Arterial stiffness, the converse of distensibility, is an emerging risk factor that has received considerable attention in the recent literature (2,3,23,37). Nondistensible arteries contribute to increased peripheral resistance, higher pulse pressures, and increased ventricular afterload (5,10,22,24). This is of clinical importance because increases in the stiffness of central elastic arteries such as the carotid artery and aorta have been associated with increased mortality and morbidity and is also now recognized as an independent risk factor for cardiovascular disease (28).
Although aerobic exercise (AE) is currently recommended as the exercise modality of preference for decreasing cardiovascular risk (2,3,8,11,16,23,24,37), the effects of resistance exercise (RE) on cardiovascular health are unclear (37). Several recent studies have shown that both acute and chronic resistance training leads to decreased arterial distensibility (AD), whereas acute and chronic AE produces increases in AD and increases in postexercise hypotension) (9,13,27,31,32). It has been suggested that factors such as endothelial function may have an impact, but investigations have not targeted these responses extensively (9,11,23,24,29,32,38). Interestingly, separate studies have shown that although an acute resistance bout leads to an increase in arterial stiffness, this may be accompanied by a decrease in blood pressure (postexercise). Altogether, this suggests that RE may elicit a potential vascular dilatory response to offset the increase in arterial stiffness possibly through changes in microvascular beds, but to date, this has not been specifically investigated.
The purpose of this study was to evaluate if acute AE and RE elicit different vascular responses and to elucidate the role of vasodilatory capacity, total peripheral resistance (TPR), heart rate (HR), and cardiac output (Q) as potential mechanisms contributing to the acute changes in AD. We hypothesized that a bout of RE will cause a larger increase in vasodilatory capacity compared to AE, combined with differential changes in AD.
Experimental Approach to the Problem
Participants visited the laboratory on 3 separate days. During the first visit, a graded maximal exercise test, body composition, and maximal strength on each RE were measured. Strength was assessed using a 10-repetition maximum (10RM) test for bench press, bent-over row, leg extension, leg curl, military (shoulder) press, biceps curl, close-grip bench press (triceps), and abdominal crunch following standard guidelines (1). Maximal aerobic capacity and strength values were used to calculate the appropriate exercise intensity for the submaximal exercise bouts. Participants were tested in the postprandial state (3 hours) and asked to refrain from alcohol and caffeine ingestion on testing days. All visits took place at the same time of the day, in the early summer season to reduce the influence of diurnal and seasonal variation.
During the second and third visits, participants rested in the supine position in a dimly lit room for 15 minutes. Pulse wave velocity (PWV) and beat-to-beat blood pressures were measured in the supine position. The participants then underwent a supervised AE or RE following standard guidelines (2). The AE and RE sessions were randomly assigned and conducted at least 72 hours apart. None of the participants engaged in any strenuous physical activity for 48 hours before the study days. The RE bout was performed at 100% of the subjects' 10RM, using 3 sets for each exercise with 90 seconds of rest between sets. The AE was performed using 30 minutes of upright cycle ergometry at 65% of peak oxygen. Participants resumed the supine position immediately after completion of the exercise protocol, and measurements of PWV and beat-to-beat BP were conducted 40 and 60 minutes after the cessation of exercise. Vasodilatory capacity was measured before and at 60 minutes after the acute exercise bouts. We did not measure vasodilatory capacity at 40 minutes, because of the potential influence of repeated inflation-deflation cycles on arterial stiffness (17).
Ten healthy, moderately active (Lipid Research Clinics Questionnaire ) men between the ages of 21 and 29 years volunteered for this study. Participants were normotensive, nonobese, and free from any known cardiovascular or metabolic disease as reported in a health questionnaire. Additionally, they were nonsmokers and were not taking any medications (including aspirin and anti-inflammatories). Subjects were informed of the experimental risks, and before participation, all subjects signed an informed consent document. All study procedures were approved by a university-based institutional review board for the use of human subjects before data collection.
