Exercise-induced Hypertension Research Articles

Hypertension during Weight Lifting Reduces Flow-Mediated Dilation in Nonathletes.

The purpose of this study was to determine whether increased intraluminal pressure is the damaging factor that reduces flow-mediated dilation (FMD) in young, healthy subjects after resistance exercise to maximal exertion. Attenuating the rise in brachial artery pressure during weight lifting by placing a blood pressure cuff on the upper arm prevents postexercise impairment of brachial artery FMD in sedentary individuals. Nine sedentary individuals who exercise once a week or less and six exercise-trained individuals who exercise three times a week or more performed leg press exercise to maximal exertion on two separate occasions. During one visit, a blood pressure cuff, proximal to the site of brachial artery measurement, was inflated to 100 mm Hg to protect the distal vasculature from the rise in intraluminal pressure, which occurs during resistance exercise. Brachial artery FMD was determined using ultrasonography before and 30 min after weight lifting. Without the protective cuff, brachial artery FMD in sedentary individuals was reduced after weight lifting (9.0% ± 1.2% prelift vs 6.6% ± 0.8% postlift; P = 0.005), whereas in exercise-trained individuals, FMD was unchanged (7.4% ± 0.7% prelift vs 8.0% ± 0.9% postlift; P = 0.543). With the protective cuff, FMD no longer decreased but rather increased in sedentary individuals (8.7% ± 1.2% prelift vs 10.5% ± 1.0% postlift, P = 0.025). An increase in FMD was also seen in exercise-trained subjects when the cuff was present (6.6% ± 0.7% prelift vs 10.9% ± 1.5% postlift, P < 0.001). Protecting the brachial artery from exercise-induced hypertension enhances FMD in sedentary and exercise-trained individuals. These results indicate that increased intraluminal pressure in the artery contributes to the reduced FMD after heavy resistance exercise in sedentary individuals.

Resting and Exercise-Induced Left Atrial Hypertension in Patients WithAtrial Fibrillation: The Causes and Implications for Catheter Ablation.

The aim of this paper was to investigate the prevalence of resting and exercise-induced left atrial hypertension (LAH) in patients with nonvalvular atrial fibrillation (AF), association of the LAH with other cardiac abnormalities, and its implications for AF catheter ablation. The clinical role of LAH in patients with established AF is largely unknown. Patients scheduled for catheter ablation of AF (n= 240; age 60 ± 10 years; 67% men, 62% paroxysmal AF) underwent detailed echocardiography, assessment of quality of life (QoL), left atrial (LA) voltage mapping, and measurement of the LA pressure at rest and during isometric handgrip exercise. After ablation they were followed forAFrecurrence for 16 ± 6 months. Resting and exercise-induced LAH (mean LA pressure >15 mmHg) occurred in 15% and 34% of the patients, respectively. Both the patients with resting and exercise-induced LAH had typical features of latent heart failure with preserved ejection fraction associated with advanced LA structural and functional remodeling. AF recurred after ablation in 45% of the patients. LAH was an independent risk factor for arrhythmia recurrence (hazard ratio: 1.7, 95% confidence interval: 1.2 to 2.2). The patients with LAH had worse baseline QoL, but they benefited significantly more from a successful ablation than the patients without LAH. Presence of either resting or exercise-induced LAH identified AF patients with a distinct clinical profile, extensive LA substrate, and different clinical response to catheter ablation. Stratification of AF patients based on the LA exercise hemodynamics could help in the future to tailor the ablation strategy.

Transcranial Doppler-determined change in posterior cerebral artery blood flow velocity does not reflect vertebral artery blood flow during exercise.

