Inverse association between arterial stiffness and perceived fatigue independent of disability status and BMI in multiple sclerosis.

INTRODUCTION: Multiple sclerosis (MS) is an immune-mediated, neurodegenerative disease of the central nervous system. Fatigue represents one of the most prevalent and limiting symptoms of MS, and is associated with vascular dysfunction, notably increased arterial stiffness. OBJECTIVE: This study examined the relationship between arterial stiffness and perceived fatigue in persons with MS. METHODS: The sample of 52 persons with MS (71.2% Female; Age: 46.7 ± 12.3 yrs.) completed arterial stiffness and fatigue assessments as baseline for an exercise training intervention. Applanation tonometry measured arterial stiffness, pulsatility and waveform characteristics, and yielded the following outcomes: carotid-femoral pulse wave velocity (cfPWV), carotid pulse-pressure (cPP), and aortic augmentation pressure (AP). Perceived fatigue was measured using the Fatigue Severity Scale (FSS). RESULTS: The mean (SD) scores for cfPWV, cPP, and AP were 7.0 ± 1.8 m/s, 35.7 ± 8.8 mmHg, 8.2 ± 6.2 mmHg, respectively. The mean (SD) FSS score was 4.6 ± 1.4 and indicated elevated fatigue. There were statistically significant (p < .05) inverse correlations between cfPWV (r = -.32), cPP (r = -.37) and AP (r = -.32) with FSS scores, and the correlations remained significant even after controlling for disability, body mass index, age, and sex. CONCLUSION: Our results indicate a consistent pattern of inverse relationships between arterial stiffness, pulsatility, and waveforms with fatigue independent of disability, body mass index, age, and sex in MS. This could be explained by lower sympathetic activation linking higher arterial stiffness, pulsatility and augmentation pressure with lower fatigue in persons with MS.

Relationships Among Heart Rate Variability, Perceived Social Support, and Hopelessness in Adults With Ischemic Heart Disease.

BACKGROUND: Lower perceived social support is associated with hopelessness in patients with ischemic heart disease (IHD). Higher perceived social support is associated with higher heart rate variability (HRV) in adults following a stressful event, but the relationship between HRV and hopelessness has not been examined in patients with IHD. The purpose of this research was to evaluate the relationships among HRV, perceived social support, and hopelessness in patients with IHD. METHODS AND RESULTS: Ninety-four participants were enrolled while hospitalized for an IHD event at a large hospital in the United States. Data collection occurred 2 weeks after hospital discharge and included the State-Trait Hopelessness Scale, ENRICHD Social Support Inventory, Patient Health Questionnaire-9, a demographic form, and a short-term HRV measurement taken at rest. Linear models were used to assess associations between variables in unadjusted and adjusted models. Most participants were men (67%), married (75%), and non-Hispanic White (96%) and underwent coronary artery bypass surgery (57%). There were inverse correlations between high frequency HRV and state hopelessness (r=-0.21, P=0.008) and root mean square of successive differences between normal heartbeats HRV and state hopelessness (r=-0.20, P=0.012) after adjusting for important covariates. High frequency and root mean square of successive differences between normal heartbeats did not show evidence of mediating the relationship between perceived social support and hopelessness. CONCLUSIONS: There were significant inverse correlations between parasympathetic measures of HRV and hopelessness. Assessing high frequency and root mean square of successive differences between normal heartbeats during early recovery following an IHD event could provide promising evidence for understanding a possible precursor to hopelessness and targets for future interventions. Registration Information: clinicaltrials.gov. Identifiers: NCT03907891, NCT05003791.

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.

Home-based exercise improves subclinical atherosclerosis marker in multiple sclerosis.

