Current guidelines of the American College of Sports Medicine/American Heart Association for physical activity and public health recommend moderate- to high-intensity resistance exercise training (RET) activities be performed at least 2 d·wk−1 to achieve health benefits separate from those achieved with aerobic activity (13). These evidence-based recommendations are supported by a substantial body of work showing the benefits of RET on muscular strength (24), reductions in bone loss (2), and improvements in glycemic control (17). Although evidence exists for the beneficial effects of RET on resting blood pressure (15) and body composition (37), its role in the improvement of other indices of cardiovascular health is less clear.
Various “nontraditional” arterial health indicators, such as central arterial stiffness, have emerged as being predictive of cardiovascular disease (CVD) risk (18,39). Aerobic exercise training can improve indices of arterial structure and function (12); however, the effect of RET on arterial stiffness is controversial, with studies reporting increases (6,19,27,31), decreases (30), or no change (4,5,15,32,35,42) after RET. A recent meta-analysis (26) and review (21) highlighted potential reasons for these inconsistent results, including the variation in training protocols and methods for determining arterial stiffness. It was suggested that in particular, young males with low baseline arterial stiffness may be susceptible to unfavorable arterial adaptations with RET (27), whereas older individuals (5) or those undertaking moderate-intensity RET protocols (42) do not experience RET-associated changes in arterial stiffness. Despite these conclusions, the original observations that RET leads to unfavorable changes in arterial stiffness profiles (27) have not since been replicated using criterion-standard measurement of arterial stiffness or different resistance exercise per repetition load.
The influence of RET load on the regulation of arterial stiffness has not been studied in depth; however, it has been suggested that heavier loads (i.e., 80% one-repetition maximum [1RM]), but not moderate loads (i.e., 50%–70% 1RM), are associated with increases in arterial stiffness (26). In comparison to these protocols, we (25,28) and others (36) have investigated lighter-load, higher-repetition (HR; 20–25 reps) RET regimes and shown similar gains in muscle mass and strength compared with heavier-load, lower-repetition (LR) protocols. It is, however, unknown if these HR RET protocols would generate changes in arterial stiffness due to an altered pressor response during exercise.
We aimed to investigate changes in arterial stiffness, using criterion-standard techniques, in response to RET protocols using LR versus HR training in young men. As previous studies have suggested that untrained males with low arterial stiffness may be more susceptible to unfavorable effects (27), we chose to study previously trained young males with normal arterial stiffness in an effort to address the role of this potential bias in the baseline arterial profile on our criterion outcomes. We hypothesized that although traditional LR training would elicit increases in arterial stiffness, the HR training would yield no changes in arterial stiffness.
Forty-six healthy, active males who had been RET for at least the past 2 yr (engaging in RET more than two sessions per week, including at least one lower body session) volunteered to participate in this study. Participants were excluded if they were obese (body mass index [BMI] ≥ 30 kg·m−2), had a history of smoking, or were taking supplements other than protein (e.g., NSAIDS, antioxidants) before starting the training protocol. The study protocol was submitted to, and approved by, the Hamilton Integrated Research Ethics Board (REB no. 14–333) and conformed to the Declaration of Helsinki concerning the use of humans as research participants. The trial was registered at https://clinicaltrials.gov/ as NCT02842593. All participants gave verbal and written consent before participation in the study.
Thirty-two participants (all reported excellent health, as assessed by standardized medical questionnaires, were nonsmokers and were free of medication, including over-the-counter medication, use) completed 12 wk of whole-body RET in a between-groups repeated-measures design, as previously described (28). Participants were randomized into one of three groups: the HR group (n = 16) performed three sets of 20–25 repetitions per set (~30%–50% of 1RM) to volitional failure; the LR group (n = 16) performed three sets of 8–12 repetitions per set (~75%–90% of 1RM) to volitional failure; and the control group (CON; n = 14) was matched for baseline fat-free mass (FFM), BMI, and strength. Muscle strength (via 1RM testing) was reassessed at weeks 4, 7, and 10 to adjust load to ensure the progression of the RET stimulus and that participants “failed” within their designated repetition range. Controls were instructed to maintain their physical activity, including RET, for a period of 12 wk. Vascular assessments for all groups (HR, LR, and CON) were completed 1 wk before and 1 wk after the intervention period (>72 h after the last training session) after an overnight fast refraining from caffeine, alcohol, and moderate-to-vigorous physical activity (including 1RM testing) >12 h before the study visit.
