The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre- or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2±1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136±2.9 vs post 132±3.4; AE, pre 141±3.8 vs post 136±3.4 mm Hg, P=0.005; diastolic BP: RE, pre 78±1.3 vs post 74±1.6; AE, pre 80±1.6 vs post 77±1.7 mm Hg, P=0.001). Central PWV increased (P=0.0001) following RE (11±0.9–12.7±0.9 m s−1) but decreased after AE (12.1±0.8–11.1±0.8 m s−1). Peripheral PWV also increased (P=0.013) following RE (RE, pre 11.5±0.8 vs post 12.5±0.7 m s−1) and decreased after AE (AE, pre 12.6±0.8 vs post 11.6±0.7 m s−1). The VC area under the curve (VCAUC) increased more with RE than that with AE (RE, pre 76±8.0 vs post 131.1±11.6; AE, pre 82.7±8.0 vs post 110.1±11.6 ml per min per s per 100 ml, P=0.001). Further, peak VC (VCpeak) increased more following resistance training compared to aerobic training (RE, pre 17±1.9 vs post 25.8±2.1; AE, pre 19.2±8.4 vs post 22.9±8.4 ml per min per s per 100 ml, P=0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.
The importance of controlling high blood pressure (BP) has been re-emphasized in a recent report of the Joint National Committee on Prevention, Detection and Treatment of High Blood Pressure,1 and a new category termed ‘pre-hypertension’ has been established, because systolic (SBP) and/or diastolic blood pressure (DBP) greater than 120/80 mm Hg still increase the risk of cardiovascular complications.1 Lifestyle changes, such as the adoption of appropriate exercise habits, are especially important for treatment and prevention of both pre- and stage-1 essential hypertension.2 Dynamic, moderately intense aerobic exercise (AE) is recommended for the prevention and treatment of high BP,3 and it has been found to decrease SBP by 10 mm Hg and DBP by 7 mm Hg in hypertensive individuals.4 The reductions in BP following AE have been shown to occur after only 1–2 weeks in individuals with elevated BP.5
Currently, resistance exercise (RE) is recommended as a complement to an aerobic training programme2, 6 and offers many benefits for the aging population, including the prevention and treatment of osteoporosis and sarcopaenia.7, 8, 9 A meta-analysis reported that dynamic resistance training reduced SBP and DBP of 4.6 and 3.8 mm Hg, respectively,10 in normotensive adults, but the haemodynamic effects of dynamic resistance training have not been studied in a hypertensive population. Confounding the recommendation employing RE as an exercise regimen, recent evidence indicates that RE may cause increased arterial stiffness in young, healthy normotensive individuals.11, 12 However, these findings are controversial, as not all studies show an increase in arterial stiffness with resistance training.13, 14 Increases in arterial stiffness, which are associated with increased mortality and morbidity, can lead to decreases in blood flow because of increased peripheral resistance.15 As arterial stiffness is related to increased pulse pressure and myocardial load, RE may potentially lead to myocardial hypertrophy.12 These changes may be further exacerbated by hypertension.16, 17
Studies investigating flow-mediated vasodilation (FMD) have shown that moderate-intensity AE significantly increased FMD in hypertensive and normotensive subjects, likely mediated through augmented endothelial function.18, 19 There is also evidence that combined AE and RE training programs can improve endothelial function;20 however, there is only one recent study that has shown an attenuated response to resistance forearm training in a cohort of hypertensive subjects, yet their results may have been confounded with the protocol acceptance of BP medications.21 Considering the potential disparate results of RE, coupled with a paucity of research regarding the effect of RE in patients with elevated BP without pharmacological intervention, there is considerable need for research studies in this area.
Therefore, the purpose of this study was to compare the haemodynamic, arterial stiffness and blood flow changes following 4 weeks of aerobic or resistance training in individuals with pre- or mild hypertension.