PURPOSE: Using a 12-week, randomized controlled trial coupled with social cognitive theory behavioral coaching, we aimed to assess the effect of a home-based aerobic training intervention versus an attention-control on aerobic fitness, subclinical atherosclerosis, and mobility in persons with MS. METHODS: Persons with MS with an expanded disability status scale score between 0 and 4 were randomized to a 12-week aerobic exercise (EX) (n = 26; 19 females; 49 yrs; 28.8 kg/m2) or attention-control (CON) condition (stretching; n = 22; 16 females; 44 yrs; 29.2 kg/m2). Aerobic capacity was assessed via a graded cycle ergometry test with indirect calorimetry. The co-primary measures of subclinical atherosclerosis assessed included carotid intima media thickness, a test of vasodilatory reactivity, and arterial stiffness. Mobility was assessed via a timed 25-foot walk test (T25FW) and a 6 min walk test. The EX group engaged in cycle ergometry 3d/wk with gradual increases in the intensity and duration of the exercise sessions. CON participated in standardized stretching designed to provide the same contact time as EX 3d/wk. Behavioral coaching took place via weekly phone/video chats to track adherence. RESULTS: Aerobic capacity, vasodilatory reactivity, and T25FW speed increased only in the EX group, 7%, 16%, and 13% (p<0.05), respectively; whereas the CON group did not change. CONCLUSION: The EX group had modest, yet significant, increases in aerobic capacity over the 12-week period, coupled with improvements in T25FW speed and vasodilatory reactivity. A home-based exercise intervention can improve outcomes of a subclinical marker of atherosclerosis, which provides a basis for examining these outcomes in persons prescreened for CVD-related comorbidities and/or mobility issues.

Older females but not males exhibit increases in cerebral blood velocity, despite similar pulsatility increases after high-intensity resistance exercise.

Sex differences in resting cerebral hemodynamics decline with aging. Given that acute resistance exercise (RE) is a hypertensive challenge, it may reveal sex-dependent abnormalities in cerebral hemodynamics. Thus, we hypothesized that cerebral blood velocity and pulsatility responses to RE would be sex-dependent in older adults. Fourteen older females and 11 males (50-68 yr) completed a high-intensity unilateral isokinetic knee flexion/extension exercise. Measurements were collected at baseline, immediately, 5- and 30-min post-RE. Blood pressure was measured via finger photoplethysmography. Mean middle cerebral artery blood velocity (MCAv) and pulsatility were assessed via transcranial Doppler ultrasound. Carotid pulsatility was obtained via duplex ultrasound. MCAv increased immediately after RE in older females [mean difference (d) = 6.02, 95% CI: 1.66 to 10.39 cm/s, P < 0.001] but not in males (d = -0.72, 95% CI: -3.83 to 5.27 cm/s, P = 0.99), followed by similar reductions 5-min post-RE in older females (d = -4.40, 95% CI: -8.81 to -0.10 cm/s, P = 0.045) and males (d = -6.41, 95% CI: -11.19 to -1.62 cm/s, P = 0.003). MCAv pulsatility increased similarly in older females (d = 0.24, 95% CI: 0.11 to 0.40, P < 0.001) and males (d = 0.38, 95% CI: 0.20 to 0.53, P < 0.001), persisting 5-min post-RE. Older females showed smaller increases in carotid pulsatility immediately after RE (d = 0.18, 95% CI: 0.03 to 0.38, P = 0.01) than males (d = 0.48, 95% CI: 0.26 to 0.68, P < 0.001). An exercise-mediated hypertensive stimulus revealed differential sex responses in MCAv and carotid pulsatility but not in cerebral pulsatility. Cerebral pulsatility findings suggest a similar sex susceptibility to cerebrovascular abnormalities following exercise-mediated hypertensive stimulus in older adults.NEW & NOTEWORTHY Sex differences in resting cerebral hemodynamics decline with advancing age as females experience larger reductions in cerebral blood velocity and steeper pulsatility increases than males. However, an exercise-mediated hypertensive stimulus might reveal sex differences in cerebral hemodynamics not apparent at rest. Following high-intensity resistance exercise, older females but not males exhibit increases in cerebral blood velocity, despite similar increases in cerebral pulsatility. The susceptibility to cerebrovascular abnormalities following exercise-mediated hypertensive stimulus appears similar between sexes.

Temporal longitudinal associations of carotid-femoral pulse wave velocity and carotid intima-media thickness with resting heart rate and inflammation in youth.

