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Original Research

Effects of a 12-Week Resistance Training Program on Arterial Stiffness: A Randomized Controlled Trial

Werner, Timothy J.; Pellinger, Thomas K.; Rosette, Vincent D.; Ortlip, Austin T.

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Journal of Strength and Conditioning Research: December 2021 - Volume 35 - Issue 12 - p 3281-3287
doi: 10.1519/JSC.0000000000003331
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Resistance training is popular, and modalities for it are commonly found in fitness centers across the world. Support for the use of resistance training comes from key recommendations developed by influential scientific committees and associations (18,22). Current guidelines suggest that healthy adults participate in strength training activities for at least 2 days a week using moderate-to-high training intensities. These recommendations are based on findings that chronic resistance training improves indices for blood pressure (BP) (27,42), insulin sensitivity (3), body composition (51), balance (21), and bone and skeletal muscle strength (57). However, its impact on other markers for cardiovascular health remains unclear.

Arterial stiffness is a strong predictor of cardiovascular disease risk (36). Identifying and characterizing stimuli that accelerate arterial stiffness and developing therapeutic strategies to delay stiffening have gained popularity in recent years. Arterial stiffness is strongly correlated with age (37), and arterial “aging” is accelerated by numerous behaviors, such as smoking (25), alcohol abuse (35), sleep deprivation (10), inactivity (45), and poor dietary patterns (58). However, aerobic exercise has consistently shown to attenuate age-associated arterial stiffening in otherwise-healthy adults (32,41). However, what is less understood is the overall impact of resistance training on age-associated arterial stiffening. Discrepancies exist within the literature on the relationship between chronic resistance training and the progression of arterial stiffness. Specifically, some (9,12,19,27,56,59), but not all (13,30,40,47), studies support exercise prescriptions with strength training activities for maintaining and improving cardiovascular health. Recent reviews (20,32) and meta-analyses (17,38) have indicated methodological issues between studies that may help to explain some of the variations across studies, such as differences in training durations, volumes, and intensity, and differences in arterial stiffness measurement techniques. In addition, it is worth mentioning that previous investigations have other methodological issues. For example, many studies did not include a full-body strength training routine, whereas others did not include a control group or a randomization process. Finally, in some studies, aerobic training was permitted during the resistance training period. This is an important issue because cardiorespiratory exercise plus strength training, otherwise known as combination training, has been shown to improve indices of arterial stiffness in several reports (32,60). Therefore, the aim of the current study was to investigate the influence of a 12-week high-intensity (HI) or high-volume (HV) training program following the guidelines of the National Strength and Conditioning Association (NSCA) (23) on several indices of arterial stiffness.


Experimental Approach to the Problem

The current study was designed to examine and compare the effects of a 12-week HI and HV resistance training program on arterial stiffness in young men. It was hypothesized that resistance training, irrespective of training regimen, would not have a clinically significant influence on arterial stiffness. To test these hypotheses, untrained subjects underwent HI and HV training consistent with the guidelines from the NSCA (23), or refrained from any physical activity for the duration of the study, which included cardiovascular training. One repetition maximum (1RM) for bench press, back squats, and seated row, body composition, seated and supine BP acquisition, carotid ultrasonography, and arterial tonometry were performed on every subject at baseline and after the study.


A total of 30 subjects, aged 18–30 years, volunteered and participated in this study from 38 individuals who were initially screened. Only men were recruited for the study to control for the potential sex-related differences. Young women have different baseline arterial stiffness values than male counterparts (37), potentially causing differences in primary outcomes (4). For instance, young women have higher augmentation indices adjusted to a heart rate of 75 b·min−1 (AIx75) while at rest (26). Furthermore, recent studies have examined potential sex-related differences with exercise. A previous investigation found acute bouts of exercise reduced pulse wave velocity (PWV) in young men only (53). A similar study reported greater reductions in aortic BP and greater increases in AIx75 only in the young male subjects (16). In addition, 4 weeks of resistance training decreased PWV by 17% in young men, but it had no effect on PWV in young women (11).

