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We aimed to provide evidence for an a priori hypothesis and sample size for subjectively assessing physical activity intensity and duration in paediatric population, adopting objective methods as the reference. We searched electronic databases, reference lists and author databases. Correlation coefficients were pooled as an indicator of agreement estimates. We found 183 agreement analyses (94.5% based on correlation coefficients) from 89 studies that met our inclusion criteria. We identified four physical activity parameters addressing intensity and two parameters addressing duration. The physical activity parameters focusing on intensity were measured only by questionnaires, and the best correlation was achieved by moderate-to-vigorous physical activity compared with a heart rate monitor. In addition, total physical activity duration had a stronger correlation with an accelerometer when measured by diaries or logs than when measured by questionnaires. In both cases, the correlation was moderate. Studies with sample sizes between 50 and 99 subjects showed measurements that were stable in both magnitude and interpretation. Our findings suggest that the agreement between subjective and objective methods for assessing physical activity intensity and duration is weak to moderate. Furthermore, sample sizes ranging from 50 to 99 subjects provide stable agreement estimates between methods.

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OBJECTIVES: The aims of this study were twofold: (i) to model changes in body mass index (BMI) of 10-18-year-old adolescents, and (ii) to investigate the effects of total physical activity (TPA), physical fitness (PF), sleep duration and fruit/vegetable consumption in BMI trajectories across time. METHODS: Data were obtained from the Oporto Growth, Health and Performance Study and comprised 6894 adolescents (3418 girls) divided into four age cohorts (10, 12, 14 and 16 years) measured annually for 3 years. BMI was computed using the standard formula (kg m(-2)); TPA was estimated with the Baecke questionnaire; PF measures included 1-mile run/walk, 50 yard dash (50YD), standing long jump (SLJ), handgrip strength (HGr) and agility shuttle run. Longitudinal changes in BMI were analyzed using the multilevel modeling approach. RESULTS: The average BMI at age of peak of height velocity was 20.7±0.07 kg m(-2) for girls (P<0.001) and 20.58±0.06 kg m(-2) for boys (P<0.001). The annual increment in BMI was 1.36±0.04 kg m(-2), P<0.001 and 1.23±0.03 kg m(-2), P<0.001 for girls and boys, respectively. PF were related to BMI trajectories in both sexes (Girls: ß1mile=0.12±0.02, P<0.001; ßSLJ=-0.01±0.00, P<0.001; ß50YD=0.28±0.05, P<0.001; ßHGr=-8.91±0.54, P<0.001; Boys: ß1mile=0.18±0.02, P<0.001; ßSLJ=-0.01±0.00, P<0.001; ß50YD=0.26±0.04, P<0.001; and ßHGr=-8.15±0.45, P<0.001). TPA only showed significant, but positive, association with girls' BMI trajectories (ß=0.10±0.03, P=0.001). After adjusting for the covariates, sleep duration and fruit/vegetable intake did not show any significant association with BMI trajectories either sex. CONCLUSIONS: BMI increased linearly with age in both gender. PF levels are negatively associated with BMI across time in both boys and girls. Therefore, promotion of PF in the adolescent years seems to be effective in the early prevention of obesity.