We examined the temporal longitudinal associations of carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT) with the risk of elevated resting heart rate (RHR) and high-sensitivity C-reactive protein (hsCRP). We studied 3,862 adolescents, mean age 17.7 (SD 0.3 yr), followed-up for 7 yr until age 24.5 (0.7) yr, from the Avon Longitudinal Study of Parents and Children, UK. RHR, fasting plasma hsCRP, cfPWV, and cIMT were repeatedly assessed and analyzed using logistic regression, linear mixed-effect, and structural equation models adjusting for important covariates. Among 3,862 adolescents [2,143 (55.5%) female], 10% and 44% were at moderate-to-high risk of elevated RHR and hsCRP at 24.5 yr, respectively. Higher cfPWV at 17.7 yr was associated with elevated RHR risk at follow-up [odds-ratio (OR) 1.58 (CI 1.20-2.08); P = 0.001], whereas cIMT at 17.7 yr was associated with elevated hsCRP risk [OR 2.30 (1.18-4.46); P = 0.014] at follow-up, only among females. In mixed model, 7-yr progression in cfPWV was directly associated with 7-yr increase in RHR [effect-estimate 6 beats/min (1-11); P = 0.017] and hsCRP. cIMT progression was associated with 7-yr increase in RHR and hsCRP. In cross-lagged model, higher cfPWV at 17.7 yr was associated with higher RHR (ß = 0.06, standard error = 3.85, P < 0.0001) at 24.5 yr but RHR at 17.7 yr was unassociated with cfPWV at 24.5 yr. Baseline cIMT or RHR was unassociated with either outcome at follow-up. Higher hsCRP at 17.7 yr was associated with higher cfPWV and cIMT at 24.5 yr. In conclusion, adolescent arterial stiffness but not cIMT appears to precede higher RHR in young adulthood, whereas elevated hsCRP in adolescence preceded higher cfPWV and cIMT.NEW & NOTEWORTHY Higher arterial stiffness but not carotid-intima media thickness in adolescence preceded higher resting heart rate in young adulthood, however, elevated high sensitivity C-reactive protein in adolescence preceded higher arterial stiffness and carotid intima-thickness in young adulthood in the temporal causal path. Low-grade inflammation during adolescence may be causally associated with the development of subclinical arteriosclerosis and atherosclerosis in young adulthood.

Blood pressure and cognition in older adults with multiple sclerosis: preliminary examination.

BACKGROUND: Comorbid conditions, particularly vascular comorbidity, are common in MS and may hasten the CNS damage and disease manifestations. We undertook a preliminary examination of the association between blood pressure (BP) and cognitive function in samples of older adults with MS and healthy controls. METHODS: Older adults with MS (n = 29) and healthy controls (n = 29) completed the Brief International Cognitive Assessment for MS (BICAMS) battery and underwent assessment of BP. The data were analyzed using the Baron and Kenny approach for examining blood pressure as an explanatory variable for group differences in cognition. RESULTS: The MS group, as expected, had significantly lower California Verbal Learning Test-II (CVLT-II) z-scores from the BICAMS and higher diastolic BP (DBP) than healthy controls. DBP had statistically significant correlations with CVLT-II z-scores in the overall sample (r = - .42) and MS subsample (r = - .51), but not healthy controls(r = - .29); the correlation was not attenuated when controlling for age and disability status in the MS subsample (pr = - .48). Group initially explained 6% of the variance in z-scores from the CVLT-II (ß = - 0.24). The inclusion of DBP accounted for an additional 14% of the variance in z-scores from the CVLT-II, and DBP(ß = - 0.39), but not group (ß = - 0.13), was a significant correlate of CVLT-II z-scores; the results were unchanged when controlling for anxiety and depression scores. CONCLUSION: Our results provide preliminary, cross-sectional support for future population-based research examining DBP, hypertension, and verbal memory in older adults with MS.

The effect of aging on carotid artery wall mechanics during maximal resistance exercise.

INTRODUCTION: Age-related stiffening of the large elastic arteries (e.g., common carotid artery [CCA]) may impair wall dynamics (i.e., strain) and amplify transmission of pulsatile blood flow into the brain with large increases in pressure that occur during maximal resistance exercise (RE). The purpose of this study was to compare CCA arterial wall dynamics, central hemodynamics, and cerebral blood velocity responses during maximal RE between young and older adults. METHODS: Thirty-one young (YA; 26 ± 5 yrs; 23.8 ± 3.3 kg/m2) and 25 older adults (OA; 60 ± 6 yrs; 30.0 ± 5.5 kg/m2) performed a unilateral maximal isokinetic knee flexion/extension exercise protocol (i.e., maximal RE). All measures were recorded at baseline and during the last 10 s of maximal RE. Common carotid artery strain, CCA strain time to peak, and CCA strain rate (i.e., variables of arterial wall dynamics) were analyzed using 2D speckle tracking software from circumferential ultrasound images. Transcranial Doppler was used to measure right middle cerebral artery (MCA) blood velocity. Non-invasive arterial blood pressure measurements were obtained using finger photoplethysmography. RESULTS: Older adults had greater reductions in CCA strain time to peak from baseline to maximal RE (345 ± 39 to 242 ± 52 ms) than YA (308 ± 35 to 247 ± 42 ms; interaction effect, p < 0.01). MCA velocity was similar between YA and OA during maximal RE (p = 0.48), despite a greater arterial pressor response in OA (p < 0.01). CONCLUSION: These data suggest cerebral blood velocity responds similarly during maximal RE among OA compared to YA, despite subtle age-related differences in the pressor and extracranial vascular response during maximal RE.

