potential mechanisms such as decreased sympathetic vasoconstrictor activity and enhanced baroreflex sensitivity, direct assessments of autonomic function were not performed. Consequently, these interpretations should be considered physiologically plausible explanations rather than definitive causal mechanisms. Such functional adaptations appear to precede, and may occur independently of measurable structural changes in body composition. The greater magnitude of hemodynamic improvement observed in hypertensive groups suggests that exercise acts as a corrective regulatory stimulus, restoring homeostatic autonomic control in individuals with elevated baseline sympathetic activity.
Although the present study examined improvements in hemodynamic variables following a 15-week structured body conditioning program, several limitations should be acknowledged. The lack of a nonexercise control group restricts the ability to draw definitive causal conclusions. Nevertheless, the within-subject repeated-measures design, together with covariate adjustment, increases confidence that the observed changes are more likely attributable to training-related adaptations rather than random variation. Dietary intake, sodium consumption, and sleep quality were not rigorously controlled. Additionally, direct measurements of arterial stiffness (e.g., pulse wave velocity), endothelial function, or HR variability were not obtained, limiting mechanistic insight. The large variability observed in respiratory rate percentage change may reflect measurement variability inherent to visual counting methods. Given the number of outcome variables examined, the potential for inflated type I error cannot be excluded. Although SBP and DBP were predefined as primary outcomes, multiple secondary physiological variables were analyzed. Therefore, the possibility of inflated type I error cannot be entirely excluded, and findings related to exploratory outcomes should be interpreted cautiously. Future studies may consider false discovery rate procedures to further enhance statistical rigor. Participants were volunteers enrolled in an academic body conditioning course, potentially reflecting a relatively health-conscious subgroup of young adults and introducing possible selection bias. Although dropout rates were relatively small, potential attrition bias cannot be entirely excluded. Furthermore, the present findings are limited to young university students and therefore should not be generalized to middle-aged or older adults, individuals receiving antihypertensive medication, or patients with comorbid cardiovascular conditions without caution. Future randomized controlled trials incorporating vascular biomarkers, autonomic indices, and dietary standardization are warranted to confirm and extend these findings.
In spite of the limitations, the 15-week structured body conditioning program significantly reduced systolic and diastolic BP in young adults with stage 1 and stage 2 hypertension, with the largest effects observed in those with higher baseline values. These antihypertensive adaptations occurred independently of substantial changes in body composition and were accompanied by significant improvements in muscular strength.

Notes

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

ACKNOWLEDGMENTS

The authors received no financial support for this article.

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Fig. 1
Differences of Δ% hemodynamic variables and respiratory rate. (A) Systolic blood pressure (SBP). (B) Diastolic blood pressure (DBP). (C) Heart rate (HR). (D) Respiratory rate (RR). Symbols a–c mean post hoc comparisons using the Bonferroni correction. NBP, normal blood pressure; EBP, elevated blood pressure; S1HTN, stage 1 hypertension; S2HTN, stage 2 hypertension.
jer-22-2-51f1.jpg
Table 1
Demographic features in all participants
Items Groups (n=85) H P-value η2

NBP (n=21) EBP (n=20) S1HTN (n=22) S2HTN (n=22)
Demographics
 Age (yr) 22.0±1.8 21.9±1.9 22.7±2.2 22.0±2.0 1.907 0.592 0.028
 Sex* 1.2±0.4 1.1±0.3 1.0±0.0 1.1±0.3 4.530 0.210 0.054
 Disease 1.2±0.7 1.4±1.1 1.5±1.7 1.4±1.7 0.730 0.866 0.007
 Family history 1.4±0.8 1.4±0.7 1.3±0.7 1.3±0.7 0.949 0.814 0.008
 Smoking 1.6±0.5 1.6±0.5 1.5±0.5 1.5±0.5 0.810 0.847 0.010
 Physical activity 1.3±0.5 1.2±0.4 1.1±0.4 1.2±0.4 3.210 0.360 0.038
 IPAQ (MET·hr/wk) 58.1±34.5 73.3±33.8 47.0±27.5 66.3±50.5 5.914 0.116 0.066
 Sleep duration (hr) 7.7±1.5 7.3±1.4 7.6±1.0 6.8±1.2 6.523 0.089 0.082