All subjects were not hypertensive and free from acute diseases. The subjects were not on any medications or supplements that may have influenced the dependent variables of the study. All subjects were weight stable (±2 kg) for at least 6 months before starting the study and had less than 6 months of resistance training experience with no differences in subject characteristics between groups (Table 1). Subjects completed a health history questionnaire and provided written informed consent before joining the study. The Salisbury University Institutional Review Board approved all study protocols.

Table 1 - Subject characteristics before and after the intervention.*
Variable Control (N = 10) High-volume group (N = 10) High-intensity group (N = 10)
Pre Post Pre Post Pre Post
Age (y) 21.2 ± 2.8 NA 20.9 ± 3.2 NA 22.9 ± 2.9 NA
Height (cm) 179.5 ± 6.2 NA 179.7 ± 4.0 NA 173.1 ± 7.7 NA
Body mass (kg) 68.1 ± 9.2 68.4 ± 10.2 77.6 ± 15.3 78.2 ± 13.9 79.6 ± 19.1 81.6 ± 19.7
BMI (kg·m−2) 21.0 ± 2.2 21.2 ± 2.6 24.1 ± 5.1 24.3 ± 4.7 26.5 ± 6.3 27.2 ± 6.6
Body fat (%) 11.8 ± 3.9 12.2 ± 4.6 15.3 ± 7.5 14.9 ± 7.3 19.7 ± 9.7 19.5 ± 10.2
Fat mass (kg) 8.1 ± 3.3 8.5 ± 4.1 12.7 ± 8.1 12.4 ± 7.6 17.3 ± 12.5 17.6 ± 13.3
Fat-free mass (kg) 60.0 ± 7.5 59.9 ± 8.0 64.9 ± 9.1 65.8 ± 8.2 62.3 ± 7.5 63.9 ± 7.4
Resting HR (b·min−1) 63 ± 8 62 ± 7 64 ± 5 62 ± 8 65 ± 8 64 ± 6
Seated systolic BP (mm Hg) 116 ± 9 123 ± 10 122 ± 13 123 ± 10 123 ± 11 122 ± 8
Seated diastolic BP (mm Hg) 72 ± 9 75 ± 6 75 ± 7 74 ± 6 74 ± 8 73 ± 6
Seated MAP (mm Hg) 86 ± 8 91 ± 7 90 ± 8 90 ± 7 90 ± 8 89 ± 6
Supine systolic BP (mm Hg) 120 ± 10 119 ± 9 124 ± 11 122 ± 8 123 ± 11 117 ± 7
Supine diastolic BP (mm Hg) 69 ± 6 69 ± 5 71 ± 7 68 ± 5 71 ± 7 68 ± 5
Supine MAP (mm Hg) 86 ± 7 86 ± 5 88 ± 7 86 ± 5 87 ± 8 84 ± 6
*BMI = body mass index; HR = heart rate; BP = blood pressure; MAP = mean arterial pressure.
Values expressed as mean ± SD.
p < 0.05 interaction effect.

Study Design and Protocol

After subjects completed the baseline testing, they were randomly assigned to control (CON; n = 10), HV (n = 10), or HI (n = 10) groups. All subjects were instructed to maintain their normal dietary intake and provided detailed 3-day diet records at baseline and follow-up. Subjects were instructed on procedures for measuring and recording food intake on 2 weekdays and 1 weekend day. The Dietary Analysis Plus (Cengage Learning, Independence, KY) was used to determine differences in energy intake, macronutrient composition, and sodium intake of each individual's diet (data not shown). Subjects in the CON group were instructed to avoid any exercise training during the study period and provided activity logs throughout the study. Subjects in the HV group performed 3–4 sets of 10–15 repetitions at 50–70% of their 1RM to volitional fatigue. Subjects in the HI group performed 2–3 sets of 3–8 repetitions at 80–90% of their 1RM to volitional fatigue. All subjects initially trained at the lower end of the repetition and load range and progressed to higher repetitions and training loads over the 12-week period. The 2-for-2 rule (23) was used to readjust training intensities based on strength gains over the course of the training period in both groups to ensure that subjects performed repetitions to failure within their designated range. Briefly, the 2-for-2 rule is a method that indicates when additional weight should be added to the exercise. Extra weight was added in the following training session if subjects were able to perform 2 additional repetitions above the goal during the last set in 2 consecutive workouts. All assessments were completed within 1 week before and 1 week after the study period. All vascular assessments were performed in the Salisbury University Human Physiology Laboratory between the 08:00 and 11:00 hours after a 12-hour fast. All strength assessments were completed in the Salisbury University Maggs Center weight room between 09:00 and 14:00 hours. Every subject refrained from tobacco use and caffeinated products for 12 hours and exercise for 24 hours before the testing sessions.