Breast cancer survivors with preserved or rescued cardiorespiratory fitness have similar cardiac, pulmonary and muscle function compared to controls.

Breast cancer survivors (BCS) have a high prevalence of cardiovascular disease and low cardiorespiratory fitness (CRF). CRF is an important predictor of survival in BCS. However, the physiological factors that contribute to low CRF in BCS have not been completely elucidated. To assess differences in physiological factors (cardiac, pulmonary, muscle function) related to CRF between BCS and controls. Twenty-three BCS and 23 age-body mass index (BMI) matched controls underwent a peak cycling exercise test to determine CRF, with physiological factors measured at resting and at peak exercise. Cardiac hemodynamics (stroke volume [SV], SVindex, heart rate [HR], cardiac output [Formula: see text], and [Formula: see text]index) were evaluated using ultrasonography. Pulmonary function was evaluated using the oxygen uptake efficiency slope (OUES), ventilation to carbon dioxide production slope [Formula: see text] and breathing reserve at peak exercise (BR). Muscle oxygenation variables (oxygenated [HbO2] deoxygenated [HHb] and total hemoglobin [Hb], and tissue oxygenation index [TSI]) were measured with near-infrared spectroscopy (NIRS). Both groups had similar CRF and similarly increased all hemodynamic variables (HR, SV, SVindex, [Formula: see text] and [Formula: see text]index) at peak exercise compared to resting (p < 0.001). BCS had higher overall HR and lower SVindex (group effect, p < 0.05). BCS had similar OUES, [Formula: see text] and BR compared to the controls. Both groups decreased TSI, and increased Hb and HHb similarly at peak exercise compared to resting (p < 0.001). Our data suggest BCS do not exhibit differences in cardiac, pulmonary, or muscle function at peak exercise compared to controls, when both groups have similar CRF and physical activity.

Safety of maximal cardiopulmonary exercise testing in individuals with sickle cell disease: a systematic review.

OBJECTIVE: We evaluated the safety of maximal cardiopulmonary exercise testing (CPET) in individuals with sickle cell disease (SCD). Maximal CPET using gas exchange analysis is the gold standard for measuring cardiopulmonary fitness in the laboratory, yet its safety in the SCD population is unclear. DESIGN: Systematic review. DATA SOURCES: Systematic search of Medline (PubMed), EMBASE, Cochrane, ClinicalTrials.gov and professional society websites for all published studies and abstracts through December 2020. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Two reviewers independently extracted data of interest from studies that assessed safety outcomes of maximal CPET in children and adults with SCD. A modified version of the Newcastle-Ottawa Scale was used to assess for risk of bias in studies included. RESULTS: In total, 24 studies met inclusion/exclusion criteria. Adverse events were reported separately or as part of study results in 36 (3.8%) of 939 participants with SCD undergoing maximal CPET in studies included. Most adverse events were related to transient ischaemic changes on ECG monitoring or oxygen desaturation during testing, which did not result in arrhythmias or other complications. Only 4 (0.43%) of 939 participants experienced pain events due to maximal CPET. CONCLUSION: Maximal CPET appears to be a safe testing modality in children and adults with SCD and can be used to better understand the physiological basis of reduced exercise capacity and guide exercise prescription in this population. Some studies did not focus on reporting adverse events related to exercise testing or failed to mention safety monitoring, which contributed to risk of bias.

Predictive equations to estimate peak aerobic capacity and peak heart rate in persons with Down syndrome.

