Effects of muscle contraction timing during resistance training on vascular function

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1 (2009) 23, & 2009 Macmillan Publishers Limited All rights reserved /09 $ ORIGINAL ARTICLE Effects of muscle contraction timing during resistance training on vascular function T Okamoto 1, M Masuhara 2 and K Ikuta 3 1 Institute of Health Science and Applied Physiology, Kinki Welfare University, Fukusaki-cho, Kanzaki-gun, Hyogo, Japan; 2 Institute of Exercise Physiology and Biochemistry, Osaka University of Health and Sport Sciences, Kumatori-cho, Sennan-gun, Osaka, Japan and 3 Institute of health and child sciences, Osaka Aoyama University, Minoh, Osaka, Japan Muscle contractions in normal resistance training are performed by eccentric (ECC, lowering phase) and concentric (CON, lifting phase) muscle contractions. However, the difference in effects of timing of muscle contraction during resistance training on arterial stiffness is unknown. This study investigated the effect of muscle contraction timing during resistance training on vascular function in healthy young adults. Thirty healthy men were randomly assigned to group of resistance training with quick lifting and slow lowering (ERT, n ¼ 10), group of resistance training with slow lifting and quick lowering (CRT, n ¼ 10) and sedentary groups (SED, n ¼ 10). The ERT and CRT groups underwent two supervised resistance-training sessions per week for 10 weeks. The ERT group performed the on set of 8 10 repetitions with 3 s ECC and 1 s CON muscle contractions. In contrast, the CRT group performed the on set of 8 10 repetitions with 1 s ECC and 3 s CON muscle contractions. Brachial ankle pulse wave velocity (bapwv) after ERT did not change from baseline. In contrast, bapwv after CRT increased from baseline (from 1049±37 to 1153±30 cm s 1, Po0.05). No significant changes in flow-mediated dilation were observed in the ERT and CRT groups. These values did not change in the SED group. These findings suggest that although both training does not deteriorate a vascular endothelial function, resistance training with quick lifting and slow lowering (that is, ERT) prevent the stiffening of arterial stiffness. (2009) 23, ; doi: /jhh ; published online 18 December 2008 Keywords: resistance training; eccentric contraction; concentric contraction; arterial stiffness; vascular endothelial function Introduction Arterial distensibility regulates fluctuations in arterial pressure and blood flow (BF). The stiffening of elastic arteries impairs this buffering function and contributes to elevations in systolic blood pressure, left ventricular hypertrophy, ischaemic coronary artery disease and reductions in arterial baroreflex sensitivity. 1 3 Increased arterial stiffness has been found to be a strong independent predictor of cardiovascular morbidity in patients with hypertension and type II diabetes, and of all-cause mortality in patients with hypertension and end-stage renal disease. 4 6 Correspondence: Dr T Okamoto, Welfare and Health Management, Institute of Health Science and Applied Physiology, Kinki Welfare University, , Takaoka, Fukusaki-cho, Kanzaki-gun, Hyogo , Japan. tokamoto@sw.kinwu.ac.jp Received 9 July 2008; revised 19 November 2008; accepted 20 November 2008; published online 18 December 2008 Resistance training is widely recommended to prevent sarcopenia and osteoporosis. 7 Resistance training is also an important physical activity that can prevent or treat lifestyle-related diseases. 8,9 Thus, resistance training can be useful for maintaining or improving physical condition. However, high-intensity resistance training reduces arterial compliance and increases arterial stiffness Muscle contractions during resistance training are performed by eccentric (ECC, lowering phase), concentric (CON, lifting phase) or isometric muscle contractions. Because ECC and CON are contraction modes accompanied by joint movement, they are widely used in typical resistance training. The human cardiovascular response increases more during high-intensity CON than during high-intensity ECC, and the CON phase is associated with endothelin-1 production and a greater increase in blood pressure than the ECC phase. 13 It has been reported that the increase in arterial stiffness associated with resistance training might be caused by endothelin In fact, a previous study reported

