Pre-hypertension (pre-HT) (Blood Pressure (BP) ≥120/80mmHg to ≤ 140/90mmHg) increases the risk of developing hypertension (HT). BP reductions following acute exercise are known as post exercise hypotension (PEH). BP and perhaps PEH shows a daily circadian rhythm. Purpose: To compare the magnitude of PEH after morning and evening aerobic exercise in adults with pre-HT. Hypothesis: The magnitude of PEH will be larger after evening versus morning exercise. Participants: Pre-HT men and women 50-65 years old. Study Design: Participants engaged in cycling exercise (60% VO2max) on two occasions: 1.5 and 11 hours following waking. Cardiovascular function was assessed for 30 minutes pre and one hour post exercise. Results: 1) Systolic PEH responses affected by TOD differed by gender. 2) Baseline Heart Rate Variability and its response to exercise differed gender but not TOD. The inconsistent significant gender and TOD differences of PEH and its mechanisms suggest that this group.

Aerobic exercise is recommended as a lifestyle intervention to reduce blood pressure (BP) in individuals with elevated BP (SBP/DBP >120/80 mmHg). However, the BP response is highly variable after both acute (SBP/DBP: –27 to 9/-8 to 7mmHg) and chronic aerobic exercise (-20 to 9/ -11 to 11.3mmHg). We attempt to identify those who are resistant or responsive to training based on their responses to acute (one-bout) exercise. 17 prehypertensive (120 to 139/80 to 89mmHg) males and females (45-60yrs) underwent acute exercise assessments before and after an 8-week walking/jogging program. The magnitude of change in BP after acute exercise significantly correlated (r=.89, p < .01) with the magnitude of change in resting BP after the training. The antihypertensive mechanisms (total peripheral resistance, baroreflex sensitivity) for acute exercise were not correlated to those for chronic exercise. Central cardiovascular controls may link BP reductions after both acute and chronic exercise.

Aerobic exercise such as cycling is known to elicit a post-exercise hypotensive (PEH) response. However, it is not known if swim exercise produces a similar effect in normotensive individuals. We tested the hypothesis that an acute bout of swimming would elicit a PEH response that is less compared to an equivalent bout of cycling. 10 trained and 11 untrained normotensive (SBP/DBP < 120/80 mmHg) individuals (23±1 years) underwent 30 min intensity-matched cycling and swimming sessions to assess changes in BP and cardiovascular responses. While PEH was similar between modalities within groups, the magnitude and temporality of change in BP following swimming was significantly different (p < 0.01) between groups, with untrained participants showing a significant PEH response. Attenuation of PEH in trained individuals was reflective of a significant increase in sympathetic outflow and slower vagal reactivation, suggesting training in an aquatic environment leads to alterations in post-exercise BP regulatory mechanisms.

Pre-hypertension (pre-HT) (Blood Pressure (BP) ≥120/80mmHg to ≤ 140/90mmHg) increases the risk of developing hypertension (HT). BP reductions following acute exercise are known as post exercise hypotension (PEH). BP and perhaps PEH shows a daily circadian rhythm. Purpose: To compare the magnitude of PEH after morning and evening aerobic exercise in adults with pre-HT. Hypothesis: The magnitude of PEH will be larger after evening versus morning exercise. Participants: Pre-HT men and women 50-65 years old. Study Design: Participants engaged in cycling exercise (60% VO2max) on two occasions: 1.5 and 11 hours following waking. Cardiovascular function was assessed for 30 minutes pre and one hour post exercise. Results: 1) Systolic PEH responses affected by TOD differed by gender. 2) Baseline Heart Rate Variability and its response to exercise differed gender but not TOD. The inconsistent significant gender and TOD differences of PEH and its mechanisms suggest that this group.