Materials and methods
Thirty moderately active, pre-hypertensive (n=13) or stage-1 (n=17) essential hypertensive men and women, but otherwise healthy between the ages of 30 and 60 years, were screened (as part of regular medical exams) and recruited by a local group of physicians. Only post-menopausal women were recruited to avoid the influence of hormonal changes during menstruation, and they were required to have a history of >12 months of amenorrhea and not under hormone replacement therapy. The patients referred by the physicians had multiple BP readings during regular office visits, usually over a 1- to 3-month period that fell into the pre- or stage-1 hypertension range. All have been screened for other cardiovascular risk factors and none met National Cholesterol Education Program (NCEP) guidelines for lipid-lowering therapy (that is, low-density lipoprotein >190 mmol/l in the absence of any risk factors except their new borderline hypertension). Also, none had diabetes (based on two fasting blood glucose 127 mmol/l or greater). Although none of the patients had glucose tolerance testing to uncover prediabetes, there was also no suspicion for prediabetes based on family history, body mass index and lab assessment. None of the subjects were taking any medication, including antihypertensives or aspirin, and all were non-smokers. The protocol was approved by the University Institutional Review Board, and all subjects gave written informed consent before participation.
Subjects reported to the Human Performance Laboratory for three separate visits. The first visit consisted of group randomization, health history and physical activity questionnaires, and tests of body composition, maximal aerobic capacity or 10 repetition maximal (10 RM) test and measurement equipment familiarization. At visit 2, subjects rested in a supine position for 15 min, followed by pulse wave velocity (PWV) and BP measurements. Blood flow and reactive hyperaemia (RH) were also measured while the subject was resting quietly. All subjects reported back to the laboratory for their post-training measurements (visit 3) between 24 and 48 h following the completion of the last exercise session. To avoid diurnal variation, all measurements were repeated at the same time of day in the post-prandial state (>3 h) and in the same order as pre-measurements.
Whole-body plethysmography (Bod Pod; Life Measurement Inc., Concord, CA, USA) was used to assess body composition,22 and body weight was measured using the Bod Pod scale. Height was measured using a stadiometer to the nearest 0.5 cm, and body mass index was calculated as weight (kg) per height2 (m2).
Maximal exercise testing
Subjects randomized to the aerobic arm of the study completed a customized peak oxygen consumption (VO2) protocol on a treadmill. Briefly, subjects started walking at a speed of 3 miles per hour for 2 min. Adjustments to the speed were made until the subject achieved a stable pace, at which point the grade was increased every 3 min until volitional fatigue was reached. Expired gases were analysed using a Quark b2 breath-by-breath metabolic cart (Cosmed, Rome, Italy). Rating of perceived exertion (RPE) and heart rate (HR) (Polar Electro Inc., Woodbury, NY, USA) were acquired once per stage. Maximal effort was achieved when subjects met three of the following criteria: (a) a final RPE score of 17 or greater on the Borg scale (rankings from 6 to 20), (b) an RER greater than 1.15, (c) no change in HR following a change in workload and/or (d) a plateau in oxygen uptake with an increase in workload (<150 ml).
Subjects randomized to the RE training completed a 10 RM. Following a brief warm-up, an estimated load was given for each exercise (leg press, lat pulldown, leg extension, chest press, leg curl, shoulder press, bicep curl, tricep press and abdominal crunch), and each subject completed no less than 3 and no more than 15 repetitions. If the subject achieved less or more than 10 repetitions, prediction tables were used to add or reduce weight until the preferred load was attained.
Central and peripheral arterial stiffness
Pulse wave velocity measurements were obtained with two MD6 bidirectional transcutaneous Doppler probes (Hokanson, Bellevue, WA, USA) in accordance with the guidelines from the Clinical Application of Arterial Stiffness Task Force 3.23 Each subject was monitored with an EKG (modified CM5), and HR data were inputted to the computer in phase with the PWV measurements and used as timing markers for PWV identification. Central PWV measures were obtained from the left common carotid artery to the left femoral artery. The distances from the carotid site to the midpoint of the manubrium sterni were subtracted from the carotid to femoral artery distance. Peripheral PWV measures were obtained from the left femoral artery to the ipsilateral superior dorsalis pedis artery. The distance between the PWV measurement locations was obtained with a tape measure and recorded to the nearest millimetre.