Estimations based on the available equations for predicting oxygen uptake (V̇o2) from treadmill speed of locomotion are not appropriate for individuals with Down syndrome (DS). We aimed at developing prediction models for peak absolute oxygen uptake (V̇o2peak) and peak heart rate (HRpeak) based on retrospective data from a healthy population with and without Down syndrome (DS). A cross-sectional analysis of V̇o2peak and HRpeak was conducted in 196 and 187 persons with and without DS, respectively, aged from 16 to 45 yr. Nonexercise data alone versus combined with HRpeak were used to develop equations predictive of absolute V̇o2peak. Prediction equations for HRpeak were also developed. Two additional samples of participants (30 with, 29 without DS) enabled model cross-validation. Relative V̇o2peak and HRpeak were lowest for persons with DS across all ages (∼40% and 20 beats·min-1, respectively). For persons with DS, V̇o2peak predictions provided no differences compared with actual values. Predicted HRpeak was similar to actual values in both groups of participants. Large limits of agreement were obtained for V̇o2peak (DS: 735, non-DS: 558.2 mL·min-1) and HRpeak (DS: 24.8, non-DS: 16.6 beats·min-1). Persons with DS exhibit low levels of V̇o2peak and HRpeak in all age groups included in this study. It is possible to estimate absolute V̇o2peak in persons with DS using nonexercise variables. HRpeak can be accurately estimated in groups of people with and without DS. Yet, because of large limits of agreement, caution is advised if using these equations for individual estimations of V̇o2peak or HRpeak in either population.NEW & NOTEWORTHY Our data show that it is possible to estimate absolute peak oxygen uptake in persons with Down syndrome using nonexercise variables. Peak heart rate can also be accurately estimated in groups of people with and without Down syndrome. However, because of large limits of agreement, caution is advised if using these equations for individual estimations of peak oxygen uptake or peak heart rate in either population.

Oral vitamin C restores endothelial function during acute inflammation in young and older adults.

Oxidative stress has been linked to reductions in vascular function during acute inflammation in young adults; however, the effect of acute inflammation on vascular function with aging is inconclusive. The aim of this study was to determine if oral antioxidant administration eliminates vascular dysfunction during acute inflammation in young and older adults. Brachial flow-mediated dilation (FMD) and carotid-femoral pulse wave velocity (PWV) were measured in nine young (3 male, 24 ± 4 yrs, 26.2 ± 4.9 kg/m2 ) and 16 older (13 male, 64 ± 5 yrs, 25.8 ± 3.2 kg/m2 ) adults before and 2-h after oral consumption of 2 g of vitamin C. The vitamin C protocol was completed at rest and 24 h after acute inflammation was induced via the typhoid vaccine. Venous blood samples were taken to measure markers of inflammation and vitamin C. Both interleukin-6 (Δ+0.7 ± 1.8 pg/ml) and C-reactive protein (Δ+1.9 ± 3.1 mg/L) were increased at 24 h following the vaccine (p < 0.01). There was no change in FMD or PWV following vitamin C administration at rest (p > 0.05). FMD was lower in all groups during acute inflammation (Δ-1.4 ± 1.9%, p < 0.01), with no changes in PWV (Δ-0.0 ± 0.9 m/s, p > 0.05). Vitamin C restored FMD back to initial values in young and older adults during acute inflammation (Δ+1.0 ± 1.8%, p < 0.01) with no change in inflammatory markers or PWV (p > 0.05). In conclusion, oral vitamin C restored endothelial function during acute inflammation in young and older adults, with no effect on aortic stiffness. The effect of vitamin C on endothelial function did not appear to be due to reductions in inflammatory markers. The exact mechanisms should be further investigated.

Assessment of Cerebrovascular Dynamics and Cognitive Function with Acute Aerobic Exercise in Persons with Multiple Sclerosis.