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To compare post-resistance exercise hypotension (PREH) and its mechanisms in normotensive and hypertensive individuals, 14 normotensives and 12 hypertensives underwent two experimental sessions: control (rest) and exercise (seven exercises, three sets, 50% of one repetition maximum). Hemodynamic and autonomic clinic measurements were taken before (Pre) and at two moments post-interventions (Post 1: between 30 and 60 min; Post 2: after 7 h). Ambulatory blood pressure (BP) was monitored for 24 h. At Post 1, exercise decreased systolic BP similarly in normotensives and hypertensives (-8 ± 2 vs -13 ± 2 mmHg, P > 0.05), whereas diastolic BP decreased more in hypertensives (-4 ± 1 vs -9 ± 1 mmHg, P < 0.05). Cardiac output and systemic vascular resistance did not change in normotensives and hypertensives (0.0 ± 0.3 vs 0.0 ± 0.3 L/min; -1 ± 1 vs -2 ± 2 U, P > 0.05). After exercise, heart rate (+13 ± 3 vs +13 ± 2 bpm) and its variability (low- to high-frequency components ratio, 1.9 ± 0.4 vs +1.4 ± 0.3) increased whereas stroke volume (-14 ± 5 vs -11 ± 5 mL) decreased similarly in normotensives and hypertensives (all, P > 0.05). At Post 2, all variables returned to pre-intervention, and ambulatory data were similar between sessions. Thus, a session of resistance exercise promoted PREH in normotensives and hypertensives. Although this PREH was greater in hypertensives, it did not last during the ambulatory period, which limits its clinical relevance. In addition, the mechanisms of PREH were similar in hypertensives and normotensives.

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This study investigated the effect of the dihydropyridine calcium channel antagonist, amlodipine, on blood pressure (BP) during resistance exercise performed at different intensities in hypertensives. Eleven hypertensives underwent 4 weeks of placebo and amlodipine (random double-blinded crossover design). In each phase, they performed knee extension exercise until exhaustion following three protocols: one set at 100% of 1 RM (repetition maximum), three sets at 80% of 1 RM, and three sets at 40% of 1 RM. Intraarterial BP was measured before and during exercise. Amlodipine reduced maximal systolic/diastolic BP values achieved at all intensities (100% = 225 ± 6/141 ± 3 vs. 207 ± 6/130 ± 6 mmHg; 80% = 289 ± 8/178 ± 5 vs. 273 ± 10/169 ± 6 mmHg; 40% = 289 ± 10/176 ± 8 vs. 271 ± 11/154 ± 6 mmHg). Amlodipine blunted the increase in diastolic BP that occurred during the second and third sets of exercise at 40% of 1RM (+75 ± 6 vs. +61 ± 5 mmHg and +78 ± 7 vs. +64 ± 5 mmHg, respectively). Amlodipine was effective in reducing the absolute values of systolic and diastolic BP during resistance exercise and in preventing the progressive increase in diastolic BP that occurs over sets of low-intensity exercise. These results suggest that systemic vascular resistance is involved in BP increase during resistance exercise, and imply that hypertensives receiving amlodipine are at lower risk of increased BP during resistance exercise than non-medicated patients.

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Due to differences in study populations and protocols, the hemodynamic determinants of post-aerobic exercise hypotension (PAEH) are controversial. This review analyzed the factors that might influence PAEH hemodynamic determinants, through a search on PubMed using the following key words: "postexercise" or "post-exercise" combined with "hypotension", "blood pressure", "cardiac output", and "peripheral vascular resistance", and "aerobic exercise" combined only with "blood pressure". Forty-seven studies were selected, and the following characteristics were analyzed: age, gender, training status, body mass index status, blood pressure status, exercise intensity, duration and mode (continuous or interval), time of day, and recovery position. Data analysis showed that 1) most postexercise hypotension cases are due to a reduction in systemic vascular resistance; 2) age, body mass index, and blood pressure status influence postexercise hemodynamics, favoring cardiac output decrease in elderly, overweight, and hypertensive subjects; 3) gender and training status do not have an isolated influence; 4) exercise duration, intensity, and mode also do not affect postexercise hemodynamics; 5) time of day might have an influence, but more data are needed; and 6) recovery in the supine position facilitates systemic vascular resistance decrease. In conclusion, many factors may influence postexercise hypotension hemodynamics, and future studies should directly address these specific influences because different combinations may explain the observed variability in postexercise hemodynamic studies.