Whole-body air displacement plethysmography (Bod Pod, Life Measurement Inc., Concord, CA, USA) was used to assess body composition (21). Height was measured using a stadiometer and recorded to the nearest 0.5 cm. Body mass index was calculated as weight (kg) divided by height (m) squared.
Maximal Aerobic Capacity
A cycle ergometry protocol was used to measure peak oxygen consumption (V̇o2peak) Participants began cycling at 50 W for 2 minutes. Intensity was then increased by 50 W every 2 minutes until volitional fatigue. Heart rate was measured using a Polar Heart Rate Monitor (Polar Electro Inc., Woodbury NY, USA). Ratings of perceived exertion (RPEs) were collected during each exercise stage and at peak exercise. Expired gases were analyzed using a Quark b2 breath-by-breath metabolic system (Cosmed, Rome Italy). Maximal effort was defined as meeting 3 of the following 4 criteria: (a) no change in HR with a change in workload, (b) a final RPE score of 17 or greater on the Borg scale (scale 6-20), (c) an respiratory exchange ratio (RER) greater than 1.15, (d) a “plateau” (increase of no more than 150 ml) in oxygen uptake with an increase in workload.
Ten Repetition Maximum Maximal Resistance Exercise
Ten repetition maximum values for REs were obtained following the guidelines of the National Strength and Conditioning Association. After a brief warm-up, a weight allowing participants to complete between 3 and 15 repetitions was applied. Then, using a prediction table extrapolating maximal loads from submaximal effort, weight was added or reduced in 2.3-kg increments to reach the appropriate load.
Regional Arterial Stiffness
The PWV measurements were conducted following the guidelines of the Clinical Application of Arterial Stiffness, Task Force III (35). Two bidirectional transcutaneous Doppler flow probes (MD6, Hokanson, Bellevue, WA, USA) were used to obtain the pulse wave between the left common carotid artery and the left femoral artery and between the left femoral artery and the ipsilateral superior dorsalis pedis artery. The distance from the carotid site to the midpoint of the manubrium sterni, from the manubrium sterni to femoral artery, and femoral to superior dorsalis pedis artery was measured with a tape measure (26). The distance from the carotid artery to the manubrium sterni was then subtracted from the manubrium to calculate femoral artery distance (34). Pulse wave velocity was determined from the foot-to-foot flow wave velocity. The foot of the doppler wave was identified at the point of systolic upstroke (28). The peak of an in-phase R wave, obtained from an electrocardiogram (ECG) (modified CM5 configuration), was used as a timing marker. We calculated the time delay between 10 simultaneously recorded flow waves and used an average of these 10 recordings. Pulse wave velocity was calculated from the distances measured and from the time delay (t) between proximal and distal foot waveforms as follows: PWV = D/(m·s−1), where D is the distance in meters and t is the time interval in seconds. The PWV calculated from the carotid to femoral artery was used as an index of central stiffness, whereas values from the femoral to superior dorsalis pedis artery were used as an index of peripheral stiffness. Data were collected in real time at a sample rate of 1,000 Hz, and the bidirectional doppler probes and the ECG were interfaced with a computer (MP100, BioPac Systems, Santa Barbara, CA, USA). All data were stored and analyzed off-line after completion of testing. In our laboratory, the day-to-day reliability coefficient for PWV is 0.98.
With the subjects in a supine position, beat-to-beat blood pressure was recorded for a 10-minute epoch via finger plethysmography (Finometer, FMS, The Netherlands). We used the Modelflow method using finger pressure to compute an aortic waveform simulating a nonlinear 3-element model of the aortic input impedance (6,36) to calculate stroke volume (SV). Integrating the computed aortic flow waveform per beat provides left ventricular SV and consequently Q by multiplying SV by the instantaneous HR (6). Total peripheral resistance was derived from mean arterial blood pressure (MAP) and Q.
