Exaggerated Blood Pressure Response Research Articles

Excessive blood pressure rise and cardiovascular remodeling in marathon runners.

Exercise-induced hypertension (EIH) is thought to be associated with increased cardiovascular (CV) risks. However, no previous studies have investigated the effects of EIH on CV systems in marathon runners without CV risk factors using both 24-hr ambulatory blood pressure (BP) monitoring and exercise stress echocardiography (ESE). This study firstly described differences in CV adaptations according to EIH assessed by both exams. Marathon runners between 35 and 64 years of age without CV risk factors were eligible. All the participants underwent both 24-hr ambulatory BP monitoring and ESE. EIH was defined as a maximal exercise systolic BP ≥210 mmHg. The EIH group (n = 19) had shorter training history and higher exercise intensity compared to the non-EIH group (n = 23). The average systolic BP was higher in the EIH group than in the non-EIH group. Left cardiac chamber size and left ventricular mass (LVM) were also higher in the EIH group compared to the non-EIH group. Maximal BP during ESE was positively correlated with both parameters. Exaggerated BP response during exercise needs to be monitored for pre-emptive measurements before it results in progressive cardiovascular maladaptation.

Beneficial Effect of Heat Treatment on the Exercise Pressor Reflex in Hindlimb Ischemia-Reperfusion: Potential Role of P2X3

PURPOSE: In peripheral artery disease (PAD), a greater blood pressure (BP) response during exercise causes cardiovascular and cerebrovascular risks. The exercise pressor reflex (EPR) is a key factor for why BP is exaggerated in PAD patients. Thus, we examined the effect of heat treatment (HT) with two temperature increments in skeletal muscle: 1.5 and 3oC on the EPR response following limb ischemia-reperfusion (IR) injury, one of the most common pathological conditions seen in PAD. In addition, the P2X3 (an ATP-sensitive receptor) in the muscle afferent dorsal root ganglion (DRG) was also evaluated. We hypothesized that IR upregulates the BP response to static muscle contraction and the protein expression of P2X3 in muscle afferent nerves. HT attenuates those exaggerated responses. METHODS: An experimental IR model was induced by 6 hours of ischemia followed by 18 hours of reperfusion in rats (IR rats). For HT groups, three HT sessions (muscle temperature increased by 1.5 or 3oC) for 30 mins/each time were applied. EPR response was evoked by static muscle contraction (30s). Protein expression of the P2X3 receptor in DRGs was examined. Data are presented as mean ± standard deviation. Results: The mean arterial pressure (MAP) response to the static muscle contraction was significantly exaggerated in rats of IR 18h (vs. Sham, P=0.018). With increasing Tm by 1.5°C, there was a promising trend that thus exaggerated BP response was attenuated (IR 18h + HT 1.5°C, n=5 vs. IR 18h rats, n=5, P=0.08). Meanwhile, the exaggerated BP response was significantly attenuated with the Tm increasing by 3°C (IR 18h + HT 3°C, n=5, vs. IR 18h rats, n=5, P=0.032). The expression of the P2X3 receptor was significantly enhanced in the DRGs of IR 18h rats (n=4, p<0.01 vs. sham, n=6). The upregulated P2X3 was suppressed in the DRGs of IR 18h rats +HT of 1.5°C (n=3, p<0.01 vs. IR 18h, n=4) and there was a promising trend that upregulated P2X3 was suppressed in the DRGs of IR 18h rats +HT of 3°C (n=3, P=0.079 vs. IR 18h, n=4). CONCLUSION: IR injury leads to upregulation of EPR response and this effect was attenuated by HT. The P2X3 signaling pathways are likely involved in the beneficial regulatory effect of HT on EPR in IR. Further data collection will be performed to test this conclusion. Supported by NIH R01 HL141198 & HL164571; AHA GRANT # 940567/Lu Qin/2022; and College of Medicine DOM Innovation and Inspiration Award. The authors sincerely thank Chunying Yang for the excellent technical assistance. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Resposta Hipertensiva ao Exercício: uma Forma de Apresentação da Hipertensão Mascarada

Blood pressure measurements outside the office allowed the identification of two opposing phenotypes, commonly known as white coat hypertension and masked hypertension (MH). Whether the hypertensive response to exertion, also called exaggerated blood pressure response to exercise, represents a marker of MH in individuals without a previous history of hypertension is not yet clear, but several follow-up studies have indicated that this finding is associated with the highest future incidence of arterial hypertension, heart failure with preserved ejection fraction and cardiovascular events. Based on data from several studies, the most used definition for hypertensive response to exertion is 210/100 mmHg for men, 190/100 mmHg for women and 220/85mmHg for male athletes and 200/80 mmHg for female athletes. Measuring BP during a low-intensity exercise session (Bruce stage I/II or 70% of maximum theoretical heart rate) also seems to define increased cardiovascular risk, with good accuracy (values >170 mmHg). When the BP values during exercise exceed normal limits, it should be suspected MH and recommended a subsequent study to revaluate BP at home and ABPM, as well as study the cardiorenal repercussion.