We examined whether a change in posterior cerebral artery flow velocity (PCAv) reflected the posterior cerebral blood flow in healthy subjects during both static and dynamic exercise. PCAv and vertebral artery (VA) blood flow, as an index of posterior cerebral blood flow, were continuously measured during an exercise trial using transcranial Doppler (TCD) ultrasonography and Doppler ultrasound, respectively. Static handgrip exercise significantly increased both PCAv and VA blood flow. Increasing intensity of dynamic exercise further increased VA blood flow from moderate exercise, while PCAv decreased to almost resting level. During both static and dynamic exercise, the PCA cerebrovascular conductance (CVC) index significantly decreased from rest (static and high-intensity dynamic exercise, -11.5 ± 12.2% and -18.0 ± 16.8%, means ± SD, respectively) despite no change in the CVC of VA. These results indicate that vasoconstriction occurred at PCA but not VA during exercise-induced hypertension. This discrepancy in vascular response to exercise between PCA and VA may be due to different cerebral arterial characteristics. Therefore, to determine the effect of exercise on posterior cerebral circulation, at least, we need to carefully consider which cerebral artery to measure, regardless of exercise mode.NEW & NOTEWORTHY We examined whether transcranial Doppler-determined flow velocity in the posterior cerebral artery can be used as an index of cerebral blood flow during exercise. However, the changes in posterior cerebral artery flow velocity during exercise do not reflect vertebral artery blood flow.

Heterogeneous Regulation of Brain Blood Flow during Low-Intensity Resistance Exercise.

The present study was designed to explore to what extent low-intensity resistance exercise-induced acute hypertension influences intracranial cerebral perfusion. Twelve healthy participants performed one-legged static knee extension exercise at 30% maximal voluntary contraction for 2 min. Blood flow to the internal and external carotid arteries (ICA/ECA) were evaluated by duplex ultrasonography. ICA blood flow increased and reached a plateau before stabilizing 60 s into exercise despite continued increases in cardiac output and arterial blood pressure. ICA conductance significantly decreased by -14.4% ±13.8% at the end of exercise (P < 0.01), whereas in contrast, ECA blood flow (P < 0.01) and conductance were shown to increase (P < 0.05). The present findings demonstrate that low-intensity resistance exercise was associated with vasodilation of the ECA that was accompanied by vasoconstriction of the ICA. We propose that the heterogeneity and reciprocal regulation of intracranial cerebral blood flow reflect an adaptive neuroprotective mechanism that serves to protect the brain and associated vasculature against the structural damage associated with resistance exercise-induced hypertension.

Delayed systolic blood pressure recovery following exercise as a mechanism of masked uncontrolled hypertension in chronic kidney disease.

Among people treated for hypertension, the presence of elevated blood pressure (BP) out of the clinic but normal BP in the clinic is called masked uncontrolled hypertension (MUCH). What causes MUCH remains unknown. The purpose of this study was to answer the question of whether patients with MUCH have an increased hemodynamic reactivity to exercise and delayed hemodynamic recovery following exercise. Four groups were compared: controlled hypertension (CH, n = 58), MUCH (n = 34) and uncontrolled hypertension (UCH, n = 12), all of which had chronic kidney disease (CKD), and a group of healthy normal volunteers who did not have hypertension or CKD (n = 16). All participants underwent assessment of 24-h ambulatory BP monitoring, BP measurement during a graded symptom-limited exercise using a cycle ergometer and BP recovery over 7 min following exercise. Exercise-induced increase in systolic BP was similar among the four groups. When compared with healthy controls, recovery of systolic BP following termination of exercise was blunted among the CKD groups in unadjusted (P < 0.0001) and adjusted (P < 0.001) models. During recovery, the healthy control group had 5.9% decline in systolic BP per minute. In contrast, MUCH had only 3.3% per minute reduction and the UCH group had 0.3% reduction per minute. A test of linear trend was significant (P = 0.002, adjusted model). Because there was no impairment in the heart rate recovery among groups, we speculate that the parasympathetic pathway appears intact among treated hypertensives with CKD. However, the failure to withdraw sympathetic tone upon termination of exercise causes ongoing vasoconstriction and delayed systolic BP recovery providing a biological basis for MUCH. Delayed recovery from exercise-induced hypertension in those with poorly controlled BP provides potentially a new target to assure round-the-clock BP control.

