Acute Effect of a Single Bout of Aerobic Exercise on Vascular and Baroreflex Function of Young Males with a Family History of Hypertension

Home , Hyperaemia

Journal of Human Hypertension (2011) 25, 311–319 & 2011 Macmillan Publishers Limited All rights reserved 0950-9240/11 www.nature.com/jhh ORIGINAL ARTICLE Acute effect of a single bout of aerobic exercise on vascular and baroreflex function of young males with a family history of hypertension

YN Boutcher, JP Hopp and SH Boutcher School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia

The effect of one single bout of aerobic exercise on À20, À40, À60 and À80 mm Hg pressures and was the vascular and baroreceptor function of individuals determined from RR interval divided by systolic blood with a family history of hypertension was investigated. pressure. Augmentation index (AIx), a measure of Forty young males, mean age 21 years, comprising wave reflection, was assessed using applanation tono- offspring with (FH þ ; n ¼ 20) and without (FHÀ; n ¼ 20) a metry, and was calculated as the ratio of augmented family history of hypertension participated in this study. pressure and pulse pressure. The peak FBF at pre- Acute exercise was performed on a stationary bike for exercise was lower in FH þ than in FHÀ subjects. Twenty 20 min at 60% of maximal oxygen uptake. Peak forearm minutes of acute cycle exercise resulted in signifi- blood flow (FBF) was assessed using plethysmography cantly increased peak FBF by 22% in FH þ and by and was determined as the highest blood flow after 11% in FHÀ subjects, whereas peak FVR of both groups 5 min of reactive hyperaemia. Cardiopulmonary baror- decreased by 17% and 11%, respectively. No change eceptor (CPBR) sensitivity was measured using lower- occurred in CPBR, CBR or AIx. It is concluded that body negative pressure (LBNP) for 5 min at À20 mm Hg. 20 min of acute cycle exercise normalised baseline CPBR was determined by calculating change of stroke FBF and forearm vasodilation during hyperaemia in volume and forearm vascular resistance (FVR) at FH þ subjects. baseline and during LBNP. Carotid baroreceptor Journal of Human Hypertension (2011) 25, 311–319; (CBR) sensitivity was assessed using neck suction at doi:10.1038/jhh.2010.62; published online 17 June 2010

Keywords: forearm blood flow; forearm vascular resistance; cardiopulmonary baroreceptor; carotid baroreceptor