Data were collected in real time by aligning the Doppler waveforms and the electrocardiogram tracings on a computer screen (MP100; BioPac Systems, Santa Barbara, CA, USA). All data were stored and analysed at a later time. PWV was measured from the foot-to-foot flow wave velocity, whereas the foot of the sound wave was identified as the point of systolic upstroke. A minimum of 10 pulse contours were recorded and manually analysed as the distances between points, and the time delay between proximal and distal foot waveforms was calculated as distance (D) divided by the change in time (m s−1). Ten pulse contours were collected and averaged. The data were analysed by an investigator who was blinded to any grouping variables. In our laboratory, the intra-class correlation coefficient for PWV on 30 subjects, calculated using both central and peripheral sites on 2 separate days, was 0.97 with a coefficient of variation (CV) of <4.0%.
Blood pressure was measured by a trained investigator by standard sphygmomanometry following a quiet rest for 15 min in the supine position. SBP and DBP were measured manually at the brachial artery after the resting period and at the start of each testing session using the first and fifth Korotkoff sounds, according to American Heart Association standards.24 HR was taken from the calculation of successive R-R intervals from the three lead EKG. An investigator, blinded to grouping and condition variables, entered the data into the computer.
Blood flow and reactive hyperaemia
Forearm blood flow (FBF) and forearm RH25 were measured using a mercury-in-silastic strain gauge plethysmograph (EC-6; DE Hokanson Inc., Issaquah, WA, USA) as described by Higashi et al.18 Briefly, the subject was positioned in the supine position with their arm elevated slightly above heart level. Following a circumference measurement of the lower left arm, a strain gauge was attached and connected to the plethysmograph. A wrist cuff was inflated to 50 mm Hg above the subjects’ SBP at 1 min before each measurement, and the hand was left occluded throughout each FBF measurement. The upper arm cuff was inflated to 52 mm Hg for 7 s of each 15-s measurement cycle using a rapid cuff inflator (EC 20; DE Hokanson Inc.) to occlude venous outflow. All data were transmitted to a computer and analysed with a Non-Invasive Vascular Program 3 Software Package (version 5.27b; DE Hokanson Inc.). Six plethysmograph measurements were averaged for baseline blood flow values at pre- and post-exercise. Following baseline flow measures, a second occlusion cuff was placed over the first upper arm cuff and was inflated for 5 min at 250 mm Hg. Again, 1 min before deflation of the upper arm cuff, a wrist cuff was inflated to 50 mm Hg above SBP and left inflated until the end of the measure. Following 5 min of occlusion, the upper arm cuff was rapidly deflated to induce RH. Following cuff release, 3 min of blood flow measures were recorded as described above. FBF was expressed as millilitre per 100 ml of tissue per minute. To avoid confounding other vascular measures, RH was conducted after all other measures were complete.
The AE training consisted of 30 min of treadmill exercise at 65% of their previously determined VO2peak, 3 days per week for 4 weeks. The 10 RM provided the basis for individual load resistance for the dynamic resistance training sessions. The resistance training exercises consisted of leg press, chest press, leg extension, lat pulldown, leg curls, shoulder press, bicep curl, tricep press and abdominal crunch, all performed on Life Fitness machine (Life Fitness Inc., Schiller Park, IL, USA) training equipment. Each subject completed 3 sets of 10 repetitions at 65% of their 10 RM, 3 days per week for 4 weeks. Each RE session took approximately 45–50 min to complete. Subjects were asked to refrain from any exercise outside of their aerobic or resistance prescription.
Treatment of the data
Vasodilatory capacity was calculated from the blood flow data as area under the curve (AUC) above baseline values using GraphPad Prism 3.02 and the trapezoidal rule on the basis of actual datum points. A 2 × 2 analysis of variance with repeated measures (exercise mode (AE vs RE) by time (pre- vs post-training)) was employed with SPSS version 14 (SPSS Inc., Chicago, IL, USA) on all dependent variables. If a significant interaction was detected, a Dunnett's post hoc test was conducted to determine the significant difference. A priori significance was set at an α<0.05, and all data are reported as means±s.e.m. Sample size for the present study was based on previous data from our laboratory gathered under similar conditions on 30 subjects. For these calculations, the STATA statistical software package was used (STATA Corporation, College Station, TX, USA), and a total of 30 subjects were required to give us adequate statistical power at a P<0.05. With a relatively small sample size, rather large differences may not reach statistical significance and may result in type II error with other secondary variables. Therefore, effect sizes (partial η2) and the F values are reported as an additional statistical parameter to aid the reader in interpretation of the findings.
