Aortic stiffness is currently recognized as an independent predictor of stroke (16), and related increases in aortic wave reflection are associated with coronary artery disease (31). Cross-sectional studies have revealed that aerobically trained individuals have lower arterial stiffness than their sedentary counterparts (6,21). This, in turn, results in a longer pressure wave-reflection time and lower intensity of the reflected pressure wave, with favorable effects on central blood pressure (6). Conversely, cross-sectional investigations have demonstrated that chronically resistance-trained (RT) males have stiffer central (18) and peripheral (3) arteries than their sedentary age-matched peers. This results in unfavorable increases in central pressure augmentation and widened pulse pressure (PP) (3,18), which may increase left ventricular (LV) load (18). Thus, although resistance exercise confers many positive health benefits and is recommended by professional medical organizations for health promotion, disease prevention, and cardiac rehabilitation (23), it may have negative effects on the vasculature and on central hemodynamics.
Maximal aerobic exercise testing has been employed to delineate physiologic differences between groups that may not be apparent at rest (9). Maximal exercise also acutely reduces peripheral muscular artery stiffness (19). The effect of a graded maximal exercise test on central elastic artery stiffness is unknown. Because RT males may have greater tonic peripheral artery stiffness (3), structural and/or functional arterial adaptations may attenuate reductions in peripheral artery stiffness after maximal aerobic exercise. This, in turn, would negatively impact central pressure wave reflections. Thus arterial reactivity to an acute stressor may be compromised in this population, but this has not been previously investigated.
The primary purpose of this study was to examine arterial stiffness and wave reflection after a maximal aerobic exercise test in young RT males and age-matched non-RT controls. Two hypotheses were to be tested: 1) acute maximal aerobic exercise would reduce central aortic pressure wave reflection (i.e., augmentation index (AIx)), central aortic stiffness, and peripheral femoral artery stiffness in all young men; and 2) reductions in central/peripheral arterial stiffness and AIx would be attenuated in RT males.
Thirty healthy young men between the ages of 18 and 30 volunteered for this study. Subject characteristics are presented in Table 1. RT participants were self-reported as engaging in a total body resistance training program for 7.2 ± 0.6 yr, more than 3 d·wk−1, with less than 1.5 h of concomitant nonvigorous aerobic activity per week. Control participants were sedentary/recreationally active and did not engage in a regular planned exercise program. Those considered recreationally active engaged in less than 1.5 h of unplanned nonvigorous physical activity per week and did not engage in any resistance training. Exclusionary criteria consisted of cardiovascular disease, diabetes, obesity, hypertension (resting blood pressure > 140/90 mm Hg), medication use (including aspirin, antiinflammatories, anabolic steroids, and other performance-enhancement agents), smoking, and orthopedic problems preventing full compliance with the study protocol, as assessed using a medical history questionnaire. Before participation in this project, all subjects gave written informed consent. This research was approved by the institutional review board of the University of Illinois at Urbana-Champaign.
Participants reported to the exercise and cardiovascular research laboratory for testing. All participants were at least 3 h postprandial and did not consume caffeine or exercise for 24 h before testing. After attainment of written consent, body anthropometrics were attained. Participants were then required to rest in the supine position for a period of 10 min in a climate-controlled room. Resting blood pressure, AIx, and central/peripheral pulse wave velocity (PWV) measures were made. Participants then underwent a graded exercise test until volitional exhaustion on a cycle ergometer. Postexercise test measures of AIx and PWV were made at 10, 20, and 30 min. Previous research has shown a nadir in reduction of lower-limb PWV to occur approximately 10 min after maximal exercise (19), hence our rationale for measurement at this time point. Previous research also suggests significant alterations in vascular wall properties to occur at 20 min (8) and 30 min (13) after acute exercise, hence our reasoning for including these time points as well. Given our purpose of comparing potential group differences, we did not examine a complete time course of arterial recovery kinetics, which has previously been reported (19). All testing was conducted at the same time of day, to reduce possible diurnal influences on physiologic parameters.
Height and weight were measured using a stadiometer (to the nearest 0.5 cm) and a beam balance platform scale, respectively. Body mass index was calculated as weight (kg) divided by squared height (m). Body circumference measures were taken with a tape measure for the following sites: neck, chest, upper arm, abdomen (at the level of the umbilicus), and thigh. All measures were made at the site of greatest circumference. This was used to compare body dimensions between groups.
Brachial artery blood pressure assessment.
Resting blood pressure was measured in the supine position by an experienced technician using standard sphygmomanometry. Because of the larger arms of the RT men, blood pressure cuff size was selected accordingly. The same technician conducted all ausculatory blood pressure measurements in all subjects. All measurements were made in duplicate, and average values recorded for analysis.