Excessive exercise habits of runners as new signs of hypertension and arrhythmia

BackgroundExcessive exercise may induce arrhythmia, and this risk is higher in middle-aged people. The study aim was to compare the exercise characteristics of middle-aged runners participating in excessive endurance exercise. MethodsThe subjects of this study were 552 runners (mean age; 49.0±7.4years) without structural heart disease who performed exercise at least twice per week, had consistently exercised for at least three years, and had finished at least five marathons. The arrhythmia runner group (ARG, n=14) and normal runner group (NRG, n=538) were compared with regard to hemodynamic response, cardiorespiratory fitness level, training history, number of finished races, finishing times, and exercise habits. ResultsThe mean resting systolic (134.0±15.8mmHg) and diastolic (85.8±10.9mmHg) blood pressure values indicated pre-hypertension, while the mean maximal SBP (213.7±27.4mmHg) values indicated exercise-induced hypertension. The VO2max was significantly higher and the maximal DBP was significantly lower in the ARG than in the NRG (p<0.05). Training history was significantly longer in the ARG than in the NRG (p<0.05), while the number of finished marathons, the finishing times in marathons and the exercise frequency per week didn't differ significantly between the two groups. Exercise intensity was significantly higher in the ARG than in the NRG (p<0.01). ConclusionsMiddle-aged long-distance runners showed pre-hypertension and exercise-induced hypertension, and the ARG had higher VO2max values, greater exercise intensities, and longer training histories than the NRG.

50대 남성의 운동 유발성 고혈압 반응과동맥경직도 간의 연관성

[PURPOSE] This study attempted to show the relationship between exercise-induced hypertension response and arterial stiffness in men aged 50 years. [METHODS] The subjects of the study were adults male with exercise induced hypertension group (n=45, age 56.22±2.60 years) and control group (n=61, age 56.01±1.57 years) who had undergone exercise test and arterial stiffness test. Exercise induces hypertension is defined as a peak systolic blood pressure ≥210mmHg during treadmill tests. Exercise stress test was conducted using modified Balke protocol. Arterial stiffness was assessed based on brachial-ankle pulse wave velocity (baPWV). [RESULTS] Exercise induced hypertension group showed significantly higher baPWV than that of control group (1416.5±154.09cm/sec vs. 1309.5±127.76cm/sec, p<.001). The peak systolic blood pressure was correlated with the resting heart rate (r=0.198, p<.05), resting systolic blood pressure (r=0.190, p<.05), and baPWV (r=0.461, p<.001). In multiple linear regression analysis, we found that the baPWV was a significant predictor of peak systolic blood pressure (β=0.429, p<.001). [CONCLUSIONS] Exaggerated blood pressure response to exercise was associated with arterial stiffness.

Antioxidants Attenuate the Exercise Induced Resetting of the Arterial Baroreflex in Healthy Human Subjects: Implications for Exercise Induced Hypertension

Patients with Exercise‐induced‐Hypertension (EiHT) exhibit exaggerated increases in arterial pressure at the onset of exercise which may prevent EiHT patients from participating in exercise training programs. EiHT is thought to occur due to dysregulated resetting of the arterial baroreflex (ABR). Prior studies in animal models demonstrate that reactive oxygen species (ROS) generated in the brainstem scavenge the sympathoinhibitory function of central Nitric Oxide (NO) and, thereby enable ABR resetting of the operating point (OP) pressure and hypertension. We tested the hypothesis that a centrally and peripherally active antioxidant cocktail (CT; composed of Vitamin E and C with Co‐Q10) will attenuate the exercise induced resetting of the ABR's centering point (CP) and OP pressures compared to the same exercise intensity performed with a vehicle placebo (PL). Seven healthy human subjects were recruited and performed 700 back‐supported semi‐recumbent dynamic leg exercise at moderate (HR at 120 beats per minute: e120) and heavy (HR at 150 beats per minute: e150) intensities. Mean arterial pressure (MAP) was continuously recorded using photoplethysmography at the finger, while HR was recorded via a three lead electrocardiogram (ECG). On experimental day 1, subjects were either given the CT or PL 1 hr. (time of peak plasma concentrations) prior to the start of exercise. On a separate experiment day 2, the subjects repeated the same exercise intensity protocol with the other test article (CT or PL) in a randomized repeated measures design. During exercise with the PL ingestion, the CP of the ABR was reset to higher MAPs from rest to e120 (100 ± 3 mm Hg to 121 ± 3 mm Hg, P&lt;0.02) but not e150 (113 ± 3 mm Hg, P=0.15). The absence of resetting at the higher work intensity was likely due to cardiovascular drift (decreasing MAP). Ingestion of the CT prior to the exercise protocols prevented the increase of the CP to higher MAPs from rest to e120 and e150 (rest: 97 ± 3 mm Hg, e120: 106 ± 3 mm Hg, e150: 106 ± 3 mm Hg, P &gt;0.21). Furthermore, the OP‐pressure of the ABR was attenuated with CT ingestion compared to PL at e120 (placebo e120: 116 ± 0.8 mm Hg, CT e120: 111 ± 0.8 mm Hg, P = 0.04). These data: (a) confirm that centrally derived ROS contribute to exercise induced ABR resetting; and (b) indicate that EiHT could be treated by ingestion of an anti‐oxidant cocktail prior to the start of exercise