Blood pressure responses to isometric handgrip exercise and post-exercise ischemia in females with no/low or high severity hot flash symptoms

Introduction: Severe menopausal hot flash symptoms are linked to the development of cardiovascular disease. Exaggerated blood pressure responses to exercise are also associated with an increased risk of hypertension and cardiovascular disease. It is unclear if females with more severe hot flash symptoms exhibit greater blood pressure responses to exercise compared to those with minimal menopausal hot flashes. We aimed to determine if there is a difference in the pressor response to isometric exercise between females with severe hot flash symptoms compared to females with no/low hot flash symptoms. We hypothesized that there will be exaggerated blood pressure responses to isometric handgrip exercise (IHG) and post-exercise ischemia (PEI) in females who have severe menopausal hot flashes compared to females with no/low hot flashes. Methods: We studied 19 female participants (age: 51±5yrs) with no history of cardiovascular disease or hypertension. The Menopausal Rating Scale (MRS) was used to assess the hot flash symptom severity and to group the participants into no/low (no-or-mild on MRS) or high (moderate-or-severe on MRS) hot flash symptom groups. Continuous blood pressure (BP) was measured via photoplethysmography and calibrated relative to a brachial arm cuff pressure. After 2 minutes of quiet rest, participants performed 2 minutes of IHG at 30% of maximal voluntary contraction, followed by 2 minutes of PEI on the exercising arm to isolate the metaboreflex. The severity groups were compared via independent samples t-tests. Results: There were 13 females in the no/low group and 6 females in the high group. Baseline heart rate (HR, no/low: 60±11 vs high: 58±8bpm), systolic (SBP, no/low:129±18 vs high: 120±14mmHg), diastolic (DBP, no/low: 72±12 vs high: 63±7mmHg) and mean BP (MBP, no/low: 91±11 vs high 82±9mmHg) were not different between groups. There were no differences in the pressor responses to IHG between groups (HR: no/low: Δ6±5 vs high: 5±4bpm, p=0.425; SBP: no/low: Δ9±5 vs high: 11±6mmHg, p=0.408; DBP: no/low: Δ5±3 vs high: 7±4mmHg, p=0.182; MBP: no/low: Δ6±3 vs high: 8±4mmHg, p=0.253). There was also no difference in the pressor response to PEI between groups (HR: no/low: Δ6±6 vs high: 4±2bpm, p=0.554; SBP: no/low: Δ11±6 vs high: 16±9mmHg, p=0.191; DBP: no/low: Δ5±3 vs high: 8±6mmHg, p=0.298; MBP: no/low: Δ7±4 vs high: 11±7mmHg, p=0.280). Conclusion: The current data show no differences in the blood pressure responses to IHG or PEI between females with different menopausal hot flash symptom severities. This suggests that pressor responses to an IHG exercise and the metaboreflex may not be notable contributors to the increased cardiovascular risk in females with severe menopausal hot flashes. NIH: K01 HL148144, NCATS UL1 TR000135, UL1 TR002377; AHA: 898649. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

What Is the Role of the Carotid Baroreflex in Exaggerating the Exercise Pressor Reflex in Male UCD-Type 2 Diabetes Mellitus Rats?