2 that, although high-intensity ECC resistance training does not change arterial stiffness, high-intensity CON resistance training increases it. 12 Therefore, in normal resistance training during which ECC and CON are repeated, it is plausible to hypothesize that increased arterial stiffness may be prevented by differences in muscular contraction timing during resistance exercise. However, because previous studies performed ECC and CON individually, 12,13 the effects of the timing of the muscle contractions during normal resistance training on arterial stiffness are unknown. In addition, muscle contraction timing during resistance training must be understood to clarify the effect of resistance exercise on arterial stiffness. Accordingly, this study investigated the effect of muscle contraction timing during resistance training on vascular function in healthy young adults. We postulated that, although resistance training with quick lifting and slow lowering can prevent vascular function deterioration, resistance training with slow lifting and quick lowering accelerates vascular function deterioration. Our findings may help to establish an important guideline by which highintensity resistance training can help prevent deterioration of vascular function. Methods Subjects The participants in this study were 30 healthy, nonsmoking, non-obese males who were not actively involved in regular physical exercise (aged 19.5±0.2 years, mean±s.e.m.). The subjects were normotensive (o140/90 mm Hg), with no signs, symptoms or history of any overt chronic diseases. Although some subjects who had exercised regularly in the past were included, most subjects had not exercised for more than 1 year. The subjects were not doing any form of resistance training nor had they performed such training previously. Table 1 shows the subjects physical characteristics. The subjects were randomly assigned to a group that performed resistance training with quick lifting and slow lowering (ERT, n ¼ 10), a group that performed resistance training with slow lifting and quick lowering (CRT, n ¼ 10) and a sedentary group (SED, n ¼ 10). The experiments were carried out with the approval of the Ethical Committee of the Kinki Welfare University. The potential risks were explained to all of the subjects in detail, and they gave their written informed consent before the experiment. Measurements The training and SED groups were studied before (baseline) and after training (10 weeks, completion of training). All of the measurements were performed at a constant room temperature ( C). Brachial ankle pulse wave velocity After the subject had rested in a supine position for at least 10 min, brachial ankle pulse wave velocity (bapwv) was measured using automatic oscillometric device (formpwv/abi, Omron-Colin Co. Ltd, Komaki, Japan). This device records the PWV, blood pressure, an electrocardiogram and heart sounds form and arterial blood pressure at both the left and right brachia and ankles. It was reported that bapwv may provide qualitatively similar information to those derived from central arterial stiffness. 15 bapwv was measured at rest in the supine position with sensory cuffs wrapped around both brachials and ankles. Before measurement, subjects abstained from caffeine and fasted for at least 4 h. The cuff, which was wrapped around both arms and ankles, was connected to a plethysmographic sensor to determine volume pulse form, and to an oscillometric sensor to measure blood pressure. The pulse volume waveforms were recorded using a semiconductor pressure sensor, with the sample acquisition frequency for PWV set at 1200 Hz. Volume waveforms for the brachium and ankle were stored for a sampling time of 10 s with automatic gain analysis and quality adjustment. Sufficient waveform data were obtained in this stored sample. The time interval between the wave front of the brachial waveform and that of ankle waveform was defined as time interval between brachium and ankle (Tba). The distance between the sampling points of the bapwv was calculated automatically according to the height of the subject. The path length from the suprasternal notch to the brachium (Lb) was obtained from superficial measurements and was expressed using the equation: Lb ¼ height of the subject (cm) The path length from the suprasternal notch to the ankle (La) was obtained from superficial measurements and was expressed using the equation: La ¼ ( height of the subject (cm) þ ). That is, bapwv was calculated as follows: bapwv ¼ (La Lb)/Tba. Because all of the participants were right-handed, we used the left bapwv value in this study. In our laboratory, the day-to-day reproducibility of the measurements for bapwv was 5.3%. Brachial artery flow-mediated dilation Brachial artery flow-mediated dilation (FMD) was assessed noninvasively as described by Corretti et al. 16 Briefly, once the basal measurements were obtained, arterial occlusion was created by inflating a cuff placed on the forearm to 240 mm Hg for 5 min. After 5 min inflation, the cuff was deflated producing a brief high-flow state resulting in artery dilatation due to increased shear stress. For the FMD scans, brachial artery diameter and brachial BF measurements were taken between 50 and 70 s after cuff deflation, and the maximal diameter was taken. 471