Resistance training protocol
The resistance exercise protocol consisted of three sets of five exercises per session that targeted all major muscle groups. Training sessions included two supersets (i.e., exercises performed in succession with no rest between exercises) and one single set, with 1-min rest periods in between each set or superset. Sets were performed until volitional failure and load was adjusted between sets to keep participants “failing” within their designated repetition range. Each workout was repeated twice per week as follows: inclined leg press, seated row, bench press, cable hamstring curl, and front planks (Monday and Thursday) and machine-guided shoulder press, bicep curls, triceps extension, wide grip pull downs, and machine-guided knee extension (Tuesday and Friday). Each participant was individually supervised by a researcher to ensure volitional failure was achieved with good exercise form. During the RET intervention, participants were asked to refrain from additional RET as well as aerobic exercise training. In addition to exercise training, participants consumed 30 g of whey protein (BioPRO, Davisco Foods International, Le Sueur, MN) twice per day. On training days, the first 30 g was ingested immediately after exercise and the second presleep. On nontraining days, participants consumed the first 30 g in the morning and the second presleep.
All participants refrained from eating >4 h, consuming alcohol and caffeine for >10 h, and exercising for >24 h before all vascular assessments. Measurements were taken in the supine position after a 10-min rest period. Single-lead ECG (PowerLab model ML 795; AD Instruments, Colorado Springs, CO) was used to monitor participants throughout the session.
FFM and % body fat were determined through air displacement plethysmography (BodPod®; COSMED Inc., Concord, CA). Measurements were taken after an overnight fast (>8 h) before and after the RET intervention.
Carotid-femoral pulse wave velocity
Measurement of carotid-femoral pulse wave velocity (cfPWV) was conducted according to the latest published guidelines (41). Pulse waves were recorded at the right common carotid and femoral arteries using applanation tonometry (model SPT-301; Millar Instruments, Houston, TX) and sampled at 2000 Hz using commercially available hardware (PowerLab model ML 795; AD Instruments). Pulse waves were band-pass filtered at 5–30 Hz to identify the foot of the waveform to calculate pulse transit time. The distance between measurement sites was determined with an anthropometric tape measure. cfPWV was determined from an average of 20 heart cycles using the equation: cfPWV = D/PTT, where D is 80% of the distance between measurement sites, and PTT is the foot-to-foot pulse transit time.
Carotid artery distensibility was assessed at the common carotid artery using combined applanation tonometry and B-mode ultrasound imaging. To estimate local blood pressure, 10 high-quality pressure waveforms were obtained at the right common carotid artery (model SPT-301; Millar Instruments). Maximum, mean, and minimum voltages were then used to predict local blood pressure, calibrated to supine brachial blood pressure (Dinamap Pre 100; Critikon LCC, Tampa, FL). Brachial blood pressure was measured in triplicate, disregarding the first measurement, and the average of the second and third measurements was taken; if the second and third measurements differed by >5 mm Hg, a fourth measurement was taken and values were averaged. Carotid maximum and minimum lumen diameters were assessed using B-mode ultrasound imaging 2–5 cm proximal to the carotid bifurcation in the lateral plane using a 12-MHz linear-array probe connected to a high-resolution ultrasound machine (Vivid Q; GE Medical Systems, Horten, Norway). A minimum of 10 heart cycles were recorded at 22.5 frames per second. After acquisition, images were stored offline in Digital Imaging and Communications in Medicine format for analysis. Lumen diameter was measured using a semiautomated edge-tracking software (Arterial Measurement System Image and Data Analysis, Tomas Gustavsson, Sweden). Equations for carotid distensibility and β-stiffness are as follows (29):
where LDmax is the maximum lumen diameter, LDmin is the minimum lumen diameter, PP is the pulse pressure, SBP is the systolic blood pressure, and DBP is the diastolic blood pressure.