Previous studies have shown that exercise evokes an excessive increase in blood pressure in individuals with type 2 diabetes mellitus (T2DM), which is mediated, in part, by an altered exercise pressor reflex. Importantly, in healthy individuals the arterial baroreflex modulates the pressor response to exercise; however, the effects of T2DM on this modulatory effect of the baroreflex remain unclear. Therefore, the purpose of this study was to characterize the arterial baroreflex function in T2DM rats and to determine whether the carotid baroreflex plays a role in exaggerating the exercise pressor reflex. We hypothesized that T2DM rats would present a baroreflex dysfunction that likely contributes to the exaggerated pressor response during muscle contraction. Experiments were performed on adult (8 ± 2 months old), male University of California Davis (UCD)-T2DM ( n=7; body weight: 640 ± 43 g) and healthy Sprague-Dawley rats ( n=3; body weight: 485 ± 29 g). Female rats were not included in this study because they become diabetic when they are much older (>10 months old). Cardiac baroreflex function was characterized in anesthetized T2DM and healthy rats using the modified Oxford technique, which involved sequential bolus infusions of sodium nitroprusside (10 μg/kg) and phenylephrine (10 μg/kg) to induce blood pressure decreases and increases, respectively. Overall cardiac baroreflex gain (i.e., slope of the relationship between systolic blood pressure and R-R interval) was calculated using logistic regression, while gains to blood pressure falling and rising were calculated separately using piecewise and linear regression. The role of the carotid baroreflex in exaggerating the exercise pressor reflex was tested by statically contracting the hindlimb muscles for 30 s after surgical sinoaortic denervation (SAD) in decerebrated T2DM ( n=1; body weight: 555 g) and healthy ( n=1; body weight: 519 g) rats. Carotid barointact T2DM ( n=8; body weight: 521 ± 38 g) and healthy rats ( n=8; body weight: 482 ± 56 g) were included as controls. The pressor responses were calculated as a change (Δ) in peak mean arterial pressure during 30 s contraction relative to baseline. Data are presented as mean ± SD. T2DM rats presented with lower overall baroreflex sensitivity (T2DM: 0.07 ± 0.02 ms/mmHg, healthy: 0.61 ± 0.81 ms/mmHg, p=0.044), as well as sensitivity to increases in blood pressure (T2DM: 0.14 ± 0.10 ms/mmHg , healthy: 0.28 ± 0.15 ms/mmHg, p=0.049) compared to healthy controls. In contrast, cardiac baroreflex gain during decreases in blood pressure were not different between groups (T2DM: 0.16 ± 0.07 ms/mmHg, healthy: 0.10 ± 0.06 ms/mmHg, p=0.109). Notably, SAD did not alter blood pressure response to muscle contraction in the T2DM rat (SAD: Δ32 mmHg vs barointact: Δ32 ± 12 mmHg), but evoked an exaggerated blood pressure response in healthy rat (SAD: Δ34 mmHg vs barointact: Δ12 ± 3 mmHg). Our preliminary findings suggest that despite an attenuated cardiac baroreflex function in T2DM rats, specifically during acute increases in blood pressure, carotid baroreflex dysfunction may not contribute significantly to the exaggerated exercise pressor reflex in diabetes. This project was supported by NIH R01 HL144723. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Exercise-induced Hypertension and Carotid Intima-media Thickness in Male Marathon Runners.

This study aimed to identify the relationship between exercise-induced hypertension and carotid artery intima-media thickness in long-distance runners. Sixty healthy male runners aged 40 to 60 years were assigned to the following three groups based on resting blood pressure and maximal systolic blood pressure during a maximal exercise test: normal blood pressure response, exercise-induced hypertension, and complex hypertension. An exaggerated systolic blood pressure response was defined as a maximal systolic blood pressure+≥+210 mmHg during the maximal exercise test, while carotid intima-media thickness was measured using B-mode ultrasonography. The carotid intima-media thickness mean values were the highest in the complex hypertension group (0.72±0.11 mm), followed by exercise-induced hypertension (0.62±0.12 mm) and normal blood pressure groups (0.55±0.13 mm), with a significant difference between the groups (p+<+0.002). In linear regression analysis, the mean intima-media thickness was independently associated with age (p=0.015) and maximal systolic blood pressure (p=0.046) but not with resting systolic blood pressure. These results suggest that exercise-induced hypertension is associated with carotid intima-media thickness, a surrogate marker of cardiovascular disease, in long-distance runners. Therefore, evaluating the blood pressure response during exercise is important for the early detection of potential cardiovascular disease risks in long-distance runners.

Assessment and management of exaggerated blood pressure response to standing and orthostatic hypertension: consensus statement by the European Society of Hypertension Working Group on Blood Pressure Monitoring and Cardiovascular Variability.

Recent evidence suggests that an exaggerated blood pressure (BP) response to standing (ERTS) is associated with an increased risk of adverse outcomes, both in young and old individuals. In addition, ERTS has been shown to be an independent predictor of masked hypertension. In the vast majority of studies reporting on the prognostic value of orthostatic hypertension (OHT), the definition was based only on systolic office BP measurements. This consensus statement provides recommendations on the assessment and management of individuals with ERTS and/or OHT. ERTS is defined as an orthostatic increase in SBP at least 20 mmHg and OHT as an ERTS with standing SBP at least 140 mmHg. This statement recommends a standardized methodology to assess ERTS, by considering body and arm position, and the number and timing of BP measurements. ERTS/OHT should be confirmed in a second visit, to account for its limited reproducibility. The second assessment should evaluate BP changes from the supine to the standing posture. Ambulatory BP monitoring is recommended in most individuals with ERTS/OHT, especially if they have high-normal seated office BP. Implementation of lifestyle changes and close follow-up are recommended in individuals with ERTS/OHT and normotensive seated office BP. Whether antihypertensive treatment should be administered in the latter is unknown. Hypertensive patients with ERTS/OHT should be managed as any other hypertensive patient. Standardized standing BP measurement should be implemented in future epidemiological and interventional studies.