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Due to differences in study populations and protocols, the hemodynamic determinants of post-aerobic exercise hypotension (PAEH) are controversial. This review analyzed the factors that might influence PAEH hemodynamic determinants, through a search on PubMed using the following key words: “postexercise” or “post-exercise” combined with “hypotension”, “blood pressure”, “cardiac output”, and “peripheral vascular resistance”, and “aerobic exercise” combined only with “blood pressure”. Forty-seven studies were selected, and the following characteristics were analyzed: age, gender, training status, body mass index status, blood pressure status, exercise intensity, duration and mode (continuous or interval), time of day, and recovery position. Data analysis showed that 1) most postexercise hypotension cases are due to a reduction in systemic vascular resistance; 2) age, body mass index, and blood pressure status influence postexercise hemodynamics, favoring cardiac output decrease in elderly, overweight, and hypertensive subjects; 3) gender and training status do not have an isolated influence; 4) exercise duration, intensity, and mode also do not affect postexercise hemodynamics; 5) time of day might have an influence, but more data are needed; and 6) recovery in the supine position facilitates systemic vascular resistance decrease. In conclusion, many factors may influence postexercise hypotension hemodynamics, and future studies should directly address these specific influences because different combinations may explain the observed variability in postexercise hemodynamic studies.

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Post-resistance exercise hypotension has been extensively described in men and women. However, gender influence on this response has not yet been clear. Gender might change post-exercise hemodynamics, since men and women respond differently during exercise. Thus, the purpose was to compare post-resistance exercise hypotension and its hemodynamic determinants in men and women. Normotensive subjects (22-male, 22-female) underwent 2 sessions: control (40 min of rest) and exercise (6 resistance exercises, 3 sets, 20 repetitions, at 40-50% of 1RM). Blood pressure, heart rate, and cardiac output were measured prior to and following interventions. Blood pressure decrease after exercise was similar between the genders. However, hemodynamic determinants responded differently in men and women. Systemic vascular resistance reduced in women (-4.6±1.9U, P<0.05), while cardiac output decreased in men (-0.6±0.2 L/min, P<0.05). This response was accompanied by a decrease in stroke volume in men (-21.6±5.1 ml, P<0.05) and a more pronounced increase in heart rate in men than in women (+11.3±1.3 vs. +6.5±1.7 bpm, P<0.05, respectively). In conclusion, post-resistance exercise hypotension was similar in men and women. However, its hemodynamic determinants differ between the genders, depending on cardiac output decrease in men and on systemic vascular resistance decrease in women.

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The purpose of this study was to investigate the effect of resistance training on resting blood pressure and heart rate variability in elderly postmenopausal women. 29 untrained, non-hypertensive elderly women were randomly assigned to 2 groups: an intervention group (n=15, 65.5±5.0 years, 57.3±6.5 kg, 156.7±5.1 cm) that underwent a supervised resistance training program (8 exercises, 2 sets, 10-15 repetitions, 3 times/week) or a control group (n=14, 66.2±4.1 years, 61.1±11.7 kg, 157.5±7.1 cm) that participated in a supervised stretching program (25-30 min/session, 2 times/week). Resting auscultatory blood pressure, heart rate variability, evaluated from short recordings in a seated position, and maximal dynamic strength (1-RM test) were measured at baseline and after 12 weeks. A group x time ANOVA revealed that muscular strength increased significantly in the resistance training group (+ 10.2% for bench press and +12.7% for leg extension, P<0.05). Systolic blood pressure was reduced significantly in the resistance training group from pre- to post-intervention period (- 5 mmHg; P<0.05), while no significant effect was noted for diastolic blood pressure and heart rate variability indexes (P>0.05). None of these variables changed in the control group throughout the study. In conclusion, a supervised resistance training program improved muscular strength and reduced systolic blood pressure without affecting diastolic blood pressure and heart rate variability in elderly postmenopausal women.