The HV and HI groups used the same training exercises including machine-guided back squats, flat bench press, seated rows, machine-guided shoulder press, bicep curls, triceps extension, standing calf raises, seated leg curls, and seated leg extension. Both groups performed all the exercises 3 times a week for the first 2 weeks with at least 1 day of rest between workouts. The training days were then divided into upper- (flat bench press, seated rows, shoulder press, biceps curls, and triceps extensions) and lower- (back squats, standing calf raises, seated leg curls, and seated leg extensions) body exercises. Subjects performed upper-body exercises 2–3 days a week and lower-body exercises 2–3 days a week for the next 10 weeks. Each subject was trained and supervised by a certified strength and conditioning specialist and was instructed to use proper form and full range of motion. Subjects recorded repetitions of each set. Individual training loads were adjusted to pace the progression based on variations in the weekly training outcomes. High-volume and HI subjects were instructed to avoid cardiovascular training for the duration of the treatment period and provided activity logs throughout the study to ensure compliance.


One Repetition Maximum Protocol

All subjects completed baseline and follow-up 1RM assessments in the same order: back squat, bench press, and seated row. The 1RM tests conformed to NSCA's regulations and guidelines (23).

Pulse Wave Velocity

Noninvasive pulse tonometers (Complior Analytic Tonometer; Alam Medical, Vincennes, France) were used to simultaneously obtain arterial pressure waveforms at the carotid, radial, and femoral arteries throughout 10 cardiac cycles. Surface distance between the carotid and femoral sites was calculated using a measuring tape to the nearest 0.5 centimeter. This process was repeated to measure arterial pressure waveforms at the carotid and radial arteries. Pulse wave velocity for the carotid-femoral (aortic PWV) and carotid-radial (brachial PWV) recordings was determined by normalizing the waveform foot-to-foot time delay to the distance between recording sites (PWV = D (cm)/Δt (sec)). Subjects remained supine for at least 10 minutes before measurements and stayed exactly as they were positioned during the tonometry acquisition sequence.

Arterial Applanation Tonometry

The carotid arterial pressure waveform and amplitude was obtained from the common carotid artery with a probe incorporating a high-fidelity strain gauge transducer (Complior Analytic Tonometer; Alam Medical). The pressure signal obtained by tonometry was calibrated by equating the carotid mean arterial pressure to the brachial artery measurement with mercury sphygmomanometry, using the transfer function. Briefly, this transfer function uses supine brachial systolic and diastolic pressure along the carotid waveforms to calculate carotid or central BP.

β-Stiffness Index

β-Stiffness index was the primary outcome in this study. In contrast to other indices, β-stiffness index is a BP-independent index of central arterial stiffness. High-resolution Doppler ultrasound was used to measured common carotid artery diameters (see below), and applanation tonometry was used to measure carotid BP (see above). β-Stiffness index is calculated as: β = (log P1/P0)/((D1 − D0)/D0), where D0 is the smallest diameter, D1 is the maximal diameter, P0 is the lowest pressure, and P1 is the maximal pressure over the cardiac cycle. The β index is expressed in arbitrary units.

Carotid Artery Ultrasonography

Left common carotid artery diameters were assessed using a Doppler ultrasound unit (Philips Sonos 4500 ultrasound system; Philips North America Corporation. Andover, MA) equipped with a linear ultrasound probe (Philips 11-3L Ultraband trapezoidal linear-array vascular transducer; Amsterdam, Netherlands) placed approximately 2 cm proximal to the bifurcation. Longitudinal B-mode images of the artery were acquired during systole and diastole, and measurements of minimal and maximal artery diameters were taken in triplicate. Diameters were measured as the distance from the intima-lumen interface of the near wall to the lumen-intima interface of the far wall.