Introduction (BP), these males with a family history of hypertension possessed abnormal vascular function. Normotensive young males with a family history of Other abnormalities possessed by normotensive hypertension have been found to possess a number young adults with a family history of hypertension of vascular abnormalities. It has been shown that are reduced cardiopulmonary and carotid barore- young normotensives with a family history of ceptor (CBR) sensitivity.3 It has also been shown that hypertension had 25% higher peripheral vascular middle-aged offspring of hypertensive parents pos- resistance than young normotensives without a 1 sessed greater arterial stiffness, measured through family history of hypertension. Similar findings augmentation index (AIx), compared with middle- were found with young males possessing a family aged individuals without a family history of hyper- history of hypertension who showed a 19% lower tension.4 However, it is undetermined whether peak forearm blood flow (FBF) and a 17% higher young adults of offspring of hypertensive parents peak forearm vascular resistance (FVR) than young 2 show elevated AIx similar to that of the middle- males without a family history of hypertension. aged. AIx increases with age, regardless of family Thus, despite demonstrating normal blood pressure history of hypertension. Acute exercise is a potential non-pharmacological therapy that may be able to reverse or normalise the Correspondence: Dr YN Boutcher, Faculty of Medicine, School of vascular dysfunction observed in young normoten- Medical Sciences, University of New South Wales, Sydney 2052, sives with a family history of hypertension. Acute Australia. E-mail: [email protected] aerobic exercise has been shown to influence Received 13 October 2009; revised 6 May 2010; accepted 11 May cardiovascular dysfunction by improving vasodila- 2010; published online 17 June 2010 tory capacity5 and reducing arterial stiffness in Acute exercise and hypertension YN Boutcher et al 312 healthy young males.6,7 The likely mechanism one or two parents or grandparents suffering from underlying these effects is enhanced release of nitric hypertension, as confirmed by anti-hypertensive med- oxide through increased blood flow.5,8 Nitric oxide ication usage. All procedures and potential risks were has been shown to increase after acute exercise by explained and participants gave their written informed improving circulating endothelial progenitor cells in consent. This study was approved by a university humans9 and regulating endothelial receptor num- human experimentation ethics committee. ber/receptor affinity in rats.10 Thus, nitric oxide may have an important role in improving vascular function. However, not all studies have shown the Anthropometric and electrode placement acute exercise–nitric oxide relationship. Equivocal Anthropometric measures included height, weight findings may be due to varying exercise modality, and skinfolds to determine body fat percentage.18 intensity, duration and subject population. Three bipolar electrocardiogram electrodes were The effect of acute exercise on cardiopulmonary applied to the participants’ chest to monitor heart baroreceptor (CPBR) and CBR function of offspring of rate (HR). Resting HR was determined by calculating hypertensives is undetermined. However, Silva the respiration rate interval from the electrocardio- 11 et al. have shown that an acute bout of exercise. for gram after 15–20 min in a supine position. Stroke 45 min at 50% of maximal oxygen uptake (VO2max) volume (SV) during baseline and lower-body nega- improved arterial baroreflex and CPBR sensitivity in tive pressure (LBNP) was measured non-invasively spontaneous hypertensive rats (SHR), whereas Brum through impedance cardiography19 using a Minnesota et al.12 found that the improvement in baroreceptor Impedance Cardiograph (Model 304B, Minnesota, sensitivity also occurred in both SHR and normoten- MN, USA) with a tetrapolar aluminium band elec- sive rats. The improvement in baroreceptor sensitivity trode configuration.20 The inner two measuring after acute exercise in SHR rats was thought to be due electrodes were located at the base of the neck and to haemodynamic change and/or sympathetic activa- at the level of the xiphistal point of the thorax.20 The tion during exercise, which led to a reduction in two outer current electrodes were placed 3–5 cm sympathetic activity after exercise.13,14 outside of the measuring electrodes, imposing a In hypertensive individuals, acute exercise has sinusoidal current of 4 mA with a frequency of been shown to produce significant post-exercise 100 kHz. SV was recorded every 25 s and was decreases in BP.15 Reduced peripheral resistance calculated using the Kubicek equation.21 Software and increased vasodilator substances have been usingensembleaveragingwasusedtoprocessthe proposed as underlying mechanisms.16 However, impedance cardiogram (COP, Microtonics Inc., Cha- whether a post-exercise reduction in BP would be pel Hill, NC, USA). The validity of impedance observed in the normotensive young individual cardiography has been established by comparing with a family history of hypertension is unknown. values with isotope/thermodilution, which correlated The effect of acute exercise on AIx in offspring of significantly.22,23 hypertensive individuals has not been explored; however, Tabara et al.17 found that there was no change in AIx after acute exercise in apparently BP healthy and sedentary elderly subjects, although AIx Systolic, diastolic and mean arterial blood pressure changed after 6 months of aerobic exercise. Thus, it (MAP) were monitored using a BP monitor (Jentow, is undetermined what effect acute exercise would Colin Electronics, Komaki, Japan) on a beat-by-beat have on the AIx of young offspring of hypertensives. basis by attaching a radial artery sensor to the left Therefore, the purpose of this study was to determine wrist. During the 5-min recovery period, after LBNP whether a 20-min bout of acute aerobic exercise could at À20 mm Hg, HR and MAP were monitored to improve vascular, carotid and cardiopulmonary baror- ensure that they had returned to baseline levels. eceptor sensitivity, as well as AIx, in normotensive young males with a family history of hypertension. Baseline FBF and peripheral resistance Baseline and peak FBF levels were measured using Methods strain-gauge plethysmography (Model EC-4, D.E. Hokanson, Inc., Bellevue, WA, USA) using the Subjects venous occlusion technique. While participants Subjects were 40 normotensive healthy young males were in the resting supine position, strain gauges, aged between 18 and 27 years, possessing either a which were 2–3 cm less than the limb circumfer- background of family hypertension (FH þ ; n ¼ 20) or no ence, were applied to the right forearm. The position family history of hypertension (FHÀ; n ¼ 20). Both of the forearm was at least 301 above heart level. groups were physically active and were involved in A venous cuff was attached to the upper arm, whereas moderate-intensity exercise (for example, jogging, an arterial cuff was attached to the wrist. A radial cycling or recreational sports) for 1–3 sessions per artery tonometry blood pressure sensor (Jentow) was week, lasting at least 30 min per session for at least 2 attached to the subjects’ left wrist to obtain beat- years. Family history of hypertension was defined as by-beat BP waveforms. Data were collected 15 min