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Moderate- to high-intensity strength training is recommended for healthy adults. In young subjects, a single session of strength training decreases blood pressure, while heart rate and cardiac work remain elevated afterwards. However, these effects have not been clearly demonstrated in elderly subjects. To investigate this issue, 16 elderly subjects each underwent a Control and an Exercise (3 sets, 8 RM, 9 exercises) session conducted in random order. Haemodynamic variables and heart rate variability were measured before and after the interventions. Systolic blood pressure did not change after the exercise session but did increase after the control session (+8.1±1.6 mm Hg, P≤0.05). Diastolic blood pressure, as well as systemic vascular resistance increased similarly after both sessions. Cardiac output and stroke volume decreased, while heart rate, rate-pressure product and the low- to high-frequency ratio of heart rate variability increased only after the exercise session ( - 0.5±0.1 L/min, - 9.3±2.0 ml,+3.8±1.6 bpm, +579.3±164.1 mmHg.bpm and +0.71±0.34, P≤0.05). Ambulatory blood pressure was similar after both sessions, while heart rate and rate pressure product remained higher after the exercise session for up to 4.5 h. After a single session of strength training, cardiac sympathetic modulation and heart rate remain elevated in elderly subjects, keeping cardiac work elevated for a long period of time.

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Blood pressure (BP) and physical activity (PA) levels are inversely associated. Since genetic factors account for the observed variation in each of these traits, it is possible that part of their association may be related to common genetic and/or environmental influences. Thus, this study was designed to estimate the genetic and environmental correlations of BP and PA phenotypes in nuclear families from Muzambinho, Brazil. Families including 236 offspring (6 to 24 years) and their 82 fathers and 122 mothers (24 to 65 years) were evaluated. BP was measured, and total PA (TPA) was assessed by an interview (commuting, occupational, leisure time, and school time PA). Quantitative genetic modeling was used to estimate maximal heritability (h²), and genetic and environmental correlations. Heritability was significant for all phenotypes (systolic BP: h² = 0.37 ± 0.10, P < 0.05; diastolic BP: h² = 0.39 ± 0.09, P < 0.05; TPA: h² = 0.24 ± 0.09, P < 0.05). Significant genetic (r g) and environmental (r e) correlations were detected between systolic and diastolic BP (r g = 0.67 ± 0.12 and r e = 0.48 ± 0.08, P < 0.05). Genetic correlations between BP and TPA were not significant, while a tendency to an environmental cross-trait correlation was found between diastolic BP and TPA (r e = -0.18 ± 0.09, P = 0.057). In conclusion, BP and PA are under genetic influences. Systolic and diastolic BP share common genes and environmental influences. Diastolic BP and TPA are probably under similar environmental influences.

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Blood pressure (BP) and physical activity (PA) levels are inversely associated. Since genetic factors account for the observed variation in each of these traits, it is possible that part of their association may be related to common genetic and/or environmental influences. Thus, this study was designed to estimate the genetic and environmental correlations of BP and PA phenotypes in nuclear families from Muzambinho, Brazil. Families including 236 offspring (6 to 24 years) and their 82 fathers and 122 mothers (24 to 65 years) were evaluated. BP was measured, and total PA (TPA) was assessed by an interview (commuting, occupational, leisure time, and school time PA). Quantitative genetic modeling was used to estimate maximal heritability (h²), and genetic and environmental correlations. Heritability was significant for all phenotypes (systolic BP: h² = 0.37 ± 0.10, P < 0.05; diastolic BP: h² = 0.39 ± 0.09, P < 0.05; TPA: h² = 0.24 ± 0.09, P < 0.05). Significant genetic (r g) and environmental (r e) correlations were detected between systolic and diastolic BP (r g = 0.67 ± 0.12 and r e = 0.48 ± 0.08, P < 0.05). Genetic correlations between BP and TPA were not significant, while a tendency to an environmental cross-trait correlation was found between diastolic BP and TPA (r e = -0.18 ± 0.09, P = 0.057). In conclusion, BP and PA are under genetic influences. Systolic and diastolic BP share common genes and environmental influences. Diastolic BP and TPA are probably under similar environmental influences.