3 472 The increase in BF after the release of the cuff was expressed as a percentage change from the baseline flow. FMD was calculated as the percentage increase in brachial artery diameter from the resting state ((DB, for basal diameter) to maximal dilatation (DM, for maximal diameter): %FMD ¼ (DM DB)/DB 100. To most effectively evaluate the stimulus-response relationship between shear rate and vasodilation, FMD was normalized for shear rate and calculated as follows: Normalized FMD ¼ %diameter/shear rate area under the curve (mean blood velocity (MBV)/diameter). Brachial artery hemodynamics Measurement of brachial artery diameter and brachial artery MBV were performed while subjects were supine in a quiet room. In all the studies, brachial artery diameter and brachial MBV were obtained after at least a 10-min rest. The investigators blinded to the experimental condition, because most of the vascular measures are dependent on who is taking them. The brachial artery diameter and brachial MBV were imaged using a B-mode ultrasonography and a 7.5 MHz convex probe (SonoSite 180PLUS, SonoSite Inc., Washington, DC, USA), at a location 3 7 cm above the antecubital fossa. Ultrasound images were recorded on a personal computer, and brachial artery diameter measurements were analysed by the use of computerized image analysis software (Scion Image Beta 4.02). Brachial artery diameter was measured from longitudinal images with lumen intima interface visualized on both (anterior and posterior) walls. Pulsed Doppler measurements for measuring brachial MBV were performed with the sample volume placed in mid-artery. Brachial MBV measurements were performed with the insonation angle o601 and were corrected for the insonation angle. The position of the transducer was marked to ensure the same position of the transducer for all measurements. Hyperaemic flow velocity was determined during Table 1 Physical characteristics of subjects Variables SED (n ¼ 10) ECC (n ¼ 10) CON (n ¼ 10) Age, years 19.7± ± ±0.3 Height (cm) 170.8± ± ±1.2 Body mass (kg m 2 ) Before training (baseline) 62.7± ± ±4.3 After training 62.7± ± ±4.0 Body mass index (kg m 2 ) Before training 21.5± ± ±1.5 After training 21.5± ± ±1.5 Body fat (%) Before training 14.2± ± ±2.6 After training 13.6± ± ±2.3 Heart rate (bpm) Before training 64±3 64±4 64±4 After training 62±3 62±3 63±4 Systolic pressure (mm Hg) Before training 120±2 118±3 117±2 After training 117±3 120±5 118±3 Mean pressure (mm Hg) Before training 85±2 86±3 83±2 After training 83±2 83±4 81±3 Diastolic pressure (mm Hg) Before training 66±2 66±2 62±2 After training 62±2 63±2 60±2 Pulse pressure (mm Hg) Before training 54±1 53±2 55±1 After training 55±1 55±4 56±2 Abbreviations: CON, concentric; ECC, eccentric; SED, sedentary. Values are mean±s.e.m. CRT, group of resistance training with slow lifting and quick lowering; ERT, group of resistance training with quick lifting and slow lowering; SED, sedentary group.

4 the first s arterial pulses after cuff deflation to establish the magnitude of the hyperaemic response. Brachial artery BF and hyperaemic BF were calculated as follows: Brachial BF ¼ (MBV) (circular area) ( ). Hyperaemic BF ¼ (hyperaemic blood velocity) (circular area) ( ). The constant is the conversion factor from metres per second to liters per minute. Moreover, brachial vascular conductance (VC) and resistance were calculated as follows: Brachial VC ¼ brachial BF/brachial mean pressure. Brachial vascular resistance (VR) ¼ brachial mean pressure/brachial BF. Blood pressure and heart rate at rest Chronic levels of blood pressure and heart rate at rest were measured using automatic oscillometric device (formpwv/abi, Omron-Colin Co. Ltd) over the brachial and dorsalis pedis arteries. Recordings were made in triplicate with subjects in the supine position. activities during the study period. Although the subjects were not observed for 24 h per day, detailed information about their behaviour was obtained using a weekly questionnaire. Statistical analysis All data are expressed as means±s.e.m. Statistical analyses were performed using the Statistica software (Statview Version 5.0J). Data were analysed by two-way analysis of variance (group period) with repeated measures. In the case of significant F-values, a Newman Keuls post hoc test was used to identify significant differences among mean values. Statistical significance was set at Po0.05. Results Changes in body composition The baseline assessments were performed after randomization. In all groups, there were no changes in body mass, body mass index and body fat throughout the intervention periods (Table 1). 