Journal of Human Hypertension Acute exercise and hypertension YN Boutcher et al 313 after the application of the strain gauge and cuffs. LBNP divided by the change in SV from baseline to Baseline FBF was obtained by inflating the venous LBNP. cuff to 50 mm Hg24 for 5 s every 15 s, whereas the arterial cuff was inflated to suprasystolic pressure and maintained for the duration of the measurement. CBR sensitivity Blood flow was determined by measuring the rate of Neck suction (NS) was applied using equipment 34 increase in volume and flow rate was expressed as a similar to the design of Ogoh et al. Two suction volume change per unit time (ml of blood flow per cups were placed over both carotid arteries. The 100 ml of tissue per min). Increase in circumference device, connected by tubing to a reservoir, was when the venous cuff was inflated is reflected by a connected to a vacuum source, which was set change in electrical resistance of the strain gauge.25 to achieve the required suction pressure. The order Baseline FBF was then determined by averaging six of NS was counter balanced (À20, À40, À60 and blood flow measurements. The blood flow wave was À80 mm Hg). NS was performed during held expira- collected and analysed through customised data tion (10–15 s) and applied for 5 s to ensure that acquisition software (BP Monitor, The University of maximal bradycardia was attained. CBR sensitivities New South Wales). Baseline FVR was calculated by were calculated from the RR interval in milliseconds dividing baseline MAP by baseline FBF. divided by systolic arterial blood pressure. Systolic arterial blood pressure instead of MAP was used in the calculation because of the ease and accuracy of 35 Peak FBF and peripheral resistance this measurement. Peak FBF was obtained through reactive hyperaemia blood flow. The protocol was a shortened version of AIx that used by Kouame´ et al.26 The venous cuff on the Before and after acute exercise, applanation tono- upper arm was inflated to 60 mm Hg above partici- metry (SphygmoCor, AtCor Medical Pth Ltd, pants’ systolic arterial blood pressure without an Sydney, Australia) was used to assess AIx. AIx is a arterial cuff (wrist cuff) and was maintained for surrogate measure of arterial stiffness, which is 5 min. To obtain peak blood flow, the venous cuff measured through pulse wave analysis. AIx was was deflated and the arterial cuff was inflated to determined by placing a tonometry sensor on a suprasystolic pressure, after which the venous cuff radial artery. Twenty consecutive wave forms were was inflated to 50 mm Hg every 5 s for 1 min. Peak recorded to analyse AIx, which was derived from FBF was determined as the highest blood flow of six the ratio of augmented pressure and pulse pressure. measurements obtained after reactive hyperaemia Applanation tonometry (SphygmoCor) is a reliable, blood flow. Reactive hyperaemia blood flow can also valid measure of arterial stiffness and has been be used to assess endothelial function in humans.27 compared against Complior and VaSera devices.36 The correlation between non-invasive reactive hyperaemia blood flow and infusion of acetylcholine (30 mg minÀ1) was 0.91.27 Peak FVR was calculated . Maximal oxygen uptake (VO2max) test by dividing peak MAP by peak FBF. Strain gauge . All subjects underwent a VO2max test using an plethysmography is a reliable measure to assess electronic bike (Monark E319, Sweden). The max- blood flow. Strain gauge plethysmography has been . imal load achieved in the VO2max test was used to compared against other methods, such as water determine the 60% maximal load required for the 28–30 31,32 plethysmography and Doppler ultrasound. acute exercise bout. Gases were collected through a Results from both devices correlated significantly. Parvomedic metabolic cart (TrueOne model 2400, ParvoMedics Inc., Utah, UT, USA). Subjects cycled at a cadence of 60–80 revolutions per minute. The CPBR sensitivity initial load was 30 watts (W) for the first minute, LBNP was applied distal to the iliac crest while then the load was increased gradually by 1 W every subjects were at rest. LBNP allows evaluation of 2 s. The test was terminated when the respiratory CPBR sensitivity by manipulation of central venous exchange ratio exceeded 1.10 or when partici- pressure (CVP). The level of LBNP was manually pants reached volitional exhaustion. The accuracy controlled to produce a reduction in CVP. At and reliability of the Parvomedic metabolic cart pressures of À20 mm Hg, CVP decreases without (TrueOne model 2400) has been verified by compar- decreasing arterial pressure and, therefore, reflects ison with the Douglas bag technique.37 decreases in CPBR sensitivity but not arterial baroreceptor sensitivity. In this study, a reduction in SV in relation to LBNP was used instead of CVP, Procedure . as the reduction in SV has been shown to be similar In session one, all subjects underwent the VO2max to that of CVP.33 After 5 min of baseline HR and test to determine the 60% load that was used BP measurement, LBNP at À20 mm Hg for 5 min in acute. exercise. In session two, at least 24 h after was applied. CPBR sensitivity was determined by the VO2max test, subjects underwent pre-exercise calculating the change in FVR from baseline to measurement of peripheral vasculature, baro-