Anthropometrics
 Height (cm) 171.0±6.6 173.8±6.8 176.7±6.6 175.2±4.6 9.602 0.022 0.110
 Weight (kg) 67.9±11.1 72.4±11.2 77.0±13.9 75.7±11.5 6.425 0.093 0.082
 Muscle mass (kg) 28.9±7.0 33.5±5.8 35.0±5.9 34.2±5.4 9.552 0.023 0.140
 Fat mass (kg) 16.2±5.1 13.4±4.1 15.4±5.4 15.5±7.2 3.233 0.357 0.035
 BMI (kg/m2) 23.1±2.6 23.9±2.7 24.5±3.3 24.6±3.4 2.708 0.439 0.040
 Fat percentage (%) 24.2±7.7 18.4±4.8 19.6±4.2 20.1±7.7 7.252 0.064 0.110
 WHR 0.8±0.0 0.8±0.0 0.9±0.0 0.9±0.1 6.528 0.089 0.082

BMR (kcal) 1,487.2±243.3 1,645.4±205.3 1,702.0±214.6 1,671.5±188.9 9.736 0.021 0.136

Values are presented as mean±standard deviation.

NBP, normal blood pressure group; EBP, elevated blood pressure group; S1HTN, stage 1 hypertension; S2HTN, stage 2 hypertension group; IPAQ, International Physical Activity Questionnaire; MET, metabolic equivalent; BMI, body mass index; WHR, waist-to-hip ratio; BMR, basal metabolic rate.

Before the experiment, comparisons between groups were performed using the Kruskal–Wallis test.

* Coded as 1 for male and 2 for female.

Coded as 1 for nothing and 2 for having.

Coded as 1 for ‘do’ and 2 for ‘don’t.’

Table 2
Repeated-measures ANCOVA results of hemodynamic variables adjusted for baseline MS and BMR
Item Groups (n=85) ANCOVA P (η2)


NBP (n=21) EBP (n=20) S1HTN (n=22) S2HTN (n=22) T G T×G T×MS T×BMR
SBP (mmHg)
 Pre 114.3±4.7 125.7±2.4 135.5±2.4 147.2±4.0 0.040 0.001 0.001 0.017 0.020
 Post 118.9±9.9 128.0±12.7 128.3±8.4 130.0±7.8 0.052 0.684 0.471 0.070 0.066
 Δ% 4.2±9.5 1.9±11.3 −5.3±6.5 −11.7±5.2

DBP (mmHg)
 Pre 68.7±8.7 71.0±5.7 76.3±8.3 80.3±10.6 0.190 0.001 0.007 0.168 0.171
 Post 70.5±8.0 72.2±9.7 73.3±8.2 73.0±9.1 0.022 0.187 0.141 0.024 0.024
 Δ% 3.8±15.1 1.9±13.4 −3.3±11.1 −8.1±12.6

Heart rate (bpm)
 Pre 81.8±15.0 74.1±12.8 79.6±11.6 83.4±13.3 0.236 0.054 0.007 0.240 0.241
 Post 74.8±10.4 75.8±14.9 83.1±10.1 78.5±13.5 0.018 0.092 0.142 0.017 0.017
 Δ% −6.9±14.1 2.9±14.3 5.5±13.8 −5.1±13.7

Respiratory rate (reps)
 Pre 20.0±4.4 20.7±5.7 22.1±7.5 23.2±6.2 0.217 0.055 0.826 0.212 0.214
 Post 20.3±5.5 19.5±6.4 22.1±8.4 21.3±6.1 0.019 0.055 0.011 0.020 0.019
 Δ% 4.0±27.5 −3.0±28.3 9.0±52.1 −6.9±16.3

Values are presented as mean±standard deviation.