Aerobic exercise is recommended as a lifestyle intervention to reduce blood pressure (BP) in individuals with elevated BP (SBP/DBP >120/80 mmHg). However, the BP response is highly variable after both acute (SBP/DBP: –27 to 9/-8 to 7mmHg) and chronic aerobic exercise (-20 to 9/ -11 to 11.3mmHg). We attempt to identify those who are resistant or responsive to training based on their responses to acute (one-bout) exercise. 17 prehypertensive (120 to 139/80 to 89mmHg) males and females (45-60yrs) underwent acute exercise assessments before and after an 8-week walking/jogging program. The magnitude of change in BP after acute exercise significantly correlated (r=.89, p < .01) with the magnitude of change in resting BP after the training. The antihypertensive mechanisms (total peripheral resistance, baroreflex sensitivity) for acute exercise were not correlated to those for chronic exercise. Central cardiovascular controls may link BP reductions after both acute and chronic exercise.

Aerobic exercise such as cycling is known to elicit a post-exercise hypotensive (PEH) response. However, it is not known if swim exercise produces a similar effect in normotensive individuals. We tested the hypothesis that an acute bout of swimming would elicit a PEH response that is less compared to an equivalent bout of cycling. 10 trained and 11 untrained normotensive (SBP/DBP < 120/80 mmHg) individuals (23±1 years) underwent 30 min intensity-matched cycling and swimming sessions to assess changes in BP and cardiovascular responses. While PEH was similar between modalities within groups, the magnitude and temporality of change in BP following swimming was significantly different (p < 0.01) between groups, with untrained participants showing a significant PEH response. Attenuation of PEH in trained individuals was reflective of a significant increase in sympathetic outflow and slower vagal reactivation, suggesting training in an aquatic environment leads to alterations in post-exercise BP regulatory mechanisms.

abstract: PURPOSE: Lean hypertension (HTN) is characterized by a mechanistically different HTN when compared to obese HTN. The purpose of this study is to assess whether body phenotype influences blood pressure (BP) responses following both acute and chronic exercise. METHODS: Obese (body mass index (BMI) > 30 kg/m2) and lean (BMI < 25 kg/m2) men with pre-hypertension (PHTN) (systolic BP (SBP) 120 - 139 or diastolic BP (DBP) 80 - 89 mm Hg) were asked to participate in a two-phase trial. Phase 1 assessed differences in post-exercise hypotension between groups in response to an acute exercise bout. Phase 2 consisted of a two-week aerobic exercise intervention at 65-70% of heart rate (HR) max on a cycle ergometer. Primary outcome measures were: brachial BP, central (aortic) BP, cardiac output (CO), and systemic vascular resistance (SVR) measured acutely after one exercise session and following two weeks of training. RESULTS: There were no differences between groups for baseline resting brachial BP, central BP, age, or VO2 peak (all P > 0.05). At rest, obese PHTN had greater CO compared to lean PHTN (6.3 ± 1 vs 4.7 ± 1 L/min-1, P = 0.005) and decreased SVR compared to lean PHTN (1218 ± 263 vs 1606 ± 444 Dyn.s/cm5, P = 0.003). Average 60-minute post-exercise brachial and central SBP reduced by 3 mm Hg in Lean PHTN in response to acute exercise (P < 0.005), while significantly increasing 4 mm Hg for brachial and 3 mm Hg for central SBP (P < 0.05). SVR had a significantly greater reduction following acute exercise in lean PHTN (-223 Dyn·s/cm5) compared to obese PHTN (-75 Dyn·s/cm5, P < 0.001). In lean subjects chronic training reduced brachial BP by 4 mm Hg and central BP by 3 mm Hg but training had no effect on the BP’s in obese subjects. Resting BP reduction in response to training was accompanied by reductions in SVR within lean (-169 Dyn·s/cm5, P < 0.001), while obese experienced increased SVR following training (47 Dyn·s/cm5, P < 0.001). CONCLUSION: Hemodynamic response to both acute and chronic exercise training differ between obese and lean individuals. / Dissertation/Thesis / Doctoral Dissertation Exercise Science 2016