Regional arterial stiffness: PWV.
All measurements were conducted following guidelines of the Clinical Application of Arterial Stiffness, Task Force III (30). A high-fidelity strain-gauge transducer (Millar Instruments, Houston, TX) was used to obtain the pressure waveform from 1) the right common carotid artery and the right femoral artery, and 2) the right femoral artery and the ipsilateral superior dorsalis pedis artery. Distances from the carotid artery sampling site to the femoral artery, carotid artery to the suprasternal notch, and femoral artery to the superior dorsalis pedis artery were measured as straight lines with a tape measure. The distance from the carotid artery to the sternal notch was then subtracted from the carotid femoral segment length to account for differences in the direction of pulse wave propagation. PWV was determined from the foot-to-foot pressure wave velocity (SphygmoCor, AtCor Medical, Sydney, Australia). PWV was calculated from the distances between measurement points and the measured time delay between 10 proximal and distal foot waveforms. The peak of an in-phase R wave, as attained from sequential ECG monitoring (CM5 configuration) was used as a timing marker. ECG recordings were also used to attain resting and recovery HR at the time of measurement. This technique has been shown to be highly reproducible (32). In our laboratory, the intraclass correlation coefficients for central and peripheral PWV measured before and after maximal aerobic exercise, calculated on two separate days, are as follows:
Pulse contour analysis.
Radial artery pressure waveforms were attained in the supine position from a 10-s epoch using applanation tonometry and a high-fidelity strain-gauge transducer (Millar Instruments, Houston, TX). Using a generalized validated transfer function, a central aortic pressure waveform was reconstructed from the aforementioned radial artery pressure waveform (SphygmoCor, AtCor Medical, Sydney, Australia). The use of a transfer function to synthesize a central pressure waveform from a peripheral radial waveform has been validated at rest and during exercise using both intraarterially (4,22,26) and noninvasively (7,27) obtained radial waveforms. Moreover, central aortic pressure waves generated from intraarterially attained radial pressure waves with a transfer function are comparable with directly measured central pressure waves attained during dynamic changes in blood pressure in response to nitroglycerin and valsalva maneuver (28). AIx was calculated as the ratio of amplitude of the pressure wave above its systolic shoulder (i.e., the difference between the early and late systolic peaks of the arterial waveform) to the total PP; the result was expressed as a percentage and was used as an index of aortic pressure wave-reflection intensity. Because AIx is influenced by HR (33), AIx values also were normalized to an HR of 75 bpm. All measurements were made in duplicate, and the mean value was used for subsequent analysis. The reproducibility of measures attained from this technique has previously been shown to be high (32). In our laboratory, the intraclass correlation coefficients for AIx and AIx75 measured before and after maximal aerobic exercise, calculated on two separate days, are as follows:
Also derived from the aortic waveform were aortic systolic blood pressure (SBP), aortic diastolic blood pressure (DBP), aortic PP, travel time of the forward pressure wave from the aorta to the peripheral reflection site and back (time delay of the reflected wave (Δt)), heart period (average length of a pressure waveform), and LV ejection duration (time for opening and closure of the aortic valve, or the time from the start of the pulse wave to the incisura). Ejection duration is presented in absolute (ms) and relative (%) values (relative to heart period). Good agreement has been found with directly measured central aortic pressure via catheterization and central pressure derived from peripheral radial pressure waveforms attained via applanation tonometry and calibrated with brachial blood pressure measured noninvasively, as employed in the present study. This has been shown both at rest (1) and during exercise (27).
Maximal aerobic capacity.
Peak oxygen consumption (V˙O2peak) was assessed using a cycle ergometry protocol. Briefly, participants began a brief warm-up by cycling against no resistance (0 W) for a period of 2 min. The first workload was set at 50 W. Intensity was increased by 30 W every 2 min thereafter until volitional fatigue was reached. HR was measured and recorded once per minute during the protocol using a Polar Heart Rate Monitor (Polar Electro Inc., Woodbury NY). Ratings of perceived exertion (RPE) were also assessed once per stage. Expired gases were analyzed using a Quark b2 breath-by-breath metabolic system (Cosmed, Rome Italy). Maximal effort was considered attained when subjects met three of the following four criteria: (a) a final RPE score of 17 or greater on the Borg scale (scale 6-20), (b) a respiratory exchange ratio greater than 1.1, (c) no change in HR with a change in workload, and/or (d) a "plateau" (increase of no more than 150 mL) in oxygen uptake with an increase in workload. All participants met a minimum of three of the aforementioned criteria.
Maximal resistance exercise.