Exaggerated blood pressure response to standing: a still underinvestigated issue.

Exaggerated blood pressure response to standing: a still underinvestigated issue.

Exercise testing unmasks exaggerated blood pressure independent of fibrinolytic response in Black but not White postmenopausal females.

Exercise testing unmasks more exaggerated systolic blood pressure responses (SBP) in Black compared with White male adults. Such responses, if translatable to females, may detect racial disparities particularly relevant during menopause. Given the endothelial involvement in BP regulation and as a source of fibrinolytic markers, it follows that fibrinolytic and BP response to exercise could be linked. Thus, we examined BP and fibrinolytic responses to exercise testing in Black and White postmenopausal females. Postmenopausal females (Black = 40; White = 41; 51-70 yr) performed maximal treadmill exercise. BP and blood draws were conducted before and immediately after exercise. Plasma samples, using minimal stasis, were analyzed for tissue plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI-1) activity and antigen, respectively. Resting SBP and fibrinolytic potential were similar between races. Black females exhibited greater increases in SBP during exercise [change (d)=75, 95% CI: 64-86 mmHg, P < 0.001] than White females (d = 60, 95% CI: 48-71 mmHg, P < 0.001). Black compared with White females had smaller changes in tPA (d = 3.27, 95% CI: 2.28-4.27 IU/mL, P < 0.001 vs. d = 5.55, 95% CI: 4.58-6.53, P < 0.001) and PAI-1 (d = -2.89, 95% CI: -4.39 to -1.40 IU/mL, P < 0.001 vs. d = -5.08, 95% CI: -6.59 to -3.61, P < 0.001) activities after exercise. SBP exercise-induced changes were not associated with tPA (r = -0.10, P = 0.42) or PAI-1 (r = 0.13, P = 0.30), without any influence of race (P > 0.05). Our findings show that maximal exercise unmasks risk factors for cardiovascular disease in Black postmenopausal females.NEW & NOTEWORTHY Exaggerated SBP responses to exercise testing are more frequent in Black than in White male adults. Such responses, if translatable to females, may detect early racial disparities arriving during menopause. Because the endothelium regulates BP and fibrinolytic responses, these could be linked during exercise. At peak exercise, Black but not White postmenopausal females had more exaggerated SPB responses regardless of reduced fibrinolytic potential. Maximal exercise unmasked risk factors for cardiovascular disease in Black postmenopausal females.

Amplified P2X3 pathway activity in muscle afferent dorsal root ganglion neurons and exercise pressor reflex regulation in hindlimb ischaemia-reperfusion.

Hindlimb ischaemia-reperfusion (IR) is among the most prominent pathophysiological conditions observed in peripheral artery disease (PAD). An exaggerated arterial blood pressure (BP) response during exercise is associated with an elevated risk of cardiovascular events in individuals with PAD. However, the precise mechanisms leading to this exaggerated BP response are poorly elucidated. The P2X3 signalling pathway, which plays a key role in modifying the exercise pressor reflex (EPR), is the focus of the present study. We determined the regulatory role of P2X3 on the EPR in a rat model of hindlimb IR. In vivo and in vitro approaches were used to determine the expression and functions of P2X3 in muscle afferent nerves and EPR in IR rats. We found that in IR rats there was (1) upregulation of P2X3 protein expression in the L4-6 dorsal root ganglia (DRG); (2) amplified P2X currents in isolated isolectin B4 (IB4)-positive muscle DRG neurons; and (3) amplification of the P2X-mediated BP response. We further verified that both A-317491 and siRNA knockdown of P2X3 significantly decreased the activity of P2X currents in isolated muscle DRG neurons. Moreover, inhibition of muscle afferents' P2X3 receptor using A-317491 was observed to alleviate the exaggerated BP response induced by static muscle contraction and P2X-induced BP response by α,β-methylene ATP injection. P2X3 signalling pathway activity is amplified in muscle afferent DRG neurons in regulating the EPR following hindlimb IR.

Different Cardio-Selective ß-Blockers and the Prevention of Exaggerated Blood Pressure Response During Exercise: A Retrospective Cross-Sectional Study.