Exercise-Induced Systemic Venous Hypertension in the Fontan Circulation

Increasingly end-organ injury is being demonstrated late after institution of the Fontan circulation, particularly liver fibrosis and cirrhosis. The exact mechanisms for these late phenomena remain largely elusive. Hypothesizing that exercise induces precipitous systemic venous hypertension and insufficient cardiac output for the exercise demand, that is, a possible mechanism for end-organ injury, we sought to demonstrate the dynamic exercise responses in systemic venous perfusion (SVP) and concurrent end-organ perfusion. Ten stable Fontan patients and 9 control subjects underwent incremental cycle ergometry-based cardiopulmonary exercise testing. SVP was monitored in the right upper limb, and regional tissue oxygen saturation was monitored in the brain and kidney using near-infrared spectroscopy. SVP rose profoundly in concert with workload in the Fontan group, described by the regression equation 15.97+ 0.073 watts per mm Hg. In contrast, SVP did not change in healthy controls. Regional renal (p <0.01) and cerebral tissue saturations (p <0.001) were significantly lower and decrease more rapidly in Fontan patients. We conclude that in a stable group of adult patients with Fontan circulation, high-intensity exercise was associated with systemic venous hypertension and reduced systemic oxygen delivery. This physiological substrate has the potential to contribute to end-organ injury.

Cardiovascular Adaptation and Side Effects in Middle-Aged Marathoners

Regular exercise brings about various positive effects on cardiovascular, oncological, psychiatric, neurological, and endocrinological systems of human body. According to exercise types with cardiovascular adaptation, endurance exercise is characterized by eccentric hypertrophy; resistance exercise is characterized by concentric hypertrophy; and the combination of the eccentric hypertrophy and concentric hypertrophy is seen in cycling and rowing. Although the cardiac functions of athletes are not different from those in general population, athletes show higher exercise capacities because of the increased diameter of ventricle. Atrial fibrillation which is the most common in middle-aged marathoners shows 5.3 times higher prevalence compared to that in general population. In addition, higher arterial stiffness is shown in marathoners, and higher resting blood pressure is shown in sub-3 hours-marathoners. Especially the runners with higher resting blood pressure or severe arrhythmia showed superior cardiopulmonary functions and excessive exercise habits when compared to the normal runners. The runners with exercise-induced hypertension are prone to show increased levels of cardiac markers by increasing cardiac muscle burden in exercise, and then be taken with resting hypertension in the future. The major cause of sudden deaths in marathon race of middle-aged marathoners is coronary artery disease (CAD), and the higher prevalence of CAD is shown in middle-aged marathoners being manifested by the exercise stress test or cardiac computed tomography. Therefore, middle-aged marathoners who regularly participate in marathon race are required to undergo annual exercise stress test, and their additional checkups for cardiovascular system should be supervised by specialized medical doctors.