Forearm Blood Flow and Reactive Hyperemia
Forearm blood flow (FBF), calf blood flow (CBF), and forearm reactive hyperemia (RH) were measured using a mercury-filled Silastic strain gauge plethysmograph (EC-6, D.E. Hokanson, Inc., Issaquah, WA, USA) as described by Higashi et al. (19). Briefly, the subjects were positioned in the supine position with their arm or leg elevated slightly above the heart level. After a circumference measurement, a strain gauge was attached to the upper left arm or left gastrocnemius and connected to the plethysmograph. A wrist or ankle cuff was inflated to 50 mm Hg above the subjects' systolic pressure at 1 minute before each measurement, and the hand or foot was left occluded throughout each FBF and CBF measurement. The upper-arm and leg cuff was inflated to 42 mm Hg for 7 of each 15-second measurement cycle using a rapid cuff inflator (EC 20, D.E. Hokanson, Inc.) to occlude venous outflow. All data were transmitted to a computer and analyzed with a Noninvasive Vascular Program 3 Software Package (version 5.27b, D.E. Hokanson). Six plethysmographic measurements were averaged for baseline blood flow values at pre, 40, and 60 minutes postexercise. After baseline flow measures, a cuff, placed around the upper-arm cuff was inflated for 5 minutes at 250 mm Hg. Again, 1 minute before deflation of the upper-arm cuff, a wrist cuff was inflated to 50 mm Hg above systolic and left inflated until the end of the measurement. After 5 minutes of occlusion, the upper-arm cuff was rapidly deflated to induce RH. After cuff release, 3 minutes of blood flow measures were recorded as described above. To avoid confounding the other vascular measures, RH was only repeated after the final 60-minute measures were completed. Forearm BF and CBF were expressed in milliliters per minute per 100 mL of tissue. Limb vascular conductance was calculated by dividing mean limb blood flow by MAP, whereas vascular resistance was MAP divided by mean limb blood flow.
Data were analyzed by SPSS v14. All results are presented as mean ± SE and measures were considered statistically significant if a p ≤ 0.05 was obtained. Hemodynamic measures and PWV were analyzed using a 2 × 2 (mode × time) analysis of variance (ANOVA) with repeated measures, evaluating the change from rest at 40 and 60 minutes. Area under the curve (AUC) was calculated using GraphPad Prism 3.02 and the trapezoidal rule on the basis of actual datum points. The significance of differences in changes from rest of the AUC values was evaluated using a dependent t-test. Significance differences from the ANOVA were followed up with a Dunn's multiple comparison test. Sample size for the present study was based on previous data from our laboratory gathered under similar conditions on 8 subjects. For these calculations, the STATA statistical software package was used (STATA Corporation, College Station, TX, USA), and a total of 10 subjects were required to give us adequate statistical power at a p ≤ 0.05 for the outcome variables of PWV and blood flow. Based on existing data from our laboratory (18), the estimated sample size of 10 subjects gives us an effect size of 0.92 and 0.88, respectively, with an alpha set at 0.05. Test-retest reliabilities in our laboratory for these 2 dependent variables is 0.98 and 0.97, respectively.
We studied 10 male subjects that were 24.9 ± 0.86 years old, 175.8 ± 1.48 cm height, weighed 76.8 ± 2.36 kg, and had a mean V̇o2 of 42.25 ± 2.2 L·kg−1·min−1 with 12.2 ± 1.44% body fat.
Cardiovascular variables are presented in Table 1. Mean arterial blood pressure did not differ between modes. There was a significant decrease in TPR after RE (p = 0.001), but there was no change in TPR after AE (Table 1). Heart rate was increased 40 and 60 minutes into recovery when compared to rest after RE, whereas HR did not change after AE. Stroke volume did not change from rest and was not different between exercise modes. However, cardiac output (p = 0.019) significantly increased at both 40 and 60 minutes of recovery after RE but did not change after AE.
Pulse Wave Velocity
Central pulse wave velocities are shown in Figure 1. After an aerobic bout, PWV decreased at both 40 (−0.45 ± 0.81 m/s −1) and 60 minutes (0.42 ± 0.61 m·s2) postexercise. However, central PWV increased after RE at both 40 (0.29 ± 0.85 m·s2) and 60 minutes postexercise (0.29 ± 0.70 m·s2). The change after RE was significantly different from the change after AE (p < 0.05, η2 = 0.381). There were no significant changes in peripheral PWVs for either exercise mode at either time point (Figure 2).