473 Body composition Body composition was determined by use of the bioelectric impedance method (HBF-362, Omron Co. Ltd). Exercise intervention Resistance training was conducted two times weekly for 10 weeks. The training programme included chest presses, arm curls, seated rowing, leg curls, leg presses and sit-ups. Before the start of training, one maximal repetition (1RM) was measured for all items except for sit-ups. Owing to the potential risks involved in 1RM testing, this test was not performed in the SED group. The load was set to 80% of 1RM. Training was conducted using five sets of 8 10 repetitions, with an inter-set rest period of 2 min. The resistance training involved five successive sets. That is, the participants performed five sets each of chest presses, arm curls, seated rowing, leg curls, leg presses and sit-ups (a total of 30 sets). The ERT group performed one set of 8 10 repetitions with 3-s ECC (lowering phase) and 1-s CON (lifting phase) muscle contractions. In contrast, the CRT group performed one set of 8 10 repetitions with 1-s ECC and 3-s CON muscle contractions. The subjects repeated the contractions at an approximately constant velocity and frequency accompanied by a metronome. The metronome, set at one tick per second, was used to keep the rhythm for the lowering and lifting phases. Except for routine activities during training, all other exercises (resistance training, anaerobic exercise and aerobic exercise) were prohibited. The SED group did not perform any exercise other than their routine Changes in 1RM All the subjects in both the ERT and CRT groups completed the training programme. There were no significant differences in the baseline 1RM among the ERT and CRT groups. Increases of 1RM in the ERT group were observed in the seated row, leg press (Po0.05), chest press, leg curl and arm curl (Po0.01). On the other hand, increases of 1RM in the CRT group were observed in the seated row, leg press, chest press, leg curl and arm curl (Po0.05). Interaction were F ¼ 7.40; Po0.01, F ¼ 4.29; Po0.05, F ¼ 5.92; Po0.05, F ¼ 5.13; Po0.05 and F ¼ 7.06; Po0.01, respectively. Percent increases for each of the exercises in ERT group were 22% in chest press, 34% in arm curl, 17% in seated row, 28% in leg curl and 18% in leg press. Percent increases for each of the exercises in CRT group were 20% in chest press, 24% in arm curl, 13% in seated row, 24% in leg curl and 16% in leg press. Moreover, chest presses, arm curls, leg curls and leg presses significantly increased after training in the ERT group compared with the CRT group (Po0.05). Changes in brachial blood pressure and heart rate Table 1 shows changes in brachial blood pressure and heart rate before and after training. There were no significant differences in the before and after training brachial blood pressure and heart rate among the three groups. Changes in bapwv Figure 1 shows changes in bapwv before and after training. There were no significant differences in the

5 474 bapwv (cm/sec) * FMD among the three groups. Brachial artery FMD and normalized FMD after training in the ERT and CRT groups had not changed from baseline. Interactions were F ¼ 1.81; NS and F ¼ 2.30; NS, respectively. Brachial artery FMD and normalized FMD in the SED group did not differ before and after training. Normalized FMD (S -1 ) %FMD Before training (Baseline) Before training (Baseline) After training Figure 1 Changes in bapwv in the SED (n), ERT ( ) and CRT (K) groups. Values are mean±s.e.m. *Po0.05 vs baseline. bapwv: brachial ankle pulse wave velocity. After training Figure 2 Changes in FMD (top) and normalized FMD (bottom) in the SED (n), ERT ( ) and CRT (K) groups. Values are mean±s.e.m. FMD: flow-mediated dilation. baseline bapwv among the three groups. bapwv after training in the ERT group had not changed from baseline. In contrast, bapwv after training in the CRT group had significantly increased from baseline (Po0.05). Interaction was F ¼ 4.63; Po0.05. bapwv in the SED group did not differ before and after training. Brachial artery FMD Figure 2 shows changes in brachial artery FMD (top) and normalized FMD (bottom) before and after training. There were no significant differences in the baseline brachial artery FMD and normalized Brachial artery hemodynamics Table 2 shows changes in brachial artery hemodynamics before and after training. There were no significant differences in the baseline hemodynamics among the three groups. However, brachial artery diameter, MBV, hyperaemic BV, BF and hyperaemic BF after training in the ERT and CRT groups had significantly increased from baseline (Po0.05, Po0.01, Po0.001). Moreover, brachial artery diameter, MBV, hyperaemic BV, BF and hyperaemic BF significantly increased after training in the ERT and CRT groups compared with SED group (Po0.05, Po0.01, Po0.001). Brachial VC after training in the ERT and CRT groups had significantly increased from baseline (Po0.01, Po0.05). Brachial vascular resistance after training in the ERT and CRT groups had significantly reduced from baseline (Po0.01, Po0.05). In addition, brachial VC significantly increased after training in the ERT and CRT groups compared with the SED group (Po0.05, Po0.01). Brachial vascular resistance significantly reduced after training in the ERT and CRT groups compared with the SED group (Po0.05, Po0.01). Brachial artery hemodynamics in the SED group did not differ before and after training. Discussion This study investigated the effect of muscle contraction timing during whole body resistance exercise on vascular function. The key novel findings were that bapwv did not change in the ERT group, but it was significantly increased