Echocardiographic image acquisition followed current guidelines (20). Parasternal short-axis images were recorded at >60 frames per second with the participant in the left lateral decubitus position using a 1.5- to 3.6-MHz phased-array probe connected to a high-resolution ultrasound machine (Vivid q; GE Medical Systems). After acquisition, images were stored offline for further analysis using commercially available software (EchoPAC 110.0.2, GE Medical Systems). Left ventricular (LV) mass, relative wall thickness (RWT), and ejection fraction were estimated using the linear cube method from LV short-axis images at the mitral valve leaflet tips (1). LV mass was allometrically scaled for FFM according to Dewey et al. (7), as well as corrected for body surface area (BSA) using the DuBois formula for comparison with normative values (20).
Statistical analyses were performed on the Statistical Package for the Social Sciences (version 20.0 for Mac; SPSS Inc., Chicago, IL). A one-way ANOVA was used to assess differences in participant characteristics at baseline. Data were checked for normality using the Kolgomorov–Smirnov test and the homogeneity of variance using the Mauchley test of sphericity. In cases where sphericity was violated, the Greenhouse-Geiser univariate model was used. A 3 × 2 mixed ANOVA (group–time) was used to test for differences in outcome variables with training. Tukey HSD post hoc test was used to probe interaction effects. Pearson correlations were used to assess the relationship between change in strength and change in PWV in an RET pooled analysis. In all analyses, the level of significance was set at α = 0.05.
Baseline participant characteristics (means ± SD) are presented in Table 1. No differences in BMI, strength, FFM, cfPWV, distensibility, or β-stiffness index were found at baseline between groups. At baseline, CON had lower DBP than LR (62 ± 4 vs 70 ± 11 mm Hg, P = 0.03), with no other differences between groups. Participants presented with normal supine blood pressure (<140/90 mm Hg) and LV geometry (LV mass index < 115 g·m−2, RWT < 0.42 cm) before RET.
Strength and body composition changes after LR and HR have been previously reported in a larger cohort, with exercise session compliance >96% in both groups (28). Changes in strength and body composition for the study participants in the present study are presented in Table 2. Leg press 1RM increased to a similar degree in both training groups (P < 0.05). Bench press 1RM increased in both LR (P < 0.05) and HR (P < 0.05), with a larger increase in LR (P < 0.05). FFM measured by air displacement plethysmography increased in both LR (P < 0.05) and HR (P < 0.05) with no difference between groups. No changes in strength or LBM were observed for CON (P > 0.05).
Supine DBP decreased in the LR group (before, 70 ± 11; after, 64 ± 7 mm Hg; P < 0.05); however, this change was not significant after controlling for elevated baseline DBP in this group. Resting heart rate was reduced in both the LR (before, 64 ± 8; after, 59 ± 8 bpm; P < 0.05) and HR (before, 58 ± 8; after, 55 ± 7 bpm; P < 0.05) groups, with no change in the CON group (before, 60 ± 8; after, 58 ± 9 bpm; P > 0.05; Table 3).
cfPWV was reduced to a similar degree in both LR (before, 6.2 ± 0.6; after, 5.8 ± 0.8 m·s−1; P < 0.05) and HR (before, 6.4 ± 0.7; after, 5.7 ± 0.6 m·s−1; P < 0.05), with no change in the control group (before, 5.9 ± 0.7; after, 6.0 ± 0.7 m·s−1; P > 0.05) (Fig. 1). The reduction in cfPWV remained significant even after adjusting for the reduction in resting heart rate and mean arterial pressure. The change in cfPWV in HR and LR was not correlated with either the change in bench press 1RM (r = −0.11, P = 0.56), or the change in leg press 1RM (r = 0.25, P = 0.18). No changes were observed in the exercise or control groups for measures of local common carotid artery distensibility or β-stiffness index (P > 0.05) (Fig. 2). A main effect of time was found for an increase in carotid pulse pressure (pooled before, 53 ± 11 mm Hg; pooled after, 57 ± 9 mm Hg; P < 0.01); however, when distensibility and β-stiffness were adjusted for the increase, there remained no change across the RET protocol. Likewise, no changes were observed for LV geometry, including LV mass, LV mass/BSA, LV mass/FFM, and RWT in any group (P > 0.05) (Figure 3).