Calf blood flow increased after RE but decreased after AE. The change after RE compared with AE was significantly different (p < 0.05, 0.44). Forearm blood flow increased after both exercise modes, but there was no difference between modes. Forearm vasodilatory capacity also changed in a similar manner between exercise modes. However, calf vasodilatory capacity increased after RE but decreased after AE, and this differential response between exercise modes was statistically significant (p < 0.05, η2 = 0.4). There was also a significant difference between exercise modes in the response to RH as the change in the AUC was significantly greater after RE (p < 0.05, η2 = 0.37) (Figure 3). A similar response was observed for the peak blood flow in response to RH, with a greater change after RE compared to AE (p < 0.05, η2 = 0.36) (Figure 4).
The most novel finding of our study was an increase in vasodilatory capacity (increased blood flow in response to RH) and increase in leg capacitance after an acute bout of RE, despite a concomitant increase in arterial stiffness. In contrast, we found that arterial stiffness decreased without a change in the maximal vasodilatory response after AE, whereas leg capacitance decreased. This observation suggests that acute exercise-induced changes in AD and vasodilation are disassociated, and changes in endothelial function are unlikely a mechanism for alterations in AD after acute exercise. Alternatively, the increase in vasodilation may be a compensatory response to the increase in arterial stiffness after acute RE.
In agreement with previous research, our results show that an acute RE bout causes central arterial stiffening with no change in distensibility in the peripheral arteries (8,9,11,16,22,32). Furthermore, the increase in central artery stiffness was associated with a decrease in TPR and an increase in vasodilatory capacity, without any significant changes in blood pressure. Mean arterial pressure was similar after both exercise modalities. Thus, changes in blood pressure per se cannot account for the differential changes in arterial stiffness after acute RE compared to AE. Several studies have suggested that because arterial stiffness was only observed in the central arteries and not in the peripheral arteries, the decrease in distensibility may only be a limited mechanical phenomenon or a transient result of acute RE (11,16,18). Also consistent with previous findings, we found that AD increases after an acute AE bout (9,11,16,18,22,32). However, we found that this increase in AD was not accompanied by an increase in vasodilatory capacity, nor was there a decrease in TPR or MAP after the aerobic bout. This implies that the changes in AD after AE may not be associated with vasodilatation of the microvascular beds.
To our knowledge, this is the first study to investigate the response of peripheral resistance arteries to RH after an acute bout of aerobic vs. resistance training. One study has shown that an acute bout of maximal AE did not change peak flow in response to RH (4), but overall blood flow was increased. This finding supports our observation that peak FBF did not increase in response to RH and thus cannot explain the decrease in arterial stiffness after AE. Additionally, contrary to the findings of Baynard et al., we did not observe an increase in the AUC for vasodilatory capacity after AE (4). This disparate finding may be related to the timing of the measurement and the intensity of the exercise, because they measured vasodilatory capacity immediately after a maximal exercise test. We measured vasodilatory capacity 60 minutes after an acute 30-minute submaximal AE bout; thus, it is possible that the residual effects of the exercise were no longer present, explaining the lack of a response in our study.
Interestingly, although we observed a decrease in AD after RE, an increase in vasodilatory capacity was detected. This was reflected as both an increase in RH-induced peak blood flow and increases in RH AUC. These observations were greater in contrast to the aerobic bout of exercise. This would suggest that the residual effects of the RE bout were still present 60 minutes into recovery. Our findings are similar to resistance training studies (8), in that as AD decreased after resistance training, stiffness was only restricted to the central arteries and there was an increase in vasodilatory capacity (increased peak flow and AUC) that was greater than what was observed in aerobically trained subjects. Moreover, the present findings are similar to those of Rakobowchuk et al. (33), who reported that whole-body resistance training significantly increased postocclusion blood flow. They concluded that because postocclusion blood flow reflects endothelial-dependent function, increases in flow were likely related to enhanced vessel endothelial function. It has been established that a 5-minute occlusion of the conduit arteries increases arterial endothelium signaling, particularly for nitric oxide (NO), and after release of the occlusive pressure increases in shear stress from increased blood flow, lead to vasodilation of the peripheral arteries (20). Thus, a possible explanation for the increased blood flow after acute RE could be attributed to the transient sheer stress experienced during the exercise (20,33). Sheer stress during exercise mediates NO signaling and release and also possibly augments the release of other endothelium-dependent dilators (prostaglandins, endothelial derived hyperpolarizing factors (EDHF), and acetylcholine [7,25,30]). Upregulation of these endothelium-dependent dilators cause an increase in RH-induced flow similar to what we observed.