The aim of this study was to analyze the role of various ß-blockers in managing exercise-induced blood pressure escalations, referred to as exaggerated blood pressure response (eBPR). Despite the importance of this phenomenon, there is limited data on the efficacy of ß-blockers in controlling eBPR. Our retrospective cohort for this study comprised 2,803 individuals who underwent treadmill tests from January 2016 to February 2018. A further subgroup analysis of 1,258 patients receiving ß-blocker treatment was performed to evaluate the influence of different ß-blockers on eBPR. The results demonstrated that ß-blockers play a significant role in mitigating the occurrence of eBPR (P = 0.026), irrespective of the specific type of ß-blocker. Additionally, no significant variance was observed in the development of eBPR among the different ß-blocker groups (P = 0.532 for systolic blood pressure (BP); P = 0.068 for diastolic BP). This finding remained consistent even among the 992 hypertensive patients, where no notable association was found between the type of ß-blocker and the development of eBPR (P = 0.736 for systolic BP; P = 0.349 for diastolic BP). It is noteworthy that patients using ß-blockers had unique clinical and demographic attributes. Our study suggests that ß-blockers can potentially deter the development of eBPR during physical activity, a benefit that is consistent across all types of ß-blockers. The study sheds light on prospective randomized studies on the use of eBPR as a new treatment target.

Correlation between blood pressure response to sub maximal exercise and left ventricular hypertrophy

There is currently no consensus on the definition of normal BP (blood pressure) increase during physical activity and thus of the exaggerated BP response to exercise. A hypertensive response to exercise (HRE) is frequently observed in individuals without hypertension or other cardiovascular disease. However, mechanisms and clinical implication of HRE is not fully explained. Endothelial dysfunction and increased afterload contribute to development of HRE. From neurohormonal aspects. Studies showed that excess stimulation of sympathetic nervous system and augmented rise of angiotensin II seems to be important mechanism in HRE [1]. However, evidences for efficacy and outcomes of treatment of HRE to submaximal exertion in individuals without hypertension or low grade hypertension is scarce and therefore warrants further studies. Presents small cohort of patients a total of 38 women and 46 men, aged 52±8 years, without evidence of cardiovascular disease, with a mean resting BP of 142±7/75±7mmHg had their BP measured at rest and during submaximal treadmill exercise. LV mass was measured using trans thoracic echocardiography. For the majority of the subjects on the initial evaluation we discovered echocardiographic evidence of concentric hypertrophy. Among the resting and exercise BP indices, sub maximal SBP was the strongest correlate of LV mass (r=0.40, P&lt;0.04). In multivariate analysis, maximal SBP was independently as-sociated with LV mass an concentric LV hypertrophy, after adjustment for lean body mass and gender. Subaximal exercise SBP is a modest but still independent predictor of LV remodeling (grade and type of LV geometry) in population with prehypertension, I and II grade hypertension. These results raise the possibility that the SBP response to sub maximal exercise is an early marker of developing LV hypertrophy.

Exaggerated Systolic Blood Pressure Increase with Exercise and Myocardial Ischemia on Exercise Stress Echocardiography.

Central Illustration : Exaggerated Systolic Blood Pressure Increase with Exercise and Myocardial Ischemia on Exercise Stress Echocardiography ESBPRE: exaggerated systolic blood pressure response to exercise; HR: heart rate; SBP: systolic blood pressure. The association between exaggerated systolic blood pressure response to exercise (ESBPRE) and myocardial ischemia is controversial and little studied in patients with established or suspected chronic coronary syndrome. To verify the relationship between myocardial ischemia and ESBPRE in patients undergoing exercise stress echocardiography (ESE). This is a cross-sectional study with 14,367 patients undergoing ESE, from January 2000 to January 2022, divided into the following 2 groups: G1, composed of patients whose peak systolic pressure increased ≥ 90 mmHg (value corresponding to the 95th percentile of the study population), and G2, patients who did not demonstrate an exaggerated hypertensive response. The groups were compared using Student's t and chi-square tests. P values < 0.05 were considered significant. Logistic regression was also performed to identify independent risk factors for myocardial ischemia, ESBPRE, complaints of typical chest pain prior to the exam, and angina during the test. Of the 14,367 patients, 1,500 (10.4%) developed ESBPRE, and 7,471 (52.0%) were female. The percentages of previous complaints of typical chest pain, angina during the test, and myocardial ischemia in patients with ESBPRE were 5.8%, 2.4% and 18.1%, compared to 7.4%, 3.9%, and 24.2%, in patients without ESBPRE, respectively (p = 0.021,p = 0.004, p < 0.001). In multivariate analysis, ESBPRE was independently associated with a lower probability of myocardial ischemia (odds ratio: 0.73; 95% confidence interval: 0.58 to 0.93; p = 0.009). Exaggerated increase in systolic blood pressure during ESE may be a marker for excluding myocardial ischemia.