Thesis (M Sport Sc (Sport Science))--University of Stellenbosch, 2009. / ENGLISH ABSTRACT: It is well-known that acute and chronic aerobic and resistance exercise results in decreased blood pressure (BP) in hypertensive individuals. There is little evidence that water exercise has a similar effect on BP response. There is also no certainty regarding the magnitude and duration of post exercise hypotension (PEH) after either land or water-based exercise. Most studies were also performed under controlled laboratory conditions and very few characterised the PEH response under real life conditions. The current study endeavoured to examine the magnitude and duration of PEH after an acute session of water- and land-based exercise during free living conditions in persons with mild to moderate hypertension. Twenty-one men and women (aged 52 ± 10 years) volunteered for the study. All participants were pre-hypertensive or hypertensive. Participants completed a no exercise control session, a water exercise session and a combined aerobic and resistance land exercise session in random order. After all three sessions, participants underwent 24 hour monitoring using an Ergoscan ambulatory BP monitoring device. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and heart rate (HR) were monitored to determine changes from resting values after each session and to compare the PEH responses between land and water exercise. Overall, the land exercise treatment caused a 3.6 mmHg lower average SBP over 24 hours than the control treatment (P = 0.04). The average difference over 24 hours between the water and control treatments was 2.2 mmHg and between land and water exercise it was 1.5 mmHg (P > 0.05). During daytime, both land and water exercise resulted in significantly lower SBP (12.7 and 11.3 mmHg) compared to the control session (2.3 mmHg). The PEH response lasted for 24 hours after land exercise and nine hours after water exercise. There was no difference in the daytime DBP for the three treatments (P > 0.05). Although all three groups showed significant reductions during night time, both exercise treatments showed greater nocturnal falls in SBP, DBP and MAP than the control treatment. / AFRIKAANSE OPSOMMING: Dit is alombekend dat akute en chroniese aërobiese- en weerstandsoefening tot ‘n afname in bloeddruk (BD) lei in persone met hipertensie. Daar is egter min getuienis dat wateroefening dieselfde effek op die bloeddruk respons het. Daar is ook nie sekerheid oor die grootte en duur van post-oefening hipotensie na water- of landoefening nie. Die meeste studies is onder gekontrolleerde laboratorium omstandighede gedoen en min resultate is beskikbaar onder alledaagse lewensomstandighede. Die huidige studie het gepoog om die grootte en duur van die post-oefening hipotensie respons in persone met ligte tot matige hipertensie onder alledaagse omstandighede na ‘n akute sessie van water- en landgebaseerde oefening te ondersoek. Een-en-twintig mans en vrouens (ouderdom 52 ± 10 jaar) het ingewillig om aan die studie deel te neem. Alle deelnemers was hipertensief of pre-hipertensief. Alle deelnemers het ‘n kontrolesessie, ‘n wateroefeningsessie en ‘n gekombineerde aërobiese en weerstands landoefensessie, in lukrake volgorde, voltooi. Na elke sessie het die deelnemers 24 uur bloeddrukmonitering met ‘n Ergoscan wandelende bloeddruk monitor ondergaan. Sistoliese bloeddruk (SBD), diastoliese bloeddruk (DBD), gemiddelde arteriële bloeddruk en harttempo (HT) is gemonitor om die veranderinge vanaf rustende waardes na elke sessie te bepaal en om die hipotensiewe respons na land- en wateroefening te vergelyk. Landoefening het ‘n 3.6 mmHg laer gemiddelde SBD oor 24 uur tot gevolg gehad in vergelyking met die kontrolesessie (P = 0.04). Die gemiddelde verskil oor 24 uur tussen die water- en kontrolesessies was 2.2 mmHg en 1.5 mmHg tussen die land en water oefensessies (P > 0.05). Gedurende die dag het beide die land- and wateroefening gelei tot beduidende laer SBD (12.7 en 11.3 mmHg) in vergelyking met die kontrolesessie (2.3 mmHg). Die post-oefening hipotensie het 24 uur geduur na die landoefening en nege uur na die wateroefening. Daar was geen verskil in DBD gedurende die dag tussen die drie groepe nie (P > 0.05).