Because our subjects were all young and healthy, it is possible that our RE bout yielded a more intense physiologic stimulus compared to the aerobic bout, but it is very difficult if not impossible to equate exercise intensity between AE and RE. Certainly, the muscle stimulus may be greater during the type of resistance training employed in our study, but it is unclear if that would be associated with a greater stimulus for blood flow and increased shear stress. It is possible that the muscle ischemic response to RE may elicit a lingering effect that may have enhanced the RH response more so than what we observed for AE. Thus, an increase in relaxing factors from local contractions may explain the differences in flow response from the resistance compared to the aerobic bout (14).
Consistent with recent findings (15), we observed a twofold increase in FBF after a single bout of AE concomitant with an increase in forearm vascular conductance. We also observed a similar response after RE. However, there were differential changes in CBF, which did not change after the aerobic bout, yet increased significantly after RE. Similarly, calf vascular conductance did not change after the aerobic bout but increased after the RE. Fisher et al. (12) found similar increases in calf vascular conductance after isometric lower limb exercise. It is possible that 30 minutes of cycling at 65% of V̇o2max was not a sufficient stimulus to elicit a significant decrease change in calf vascular conductance creating the exercise mode difference. However, it is also possible that the acute response to RE is greater because of the potential stimulatory effects on the endothelium discussed above. Alternatively, it is also possible that RE increases production of other vasodilators not seen after AE. An increased expression in endothelial-derived relaxing factors is a favorable change that may decrease cardiovascular risk.
A limitation to the interpretation of the results of this study is that matching the exercise intensity of the RE vs. AE is difficult at best. Therefore, our exercise and intensity choices were guided by guidelines from the American College of Sports Medicine Position Stand (2) and conducted as sessions commonly practiced.
In conclusion, an acute bout of RE increased central arterial stiffness in young, healthy normotensive men, whereas an aerobic bout increased central AD. Resistance exercise also produced an increase in RH-induced blood flow that was not seen after the aerobic bout. This suggests that RE may produce compensatory peripheral vascular effects, offsetting the increase in central arterial stiffness, while keeping blood pressure fairly constant after an acute exercise bout. Future studies that measure endothelial function specifically may provide further evidence to suggest whether mechanisms responsible for enhanced blood flow are either a transient compensatory response to arterial stiffness or an increase in signaling of endothelium-dependent dilators after acute RE.
There is a great need to compare exercise modes directly in current research, especially because acute bouts of exercise have divergent effects on the systemic physiology. The present study indicates that an acute bout of RE shows many favorable cardiovascular benefits and should therefore be considered as part of a daily exercise training program. Further, for the clinical end user, RE may offer greater benefits from the increases in blood flow to active muscles and could be implemented as companion to an aerobic training regimen.
This study was funded in part by a Michael Pollock Grant from Life Fitness (PI, Scott R. Collier). The author would like to express thanks to the subjects that participated in this study.
1. Ainsworth, BE, Jacobs, DR Jr, and Leon, AS. Validity and reliability of self-reported physical activity status: The Lipid Research Clinics questionnaire. Med Sci Sports Exerc
25: 92-98, 1993.
2. American College of Sports Medicine Position Stand. The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness, and flexibility in healthy adults. Med Sci Sports Exerc
30: 975-991, 1998.
3. Baechle, TR, Earle, RW, and National Strength and Conditioning Association (USA). Essentials of Strength Training and Conditioning
. Champaign, IL: Human Kinetics, 2000, pp. xiii, 658.