Effects of Ultra-Marathon Running on Pro-inflammatory, Anti-inflammatory and Endothelial Function Factors in Athletes with Exercise-induced Hypertension

Effects of Ultra-Marathon Running on Pro-inflammatory, Anti-inflammatory and Endothelial Function Factors in Athletes with Exercise-induced Hypertension

Association Between an Exaggerated Exercise Blood Pressure Response and Mortality and Cardiovascular Events in Older Adults with Known or Suspected Coronary Artery Disease

To the Editor: The relationship between exercise-induced hypertension and cardiovascular outcomes remains controversial. Several studies have shown an association between an exaggerated rise in systolic blood pressure (SBP) during exercise with the subsequent development of cardiovascular events,1-3 whereas others evaluating individuals with known or suspected coronary artery disease (CAD) differ in their findings.4-7 The purpose of this study was to examine the association between exercise-induced hypertension and all-cause mortality and cardiovascular events in elderly adults with known or suspected CAD. From March 1, 1995, to June 28, 2013, 6,104 community-based individuals aged 65 and older with known or suspected CAD underwent treadmill exercise echocardiography. Those who had received beta-blockers within 48 hours before the tests (because of their blunting effect on exercise-induced rise in SBP) and those in whom SBP did not increase with exercise above baseline values (because of the association between an exercise-induced hypotensive response and worse prognosis) were excluded.8 The final study population consisted of 4,511 individuals. The Comité Ético de Investigación Clínica de Galicia approved the investigation. Exercise echocardiography was performed as previously described.9 Blood pressure was measured at rest and at each stage of the protocol. Peak SBP was defined as maximum SBP obtained during exercise. An exaggerated exercise-induced SBP response (EESBPR) was defined as a peak SBP greater than 220 mmHg.6 Outcomes were all-cause mortality, myocardial infarction (MI), and stroke. Median follow-up was 3.6 years (interquartile range 0.2–8.1 years). Cox proportional hazards models were used to assess the association between EESPBR and outcomes. Covariates were sex, age, cardiovascular risk factors, prior MI, prior coronary revascularization, antihypertensive drugs, atrial fibrillation, left ventricular ejection fraction, baseline SBP, peak heart rate, exercise-induced chest pain, ischemic electrocardiographic changes, exercise workload, and echocardiographic ischemia. Two thousand five hundred twenty-nine participants (56.1%) were male, and 2,770 (61.4%) had a history of hypertension. EESBPR developed in 165 (3.7%). Participants with EESBPR were more likely to have resting hypertension and less likely to have previously diagnosed CAD. There were no significant differences between the groups regarding resting heart rate or likelihood of submaximal tests. During follow-up, 1,104 participants died. Annualized mortality was 3.5% in participants with EESBPR and 5.3% in those without (p = .002, Figure 1). Four hundred sixty-four participants experienced MI, and 145 had at least one stroke of any type. Annualized rates of MI, stroke of any type, ischemic stroke, and hemorrhagic stroke were 2.3%, 0.7%, 0.7%, and 0.1% in participants with EESBPR and 2.3%, 0.84, 0.6% and 0.2% in those without, respectively (P > .05 for all comparisons). In Cox regression analysis, EESBPR remained independently associated with lower risk of all-cause mortality (hazard ratio = 0.64, 95% confidence interval = 0.46–0.89, P = .008). There were no significant associations between EESBPR and MI, stroke of any type, ischemic stroke, or hemorrhagic stroke after multivariate adjustments. EESBPR was associated with longer survival in a series of elderly adults referred for exercise echocardiography for clinical reasons; no significant association was found between EESBPR and subsequent risk of MI or stroke in this population. Some prior studies performed in asymptomatic healthy subjects found that an exercise-induced BP response was associated with higher risk of cardiovascular events.1-3 Although these studies contrast with the current results, there are important differences in participant characteristics, in the definition of the variables evaluated, and in the technique used. Individuals with a history of CAD were generally excluded, and there was no consensus on normal values for exercise-induced SBP response. Nevertheless, other studies, particularly those evaluating individuals with known or suspected CAD, did not find an association between exercise-induced hypertension and worse prognosis.4-7 Furthermore, the current investigation complements and expands the results of a previous study10 that found that an increase in SBP during exercise was associated with longer survival in a group of 382 individuals aged 75 years old. Discrepancies between studies may be due, at least in part, to the different physiopathological pathways leading to an exercise-induced rise in SBP. An increase in cardiac output or an insufficient decrease in systemic vascular resistance may provoke EESBPR, and the theoretical effects of both mechanisms on outcome are opposite (beneficial for the former, detrimental for the latter). It may be that the predominant mechanism leading to the survival benefit observed in elderly adults with known or suspected CAD who exhibit EESBPR would be an enhanced exercise-induced increase in cardiac output. Conflict of Interest: The authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: MCBM: study concept and design, acquisition of subjects and data, data analysis and interpretation, preparation of manuscript. ABM, JP: study concept and design, acquisition of subjects and data, data analysis and interpretation, review of manuscript. Sponsor's Role: The study had no external funding.