After maximal aerobic exercise testing and postexercise data acquisition, one-repetition maximum values for the bench press were ascertained as previously described (8). Relative strength was calculated as absolute weight lifted in kilograms divided by absolute body weight in kilograms.
All data are reported as means ± SEM. A priori significance was set at an alpha < 0.05. Significant differences for descriptive variables (age, height, weight, body circumference measures, body mass index, body surface area, one-repetition maximum) between RT and non-RT males were assessed by one-way analysis of variance (ANOVA). A 2 × 4 (2 groups × 4 time points) ANOVA with repeated measures was used to assess differences in all dependent variables over time. Whenever significant interactions were detected, Fisher's least significant difference was used for post hoc comparisons. All data analyses were carried out using Statistical Package for the Social Sciences (version 12.0.1, SPSS, Inc., Chicago, IL).
Subject characteristics are shown in Table 1. Both groups were matched for age, height, and V˙O2peak. RT men were significantly heavier and had significantly greater body surface area and greater neck, chest, arm, and thigh circumferences (P < 0.05). Both groups had similar waist circumferences. Absolute and relative strength of the RT men was significantly greater than for non-RT controls (P < 0.05). The length of the graded maximal exercise test (Table 1: EX test time) was not different between groups (P > 0.05).
There were no group differences in any resting hemodynamic or arterial parameter. Similarly, HR, heart period, ejection duration, and central/peripheral hemodynamic and all arterial parameters in both groups responded in a similar fashion to exercise (i.e., no group-by-time interaction was detected for any outcome variable). Peripheral PWV was reduced at 10 min after and did not recover to resting values by 30 min after exercise (Fig. 1, P < 0.05). There was no change in AIx at 10 min after exercise (Fig. 1). AIx was reduced at 20 and 30 min after exercise (Fig. 1, P < 0.05). AIx75 increased after exercise, peaking at 10 min after exercise and remaining elevated 30 min after (P < 0.05). There was no change in central PWV or Δt (P > 0.05).
After exercise, there were no significant changes, compared with at rest, in central or peripheral SBP (Table 2). Peripheral DBP was reduced 10 and 20 min after exercise (P < 0.05), returning to resting values 30 min after exercise. Central DBP was reduced 10 min after exercise (P < 0.05) and returned to resting values by 20 min after exercise. Central and peripheral PP were increased at 10 min after exercise (P < 0.05) and had returned to resting values by 20 min after exercise (Table 3).
HR remained above resting values at all time points measured after maximal aerobic exercise (Table 3, P < 0.05). Similarly, heart period was reduced at all time points measured after maximal aerobic exercise (Table 3, P < 0.05). There was no change in absolute LV ejection duration. However, relative ejection duration was higher than resting values at all time points measured (Fig. 1, P < 0.05).
The major findings of the present study are that 1) resting central and peripheral artery stiffness and central pressure wave reflection are similar in young RT and non-RT men, and 2) arterial reactivity to a maximal aerobic exercise test is also similar in RT and non-RT men, with both groups exhibiting similar reductions in peripheral artery stiffness and central pressure wave reflection.
There were no differences in resting central/peripheral artery stiffness or wave reflection in young RT men compared with young non-RT men, and this is different from previous findings (3,21). Our findings do support those of Miyachi et al. (18), who note no differences in peripheral femoral artery compliance or central carotid compliance/AIx between young RT and sedentary men, despite differences in LV geometry. Similarly, Lane et al. (14) found no difference in AIx between young RT athletes (i.e., bodybuilders) and sedentary controls. Although participants in the present investigation had been training intensely for approximately 7 yr, it seems that aging per se may be a stronger modulator of resistance training-induced increases in arterial stiffness than absolute years of training. Greater age-related reductions in arterial compliance have been reported in RT men (18). Young RT men and sedentary men also have similar endothelial-dependent vasodilation in response to inhaled salbutamol and similar endothelial-independent vasodilation in response to sublingual glycerol trinitrate (14). Previous reports also have noted similar vasodilatory capacity of the microvasculature, a marker of endothelial reactivity, after maximal exercise in RT and endurance-trained men (2). Thus, our findings and those of others support the notion that vascular responsiveness to an acute maximal aerobic exercise stressor is not impaired in young RT men.
Prospective studies examining the vascular response to resistance training remain controversial. To date, several investigations have found increases in central artery stiffness with resistance training interventions (5,12,17), whereas others have not (15,25). Similarly, Rakobowchuk et al. (24) note no change in endothelial function (as assessed via brachial artery flow-mediated dilation) after a resistance training intervention in young, healthy men. Our cross-sectional findings would support the contention that chronic resistance training is not detrimental to vascular health in young, healthy men.