4. Baynard, T, Miller, WC, and Fernhall, B. Effects of exercise on vasodilatory capacity
in endurance- and resistance-trained men. Eur J Appl Physiol
89: 69-73, 2003.
5. Benetos, A, Waeber, B, Izzo, J, Mitchell, G, Resnick, L, Asmar, R. Influence of age, risk factors, and cardiovascular and renal disease on arterial stiffness
: Clinical applications. Am J Hypertens
15: 1101-1108, 2002.
6. Bogert, LW and van Lieshout, JJ. Non-invasive pulsatile arterial pressure and stroke volume changes from the human finger. Exp Physiol
90: 437-446, 2005.
7. Busse, R, Edwards, G, Feletou, M, Fleming, I, Vanhoutte, PM, and Weston, AH. EDHF: Bringing the concepts together. Trends Pharmacol Sci
23: 374-380, 2002.
8. Collier, SR, Kanaley, JA, Carhart, R Jr, Frechette, V, Tobin, MM, and Hall, AK. 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
9. Cortez-Cooper, MY, DeVan, AE, Anton, MM, Farrar, RP, Beckwith, KA, and Todd, JS. Effects of high intensity resistance training on arterial stiffness
and wave reflection in women. Am J Hypertens
18: 930-934, 2005.
10. Dart, AM and Kingwell, BA. Pulse pressure-A review of mechanisms and clinical relevance. J Am Coll Cardiol
37: 975-984, 2001.
11. DeVan, AE, Anton, MM, Cook, JN, Neidre, DB, Cortez-Cooper, MY, and Tanaka, H. Acute effects of resistance exercise
on arterial compliance. J Appl Physiol
98: 2287-2291, 2005.
12. Fisher, JP, Sander, M, MacDonald, I, and White, MJ. Decreased muscle sympathetic nerve activity does not explain increased vascular conductance during contralateral isometric exercise in humans. Exp Physiol
90: 377-382, 2005.
13. Fisher, MM. The effect of resistance exercise
on recovery blood pressure in normotensive and borderline hypertensive women. J Strength Cond Res
15: 210-216, 2001.
14. Green, DJ, Bilsborough, W, Naylor, LH, Reed, C, Wright, J, O'Driscoll, G, et al. Comparison of forearm blood flow
responses to incremental handgrip and cycle ergometer exercise: Relative contribution of nitric oxide. J Physiol
562: 617-628, 2005.
15. Harvey, PJ, Morris, BL, Kubo, T, Picton, PE, Su, WS, Notarius, CF, et al. Hemodynamic after-effects of acute dynamic exercise in sedentary normotensive postmenopausal women. J Hypertens
23: 285-292, 2005.
16. Heffernan, KS, Collier, SR, Kelly, EE, Jae, SY, and Fernhall, B. Arterial stiffness
and baroreflex sensitivity following bouts of aerobic and resistance exercise
. Int J Sports Med
28: 197-203, 2007.
17. Heffernan, KS, Edwards, DG, Rossow, L, Jae, SY, and Fernhall, B. External mechanical compression reduces regional arterial stiffness
. Eur J Appl Physiol
101: 735-741, 2007.
18. Heffernan, KS, Rossow, L, Jae, SY, Shokunbi, HG, Gibson, EM, and Fernhall, B. Effect of single-leg resistance exercise
on regional arterial stiffness
. Eur J Appl Physiol
98: 185-190, 2006.
19. Higashi, Y, Sasaki, S, Kurisu, S, Yoshimizu, A, Sasaki, N, Matsuura, H, et al. Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects: Role of endothelium-derived nitric oxide. Circulation
100: 1194-1202, 1999.
20. Hutcheson, IR and Griffith, TM. Release of endothelium-derived relaxing factor is modulated both by frequency and amplitude of pulsatile flow. Am J Physiol
261: H257-H262, 1991.
21. Katch, F, Michael, ED, and Horvath, SM. Estimation of body volume by underwater weighing: Description of a simple method. J Appl Physiol
23: 811-813, 1967.