Journal of Human Hypertension Acute exercise and hypertension YN Boutcher et al 314 receptor sensitivity and AIx in a supine position. body mass index, body fat percentage, BP and For both sessions, all subjects were required to similar aerobic fitness levels (Table 1). refrain from eating, smoking and ingesting caffeine and alcohol for at least 3 hours. Initial assessment was started with the pre-exercise measurements of Pre- and post-exercise response between groups FBF, SV and BP. CPBR sensitivity was then assessed There was no significant difference in baseline FBF through the application of 5 min of LBNP at at pre- and post-exercise between groups; how- À20 mm Hg. During application of LBNP, SV, FBF ever, baseline FBF was enhanced significantly after and BP were recorded continuously. Thereafter, the exercise in both groups, Po0.05 (Figure 1a; Table 2). assessment of CBR sensitivity was performed using Baseline FVR of FH þ subjects (55.8±4.4 mm Hg ml NS after a 5 min recovery of LBNP. Four different per 100 ml of tissue per min) at pre–exercise was negative pressures (À20, À40, À60 and À80 mm Hg) 29% higher than that of FHÀ subjects (43.1±3.6 mm were used to stimulate the CBR. Three repetitions of Hg per ml per 100 ml of tissue per min), P ¼ 0.03 NS for 5 s at each stage with 1-min intervals between (Figure 1b). However, after acute exercise, FVR of repetitions were performed during held expiration FH þ subjects (29.8±3.2 mm Hg per ml per 100 ml of between 10–15 s. The order of LBNP and NS was tissue per min) was reduced to a level similar to that counterbalanced. Once the pre-exercise measure- of FVR of FHÀ subjects (29.3±4.1 mm Hg per ml per ments were completed, subjects moved to the bike. 100 ml of tissue per min; Figure 1b). Twenty minutes. of one single bout of exercise at 60% of VO2max on the stationary bike was then performed after pre-exercise measurement of FBF, Pre- and post-hyperaemia stimuli between groups CPBR and CBR sensitivities, and AIx. Thereafter, a Peak FBF at pre-exercise of FH þ subjects (22.3± 30-min recovery period was allowed before the 0.9 ml per 100 ml of tissue per min) was 27% lower measurement of post-exercise response. than that of FHÀ subjects (28.4±1.6 ml per 100 ml of tissue per min), P ¼ 0.003 (Figure 1a), whereas Statistical analysis Subject characteristics and baseline cardiovascular Peak 35 Peak variables were compared using independent t-tests. FH- * An independent t-test was also performed on change 30 ) + * scores (baseline-LBNP) of FBF, FVR, CPBR and CBR -1 FH sensitivities, and AIx. Dependent t-tests were also 25 .min

performed on FBF and CPBR for each group. Mixed -1 between-within analysis of variance was performed 20 on NS, then Bonferroni adjustment was used to compare the main effects during NS. The statistical 15 analysis was considered significant when the prob- 10 Forearm blood flow ability level was o0.05. Baseline

(ml.100 ml tissue Baseline 5 ** Results 0 Pre exercise Post exercise There were no significant differences in subject 70 Baseline characteristics and in baseline cardiovascular para- FH-