Modulation of acute transient exercise-induced hypertension after oral administration of four angiotensin-converting enzyme inhibitors in normotensive horses

Changes in blood pressure (BP) during acute hypertension in response to angiotensin-converting enzyme inhibitors (ACEIs) have not been investigated in normotensive horses. In this study, six healthy horses were subjected to five trials, consisting in a treadmill exercise workload of 8 m/s for 1 min, 2 h after oral administration (PO) of placebo (0 mg/kg), enalapril (2.0 mg/kg), quinapril (1.0 mg/kg), ramipril (0.2 mg/kg) or benazepril (0.5 mg/kg). Serum angiotensin converting enzyme (ACE) activity was measured and systolic (SBP) and diastolic (DBP) blood pressures were recorded at rest (R), 2 h after placebo or ACEI administration (pre-E) and within the first 20 s after exercise (post-E).Mean maximum serum ACE inhibition 2 h after PO administration was 4.8% (placebo), 39.4% (enalapril), 46.4% (quinapril), 55.0% (ramipril) and 71.68% (benazepril). There were no significant differences in serum ACE inhibition between enalapril and quinapril. SBP and DBP at times R and pre-E were not different in any of the five trials. In response to exercise, SBP increased by 67.6% (placebo), 52.7% (enalapril), 43.1% (quinapril), 26.6% (ramipril) and 4.2% (benazepril). In response to exercise, DBP increased by 20.6, 13.2, 11.7, 16.6 and 3.7% after placebo, enalapril, quinapril, ramipril and benazepril administration, respectively. Serum ACE activity changed during exercise, but statistical significance was not achieved. In conclusion, administration of PO benazepril at a dose of 0.5 mg/kg modulated physiological hypertension induced by exercise in horses that were otherwise normotensive.

3B.04

Objective: To evaluate endothelial function in normotensive adolescents with exaggerated blood pressure response during exercise. Design and method: This was a cross-sectional study conducted with 157 high school students (80 boys and 77 girls), aged between 13 to 18 years old (15.0 ± 1.6), normotensive, without smoking habits, non-obese, normolipidemic and normal glucose. An exaggerated blood pressure response was defined as a systolic pressure rise of more than 70 mm Hg, during the treadmill test with Bruce protocol. The endothelial function was assessed through endothelium-dependent vasodilation with reactive hyperemia test by high-resolution vascular ultrasound. The cohort was split into quartiles, according to flow-mediated dilation (FMD). The study comparison was made between the lowest quartile versus the rest of them. Results: An exaggerated blood pressure response was observed in 13 adolescents (8.3%), 10 (13.0%) females and 3 (3.8%) males (P = 0.036). For adolescents in the lowest FMD quartile, a higher prevalence of exaggerated blood pressure response was observed, in comparison with the others quartiles (17.5 vs 5.1%, respectively; P = 0.014). Even after adjustment for factors known to affect endothelial function, the logistic regression analysis revealed that an exercise-induced hypertension was a predictor of impaired FMD (OR = 3.924; I.C. 95%: 1.233–12.488). Conclusions: Normotensive adolescents with exercise-induced hypertension have impaired endothelium-dependent vasodilation. Exercise blood pressure may thus be a useful marker of nitric oxide bioactivity, and hence an important cardiac prognostic factor.