22. Kingwell, BA. Large artery stiffness: Implications for exercise capacity and cardiovascular risk. Clin Exp Pharmacol Physiol
29: 214-217, 2002.
23. Kingwell, BA, Berry, KL, Cameron, JD, Jennings, GL, and Dart, AM. Arterial compliance increases after moderate-intensity cycling. Am J Physiol
273: H2186-H2191, 1997.
24. Kingwell, BA and Gatzka, CD. Arterial stiffness
and prediction of cardiovascular risk. J Hypertens
20: 2337-2340, 2002.
25. Koller, A, Huang, A, Sun, D, and Kaley, G. Exercise training augments flow-dependent dilation in rat skeletal muscle arterioles. Role of endothelial nitric oxide and prostaglandins. Circ Res
76: 544-550, 1995.
26. Liang, YL Teede, H, Kotsopoulos, D, Shiel, L, Cameron, JD, and Dart, AM, et al. Non-invasive measurements of arterial structure and function: Repeatability, interrelationships and trial sample size. Clin Sci
95: 669-679, 1998.
27. MacDonald, JR MacDougall, JD, Interisano, SA, Smith, KM, McCartney, N, and Moroz, JS, et al. Hypotension following mild bouts of resistance exercise
and submaximal dynamic exercise. Eur J Appl Physiol Occup Physiol
79: 148-154, 1999.
28. Mackenzie, IS, Wilkinson, IB, and Cockcroft, JR. Assessment of arterial stiffness
in clinical practice. QJM
95: 67-74, 2002.
29. Maeda, S, Iemitsu, M, Miyauchi, T, Kuno, S, Matsuda, M, and Tanaka, H. Aortic stiffness and aerobic exercise: Mechanistic insight from microarray analyses. Med Sci Sports Exerc
37: 1710-1716, 2005.
30. Martin, CM, Beltran-Del-Rio, A, Albrecht, A, Lorenz, RR, and Joyner, MJ. Local cholinergic mechanisms mediate nitric oxide-dependent flow-induced vasorelaxation in vitro. Am J Physiol
270: H442-H446, 1996.
31. McCartney, N, McKelvie, RS, Martin, J, Sale, DG, and MacDougall, JD. Weight-training-induced attenuation of the circulatory response of older males to weight lifting. J Appl Physiol
74: 1056-1060, 1993.
32. Miyachi, M, Kawano, H, Sugawara, J, Takahashi, K, Hayashi, K, and Yamazaki, K, et al. Unfavorable effects of resistance training on central arterial compliance: A randomized intervention study. Circulation
110: 2858-2863, 2004.
33. Rakobowchuk, M, McGowan, CL, de Groot, PC, Bruinsma, D, Hartman, JW, and Phillips, SM, et al. Effect of whole body resistance training on arterial compliance in young men. Exp Physiol
90: 645-651, 2005.
34. Vaitkevicius, PV, Fleg, JL, Engel, JH, O'Connor, FC, Wright, JG, and Lakatta, LE, et al. Effects of age and aerobic capacity on arterial stiffness
in healthy adults. Circulation
88: 1456-1462, 1993.
35. Vaitkevicius, PV, Duprez, D, Starmans-Kool, MJ, Safar, ME, Giannattasio, C, and Cockcroft, J, et al. Effects of age and aerobic capacity on arterial stiffness
in healthy adults. Circulation
88: 1456-1462, 1993.
36. Wesseling, KH, Jansen, JR, Settels, JJ, and Schreuder, JJ. Computation of aortic flow from pressure in humans using a nonlinear, three-element model. J Appl Physiol
74: 2566-2573, 1993.
37. Williams, MA, Haskell, WL, Ades, PA, Amsterdam, EA, Bittner, V, and Franklin, BA, et al. Resistance exercise
in individuals with and without cardiovascular disease: 2007 update: A scientific statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism. Circulation
116: 572-584, 2007.
38. Zieman, SJ, Melenovsky, V, and Kass, DA. Mechanisms, pathophysiology, and therapy of arterial stiffness
. Arterioscler Thromb Vasc Biol
25: 932-943, 2005.