) +

meters between groups. Both groups had normal -1 FH 60 .min

Table 1 Physical characteristics and baseline cardiovascular -1 50 levels of young males with (FH+; n ¼ 20) and without (FHÀ; n ¼ 20) a family history of hypertension 40 Baseline Variable FH+ (n ¼ 20) FHÀ (n ¼ 20) ** 30

Age (years) 22.2 (0.5) 21.3 (0.6) 20 Height (cm) 175.0 (1.2) 177.9 (1.3) Peak Weight (kg) 67.6 (1.7) 70.4 (2.2) Peak Forearm vascular resistance 10 Body mass index (kg mÀ2) 21.9 (0.7) 22.2 (0.5) (mmHg.ml.100 ml tissue * * Body. fat percentage (%) 16.0 (0.8) 15.9 (0.8) * À1 0 VO2max (l min ) 2.7 (0.12) 3.0 (0.14) . À1 À1 Pre exercise Post exercise VO2max (ml kg min ) 40.9 (1.9) 42.7 (1.5) Resting heart rate (b minÀ1) 66.9 (2.0) 67.0 (1.8) Figure 1 Baseline and peak forearm blood flow (a) and baseline Systolic blood pressure (mm Hg) 119.4 (2.3) 120.7 (1.4) and peak forearm vascular resistance (b) of young males with Diastolic blood pressure (mm Hg) 69.3 (1.9) 67.8 (1.1) (FH þ ) and without (FHÀ) a family history of hypertension before and after 20 min of acute exercise. (*) indicates values that are . w Abbreviation: VO2max, maximal oxygen uptake. significantly different from pre (Po0.05); indicates values that Data are mean and standard errors of the means. are significantly different from those of FHÀ subjects (Po0.05).

Journal of Human Hypertension Acute exercise and hypertension YN Boutcher et al 315 Table 2 Baseline pre- and post-cardiovascular measures following hyperaemia stimuli, cardiovascular measures to LBNP and baroreceptor response to stimuli of young males with (FH+; n ¼ 20) and without (FHÀ; n ¼ 20) a family history of hypertension

Variable FH+ (n ¼ 20) FHÀ (n ¼ 20)

Pre Post Pre Post

Baseline Forearm blood flow (ml per 100 ml of tissue per min) 1.6 (0.2) 3.3 (0.3)* 2.1 (0.2) 3.0 (0.3)* Forearm vascular resistance (mm Hg ml per 100 ml of tissue per min) 55.8 (4.4) 29.8 (3.2)* 43.1 (3.6) 29.3 (4.1)* Mean arterial pressure (mm Hg) 82.2 (1.5) 81.3 (1.2) 83.0 (1.2) 82.2 (1.1) Stroke volume (ml) 107.4 (3.8) 93.0 (4.4)* 115.4 (4.6) 91.4 (5.4)* Augmentation index (%) À2.8 (2.3) À2.6 (2.0) À3.6 (2.3) À5.4 (1.9)

Hyperaemia stimuli Peak forearm blood flow (ml per 100 ml of tissue per min) 22.3 (0.9) 27.1 (1.6)* 28.4 (1.6) 31.4 (1.9)* Peak forearm vascular resistance (mm Hg ml per 100 ml of tissue per min) 3.5 (0.2)w 2.9 (0.2)* 2.8 (0.2) 2.5 (0.1)* Mean arterial pressure (mm Hg) 76.6 (1.6) 76.5 (2.5) 74.0 (1.3) 75.4 (1.8)

Lower body negative pressure Forearm blood flow (ml per 100 ml of tissue per min) 1.2 (0.1) 1.9 (0.2) 1.4 (0.1) 2.1 (0.2) Forearm vascular resistance (mm Hg ml per 100 ml of tissue per min) 73.9 (5.4) 49.8 (4.9) 60.0 (4.7) 45.1 (4.3) Mean arterial pressure (mm Hg) 83.1 (1.9) 78.6 (1.6) 78.0 (1.6) 78.2 (1.7) Stroke volume (ml) 89.3 (4.3) 80.4 (3.6)* 97.3 (5.2) 79.2 (5.3)*