Resting Seated and Supine Blood Pressure

Recordings were made under quiet, comfortable ambient (∼24° C) laboratory conditions. All BP measurements conformed strictly to American Heart Association guidelines (5). Briefly, measurements were made by auscultation over the brachial artery using an automated sphygmomanometer (Welch Allyn, New York) after a 5–10-minute rest period in the seated or supine position. The first phase and fifth phase of the Korotkoff sounds were used to determine systolic and diastolic BP, respectively. Blood pressure was measured every 2 minutes and averaged and recorded when systolic and diastolic BPs were within 6 mm Hg on 3 consecutive measurements.

Body Mass and Composition

Body mass was measured on a scale (Detecto 439 Physician Beam Scale; Detecto, Webb City, MO) accurate to ±0.1 kg before breakfast and after attempting to void. Subjects wore standard shorts and T-shirts at the time of weighing. Body height was measured with a stadiometer (Detecto 439 Physician Beam Scale). Total fat and fat-free mass were measured in all subjects using skinfold calipers. A total of 7 skinfold sites including chest, triceps, subscapular, suprailiac, abdominal, thigh, and calf were measured on the right side of the body following the guidelines described elsewhere (2). The sum of the skinfold thicknesses was used to calculate body density from the 7-site formula (2).

Statistical Analyses

All statistical analyses were conducted with SPSS (IBM SPSS version 24; SPSS Inc., Chicago, IL). A mixed-model 3 × 2 repeated-measures analysis of variance was used to examine the between- and within-group (CON vs. HI vs. HV) differences for dependent variables of interest and time (pre-intervention vs. post-intervention). Post hoc analyses were performed on significant F-ratios with Tukey's honestly significant difference. All data are expressed as mean ± SD with 95% confidence intervals (CIs). The standardized mean differences (Cohen's d) were calculated, and threshold values were reported as: 0.2–0.6, small; 0.6–1.2, moderate; 1.2–2.0, large; and 2.0–4.0, very large (28). The level of significance was set a priori at p ≤ 0.05.


Arterial stiffness variables for baseline and after the intervention are listed in Tables 1 and 2. There were no significant baseline differences in any of the anthropometric data or in any indices for PWV, peripheral BP, central BPs, β-stiffness index, and arterial compliance between the groups (all p > 0.05). There was a baseline difference in bench press performance between the CON, and the HI and HV groups (p < 0.05), which is listed in Table 3.

Table 2 - Stiffness variables before and after the intervention.*
Variable Control (N = 10) High-volume group (N = 10) High-intensity group (N = 10)
Pre Post Pre Post Pre Post
C-F PWV (m·s−1) 6.6 ± 0.9 6.6 ± 0.9 6.5 ± 0.8 6.9 ± 1.5 7.0 ± 2.1 8.0 ± 1.7
C-R PWV (m·s−1) 9.4 ± 2.1 9.8 ± 2.0 9.2 ± 1.0 9.3 ± 3.2 9.7 ± 2.1 10.7 ± 1.4
Central systolic BP (mm Hg) 118 ± 12 117 ± 11 123 ± 10 122 ± 14 116 ± 11 110 ± 16
Central diastolic BP (mm Hg) 69 ± 6 69 ± 5 71 ± 8 68 ± 5 71 ± 7 68 ± 5
Central MAP (mm Hg) 85 ± 6 85 ± 5 88 ± 7 88 ± 9 86 ± 8 82 ± 8
Central PP (mm Hg) 48 ± 13 47 ± 8 53 ± 11 54 ± 13 47 ± 10 40 ± 9
β-SI (U) 7.26 ± 4.44 6.36 ± 3.12 6.54 ± 1.94 6.54 ± 2.1 6.1 ± 3.26 5.33 ± 2.64
AC (mm2·mm Hg × 10−1) 0.012 ± 0.006 0.011 ± 0.003 0.012 ± 0.004 0.011 ± 0.003 0.016 ± 0.009 0.017 ± 0.009
*C = carotid; F = femoral; R = radial; PWV = pulse wave velocity; BP = blood pressure; MAP = mean arterial pressure; PP = pulse pressure; β-SI = β-stiffness index; AC = arterial compliance.
Values expressed as mean ± SD.