Os efeitos da hidratação sobre a pressão arterial (PA) e seus mecanismos hemodinâmicos e autonômicos pós-exercício foram pouco estudados e os resultados são controversos. Esse estudo avaliou esses efeitos, em normotensos jovens após uma sessão de exercício aeróbico. Assim, 16 rapazes submeteram-se a quatro sessões experimentais, realizadas em ordem aleatória: controle sem hidratação, exercício sem hidratação, controle com hidratação e exercício com hidratação. Nas sessões com hidratação, os sujeitos ingeriam 1l de água na noite anterior, 500ml 60min antes da intervenção (exercício ou repouso) e mais 1ml por 1g de massa corporal perdida logo após a intervenção. O exercício foi realizado por 45min em ciclo ergômetro em 50% do VO2pico. Em todas as sessões as PA sistólica (S), média (M) e diastólica (D), o débito cardíaco (DC), a frequência cardíaca (FC) e as variabilidades da FC e da PA foram medidos antes e após as intervenções. O exercício diminuiu a PAS e o volume sistólico (VS) e impediu os aumentos da FC, da PAD, da PAM e da sensibilidade baroreflexa, que ocorreram na sessão controle. A hidratação não modificou as respostas hemodinâmicas e autonômicas após o exercício. Em conclusão, em sujeitos jovens normotensos, a hidratação não modificou o efeito hipotensor promovido pelo exercício aeróbico no período de recuperação, não afetando seus mecanismos hemodinâmicos e autonômicos / The effects of hydration on post-exercise blood pressure (BP) and hemodynamic and autonomic mechanisms were poorly studied and results are controversial. This study evaluated these effects in young normotensives after an acute bout of aerobic exercise. Sixteen young men underwent four sessions in a random order: control without hydration, exercise without hydration, control with hydration and exercise with hydration. In the hydration sessions, subjects drank 1l of water in the night before, 500 ml 60 min before the intervention (rest or exercise) and 1ml for 1g of body mass lost immediately after the intervention. In exercise sessions, they exercised for 45 min on a cycle ergometer at 50% of VO2peak. Systolic (S), diastolic (D) and mean (M) BP, as well as cardiac output (CO), heart rate (HR), and HR and BP variabilities were measured before and after the interventions. Exercise produced a significant reduction in SBP and stroke volume (SV), and abolished the increase in HR, DBP, MBP and baroreflex sensitivity that occurred in the control sessions. Hydration did not change hemodynamic and autonomic responses after exercise. In conclusion, in healthy young subjects, hydration did not modify the hypotensive effect promoted by the aerobic exercise during the recovery period, not affecting its hemodynamic and autonomic mechanisms