Data are mean and standard errors of the means. *Significantly different from pre (Po0.05); wsignificantly different from FHÀ (Po0.05). peak FVR (after hyperaemia stimulus) at pre- Exercise Combined - + þ Pre Post FH and FH exercise of FH subjects (3.45±0.2 mm Hg.ml per 0.0 100 ml of tissue per min) was 24% higher than that of FHÀ subjects (2.78±0.2), P ¼ 0.012 (Figure 1b). -0.5 After 20 min of acute exercise, both groups showed an improvement in peak FBF and peak FVR. -1.0 þ

In FH subjects, peak FBF was significantly in- SV) Δ -1.5 creased by 22%, t(17) ¼ 4.2, P ¼ 0.001, and peak FVR FH- Pre FH+

was decreased by 17%, t(17) ¼ 2.9, P ¼ 0.009. How- FVR/ ever, there were no significant differences in both Δ -2.0 peak FBF and peak FVR between groups, P40.05 -2.5

(Figures 1a and b). MAP levels during peak FBF at CPBR ( FH+ Post þ pre- and post-exercise were similar between FH -3.0 (pre: 76.6±1.6 mm Hg; post: 76.5±2.5 mm Hg) and * FHÀ (pre: 74.0±1.3 mm Hg; post: 75.4±1.8 mm Hg) -3.5 individuals. FH- -4.0 Figure 2 Cardiopulmonary baroreceptor (CPBR) sensitivity of Pre- and post-exercise response to LBNP between young males with (FH þ ) and without (FHÀ) a family history groups of hypertension before and after 20 min of acute exercise. Baseline FBF at pre- and post-exercise was signifi- (*) indicates values that are significantly different from pre cantly reduced in response to LBNP in both groups. (Po0.05). At pre-exercise, FBF was reduced by 25% in FH þ and by 33% in FHÀ subjects, whereas at post- groups. The CPBR of both groups was significantly exercise, FBF was reduced by 42% in FH þ and by more sensitive, t(39) ¼ 2.6, P ¼ 0.013, after exercise 30% in FHÀ subjects (Table 2). The decrease of FBF (Figure 2). to LBNP at pre- and post-exercise was also followed At pre-exercise, the absolute values of CBR in FHÀ by increases in FVR. FVR was increased by 32% and subjects were higher throughout NS stimulation; 39% in FH þ and FHÀ subjects, respectively, at pre- however, the difference between groups was not exercise. At post-exercise, FVR was increased by significant, F (1,38) ¼ 3.6, P ¼ 0.07 (Figure 3). Simi- 67% in FH þ and by 54% in FHÀ subjects (Table 2). larly, there was no significant difference bet- SV was also found to decrease significantly in ween groups at post-exercise. However, there was a relation to LBNP in both groups. The MAP response significant time main effect throughout the NS, to LBNP at pre- and post-exercise, however, was F (3,111) ¼ 6.9, P ¼ 0.000, which indicated dec- similar in both groups (Table 2). reased CBR sensitivity after exercise in both groups There were no significant differences in CPBR (Figure 3). Following exercise, there was a non- sensitivity at pre- and post-exercise between significant decrease in AIx by 7% in FH þ and by

Journal of Human Hypertension Acute exercise and hypertension YN Boutcher et al 316 10.0 FH- FH+ vasodilatory capacity by reducing both baseline and peak FVR. This study shows that one single 9.5 bout of moderate exercise can significantly increase

Pre exercise vasodilatory capacity. The fact that reduced vasodi- 9.0 latory capacity of FH þ individuals was improved 8.5 with one bout of aerobic exercise suggests that Post exercise * vasodilatory capacity could be enhanced if this type 8.0 of exercise was performed regularly. (RR interval/SBP) 7.5