Association of central blood pressure with an exaggerated blood pressure response to exercise among elite athletes

PurposeThe systolic blood pressure/workload (SBP/MET) slope was recently reported to be a reliable parameter to identify an exaggerated blood pressure response (eBPR) in the normal population and in athletes. However, it is unclear whether an eBPR correlates with central blood pressure (CBP) and vascular function in elite athletes.MethodsWe examined 618 healthy male elite athletes (age 25.8 ± 5.1 years) of mixed sports with a standardized maximum exercise test. CBP and vascular function were measured non-invasively with a validated oscillometric device. The SBP/MET slope was calculated and the threshold for an eBPR was set at > 6.2 mmHg/MET. Two groups were defined according to ≤ 6.2 and > 6.2 mmHg/MET, and associations of CBP and vascular function with the SBP/MET slope were compared for each group.ResultsAthletes with an eBPR (n = 180, 29%) displayed a significantly higher systolic CBP (102.9 ± 7.5 vs. 100 ± 7.7 mmHg, p = 0.001) but a lower absolute (295 ± 58 vs. 384 ± 68 W, p < 0.001) and relative workload (3.14 ± 0.54 vs. 4.27 ± 1.1 W/kg, p < 0.001) compared with athletes with a normal SBP/MET slope (n = 438, 71%). Systolic CBP was positively associated with the SBP/MET slope (r = 0.243, p < 0.001). In multiple logistic regression analyses, systolic CBP (odds ratio [OR] 1.099, 95% confidence interval [CI] 1.045–1.155, p < 0.001) and left atrial volume index (LAVI) (OR 1.282, CI 1.095–1.501, p = 0.002) were independent predictors of an eBPR.ConclusionSystolic CBP and LAVI were independent predictors of an eBPR. An eBPR was further associated with a lower performance level, highlighting the influence of vascular function on the BPR and performance of male elite athletes.

IMPACT OF POST-COVID MENTAL STRESS DISORDERS ON BLOOD PRESSURE RESPONSE TO EXERCISE

Objective: Patients recovered from COVID-19 are at high risk of developing mental stress disorders over the long-term. Post-traumatical stress disorders (PTSD) are associated with increased BP and hypertension incidence. We tested the hypothesis that PTSD, occurring in patients after hospital discharge for severe COVID-19, is associated with an impaired BP response to exercise. Design and method: 108 patients previously hospitalized for severe COVID-19 were evaluated after 5 months from hospital discharge. A Revised Impact of Event Scale (IES-r) score&gt;33 indicated probable COVID-related PTSDs All subjects underwent maximal cardio-pulmonary exercise test on a cycle ergometer with incremental ramp protocol. Submaximal BP was recorded after 4 minutes, at a workload threshold of 75W. Results: 95 subjects (mean age 58±10 years, 71% men) had complete data. Mean baseline BP was 128/82±12/11 mmHg. 51% were hypertensive. 32% had a IES-r score&gt;33 (PTSD group). These patients were more frequently women (45% vs 20%, p = 0.01), whereas no differences in terms of age, BMI, hypertension history, other CV risk factors or diseases were found compared to non-PTSD group. Baseline BP did not differ between PTSD and non-PTSD groups (127/82±10/8 mmHg vs 129/82±15/9 mmHg, p = 0.43/0.88). By contrast, submaximal exercise SBP (eSBP) was increased in PTSD vs non-PTSD group (155±16 mmHg vs 146±14 mmHg, p&lt;0.05). A strong sex-specific effect was found, being eSBP higher in PTSD vs non-PTSD women, but not in PTSD vs non-PTSD men (p for sex interaction = 0.01). Intrusion symptoms, such as unwanted and upsetting memories, nightmares and flashbacks, were more markedly associated with increased BP response to exercise. Conclusions: In people with mental stress disorders related to previous COVID-19 hospitalization, we showed increased submaximal BP during exercise. This finding showed a sex-specific association, being observed in women but not in men. Mental stress disorders could negatively impact on future CV risk in post-COVID-19 women through an exaggerated BP response to physical stressors.

Submaximal Exercise Response is Associated with Future Hypertension in Patients with Coarctation of the Aorta.