Table 3 - Maximal strength at baseline and after the intervention.*
Variable Control (N = 10) High-volume group (N = 10) High-intensity group (N = 10)
Pre Post Pre Post Pre Post
Back-squat 1RM (kg)§ 77.0 ± 23.9 80.7 ± 23.3 82.3 ± 35.9 103.0 ± 38.3 81.1 ± 16.6 112.7 ± 10.7
Bench press 1RM (kg)§ 54.5 ± 14.4 54.0 ± 17.1 70.0 ± 31.6 84.5 ± 32.4 66.1 ± 13.6 83.2 ± 13.3
Seated row 1RM (kg)§ 58.3 ± 14.7 57.8 ± 14.5 69.1 ± 20.9 77.7 ± 22.9 65.9 ± 5.8 78.2 ± 7.6
*1RM = 1 repetition maximum.
Values expressed as mean ± SD.
p < 0.05 time effect.
§p < 0.05 interaction effect.
Baseline difference with control (p < 0.05).

After the intervention, there were no significant changes in body mass, body fat percent, fat mass, and fat-free mass between the groups (all p > 0.05). However, the HI group experienced a significant increase in body mass index compared with the CON group (mean, 27.8; 95% CI 20.6–34.9, vs. mean, 20.9; 95% CI 19.4–22.5, respectively; p < 0.05, effect size [ES] = 1.2). There were no significant changes in heart rate, seated and supine resting BPs, and mean arterial pressures between the groups (all p > 0.05).

After the intervention, both the HI and HV groups significantly increased their maximal back squat (mean, 112.7; 95% CI 100.0–124.0, ES = 1.76, vs. mean, 103.0; 95% CI 81.9–113.6, ES = 0.7, respectively; p < 0.05), bench press (mean, 83.2; 95% CI 71.7–99.0, ES = 1.89, vs. mean, 84.5; 95% CI 57.9–95.5, ES = 1.18, respectively; p < 0.05), and seated row (mean, 78.2; 95% CI 60.1–86.4, ES = 1.75, vs. mean, 84.5; 95% CI 52.3–90.9, ES = 1.04, respectively; p < 0.05), respectively, from baseline and compared with the CON group. There were no significant differences in the strength improvements between the HI and HV groups (all p > 0.05). The CON group did not experience any significant changes in the maximal back squat, bench press, and seated row after the study period (all p > 0.05).

After the intervention, there were no significant differences in variables for PWV (Table 1 and Figure 1), central systolic and diastolic BPs (Table 1), central mean arterial and pulse pressure (PP) (Table 1), β-stiffness index (Table 2), and arterial compliance (Table 2) between and within the groups (all p > 0.05).

Figure 1.:
The percent change of CF PWV after 12 weeks of conditioning. C = carotid; F = femoral; PWV = pulse wave velocity. *p < 0.05 time effect.


This study shows that indices for arterial stiffness were unaffected by 12 weeks of resistance training regardless of training volume or intensity in untrained, healthy men. These findings are comparable with some (6,9,56), but not all (8,39,40,47), previous studies. The differences between the current training programs and the ones used in previous studies may explain some of the disparate results. Many previous studies used fewer exercises (9,50), higher sets (13), or lower training frequencies (49,64), all of which are not commonly recommended for optimal muscular strength and size gains (23). Another important attribute of the study was controlling for cardiovascular training in all groups, including CON, during the study period. Most of the previous studies did not control for additional activity. It is well known when strength and endurance training are combined, the beneficial effects of cardiovascular training recuse the vascular system from potentially negative side effects of resistance training (4,30,41,48). This is thought to occur through improved endothelial expression of nitric oxide synthase (15), increased blood flow (29), and shear stress (46). Thus, the previous findings are subject to interpretation. Our findings support the theory that arterial compliance remains uncompromised following a chronic strength and conditioning protocol, even in the absence of cardiovascular training. Indeed, the results have potential important clinical implications, as current physical activity guidelines endorse the use of resistance training in all healthy populations (24,43,63).