Ten men and five women were randomized into each training group. There were no significant differences in any of the subject characteristics before training, and no significant changes in weight or body composition occurred with the training programs (Table 1). Subject adherence to the supervised training sessions was >99%.
Resting haemodynamic variables are presented in Table 2.
Pulse wave velocity
Central PWV (Figure 1a) showed a significant exercise mode-by-time interaction (P=0.0001). Pretraining, no significant differences in PWVc–f were observed between groups; however, following the AE, PWVc–f significantly decreased from a mean of 12.1±0.8 m s−1 at pre values to 11.1±0.8 m s−1 post-training (P=0.002, η2=0.48, F=25.5). In contrast, RE significantly increased PWVc–f from 11.0±0.9 to 12.7±0.9 m s−1 (P=0.003). Peripheral PWV showed a significant interaction (P=0.013, η2=0.2, F=7.0), as RE increased and AE decreased transit time (AE, pre 12.6±0.8 m s−1 to post 11.6±0.7 m s−1; RE, pre 11.5±0.8 m s−1 to post 12.5±0.7 m s−1, respectively, Figure 1b). As there were slight differences between groups in baseline PWV (not significantly different), we also conducted an analysis of covariance on the post-PWV means using the baseline PWV values as the covariate. This analysis did not change our findings, as the corrected means for both central and peripheral PWV were highly significant between groups (P<0.0001 and P<0.017, respectively). We also included age as covariate in the repeated measures to ensure that we controlled for the influence of age. This also did not change any of our results.
Forearm blood flow and vascular conductance
Peak FBF following RH increased with both training types (P=0.04, power=0.93, η2=0.58, F=11.2; Figure 2b), but RE showed a greater increase than AE (AE 19% increase; RE 52% increase). Blood flow AUC following RH showed a significant exercise training mode-by-time interaction (P=0.04, F=6.4). There was a greater increase in vasodilatory capacity following RE compared to AE (AE, pre 82.7±8.05 to post 110.1±11.6; RE, pre 76±8.0 to post 131.1±11.6 ml·per 100 ml per min, respectively; Figure 2c).
Exercise training is an intervention that can decrease cardiovascular risk factors without negative side effects. This study found that RE resulted in increased arterial stiffness, whereas AE training decreased arterial stiffness in individuals with pre- to essential hypertension, despite similar reductions in BP. Furthermore, vasodilatory capacity, as measured by both peak and AUC FBF in response to RH, increased following both training modes, but these changes were greater following resistance training. Interestingly, these vascular changes all occurred without weight loss by either group. Thus, the training induced changes in arterial stiffness do not appear to be associated with changes in BP, vasodilatory capacity and body weight.
We found that as little as 4 weeks of exercise training can decrease SBP (mean decrease 4.6 mm Hg), which is identified as the primary goal in hypertension therapy.1 Likewise, DBP also decreased in both training groups along with a decrease in mean arterial pressure (DBP −3.1 mm Hg and mean arterial pressure −3.2 mm Hg). Our findings are similar to those reported in the Heritage family study,26 which showed small changes (<3 mm Hg) in resting SBP and DBP in normotensive to mildly hypertensive subjects following a longer and progressively more intense training programme (20 weeks, 55–75% VO2max). Hagberg et al.27 also demonstrated a decrease in SBP (20 mm Hg) in hypertensive men following 9 months of low- to moderate-intensity aerobic training, with a concomitant decrease in DBP (11–12 mm Hg). One previous study28 reported that 4 months of endurance training in middle-aged men resulted in no changes in resting SBP and <5 mm Hg decrease in resting DBP. Our results support these earlier studies,27, 28 indicating that exercise training has beneficial effects in individuals with pre- to stage-1 hypertension (mean BP 139/79 mm Hg) with as little as 4 weeks of moderate-intensity exercise. Our 3–4 mm Hg decreases in DBP and SBP parallel those recently reported in a meta-analysis by Fagard,29 who has shown that AE decreases in BP in normotensives of −3.0 (SBP) mm Hg and −2.4 (DBP) mm Hg with even greater reductions in resting BP in hypertensives (−6.9 and −4.9 mm Hg in SBP and DBP, respectively). Also, our 4 mm Hg mean decreases in SBP and DBP are in line with those published in a second meta-analysis of resistance training effects on resting BP.30 These authors reported significant decreases of 3.0 and 4 mm Hg in resting SBP and DBP, respectively.