Hypertension (HTN) is common in patients with a history of coarctation of the aorta (CoA) and remains underrecognized and undertreated. Studies in the non-coarctation otherwise healthy adult population have correlated an exaggerated blood pressure response during mild to moderate exercise with subsequent diagnosis of HTN. The goal of this study was to determine if blood pressure response to submaximal exercise in normotensive CoA patients correlated with development of HTN.Retrospective chart review was performed in individuals ≥ 13 years old with CoA and no diagnosis of HTN at time of cardiopulmonary exercise testing (CPET). Systolic blood pressure (SBP) during CPET at rest, submax 1 (stage 1 Bruce or minute 2 bicycle ramp), submax 2 (stage 2 Bruce or minute 4 bicycle ramp), and peak were recorded. The primary composite outcome was HTN diagnosis or initiation of anti-hypertensive medications at follow up.There were 177 patients (53% female, median age 18.5 years), of whom 38 patients (21%) met composite outcome during a median follow up of 46 months. Men were more likely to develop hypertension. Age at repair and age at CPET were not significant covariates. At each stage of CPET, SBP was significantly higher in those who met the composite outcome. Submax 2 SBP ≥ 145 mmHg was 75% sensitive, 71% specific in males and 67% sensitive, 76% specific in females for development of composite outcome.Our study shows an exaggerated SBP response to submaximal exercise may portend an increased risk of developing hypertension during short- to mid-term follow up.

Purinergic 2X Receptors Contribute to the Exaggerated Mechanoreflex in Rats with Heart Failure

Skeletal muscle contraction stimulates mechanically activated channels on the sensory endings of thin fiber muscle afferents which evokes reflex increases in sympathetic nerve activity and blood pressure. This reflex is termed the mechanoreflex and its activation in healthy populations plays a key role in facilitating oxygen delivery to contracting muscles and exercise performance. However, mechanoreflex activation in patients with heart failure with reduced ejection fraction (HF-rEF) results in excessive peripheral vasoconstriction and impaired limb blood flow during exercise. Recent evidence in a rat model of HF-rEF demonstrated that hindlimb arterial injection of PPADS, an antagonist for ATP-sensitive purinergic 2X (P2X) receptors, reduced thin fiber muscle afferent responsiveness to static hindlimb muscle stretch (a model of mechanoreflex activation isolated from contraction-induced metabolite production) to a greater extent in HF-rEF rats than in healthy counterparts. Those data suggest that, in HF-rEF, P2X receptor stimulation results in the sensitization of co-localized mechanically activated channels on the sensory endings of muscle afferents. To date, however, those electrophysiological findings have not been extended to reflex experiments investigating the cardiovascular consequences of mechanoreflex activation. Accordingly, we sought to determine the role played by P2X receptors in evoking the exaggerated blood pressure response to isolated mechanoreflex activation in HF-rEF rats. We hypothesized that hindlimb arterial injection of the P2X receptor antagonist PPADS (5mg) would reduce the integrated area under the blood pressure signal (the blood pressure index: BPI) evoked during 30 seconds of static hindlimb skeletal muscle stretch in decerebrate, unanesthetized HF-rEF rats to a greater extent than in healthy rats. Experiments were performed six to eight weeks following either a coronary artery ligation surgery to induce myocardial infarction and HF-rEF ( n=8M/2F; ejection fraction 37±6%) or a sham procedure ( n=1M/4F; ejection fraction 84±4; P&lt;0.01versus HF-rEF). In sham rats, P2X receptor blockade had no effect on the BPI response to hindlimb muscle stretch (control: 197±67, PPADS: 211±159mmHg⋅s; p=0.46). Conversely, in HF-rEF rats P2X receptor blockade reduced the BPI response to hindlimb muscle stretch (control: 425±60, PPADS: 257±83mmHg⋅s; p=0.01). The integrated area of the muscle tension signal during the stretch maneuver (tension-time-index; TTI) was not different between control and P2X receptor blockade conditions in either sham (control: 20±2, PPADS: 21±2kg·s; P=0.31) or HF-rEF (control: 24±2, PPADS: 25±2kg·s; P=0.09) rats. The data suggest that P2X receptors on the sensory endings of thin fiber muscle afferents do not play a role in the cardiovascular responses to mechanoreflex activation in health, but contribute importantly to the cardiovascular responses to mechanoreflex activation in HF-rEF. This work was supported by the National Institutes of Health (NIH) R01HL142877 to S.W.C. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Exaggerated blood pressure response to standing in young-to-middle-age subjects: prevalence and factors involved