We discovered reductions in central arterial stiffness (cfPWV) with 12 wk of RET, in previously trained young males, regardless of whether the per-repetition load lifted was heavier or lighter. In direct contrast to previous studies, we observed no change in local carotid distensibility and no changes in LV geometry (27). Our findings, using strict criterion outcome measures, help to address the conflicting results reported previously and support the theory that vascular adaptations after RE are region-dependent and are not deleterious to vascular health.
Previous studies have reported varied arterial responses to RET, dependent on age, health status, and training intensity (26). There is evidence of disparity between studies using local measures of arterial stiffness (e.g., carotid distensibility and β-stiffness), whole-body arterial stiffness (e.g., brachial-ankle PWV), and central arterial stiffness (e.g., cfPWV). Nonetheless, of these measures, only cfPWV is recognized as an independent predictor of CVD risk (41), with a 1-m·s−1 increase in aortic PWV being associated with a 7% increase in CVD risk (3). Despite an expressed concern that resistance-type exercise may elevate arterial stiffness (27), relatively few of the previously published randomized control trials have focused on validated indices of CVD risk (5,42). For this reason, we chose to assess both cfPWV and local common carotid distensibility to more definitively address the thesis that regional differences in stiffness may account for the uncertainty in this area of research. We observed an approximately 0.5-m·s−1 decrease in cfPWV in the present study, indicative of a beneficial effect of performing resistance exercise to volitional failure (regardless of load per repetition) on the central elastic arteries. Exercise-induced reductions in arterial stiffness have been suggested to account for a portion of the risk reduction conferred by exercise (11). Although we were not able to quantify an independent risk score in our cohort, our exercise intervention appeared to have had a significant positive effect on the central arteries. As only one study has previously shown improvements in arterial stiffness, measured as brachial-ankle PWV, after low-intensity RET (30), it is still unclear whether these observations translate into improved cardiovascular health in the long term. What is clear, however, is that our data do not support the suggestion that RET adversely affects arterial function, as previously suggested (27).
We hypothesized that the LR training would result in increases in arterial stiffness because of exposure to large intermittent increases in central blood pressure (22), which may shift the load-bearing properties of the arterial wall to become stiffer due to fibrosis (29). We did not quantify the blood pressure response during exercise, but previous studies indicate that lifting loads >80% MVC (involving a Valsalva maneuver) elicit greater increases in invasively measured blood pressure compared with lower loads (22). In addition, repeated Valsalva maneuvers, rather than RE per se, have a greater acute effect on measures of central and peripheral PWV (16). Although previous studies have pointed toward the beneficial effects of lighter-load versus heavier-load RET on arterial stiffness (30), we observed a uniform reduction in arterial stiffness across both our RE intervention groups with concomitant increases in strength and decreases in resting heart rate. Regardless of the RET protocol, the change in strength across the intervention did not account for the change in cfPWV, as previously suggested from cross-sectional analyses (9). Both RET protocols in this study would be considered “high intensity,” and they provided a substantial stimulus as evidenced by the changes in strength observed, despite the training history of the participants. Our lack of observed increases in PWV with training, compared with previous studies (6,27,31) cannot therefore be attributed to a lack of sufficient RET stimulus. Instead, we speculate that the responses are due to arterial structural remodeling and/or changes in local smooth muscle tone and vasodilatory capacity, although structural changes are difficult to detect within only 3 or 4 months of an exercise intervention (40). The reduction in resting heart rate in both RET groups suggests a slight reduction in sympathetic tone in response to the exercise training. Endothelial function has also previously been shown to improve with RET (23), although these findings are not universal (33). Therefore, we speculate that it is likely the cardiovascular stimuli during exercise, rather than the muscular adaptations, that are driving vascular changes across the RET protocols; however, this remains to be examined. Regardless of the changes to arterial stiffness during an RET program, improvements in sympathetic tone and endothelial function may confer additional CVD risk reduction. Future studies should focus on the blood pressure response as well as the resting changes to vascular tone and function to fully quantify how RET affects the CVD risk profile.