Previous studies have shown mixed results examining the effects of resistance training on resting BP in a pre- or stage-1 essential hypertensive cohort, but few used a drug-free population.31, 32 One previous study32 compared 6 months of RE and AE and found only modest benefits from AE on SBP or DBP in older men and women. The discrepancy between these findings and ours may be due to the older ages of their subjects (70–79 years) when compared to our cohort and their RE intensity choice (one set to failure of 8–12 repetitions, 3 days per week). Possibly, one exercise set to muscular failure may be too strenuous an intensity for reducing BP.33 The reductions in BP found in the present study are clinically relevant, as a significant reduction in SBP of 3 mm Hg for normotensives has been shown to reduce cardiac morbidity by greater than 5%, stroke by 8–14% and all-cause mortality by 4%.34 Thus, our data demonstrate that moderate-intensity RE can be used in lieu of AE in a pre-hypertensive population to lower BP, and this is accomplished without weight loss.
Aerobic exercise training increases central arterial compliance in young normotensive subjects.35 AE training has also been shown to slow or lessen the progression of arterial stiffness associated with aging.36, 37 Our findings demonstrated that 4 weeks of moderate-intensity AE training decreased central arterial stiffness by 9.5% and peripheral stiffness by 8.5%. In contrast, Kraft et al.38 in a cross-sectional study found no relationship between aerobic fitness and stiffness of the descending aorta, whereas in normotensive subjects, fitness was related to decreased stiffness. However, the hypertensive subjects were much older than the subjects in our study, and in the small subset of subjects under 50 years of age, the correlation between aerobic fitness and aortic stiffness was similar to that in their normotensive subjects, although not statistically significant, probably due to a lack of power in this subset. Previous training studies in subjects with isolated systolic hypertension have reported no changes in arterial compliance following AE training.38, 39, 40 One possible difference between these studies and our study was the pre-training mean BP, and the age of our subjects was lower than the age of subjects in the previous studies. The lower age of our subjects is the most likely explanation for the divergent findings, as age alone increases arterial stiffness even in well-trained individuals.36, 37 As previous studies on older subjects with hypertension have not shown any changes in arterial stiffness with aerobic training, this might also suggest that there is a ‘point of no return’ possibly related to the length of time hypertension has been present in combination with age. Our findings would suggest that early diagnosis and intervention are essential for beneficial changes in arterial stiffness to occur in hypertensive or pre-hypertensive subjects.
In contrast to our findings on arterial stiffness with AE, RE training increased arterial stiffness in both the elastic central arteries (14.5%) and the peripheral muscular arteries (8.7%) following resistance training. Similar findings have been seen with increases in stiffness in the central arteries following resistance training in both acute and training studies.12, 41 Miyachi et al.11 reported a 19% decrease in central arterial compliance following 4 months of strength training in 14 young men compared to sedentary controls, but with no changes in peripheral compliance. It should be noted that not all studies have shown an increase in central arterial stiffness following resistance training,42 but these studies included different populations and employed a different exercise prescription. We also observed small but significant increases in peripheral stiffness following 4 weeks of resistance training. This increase may have been significant because of the increase in sample size compared to the smaller subject numbers in previous studies. It is also possible that changes in inflammatory markers or oxidative stress mediated the increase in PWV following resistance training, as acute RE increases inflammatory responses43 and oxidative stress.44
The increase in PWV may also be due to elevations in sympathetic outflow, typical of a hypertensive population. Increases in sympathetic outflow can lead to further increases in vascular tone, possibly potentiating the effect of increased peripheral vascular stiffness.45 Although Carter et al.46 found no statistically significant increase in muscle sympathetic nerve activity (MSNA) following resistance training in young subjects, the bursts per min and bursts per 100 heart beats increased by 12.5 and 35%, respectively, whereas there was a 0% change in the control group. This would suggest that the lack of statistical significance was a function of statistical power and not a lack of physiologic effect. Our finding of increased vascular conductance following the resistance training might also suggest that an increase in sympathetic tone was unlikely, but changes in vascular conductance and sympathetic tone have been shown to be dissociated.47
Several studies have also shown an increase in parasympathetic tone following resistance training,48, 49, 50 which may argue against an increase in sympathetic tone as an explanation for our findings. However, Figueroa et al.48 studied women with fibromyalgia, a vastly different population than hypertensives. As they observed a decrease in pain concomitant with an increase in heart rate variability (HRV) and indices of vagal tone and these changes were related, it is likely that the improvement in vagal tone was really a function of the decrease in pain. This is supported by findings from Heffernan et al.,49 who found no changes in HRV indices of vagal tone following resistance training. This study did, however, find an increase in HR recovery, supporting a potential increase in vagal tone with resistance training, a finding also supported by Otsuki et al.50 Furthermore, it is likely that resistance training increases both parasympathetic and sympathetic tone; thus, these changes in autonomic function do not need to be reciprocal.49 A further increase in arterial stiffness can be more detrimental to individuals presenting with elevated BP, as many already show increases in arterial stiffness51 and increased peripheral resistance, further increasing cardiac risk.52 We found differential changes between arterial stiffness and BP in our pre- to stage-1 hypertensive population.