Our finding that both HV and HI protocols significantly increase maximal strength is consistent with other studies using similar training durations, volumes, and intensity, thus supporting the effectiveness of the training protocols (6,56). Subjects were instructed to avoid participating in any additional training, including resistance training, beyond the weekly prescribed routines. Adherence to the protocols was ∼96% based on the training logs.

Chronic resistance training is speculated to augment arterial stiffness through a sympathetic adrenergic vasoconstrictor effect (54,55) and by increased exposure to higher, intermittent central BPs that would stimulate collagen development and fibrosis in and around the central arteries (33,44). Blood pressure during each set of resistance training has been found to be as high as 320/250 mm Hg (34). This abrupt change in both the anatomy and physiology of the vessel would strengthen the integrity of the walls, while at the same time limit the amount of expansion and recoil during systole and diastole, respectively. As a result, central systolic pressures should increase, whereas central diastolic pressure should decline after a period of training. The current study shows no significant changes in central BP over time and between groups. A logical argument could be made that the treatment duration was not long enough to experience such a change (61). This is why an untrained population was selected for the study. This population was found to be more susceptible to the stiffening process because of their limited exposure to such stimuli (40). In fact, mean arterial pressure showed a downward, albeit nonsignificant, trend in the highest intensity group.

The differences between the present findings and that of others may be due to the techniques used to assess arterial changes. The use of central PWV, the gold-standard measurement for systemic arterial stiffness (31,62), and β-stiffness index, a BP-independent, local measurement of arterial stiffness, both confirmed the absence of any clinically significant changes to vascular compliance. An increase of 1 m·s−1 in PWV translates into a 7% increase in cardiovascular disease risk (7) and was reported in several other trials (11,14,50). However, many of the previous studies did not account for both these indices, and this could explain some of the discrepancies between the findings (12,40). Our results show an increasing trend in CF PWV in the HI group; however, it never reached the level of significance (p = 0.09). β-Stiffness index was reduced to 5.33 U in the HI group, possibly indicating an impact of BP on the central PWV. Furthermore, central PP was significantly increased in the HV group. It is unclear why this occurred but has been reported elsewhere (8). Possible mechanisms for the increase in central PP include alterations in angiotensin II and vasopressin and increased sympathetic activity to the kidneys and arterial media. Further research is needed to help address these discrepancies.

Several limitations warrant consideration. First, because of the dynamics of a particular academic semester, our treatment duration of 12 weeks may not have been long enough to evoke clinically significant changes in indices of arterial stiffness. Few others had extended study periods and found opposing results (12,40). Second, only young, healthy men were included in this study. Care must be taken when attempting to extrapolate these results to women, other age groups, and those suffering from chronic disease. Finally, although the ergogenic supplementation and anabolic steroid use were screened for at the beginning of the study, we were unable to confirm no history of use. Some nutritional supplements have minimal-to-no effect on arterial stiffness; however, little research has been conducted on many of the ergogenic supplements and is a potential area of research (52). Anabolic steroid abuse is a known contributor to vascular pathologies, and the progression of stiffness is associated with duration of use (1).

In conclusion, 12 weeks of muscular strength training does not appear to increase arterial stiffness in young, otherwise-healthy, untrained men. Although previous studies have shown negative effects of resistance training on indices of arterial stiffness, our results indicate no significant effects on vascular profiles from both HI and HV programs. Therefore, resistance training can be used safely alone or as part of a balanced exercise program. Further research is needed to uncover the interactions between longer duration programs and periodization models.

Practical Applications

The current results suggest that resistance training, independent of load and volume, has minimal impact on indices of arterial stiffness. As a result, resistance training protocols should continue to be used in the development and maintenance of cardiovascular health. It is important to note these protocols can be applied with or in the absence of cardiorespiratory exercise training without any impetus on vascular compliance. Thus, clinicians and practitioners can safely apply these protocols to healthy clientele.


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central arterial blood pressure; pulse wave velocity; beta-stiffness index; resistance exercise

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