The study of left ventricular hypertrophy in ECG and QT dispersion in marathon runner with exercise-induced hypertension.

The study of left ventricular hypertrophy in ECG and QT dispersion in marathon runner with exercise-induced hypertension.

Exercise-induced intracranial hypertension due to insufficient jugular vein drainage treated with a stent (P1.305)

Exercise-induced intracranial hypertension due to insufficient jugular vein drainage treated with a stent (P1.305)

Does exercise-induced hypertension reliably predict established hypertension?

Background: Hypertension is a well recognised and modifiable risk factor for cardiovascular disease and stroke, affecting close to 40% of adults globally. Hypertension is usually asymptomatic and early detection allows appropriate management to reduce the associated risks. Blood pressure (BP) increases with physical exertion, and normal values in exercise stress testing (EST) exist. The relationship to established hypertension in patients where BP rise exceeds these values has not been well described. The aim of this retrospective study was to examine the relationship of BP response during EST to hypertension status as defined using the 24 hour average BP from ambulatory blood pressure monitoring (ABPM). Methods: BP data of 723 adult patients (mean age 61 yrs; 415 male) undergoing contemporaneous EST and ABPM were retrospectively analysed. An abnormal EST response was defined as peak systolic BP ≥ 210 mmHg. Established hypertension was defined as ABPM ≥ 130/80 mmHg. EST response was then compared to ABPM. Results: 312 patients had an abnormal BP response during EST and 227 (73%) of these had an abnormal ABPM. 411 patients had a normal BP response during EST and 217 (53%) had a normal ABPM, however 194 (47%) had an abnormal ABPM. Conclusions: While an abnormal BP response during EST often predicts established hypertension (PPV 73%), a normal BP response during EST does not exclude established hypertension (NPV 53%).

Loss of functional endothelial connexin40 results in exercise-induced hypertension in mice.

During activity, coordinated vasodilation of microcirculatory networks with upstream supply vessels increases blood flow to skeletal and cardiac muscles and reduces peripheral resistance. Endothelial dysfunction in humans attenuates activity-dependent vasodilation, resulting in exercise-induced hypertension in otherwise normotensive individuals. Underpinning activity-dependent hyperemia is an ascending vasodilation in which the endothelial gap junction protein, connexin (Cx)40, plays an essential role. Because exercise-induced hypertension is proposed as a forerunner to clinical hypertension, we hypothesized that endothelial disruption of Cx40 function in mice may create an animal model of this condition. To this end, we created mice in which a mutant Cx40T152A was expressed alongside wildtype Cx40 selectively in the endothelium. Expression of the Cx40T152A transgene in Xenopus oocytes and mouse coronary endothelial cells in vitro impaired both electric and chemical conductance and acted as a dominant-negative against wildtype Cx40, Cx43, and Cx45, but not Cx37. Endothelial expression of Cx40T152A in Cx40T152ATg mice attenuated ascending vasodilation, without effect on radial coupling through myoendothelial gap junctions. Using radiotelemetry, Cx40T152ATg mice showed an activity-dependent increase in blood pressure, which was significantly greater than in wildtype mice, but significantly less than in chronically hypertensive, Cx40knockout mice. The increase in heart rate with activity was also greater than in wildtype or Cx40knockout mice. We conclude that the endothelial Cx40T152A mutation attenuates activity-dependent vasodilation, producing a model of exercise-induced hypertension. These data highlight the importance of endothelial coupling through Cx40 in regulating blood pressure during activity.

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the “cardiac fatigue” caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. Methods: We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. Results: When comparing triathletes with LVM <220g and athletes with LVM >220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2max) 57.3 ±7.5ml/min/kg vs. 59.8±9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Conclusion: Significant left ventricular hypertrophy with LVM >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the "cardiac fatigue" caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. When comparing triathletes with LVM <220g and athletes with LVM >220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2max) 57.3 ±7.5ml/min/kg vs. 59.8±9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Significant left ventricular hypertrophy with LVM >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.