Consistent with our findings, AE has been shown to increase FMD in both normotensive and hypertensive subjects.18, 53, 54 Others have also found that resistance training can increase FMD in young, healthy normotensive individuals and obese women.18, 53, 54 To our knowledge, the current study is the first to investigate the effects of aerobic vs resistance training on RH of the resistance arteries in an unmedicated hypertensive cohort. Although we observed a decrease in arterial distensibility following 4 weeks of moderate-intensity resistance training, a concomitant increase in vasodilatory capacity was observed. This was reflected in the increases in peak flow and AUC in the resistance-trained group, which were greater than in the aerobic group. Increases in vasodilatory capacity are due to factors such as nitric oxide availability, the presence of antegrade or retrograde flow and an intact endothelial lining.55, 56, 57 Resistance training may upregulate nitric oxide signalling more than aerobic training, leading to greater increases in flow,58 and possibly signal other endothelium-dependent dilators (prostaglandins, endothelium-derived hyperpolarizing factor and acetylcholine),58, 59, 60 leading to an increase in RH-induced flow. If so, this is likely related to the repeated shear stress experienced in the arm during resistance training, whereas the generalized effect from leg training may not have been as great. The specific mechanism for such an increase in signalling, if unrelated to the specific muscle mass used, remains unclear, but the increase in FMD may be a compensatory adjustment resulting from the increase in arterial stiffness following the resistance training.
Our study is limited by a relatively small number of subjects; however, our significant findings support future work on a larger scale in this area. The lack of a true, non-exercising control group could make the interpretation of our data difficult, especially as the groups initially exhibited slightly different PWV (although this was not statistically significant) and changed in a manner consistent with regression towards the mean. However, the day-to-day CV of PWV was less than 4% in our lab, suggesting that our findings were not due to measurement error. Furthermore, the intent of our study was to evaluate possible differences in the response to aerobic compared to resistance training; thus, a non-exercising control group would add little to this purpose other than showing the stability of the measurements. As we found differential arterial responses between the training modes, a non-exercising control group would have made our conclusion stronger but would not have changed our interpretation of the findings. Another limitation of the present study was the lack of maximal exercise post-testing to determine if there was a training effect. However, we did not anticipate that 4 weeks of moderate exercise would significantly alter maximal exercise testing responses, and our results still show the haemodynamic and arterial changes from participation in a standard, moderate-intensity exercise programme using exercise and intensity choices following guidelines for standard exercise prescriptions.61
In conclusion, both AE and RE training can decrease mean arterial pressure, without a concomitant mean weight loss in either group. RE training, however, produces increased central and peripheral arterial stiffness in a population with pre- and stage-1 essential hypertension, whereas AE training decreased arterial stiffness, yet both forms of training produced similar changes in BP. Although both training modes produced an increase in RH, resistance training produced greater increases in vasodilatory capacity than aerobic training. This suggests that although increases in arterial stiffness occur with RE, it seems there is a compensatory increase in flow in the microvasculature that may offset the increases in arterial stiffness. Further, the increase in vasodilatory capacity following short-term resistance training may not be a compensatory response to decreased central arterial distensibility but a local microvascular phenomenon.
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Collier, S., Kanaley, J., Carhart, R. et al. Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives. J Hum Hypertens 22, 678–686 (2008). https://doi.org/10.1038/jhh.2008.36
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