ANCOVA, analysis of covariance; MS, muscle mass; BMR, basal metabolic rate; SBP, systolic blood pressure; DBP, diastolic blood pressure; NBP, normal blood pressure group; EBP, elevated blood pressure group; S1HTN, stage 1 hypertension group; S2HTN, stage 2 hypertension group; T, time; G, group.

Table 3
Repeated-measures ANCOVA results of body composition adjusted for baseline MS and BMR
Item Group (n=85) ANCOVA P (η2)


NBP (n=21) EBP (n=20) S1HTN (n=22) S2HTN (n=22) T G T×G T×MS T×BMR
Weight (kg)
 Pre 67.9±11.1 72.4±11.2 77.0±13.9 75.7±11.5 0.659 0.487 0.738 0.639 0.646
 Post 67.8±11.5 72.4±11.7 77.8±14.9 75.9±11.0 0.002 0.030 0.016 0.003 0.003
 Δ% −0.3±3.0 −0.0±3.8 0.9±4.4 0.5±4.0

Fat mass (kg)
 Pre 16.2±5.1 13.4±4.1 15.4±5.4 15.5±7.2 0.787 0.468 0.621 0.834 0.830
 Post 16.0±5.4 12.7±5.0 15.0±5.5 14.4±7.3 0.001 0.031 0.022 0.001 0.001
 Δ% −1.0±12.7 −6.1±21.4 −2.1±12.8 −7.4±13.6

 Pre 23.1±2.6 23.9±2.7 24.5±3.3 24.6±3.4 0.648 0.721 0.498 0.651 0.652
 Post 23.0±2.8 23.9±2.9 24.9±3.5 24.6±3.4 0.003 0.017 0.029 0.003 0.003
 Δ% −0.3±3.2 0.1±4.0 1.3±2.9 0.2±3.9

BMI (kg/m2)
 Pre 24.2±7.7 18.4±4.8 19.6±4.2 20.1±7.7 0.782 0.358 0.607 0.864 0.853
 Post 23.8±7.5 17.5±6.0 18.8±4.3 18.6±8.0 0.001 0.040 0.023 0.001 0.001
 Δ% −0.9±11.3 −6.1±20.0 −3.6±11.5 −7.9±11.7

WHR
 Pre 0.8±0.0 0.8±0.0 0.9±0.0 0.9±0.1 0.671 0.243 0.509 0.838 0.794
 Post 0.8±0.0 0.8±0.1 0.9±0.1 0.9±0.1 0.002 0.051 0.029 0.001 0.001
 Δ% 0.0±3.6 −0.6±6.8 −0.5±3.0 −1.6±3.7

Values are presented as mean±standard deviation.

ANCOVA, analysis of covariance; MS, muscle mass; BMR, basal metabolic rate; NBP, normal blood pressure group; EBP, elevated blood pressure group; S1HTN, stage 1 hypertension group; S2HTN, stage 2 hypertension group; T, time; G, group; BMI, body mass index; WHR, waist-to-hip ratio.

Table 4
Repeated-measures ANCOVA results of body circumference adjusted for baseline MS and BMR
Item Group (n=85) ANCOVA P (η2)


NBP (n=21) EBP (n=20) S1HTN (n=22) S2HTN (n=22) T G T×G T×MS T×BMR
Abdomen girth (cm)
 Pre 78.7±9.0 78.4±7.4 82.8±8.7 81.7±10.0 0.123 0.074 0.363 0.134 0.131
 Post 79.2±9.3 78.5±8.6 84.7±8.4 80.9±8.7 0.030 0.084 0.039 0.028 0.029
 Δ% 0.8±6.6 0.2±5.4 2.5±7.0 −0.5±6.8

Hip girth (cm)
 Pre 96.9±4.7 97.3±6.0 99.1±6.7 99.1±9.2 0.500 0.052 0.649 0.489 0.495
 Post 98.3±5.6 97.3±6.4 100.3±7.2 99.3±5.6 0.006 0.052 0.021 0.006 0.006
 Δ% 1.5±3.5 0.1±3.6 1.3±4.7 0.7±7.8