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BACKGROUND: Exercise training is recommended as the first-line therapy for intermittent claudication patients. However, the effects of exercise therapy on cardiovascular function of these patients have been poorly studied. The aim of this study is to compare the effects of walking and strength training on cardiovascular responses assessed at rest and during exercise in patients with intermittent claudication. PATIENTS AND METHODS: Thirty-four patients with stable symptoms of intermittent claudication were randomized into two groups: strength training (ST) consisting of eight exercises, three sets of 10 repetitions, intensity of 11 - 13 on 15-grade Borg scale, 2-min interval between sets; and walking training (WT) consisting of walking on a treadmill, 15 bouts of 2-min, intensity of 11 - 13 on 15-grade Borg scale, with a 2-min interval between bouts. Before and after 12 weeks, blood pressure, heart rate and rate pressure product were measured at rest and during a progressive treadmill test until maximal claudication pain. RESULTS: Fifteen patients in each group completed the training program. After the training programs, resting systolic blood pressure (ST:-6 ± 13 mmHg and WT:-3 ± 18 mmHg, P = .04), heart rate (ST: -6 ± 10 bpm and WT:-2 ± 9 bpm, P = .03), and rate pressure product (ST:-1485 ± 1442 mmHg*bpm and WT:- 605 ± 2145 mmHg*bpm, P = .01) decreased significantly and similarly in both groups. Submaximal systolic blood pressure (ST: -14 ± 23 mmHg and WT:-6 ± 23 mmHg, P = .02), and rate pressure product (ST:-1579 ± 3444 mmHg*bpm and WT: -1264 ± 3005 mmHg*bpm, P = .04) decreased significantly and similarly in both groups. There were no changes in submaximal heart rate after ST and WT. Maximal systolic blood pressure, heart rate, and rate pressure product did not change in either group, although maximal exercise time increased similarly in the ST and WT groups (+31 ± 19 %, and +31 ± 32 %, respectively, P < .01). CONCLUSIONS: Strength and walking trainings promoted similar increases in walking capacity and decreases in resting and submaximal exercise cardiovascular load.

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Resistance training increases muscle strength in older adults, decreasing the effort necessary for executing physical tasks, and reducing cardiovascular load during exercise. This hypothesis has been confirmed during strength-based activities, but not during aerobic-based activities. This study determined whether different resistance training regimens, strength training (ST, constant movement velocity) or power training (PT, concentric phase performed as fast as possible) can blunt the increase in cardiovascular load during an aerobic stimulus. Older adults (63.9 ± 0.7 years) were randomly allocated to: control (N = 11), ST (N = 13, twice a week, 70-90 percent 1-RM) and PT (N = 15, twice a week, 30-50 percent 1-RM) groups. Before and after 16 weeks, oxygen uptake (VO2), systolic blood pressure (SBP), heart rate (HR), and rate pressure product (RPP) were measured during a maximal treadmill test. Resting SBP and RPP were similarly reduced in all groups (combined data = -5.7 ± 1.2 and -5.0 ± 1.7 percent, respectively, P < 0.05). Maximal SBP, HR and RPP did not change. The increase in measured VO2, HR and RPP for the increment in estimated VO2 (absolute load) decreased similarly in all groups (combined data = -9.1 ± 2.6, -14.1 ± 3.9, -14.2 ± 3.0 percent, respectively, P < 0.05), while the increments in the cardiovascular variables for the increase in measured VO2 did not change. In elderly subjects, ST and PT did not blunt submaximal or maximal HR, SBP and RPP increases during the maximal exercise test, showing that they did not reduce cardiovascular stress during aerobic tasks.