PurposeTo investigate the prevalence of orthostatic hypertension and the association of the blood pressure (BP) level, supine BP decline, and white-coat effect with the orthostatic pressor response.MethodsWe studied 1275 young-to-middle-age individuals with stage-1 hypertension. Orthostatic response was assessed three times over a 3 month period. The white-coat effect was assessed at baseline and after 3 months, and was calculated as the difference between office and average 24 h BP. In 660 participants, urinary epinephrine and norepinephrine were also measured.ResultsAn orthostatic systolic BP increase ≥ 20 mmHg was observed in 0.6–1.2% of the subjects during the three visits. Using the 20 mmHg cut-off, the prevalence of orthostatic hypertension was 0.6%. An orthostatic BP increase of ≥ 5 mmHg was found in 14.4% of participants. At baseline, the orthostatic response to standing showed an independent negative association with the supine BP level (p < 0.001), the supine BP change from the first to third measurement (p < 0.001), and the white-coat effect (p < 0.001). Similar results were obtained in the 1080 participants assessed at the third visit. Urinary epinephrine showed higher values in the top BP response decile (systolic BP increase ≥ 6 mmHg, p = 0.002 versus rest of the group).ConclusionAn orthostatic systolic BP reaction ≥ 20 mmHg is rare in young adults. However, even lower BP increases may be clinically relevant. The BP level, the supine BP decline over repeated measurement, and the white-coat effect can influence the estimate of the BP response to standing and should be considered in clinical and pathogenetic studies.

Does light physical activity reduce blood pressure responses to laboratory stressors?

Individuals exhibiting exaggerated blood pressure responses to stress are at increased risk for later cardiovascular disease. Engagement in brief bouts of moderate-to-vigorous physical activity may reduce instances of these exaggerated blood pressure responses. While observational work has shown that periods of light physical activity may also be associated with reduced blood pressure responses to stress in daily life, the few experimental studies involving light physical activity have methodological limitations that temper conclusions. The current investigation sought to understand the effects of brief bouts of light physical activity on blood pressure responses to psychological stress. In a between-person, single-session experimental design, 179 healthy, young adults were randomized to 15 min of light physical activity, moderate physical activity, or sitting before engaging in a 10-min computerized Stroop Color-Word Interference Task. Blood pressure readings were collected throughout the study session. Surprisingly, the light physical activity participants showed higher systolic blood pressure responses to stress than control participants by 2.9 mmHg (F (2, 174)=3.49, ηp 2 =0.038, p=.03), whereas no significant differences were shown between moderate physical activity and control groups (F (2, 174)=2.59, ηp 2 =0.028, p=.078). These findings show that light physical activity may not be related to reduced blood pressure responses to stress in an experimental session involving healthy, college-aged adults and question the extent to which brief bouts of physical activity may reduce acute blood pressure responses to stress.

Masked Hypertension and Exaggerated Blood Pressure Response to Exercise: A Review and Meta-Analysis

Whether exaggerated blood pressure response (EBPR) to exercise represents a marker of masked hypertension (MH) in individuals with no prior history of hypertension is still unclear. We investigated this issue through a review and a meta-analysis of studies providing data on this association in normotensive individuals undergone both to dynamic or static exercise and to 24 h blood pressure monitoring (ABPM). A systematic search was performed using Pub-Med, OVID, EMBASE, and Cochrane library databases from inception up to 31 December 2022. Studies were identified by using the following search terms: "masked hypertension", "out-of-office hypertension", "exercise blood pressure", "exaggerated blood pressure exercise", "exercise hypertension". Nine studies including a total of 387 participants with MH and 406 true normotensive controls were considered. Systolic BP (SBP) and diastolic BP (DBP) at rest were significantly higher in MH individuals than in sustained normotensives: 126.4 ± 1.4/78.5 ± 1.8 versus 124.0 ± 1.4/76.3 ± 1.3 mmHg (SMD: 0.21 ± 0.08, CI: 0.06-0.37, p = 0.007 for SBP; 0.24 ± 0.07, CI: 0.08-0.39, p = 0.002 for DBP). The same was true for BP values at peak exercise: 190.0 ± 9.5/96.8 ± 3.7 versus 173.3 ± 11.0/88.5 ± 1.8 mmHg (SMD 1.02 ± 0.32, CI: 0.39-1.65, p = 0.002 for SBP and 0.97 ± 0.25, CI: 0.47-1.96, p < 0.0001 for DBP). The likelihood of having an EBPR was significantly greater in MH than in their normotensive counterparts (OR: 3.33, CI: 1.83-6.03, p < 0.0001). Our meta-analysis suggests that EBPR reflects an increased risk of MH and that BP measurement during physical exercise aimed to assess cardiovascular health may unmask the presence of MH. This underscores the importance of BP measured in the medical setting at rest and in dynamic conditions in order to identify individuals at high cardiovascular risk due to unrecognized hypertension.