Upper arm girth (cm)
 Pre 28.5±3.8 31.0±3.2 31.8±4.1 31.4±5.2 0.868 0.681 0.599 0.899 0.899
 Post 28.6±3.6 32.0±4.4 32.3±4.0 33.0±4.4 0.001 0.019 0.023 0.001 0.001
 Δ% 1.0±6.9 3.2±8.8 2.2±10.2 6.2±12.3

Forearm girth (cm)
 Pre 24.5±3.7 26.5±2.5 26.5±2.4 26.6±2.6 0.272 0.406 0.820 0.245 0.254
 Post 24.5±2.9 26.8±2.9 26.8±2.6 27.5±2.2 0.015 0.036 0.012 0.017 0.016
 Δ% 0.8±10.2 1.1±7.7 1.2±8.3 3.7±9.8

Thigh girth (cm)
 Pre 51.3±5.7 54.5±4.1 55.0±4.1 53.5±5.8 0.209 0.842 0.517 0.218 0.214
 Post 51.3±4.7 53.8±6.4 54.2±5.4 54.4±4.3 0.020 0.010 0.028 0.019 0.019
 Δ% 0.6±7.3 −1.4±7.6 −1.3±7.2 2.3±8.3

Calf girth (cm)
 Pre 37.1±4.3 38.1±3.6 38.4±3.4 38.8±3.5 0.113 0.787 0.672 0.123 0.120
 Post 37.4±2.8 38.2±3.8 39.1±3.4 38.7±3.8 0.031 0.013 0.019 0.030 0.030
 Δ% 1.5±8.5 0.5±7.4 1.8±4.4 −0.2±6.1

Values are presented as mean±standard deviation.

ANCOVA, analysis of covariance; MS, muscle mass; BMR, basal metabolic rate; NBP, normal blood pressure group; EBP, elevated blood pressure group; S1HTN, stage 1 hypertension group; S2HTN, stage 2 hypertension group; T, time; G, group.

Table 5
Repeated-measures ANCOVA results of physical fitness adjusted for baseline MS and BMR
Item Group (n=85) ANCOVA P (η2)


NBP (n=21) EBP (n=20) S1HTN (n=22) S2HTN (n=22) T G T×G T×MS T×BMR
Left grip strength (kg)
 Pre 32.8±9.9 39.3±7.7 41.9±6.6 42.0±7.7 0.854 0.389 0.301 0.920 0.999
 Post 34.3±10.3 41.7±8.2 42.5±8.8 43.6±8.9 0.001 0.037 0.045 0.001 0.001
 Δ% 5.3±11.3 6.3±8.6 1.5±11.7 3.8±9.4

Right grip strength (kg)
 Pre 34.5±10.7 42.6±8.4 44.3±6.8 44.7±9.0 0.292 0.250 0.874 0.320 0.317
 Post 35.9±10.7 43.3±8.1 45.7±6.7 45.8±9.7 0.014 0.050 0.009 0.012 0.013
 Δ% 5.1±11.4 2.4±11.1 3.8±9.5 2.8±9.8

VO2max (mL/kg/min)
 Pre 37.2±6.8 40.8±6.1 37.6±5.3 36.3±6.3 0.172 0.023 0.017 0.972 0.929
 Post 40.1±5.1 40.2±7.1 35.8±3.9 38.6±6.4 0.023 0.113 0.120 0.001 0.001
 Δ% 9.7±15.6 −1.1±13.8 −3.7±12.3 7.5±15.9

All data represents mean±standard deviation.

ANCOVA, analysis of covariance; MS, muscle mass; BMR, basal metabolic rate; NBP, normal blood pressure group; EBP, elevated blood pressure group; S1HTN, stage 1 hypertension group; S2HTN, stage 2 hypertension group; T, time; G, group; VO2max, maximum oxygen uptake.

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