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Resistance training increases muscle strength in older adults, decreasing the effort necessary for executing physical tasks, and reducing cardiovascular load during exercise. This hypothesis has been confirmed during strength-based activities, but not during aerobic-based activities. This study determined whether different resistance training regimens, strength training (ST, constant movement velocity) or power training (PT, concentric phase performed as fast as possible) can blunt the increase in cardiovascular load during an aerobic stimulus. Older adults (63.9 ± 0.7 years) were randomly allocated to: control (N = 11), ST (N = 13, twice a week, 70-90% 1-RM) and PT (N = 15, twice a week, 30-50% 1-RM) groups. Before and after 16 weeks, oxygen uptake (VO(2)), systolic blood pressure (SBP), heart rate (HR), and rate pressure product (RPP) were measured during a maximal treadmill test. Resting SBP and RPP were similarly reduced in all groups (combined data = -5.7 ± 1.2 and -5.0 ± 1.7%, respectively, P < 0.05). Maximal SBP, HR and RPP did not change. The increase in measured VO(2), HR and RPP for the increment in estimated VO(2) (absolute load) decreased similarly in all groups (combined data = -9.1 ± 2.6, -14.1 ± 3.9, -14.2 ± 3.0%, respectively, P < 0.05), while the increments in the cardiovascular variables for the increase in measured VO(2) did not change. In elderly subjects, ST and PT did not blunt submaximal or maximal HR, SBP and RPP increases during the maximal exercise test, showing that they did not reduce cardiovascular stress during aerobic tasks.

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Blood pressure (BP) assessment during resistance exercise can be useful to avoid high BP, reducing cardiovascular risk, especially in hypertensive individuals. However, non-invasive accurate technique for this purpose is not available. The aim of this study was to compare finger photoplethysmographic (FPP) and intra-arterial BP values and responses during resistance exercise. Eight non-medicated hypertensive subjects (5 males, 30-60 years) were evaluated during pre-exercise resting period and during three sets of the knee extension exercise performed at 80% of 1RM until fatigue. BP was measured simultaneously by FPP and intra-arterial methods. Data are mean+/-SD. Systolic BP was significantly higher with FPP than with intra-arterial: at pre-exercise (157+/-13 vs. 152+/-10 mmHg; p<0.01) and the mean (202+/-29 vs. 198+/-26 mmHg; p<0.01), and the maximal (240+/-26 vs. 234+/-16 mmHg; p<0.05) values achieved during exercise. The increase in systolic BP during resistance exercise was similar between FPP and intra-arterial (+73+/-29 vs. +71+/-18 mmHg; p=0.59). Diastolic BP values and increases were lower with FPP. In conclusion, FPP provides similar values of BP increment during resistance exercise than intra-arterial method. However, it overestimates by 2.6+/-6.1% the maximal systolic BP achieved during this mode of exercise and underestimates by 8.8+/-5.8% the maximal diastolic BP.

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UNLABELLED: The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C-40 min of rest), low- (E40%-40% of 1 repetition maximum, RM), and high-intensity (E80%-80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF(R-R)nu) and high-frequency (HF(R-R)nu) components of the R-R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (-6 +/- 1 and -8 +/- 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (-0.4 +/- 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (-11 +/- 2 vs. -17 +/- 2 ml/beat, and +17 +/- 2 vs. +21 +/- 2 bpm, P < 0.05). LF(R-R)nu increased, while ln HF(R-R)nu decreased in both exercise sessions. IN CONCLUSION: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.