Carotid baroreceptor sensitivity CPBR sensitivity 7.0 It was expected that FH þ subjects would exhibit -20 -40 -60 -80 less-sensitive CPBR than would FHÀ subjects. How- Figure 3 Carotid baroreceptor sensitivity of young males with ever, in contrast to a previous study,3 CPBR þ À (FH ) and without (FH ) a family history of hypertension before sensitivity of both groups was similar. Both groups (FHÀ:K;FHþ : J) and after (FHÀ:m;FHþ : D) 20 min of acute exercise. (*) indicates values that are significantly different from showed enhanced CPBR sensitivity after acute pre (Po0.05). exercise. This result seems to be a novel finding, although it is in agreement with a chronic training study that has shown that regular exercise improves 50% in FHÀ subjects. Young FHÀ subjects had lower CPBR sensitivity in normotensive and hypertensive absolute values of AIx at pre- and post-exercise rats.12 In humans, Takeshita et al.39 showed that compared with FH þ subjects; however, the differ- young athletes had a higher CPBR baroreflex control ence between groups was not significant. Both of FVR than non-athletes. The ability of exercise to groups showed normal AIx levels (Table 2). have a major role in maintaining healthy CPBR is also supported by Giannattasio et al.40 who showed that detraining leads to impaired CPBR in athletes. Aerobic fitness and CBR sensitivity Thus, in the present study, the young age of When the participants were divided into low (25– the participants and their involvement in regular À1 À1 À1 À1 43.9 ml kg min ) and high. (444 ml kg min ) physical activity may have prevented or delayed fitness (on the basis on their VO2max), regardless the development of reduced CPBR sensitivity in of familial history of hypertension, significant FH þ subjects. The fact that FH þ participants were differences in CBR between low- and high-fitness physically active may suggest that exposure to groups were found at pre-exercise, F (1,38) ¼ 12.2, chronic exercise can positively influence CPBR P ¼ 0.001, and post-exercise, F (1,37) ¼ 4.5, sensitivity. P ¼ 0.041. Low-fitness participants had lower CBR The short duration of exercise in this study compared with high-fitness participants. (20 min) may have affected the magnitude of improvement in CPBR. For example, Silva et al.11 Discussion have shown that. an acute bout of exercise for 45 min at 50% of VO2max led to increased baroreflex The acute effect of aerobic exercise on vascular, bradycardia in SHR, whereas exercise training. for baroreceptor sensitivities and AIx in young normo- 5 days a week for 60 min at 50% of VO2max tensive males with (FH þ ) and without (FHÀ)a attenuated hypertension, concomitant with im- family history of hypertension was examined. The proved arterial baroreflex and CPBR sensitivity in 11 major finding was that acute exercise increased the SHR. Thus, acute exercise duration greater than vasodilatory capacity of FH þ subjects. 20 min may be needed to produce changes in CPBR sensitivity.

Peak FBF and vascular resistance (FVR) The low peak FBF possessed by FH þ subjects in this CBR sensitivity study is in agreement with previous research.1,3,38 There was no significant difference in CBR sensi- Consistently, both FH þ males1,38 and females3 have tivity between groups at pre- and post-exercise; FH þ possessed lower peak FBF compared with indivi- subjects, however, showed a tendency to possess duals without a family history of hypertension. less CBR sensitivity at both pre- and post-exercise. Thus, individuals with a family history of hyperten- The slightly impaired CBR control of HR in FH þ sion have reduced ability to vasodilate their arter- subjects may be an early indication of baroreflex ioles in response to hyperaemia. Endothelial abnormality. The results of this study do not support dysfunction and hereditary may have contributed those of Ookuwa et al.3 who found that young FH þ to this condition. This reduced arteriolar vasodila- subjects had significantly reduced CBR sensitivity tory ability was also accompanied by higher FVR compared with FHÀ subjects. Differences in metho- in response to hyperaemia (peak FVR). However, dology and subject’s gender may have influenced one single bout of moderate exercise improved the results. The similarity in CBR sensitivity of both