in the CRT group. In contrast, FMD did not change in both the ERT and CRT groups. These findings suggest that, although arterial stiffness was changed by muscle contraction timing during resistance training, vascular endothelial function did not change. Muscle contractions during dynamic resistance training are performed by ECC and CON muscle contractions. Because ECC contractions exert a much greater muscle force than CON contractions, ERT has the capability of overloading the muscle to a greater extent, which can result in greater increases in strength and size In this study, an increase in 1RM was observed both in the ERT and CRT groups, but the degree of increase was greater in the ERT than in the CRT group. These results suggest that ERT, which had a quick lifting and

6 Table 2 Changes in brachial artery hemodynamics before and after training 475 Variables SED (n ¼ 10) ECC (n ¼ 10) CON (n ¼ 10) Interaction Brachial artery diameter (mm) Before training 3.9± ± ±0.2 F ¼ After training 3.9± ±0.2**,ww 4.2±0.2**,ww Po0.001 Brachial artery mean blood velocity (cm s 1 ) Before training 4.56± ± ±0.25 F ¼ 4.5 After training 4.51± ±0.19*,w 4.77±0.23*,w Po0.05 Brachial artery hypermic blood velocity (cm s 1 ) Before training 25.52± ± ±3.32 F ¼ 5.36 After training 25.02± ±3.55*,w 28.78±3.21*,w Po0.001 Brachial artery blood flow (ml m 1 ) Before training 33.4± ± ±3.9 F ¼ After training 32.8± ±4.1***,www 40.0±5.1***,www Po Brachial artery hypermic blood flow (ml m 1 ) Before training 243.8± ± ±16.1 F ¼ 8.87 After training 237.7± ±66.4**,ww 312.0±55.6*,w Po0.001 Vascular conductance (ml m 1 mm Hg 1 ) Before training 0.39± ± ±0.06 F ¼ 6.96 After training 0.40± ±0.08*,w 0.50±0.07*,w Po0.01 Vascular resistance (mm Hg ml 1 m 1 ) Before training 2.59± ± ±0.43 F ¼ 8.21 After training 2.54± ±0.33*,w 2.03±0.26*,w Po0.01 Abbreviations: CON, concentric; ECC, eccentric; SED, sedentary. Values are mean±s.e.m. CRT, group of resistance training with slow lifting and quick lowering; ERT, group of resistance training with quick lifting and slow lowering; SED, sedentary group. *Po0.05 vs before training, **Po0.01 vs before training, ***Po0.001 vs before training, w Po0.05 vs SED group, ww Po0.01 vs SED group, www Po0.001 vs SED group. slow lowering, may have provided a greater training effect. Pulse wave velocity, which is an index of arterial stiffness, 20,21 is known to be a strong independent predictor of cardiovascular morbidity in patients with hypertension and type II diabetes, and of all-cause mortality in patients with hypertension and end-stage renal disease. 4 6 Therefore, the prevention and treatment of arterial stiffness are of paramount importance. A simple, noninvasive method to automatically measure bapwv was recently developed to screen large populations; 22 bapwv, a noninvasively measurable PWV, was strongly associated with aortic PWV. 23 Thus, muscular arterial stiffness may influence aortic PWV. Therefore, it was considered that bapwv, which is an index of peripheral muscular arterial stiffness, may provide qualitatively similar information to that derived from central arterial stiffness. 15 Aerobic exercise training combined with resistance training has been shown to prevent the muscular arterial stiffening of resistance training. 24 However, high-intensity resistance training increased arterial stiffness On the basis of these results, resistance training may have to be prescribed carefully. The results of this study indicated that CRT increases arterial stiffness, whereas ERT suppresses arterial stiffness increases. Thus, differences in the timing of muscular contraction affected arterial stiffness. Acute intermittent elevations in arterial blood pressure during resistance exercise decrease elastin and increase collagen, 25 which regulate the elasticity of the artery. The changes in blood pressure during resistance exercise are related to the lifting (CON) and lowering (ECC) of the load. Blood pressure during normal resistance training increases to maximal values due to the resistance encountered during the lifting phase, and then it declines during the lowering phase. 26 Therefore, it is possible to hypothesize that prolongation of the lowering phase decreases the blood pressure sufficiently to suppress further increase of the blood pressure during the lifting phase. Resistance training is a powerful stimulator of sympathetic nervous system activity, which may intensify vasoconstriction through a sympathetic adrenergic vasoconstrictor effect. 27,28 Sympathetic nervous activity during ECC muscle activity has been shown to be lower than that during CON muscle activity. 29 Although sympathetic nervous activity was not measured in this study, it may have contributed to the increased arterial stiffness, because low muscle sympathetic nerve activity caused by ERT suppresses the vascular smooth muscle tension level. That is, these intermittent decreases in arterial blood pressure during the lowering phase may suppress arterial stiffening.