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Insulin infusion causes muscle vasodilation, despite the increase in sympathetic nerve activity. In contrast, a single bout of exercise decreases sympathetic activity and increases muscle blood flow during the postexercise period. We tested the hypothesis that muscle sympathetic activity would be lower and muscle vasodilation would be higher during hyperinsulinemia performed after a single bout of dynamic exercise. Twenty-one healthy young men randomly underwent two hyperinsulinemic euglycemic clamps performed after 45 min of seated rest (control) or bicycle exercise (50% of peak oxygen uptake). Muscle sympathetic nerve activity (MSNA, microneurography), forearm blood flow (FBF, plethysmography), blood pressure (BP, oscillometric method), and heart rate (HR, ECG) were measured at baseline (90 min after exercise or seated rest) and during hyperinsulinemic euglycemic clamps. Baseline glucose and insulin concentrations were similar in the exercise and control sessions. Insulin sensitivity was unchanged by previous exercise. During the clamp, insulin levels increased similarly in both sessions. As expected, insulin infusion increased MSNA, FBF, BP, and HR in both sessions (23 +/- 1 vs. 36 +/- 2 bursts/min, 1.8 +/- 0.1 vs. 2.2 +/- 0.2 ml.min(-1).100 ml(-1), 89 +/- 2 vs. 92 +/- 2 mmHg, and 58 +/- 1 vs. 62 +/- 1 beats/min, respectively, P < 0.05). BP and HR were similar between sessions. However, MSNA was significantly lower (27 +/- 2 vs. 31 +/- 2 bursts/min), and FBF was significantly higher (2.2 +/- 0.2 vs. 1.8 +/- 0.1 ml.min(-1).100 ml(-1), P < 0.05) in the exercise session compared with the control session. In conclusion, in healthy men, a prolonged bout of dynamic exercise decreases MSNA and increases FBF. These effects persist during acute hyperinsulinemia performed after exercise.

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AIM: Although postexercise hypotension (PEH) has already been extensively demonstrated, the influence of exercise intensity on its magnitude and mechanisms is still controversial. METHODS: Twenty-three normotensive subjects were submitted to a control (45 minutes of rest) and 3 exercise sessions (cycle ergometer, 45 minutes at 30%, 50% and 75% of .VO(2peak)) to investigate the role of exercise intensity on PEH. Blood pressure (BP - auscultatory), heart rate (HR - ECG), and cardiac output (CO - CO2 rebreathing) were measured before and after the control and exercise sessions. RESULTS: Systolic BP decreased significantly after exercise at 50% and 75% of .VO(2peak). Diastolic BP increased significantly during the control session, did not change after exercise at 30% of .VO(2peak), and decreased significantly after exercise at 50% and 75% of .VO(2peak). This fall was greater and longer after more intense exercise. CO and systemic vascular resistance (SVR) responses were similar between sessions, CO increased whereas SVR decreased significantly. Stroke volume (SV) increased and heart rate (HR) decreased following control and exercise at 30% of .VO(2peak) whereas SV decreased and HR increased after exercise at 50% and 75% of .VO(2peak). CONCLUSION: PEH is greater and longer after more intense exercise. BP profile is followed by a decrease in SVR and an increase in CO, what was not influenced by previous exercise. The increase in CO is caused by an increase in SV after rest and low intensity exercise and by an increase in HR after moderate and more intense aerobic exercise.

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To study the relationship between the sympathetic nerve activity and hemodynamic alterations in obesity, we simultaneously measured muscle sympathetic nerve activity (MSNA), blood pressure, and forearm blood flow (FBF) in obese and lean individuals. Fifteen normotensive obese women (BMI = 32.5 +/- 0.5 kg/m2) and 11 age-matched normotensive lean women (BMI = 22.7 +/- 1.0 kg/m2) were studied. MSNA was evaluated directly from the peroneal nerve by microneurography, FBF was measured by venous occlusion plethysmography, and blood pressure was measured noninvasively by an autonomic blood pressure cuff. MSNA was significantly increased in obese women when compared with lean control women. Forearm vascular resistance and blood pressure were significantly higher in obese women than in lean women. FBF was significantly lower in obese women. BMI was directly and significantly correlated with MSNA, blood pressure, and forearm vascular resistance levels, but inversely and significantly correlated with FBF levels. Obesity increases sympathetic nerve activity and muscle vascular resistance, and reduces muscle blood flow. These alterations, taken together, may explain the higher blood pressure levels in obese women when compared with lean age-matched women.

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