Journal of Human Hypertension Acute exercise and hypertension YN Boutcher et al 317 groups in response to NS could be explained by self-reported family history by participants. their young age. Interestingly, when the participants Although this questionnaire has been used in were divided into low. and high aerobic fitness (on previous published studies, more reliable measures, the basis of their VO2max), regardless of familial such as assessment of parent’s BP, should be used to history of hypertension, significant differences in identify family history of hypertension. In conclu- CBR between the low- and high-fitness group were sion, 20 min of acute cycle exercise decreased FVR found at pre- and post-exercise. Thus, low-fitness and increased FBF response to hyperaemia, normal- participants had lower CBR compared with high- ising these responses in FH þ subjects. Moreover, fitness participants. This finding is in agreement it increased CPBR and decreased CBR sensitivity, with that of Barney et al.41 who found that highly fit but did not change AIx in normotensive subjects, subjects had higher CBR sensitivity compared with regardless of the presence of familiar history of sedentary subjects. Therefore, in the present study, hypertension. as both groups (FH þ and FHÀ) consisted of low- and high-fitness individuals, significant differences should not be expected. It seems that participation in physical activity may prevent reduced CBR What is known about topic sensitivity in FH þ subjects. Regardless of hyperten- K Individuals with a family history of hypertension possess elevated forearm vascular resistance and low CPBR and sion background, both groups showed reduced CBR CBR sensitivity. sensitivity after exercise. This finding is in agree- K Acute exercise elevates forearm vasodilation in healthy ment with previous studies that have shown that young males without a family history of hypertension. acute aerobic exercise consistently reduces barore- 42,43 What this study adds ceptor sensitivity. The physiological mechan- K Peak forearm blood flow of individuals with a family isms for reduced CBR sensitivity after aerobic history of hypertension (FH+) was improved following exercise are undetermined, although Heffernan acute exercise et al.44 showed that central arterial stiffness was K Baseline and peak forearm vascular resistance (measured by + decreased after a bout of aerobic exercise. However, reactive hyperaemia) of FH was reduced following acute exercise. in the present study, arterial stiffness was not K Acute exercise increased CPBR sensitivity in individuals reduced after exercise, suggesting that it may not with and without a family history of hypertension. be the major contributor to the decrease in CBR sensitivity after 20 min of moderate aerobic cycle exercise. Lack of post-exercise hypotension observed in this study may have possibly been caused by the Conflict of interest shorter exercise time (20 min) than that used in The authors declare no conflict of interest. previous studies,11,45 or could be because subjects had normal BP to begin with. Twenty minutes . References of exercise at 60–70% of VO2max, however, has been previously shown to reduce mean arterial 1 Takeshita A, Imaizumi T, Ashihara T, Yamamoto K, 46 pressure in hypertensive rats. It seems that a Hoka S, Nakamura M. Limited maximal vasodilator longer duration of acute exercise is needed to capacity of forearm resistance vessels in normotensive observe post-exercise hypotension. Furthermore, young men with a familial predisposition to hyperten- Jones et al.15 have shown that post-exercise hypo- sion. Cir Res 1982; 50: 671–677. tension at intermittent exercise, three repetitions for 2 Boutcher YN, Park YJ, Boutcher SH. Vascular and . baroreceptor abnormalities in young males with a 10 min with 10 min intervals at 70% of VO2peak, was higher than that of 30 min of continuous family history of hypertension. Eur J Appl Physiol cycling. Time of exercise also seems to affect the 2009; 107: 653–658. 3 Ookuwa H, Takata S, Ogawa J, Iwase N, Ikeda T, Hattori magnitude of post-exercise hypotension, as inter- N. Abnormal cardiopulmonary baroreflexes in normo- mittent exercise in the afternoon (08.00–16.00 h) had tensive young subjects with a family history of essential a greater post-exercise hypotension effect than hypertension. J Clin Hypertens 1987; 3: 596–604. morning exercise (04.00–08.00 h). 4 Yasmin, Falzone R, Brown MJ. Determinants of arterial The similar response in AIx at pre- and post- stiffness in offspring of families with essential hyper- exercise for both groups indicates that arterial tension. Am J Hypertens 2004; 17: 292–298. stiffness development is mostly influenced by age. 5 Kingwell BA, Sherrard B, Jennings GL, Dart AM. Four As both groups were young and of similar age, weeks of cycle training increases basal production of changes in AIx were not expected. Thus, it is nitric oxide from the forearm. Am J Physiol 1997a; 272: apparent that peripheral rather than central vascular H1070–H1077. 6 Kingwell BA, Berry KL, Cameron JD, Jennings GL, changes occur earlier in young FH þ compared with À Dart AM. Arterial compliance increases after moderate- young FH . intensity cycling. Am J Physiol 1997b; 273: H2186–H2191. One of the limitations of this study was that there 7 Cameron JD, Dart AM. Exercise training increases total was no control condition in which subjects did systemic arterial compliance in humans. Am J Physiol not perform exercise. Another limitation was the Heart Circ Physiol 1994; 266: H693–H701.

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