This thesis presents four studies investigating the phenomenon of post exercise hypotension in the human condition of pre (borderline)-hypertension. Study one investigated the effects of an acute bout of 30-minutes upright cycling on post exercise haemodynamics and compared the results to a non-exercise control condition. 9 pre-hypertensive males, mean arterial pressure (MAP) = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied for 6 hours following 30-minutes of cycle exercise at 70% maximal oxygen consumption and following 30-minutes of seated rest. Results demonstrate that moderate intensity exercise exerts a modest fall (~6 mmHg) in arterial pressure with the hypotension sustained for 6-hours post exercise. The fall in arterial pressure equates to a significantly reduced after load when compared to both pre-exercise baseline and non-exercise control data taken at the same time of day. The arterial pressure responses transcended into a sustained reduction (20%) in systemic vascular resistance and reciprocal increase in vascular conductance for up to 2-hours post-exercise. Venous atrial natriuretic peptide (ANP) demonstrated an elevation (44%) following exercise and a significant decline (33%) in the post-exercise period mirroring the haemodynamic response. This research reveals that acute exercise is capable of sustained reductions in arterial pressure and vascular resistance beyond the usual labile fluctuations and that the octapeptide ANP may exert a modulatory influence over the post-exercise response. Increases in 02 tension beyond the physiological range induces complex effects on the circulatory system with a dominant vasoconstriction following hyperoxia. The purpose of study 2 was to assess the effects of hypoxic (16% 02) and hyperoxic (50% 62) exercise on subsequent haemodynamic control when compared with normoxia. 9 pre-hypertensive males, MAP = 106 ± 5 mmHg (50 ±10 yr), not on medication, performed 30-minutes of cycle exercise at 70% normoxic maximal oxygen consumption in hypoxia (16% O 2 ), hyperoxia (50% O 2) and normoxia(21% O2 ). Hyperoxic exercise blunted post-exercise haemodynamics by significantly attenuating the reductions (from normoxic baseline) in SVR (-45%, PO.05 vs. normoxic & hypoxic exercise immediately post-exercise) that persisted throughout 120-minutes recovery in normoxia (-35% vs. normoxic & hypoxic exercise, during recovery) and elicited a mildly hypertensive effect, with regards to MAP, whereas normoxic and hypoxic exercise elicited a hypotension compared to baseline (P < 0.05). Circulating ANP was decreased in the hyperoxic trial when compared with normoxic and hypoxic exercise [24.3 (13.4) v. 31.5 (16.3) and 29.6 (13.9) pg/ml, respectively; P < 0.05, pooled for state]. Changes in MAP were related to changes in ANP concentration only following hyperoxic exercise (r = 0.50, P < 0.01). These findings indicate that acute modest hyperoxia reflexively induces measurable physiological derangement partly explained by decreased circulating concentrations of ANP. Study three determined the role of free-radical mediated oxidative stress and redox regulation of circulating NO metabolism as a primary modulator of vascular tone following exercise in pre-hypertensive humans. Utilising the same cohort and exercise protocol as in study 1 venous blood was sampled from an antecubital vein. Plasma NO metabolites nitrate (NO" 3 ) and nitrite (NO"2 ) were determined fluorometrically, whilst S-Nitrosothiol (RSNO) concentrations were assayed by the Saville reaction Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). Exercise led to a delayed increase in LOOH by 60- minutes post-exercise (0.69 ± 0.13 v. 0.86 ± 0.18 umol/1, respectively, P < 0.05), that remained elevated until termination of the trial 6-hours post-exercise. NO'a significantly fell below baseline by 120-minutes post-exercise (10.8 ± 3.3 v. 1.1 ±1.1 u.mol/1, respectively, P < 0.05), remaining attenuated for the remainder of the study.NO'i and RSNO were unmodified in the post-exercise period. In parallel to this finding the data also indicates a significant blunting in the hyperaemic response [SVR decreased from a 31% reduction immediately (within 1-minute) post-exercise to -13 and 8% at 60- and 120-minutes post-exercise, respectively, P < 0.05] and reversal of the hypotension (P < 0.05) over the same time frame as the augmented lipid peroxidation and attenuated circulating NO~3. These results indicate that augmented oxidative stress exerts a deleterious effect on post-exercise haemodynamics and implicates a potential redox regulation pathway of NO as being a mechanism by which free radical-induced oxidative stress blunts the degree of PEH in the recovery period. The final study investigated the potential role of a redox-mediated regulation of circulating NO bioavailability as a modulator of the augmented vasoconstriction following hyperoxic exercise. The same cohort and exercise protocol were employed as in study 2 and venous blood was assayed for NO"3 , NO'a, RSNO, LOOK, & lipid /water-soluble antioxidant concentrations. Similar adverse haemodynamic effects were noted following hyperoxic exercise as reported previously in study 2. RSNO showed a significant increase following hypoxic exercise only (P < Q.Q5, state x time, interaction), whereas NO~3, NO~2 and LOOH failed to differ between conditions (P > 0.05, main effect for state [02] and state x time, interaction effects). Ascorbic acid was mobilised in response to hyperoxic exercise when compared to normoxia (P < 0.05, main effect for state [O2] and state x time, interaction effects) being significantly elevated by 120-minutes post-exercise in hyperoxia compared to normoxia and hypoxia [75.1 (31) v. 39.5 (18.3) v. 46.7 (14.2) |amol/l, respectively, P < 0.05]. This data demonstrates an effective endogenous antioxidant response and argues against a redox regulation pathway of NO metabolism as a primary mediator of blunted vasodilatation in this scenario. This elucidates a more complex regulation of arterial tone, resulting from a metabolic pathway independent of NO in older subjects with pre-hypertension. This work demonstrates that (1) aerobic exercise exerts a hypotensive effect in humans with pre-hypertension, (2) ANP plays a part in the vasodilatation following exercise, (3) Free-radical mediated oxidative stress & subsequent modulation of NO metabolism exerts a deleterious influence on post-exercise haemodynamics (4) Acute hyperoxic exercise induces a sustained vasoconstriction that is mediated via circulating ANP concentration but not by redox regulation of NO metabolism.