Studies with participants with reduced arterial stiffness at study entry have showed marked increases with training (27) when compared with those with normal baseline stiffness values (32). In the present study, we recruited previously trained healthy young males with normal arterial stiffness to avoid having a low baseline stiffness affecting vascular outcome. Our participants presented with favorable arterial profiles, falling slightly above the 50th age- and sex-specific percentiles for carotid distensibility (8) and cfPWV (39), respectively. Thus, our subjects would be classified as being at low risk for future cardiovascular events (i.e., blood pressure < 140/90, cfPWV < 10 m·s−1). We also propose that, compared with other studies (27), our subjects’ arterial stiffness was such that our results were not affected by low (or high) stiffness, which may account for why we observed the positive changes in arterial function in-line with previous observations (32).
LV mass has previously been shown to be related to central arterial stiffness independent of blood pressure (34), representing one deleterious consequence of a reduction in the pressure buffering capacity of central elastic arteries. We observed no echocardiographic evidence to support the thesis of RET-induced LV remodeling in previously resistance exercise trained young men, similar to previous reports in young nonathletes (38). As baseline LV characteristics were at the upper end of normal values (HR: LV mass = 88.60 ± 10.88 g·m2, RWT = 0.40 ± 0.08 cm; LR: LV mass = 92.11 ± 21.59 g·m2, RWT = 0.37 ± 0.08 cm) (20), our subjects, a group of previously resistance exercise trained young men, may have already had some degree of cardiac hypertrophy thereby limiting the changes associated with the training protocols. We were unable to quantify the pressure stimulus induced by our protocols; however, we speculate that the HR protocol would have resulted in relatively smaller increases in afterload, which when coupled with prolonged increases in thoracic pressure (i.e., 25–30 repetitions), would result in a relatively stable LV transmural pressure thereby preventing substantial stimulus for cardiac remodeling (14).
Several limitations should be acknowledged. Although only men were included in this study, similar discrepancy for the effects of RET on arterial stiffness exists for women, which has not been thus far addressed in the literature. Diet was not controlled in this study; however, 3-d diet records showed no change in intake of macronutrients or energy across the training intervention (28). As the control group did not consume whey protein supplements, we were not able to control for the effect of whey protein ingestion on arterial stiffness. Whey protein has been shown to have a small effect on blood pressure and endothelial function in overweight and hypertensive individuals with poor baseline vascular function (10); however, the effects in trained young men are unknown. As our participants presented with normal resting blood pressure and normal arterial stiffness, it is unlikely that whey supplementation can explain the reduction in central arterial stiffness observed in the present study. Although no participants reported anabolic steroid use before enrollment in the study, we are not able to confirm history of use. Anabolic steroids have been shown to be associated with reduced arterial elasticity and elicit concentric remodeling of the left ventricle and substantial thickening of the LV posterior wall (14). We were not able to assess the test–retest reliability of the primary outcomes in this study, although the inclusion of an age-matched control group improves the design of this study to account for biological (and measurement) variation that would have occurred during the training period.
In a group of previously resistance exercise-trained young men, we report that 12 wk of whole-body RET, using disparate loading schemes, resulted in a reduction in central arterial stiffness without altering local elastic properties at the carotid artery or LV mass and RWT. Although previous groups have shown unfavorable effects of RET on the vasculature, our results indicate that positive alterations in the vascular profile can occur with both high- and low-load RET protocols in previously resistance exercise-trained young men. These results support the role of RET in the promotion of cardiovascular health status, particularly in individuals previously exposed to resistance-type exercise.
The authors thank the study participants and the undergraduate volunteers for their time and effort. This study was supported by funding from the Natural Sciences and Engineering Research Council of Canada to S. M. P. (grant no. RGPIN-2015-04613) and M. J. M. (DG no. 238819-13). S. M. P. thanks the Canada Research Chairs Program for their support.
The authors have no conflicts of interest to declare. The results of the present study do not constitute endorsement by the American College of Sports Medicine. The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.
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