After maximal aerobic exercise in the present study, there were reductions in peripheral PWV that were consistent with previous findings (19). Interestingly, there were no changes in central artery stiffness or reflection time; this was a novel finding. Thus, although submaximal cycling exercise has been shown to acutely reduce central artery stiffness (8,13), maximal exercise may not have an effect on large central-artery properties.
Concomitant with reductions in peripheral PWV were reductions in AIx. With each cardiac cycle, an incident pressure wave traverses the aorta, arriving at areas of impedance mismatch in the periphery (20). The pressure wave is reflected back from these areas to the left ventricle and, depending on reflection time and/or intensity, may either augment systolic (i.e., early arrival) or diastolic (i.e., late arrival) pressure (20). Thus, AIx is a composite of intensity/magnitude as well as timing of reflected pressure waves, and it can be influenced by several factors, including aortic stiffness, peripheral muscular artery stiffness, arteriolar vasomotion, and LV ejection (20). Because there was no change in aortic stiffness (i.e., central PWV and Δt), it is likely that the reductions in wave reflection seen in the present study were related to reductions in peripheral PWV stemming from muscular artery/arteriolar vasodilation. However, alterations in peripheral PWV cannot explain all the changes in wave reflection, because there was no change in AIx at 10 min after exercise concomitant with the greatest reductions in peripheral PWV.
There is an inverse relationship between HR and AIx; this is independent of arterial stiffness (33). However, changes in HR also cannot account for all changes noted in AIx, because HR was greatest at 10 min after exercise, concomitant with no change in AIx. In young individuals, pacing studies have revealed that for every 10-bpm increase in HR, there is a reduction in AIx of approximately 5.6% (33). Thus, in the present investigation, an increase in HR by approximately 30-40 bpm at 10 min after exercise would be expected to reduce AIx by approximately 15-20%, but this was not the case. According to the results attained from HR-corrected AIx (AIx75), it would seem that wave reflection increased after exercise. However, given the very different physiologic state of the system after exercise, this measure may be contrived and may not truly reflect cardiac load and true wave-reflection properties. AIx75 may be applied more aptly when comparing groups of individuals who have different resting HR.
An explanation for the discrepancy in AIx after exercise may be related to LV function. After exercise, HR was increased and heart period shortened. Although absolute LV ejection duration remained the same after exercise because of a shorter heart period, the relative ejection duration (% ED relative to total heart period) was increased. Thus, unlike resting conditions, whereby systole comprised approximately 30% of the heart period, postexercise systole consumed approximately 50% of the heart period (Fig. 2). With a greater proportion of time spent in systole, and a likely reduction in time for diastolic decay (reduced diastole), measurement of the reflected wave and occurrence of the inflection point has a greater likelihood of transpiring during late systole instead of early diastole, as is seen at rest. This is supported by our finding of a significant reduction in central DBP at 10 min after exercise that returned to resting values by 20 min after exercise. Indeed, LV outflow pattern has been shown to be as important as ascending aortic impedance parameters for late systolic-pressure augmentation (10). Thus, the intensity of reflected waves is not the only determinant of the AIx inflection point, and it may be affected independently by LV outflow pattern (10). Future research that assesses stroke volume and cardiac output after exercise, as it relates to AIx, is warranted. Overall, with respect to the present study, whether examining AIx or AIx75, wave reflection does not seem to differ between young RT and non-RT men, either at rest or in response to maximal aerobic exercise.
One potential limitation of this study is that we did not directly assess blood markers for anabolic agent use in our RT men. All men were steroid free according to their self-reports on the questionnaire. Anabolic steroid abuse has been associated with increased arterial stiffness (11) and reduced vasodilation (14) in RT men. Thus, if some of our RT men had been taking steroids, it would have manifested as greater resting stiffness and an attenuated reduction in peripheral stiffness after exercise compared with our non-RT controls, but this was not the case. All individual values at rest and in response to exercise were comparable between groups. Another limitation is that we did not assess serum lipid profiles or plasma glucose in our participants; these factors may impact PWV and AIx. If any of our participants were dyslipidemic or diabetic, group differences would potentially disappear because of this bias. This would impact our overall findings and conclusions. Given the cross-sectional nature of this investigation, direct cause-and-effect relationships regarding resistance training cannot be inferred.
In conclusion, resting arterial parameters and arterial reactivity to an acute exercise stressor is similar in young, highly trained RT and non-RT men. More research is needed to examine arterial reactivity in response to acute stressors in older RT individuals.
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Keywords:©2007The American College of Sports Medicine
AUGMENTATION INDEX; PULSE WAVE VELOCITY; RESISTANCE EXERCISE; CARDIOVASCULAR