7 476 Assessment of brachial artery FMD is widely used as a noninvasive bioassay of stimulated, nitric oxide-mediated, conduit artery vasodilator function in vivo, and it is associated with cardiovascular health. As the health of the endothelium plays a pivotal role in the maintenance of vascular tone and reactivity, 30 it is important to maintain an intact and functional vascular endothelium. In contrast with the arterial stiffness findings, in this study, both ERT and CRT did not change FMD. These results are consistent with those of a previous study. 31 However, the previous study increased the training load stepwise during the training period. As this study involved a high-intensity training load from the start, our findings are important. Moreover, Kawano et al. 32 reported the effect of resistance training with arterial stiffening on endothelial function of the carotid artery using the cold pressor test; they found that, although arterial stiffening is observed in regular resistance-trained men, there were no significant differences in the percentage change of the carotid arterial diameter in response to the cold pressor test between resistance-trained men and control subjects. Thus, resistance training does not affect vascular function, which maintains intact endothelial function. These findings are consistent with those of a previous study that showed that chronic resistance training may protect against the adverse effects of acute resistance exercise-associated hypertension by preserving vascular endothelial function. 33 Our observations, as well as those of others, 32 may reflect obvious differences in the mechanisms responsible for endothelial regulation of arterial tone on changes in arterial stiffness and/or vascular endothelial function caused by resistance training. Brachial artery diameter in the ERT and CRT groups changed significantly from baseline. Recent studies reported that resistance training or aerobic training increased brachial and femoral artery diameter. 31,34 36 These results suggest that both types of training cause enlargement at the level of the major conduit arteries. The present findings extend these results from endurance-trained individuals to those who perform resistance training. Moreover, brachial hemodynamics in the ERT and CRT groups changed significantly from baseline. Short-term resistance training increases basal femoral BF and VC, which suggests that resistance training affects basal limb perfusion through a mechanism related to its effects on glucose uptake. 35 Therefore, hemodynamic improvement induced by resistance training is clinically important. However, the physiological mechanisms underlying the changed hemodynamics during resistance training remain obscure. Further long-term intervention studies are needed to determine the beneficial effects of resistance training on vascular endothelial function. Several other important limitations of this study should be emphasized. This study investigated the effect of ERT and CRT on vascular function in male adult subjects, and the number of subjects was small (n ¼ 10, ERT, CRT and SED, respectively). Performing power analysis and sample size estimation is an important aspect of experimental design. The sample power in this study was This means that 71% of studies would be expected to yield a significant effect, rejecting the null hypothesis that the odds are 1.0, and suggesting that this study has substantial (but not adequate) statistical power. Therefore, larger studies involving both male and female subjects will be needed to generalize our findings. In conclusion, these findings showed that, although CRT increased arterial stiffness, ERT did not change it. However, both types of training maintained vascular endothelial function. These findings suggest that, although both types of training were not associated with deterioration in vascular endothelial function, ERT prevented increased arterial stiffness. Thus, resistance training with quick lifting and slow lowering may prevent arterial stiffening. What is known on this topic K Although high-intensity ECC resistance training does not change arterial stiffness, high-intensity CON resistance training increases it. 12 K The effects of the timing of the muscle contractions during normal resistance training on arterial stiffness are unknown. What this study adds K Brachial ankle pulse wave velocity did not change in the ERT group, but it was significantly increased in the CRT group. K Flow-mediated dilation did not change in both the ERT and CRT groups. K Resistance training with quick lifting and slow lowering may prevent arterial stiffening. Acknowledgements This research was partially supported by the Ministry of Education, Science, Sports and Culture, Grant-in-Aid for Young Scientists (B), , References 1 Tanaka H, Dinenno FA, Hunt BE, Jones PP, DeSouza CA, Seals DR. Hemodynamic sequelae of age-related increases in arterial stiffness in healthy women. Am J Cardiol 1998; 82: Safar ME, London GM. 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