BACKGROUND: Cognitive dysfunction in multiple sclerosis (MS) may partially stem from inadequate cerebral blood flow. Cerebral blood flow and cognitive function improve with aerobic exercise in healthy adults. The effect of aerobic exercise on cerebrovascular hemodynamics and cognitive performance in persons with MS is unclear. The acute effect of aerobic exercise versus quiet rest on cerebrovascular hemodynamics and cognitive performance in relapsing-remitting MS was examined. METHODS: Sixteen adults with relapsing-remitting MS underwent cerebrovascular hemodynamics and cognitive performance testing before, 2 minutes after, and 30 minutes after aerobic exercise (20-minute treadmill walking, 60% peak oxygen consumption) and a time-matched seated control. Brachial blood pressure was obtained via an oscillometric cuff. Right middle cerebral artery (MCA) blood velocity was measured via transcranial Doppler and used to calculate mean velocity, pulsatility index (PI), and conductance. Carotid artery stiffness was measured via ultrasonography and tonometry. Cognitive performance (accuracy, reaction time) was assessed using a modified flanker task. RESULTS: Exercise elicited significant increases in mean pressure and carotid artery stiffness and decreases in MCA conductance at 2 minutes after exercise, which subsided by 30 minutes (P < .05). Exercise did not significantly alter MCA PI. Flanker reaction time decreased during posttesting in both conditions (P < .05). There were no condition × time interactions for cognitive performance. CONCLUSIONS: Persons with MS seem resilient to exercise-induced acute changes in MCA PI despite transient carotid stiffening, potentially via reductions in MCA conductance. These data suggest that changes in cognitive performance after acute aerobic exercise are not directly related to transient cerebrovascular responses in persons with MS.

ActiGraph and Short-term Heart Rate Variability Study Protocol: Amended for the COVID-19 Pandemic.

BACKGROUND: ActiGraph accelerometry is widely used in nursing research to estimate daily physical activity. Heart rate variability (HRV), a measure of autonomic modulation, can be assessed in conjunction with the ActiGraph using a Polar H7 Bluetooth heart rate monitor. There is a paucity of nursing literature to guide nurse researchers' protocol development when using the ActiGraph to assess both physical activity and short-term HRV via its Bluetooth capabilities. OBJECTIVES: The aim of this study was to describe a standardized research ActiGraph and HRV (ActiGraph HRV) protocol for an ongoing randomized controlled trial to measure physical activity and short-term HRV in patients with ischemic heart disease who report hopelessness. METHODS: We outline the study protocol for the standardization of reliable and rigorous physical activity and HRV data collection using the ActiGraph wGT3X-BT and Polar H7 Bluetooth heart rate monitor, and data analysis using ActiLife and Kubios software programs. RESULTS: Sixty-four participants enrolled in the randomized controlled trial to date, and 45 (70.3%) have completed or are actively participating in the study. Heart rate variability data have been collected on 43 of the 45 participants (96%) to date. During the first data collection time point, 42 of 44 participants (95.5%) wore the ActiGraph for a minimum of 5 valid days, followed by 28 of 31 participants (90.3%) and 25 of 26 participants (96.2%) at subsequent data collection time points. The intraclass correlation for physical activity in this study is 0.95 and 0.98 for HRV. DISCUSSION: Revisions to the protocol were successfully implemented at the onset of the COVID-19 pandemic for data collection using social distancing. The protocol was additionally amended in response to an unanticipated problem with ActiGraph battery life using Bluetooth technology. Use of the ActiGraph HRV protocol has led to a reliable and rigorous measurement of physical activity and HRV for patients with ischemic heart disease who report hopelessness in this randomized controlled trial. CONCLUSION: We provide an ActiGraph HRV protocol that can be adapted as a model in the development of ActiGraph HRV protocols for future nursing research in community and home-based settings while maximizing social distancing in the current and future pandemics.

Blunted autonomic response to standing up and head-up tilt in individuals with intellectual disabilities.

Previous research suggests individuals with intellectual disabilities (ID) may experience autonomic dysfunction, however, this has not been thoroughly investigated. The aim of this study was to compare the autonomic response to standing up (active orthostasis) and head-up tilt (passive orthostasis) in individuals with ID to a control group without ID. Eighteen individuals with and 18 individuals without ID were instrumented with an ECG-lead and finger-photoplethysmography for continuous heart rate and blood pressure recordings. The active and passive orthostasis protocol consisted of 10-min supine rest, 10-min standing, 10-min supine recovery, 5-min head-up tilt at 70°, followed by 10-min supine recovery. The last 5 min of each position was used to calculate hemodynamic and autonomic function (time- and frequency-domain heart rate and blood pressure variability measures and baroreflex sensitivity). Individuals with ID had higher heart rate during baseline and recovery (P < 0.05), and an attenuated hemodynamic (stroke volume, heart rate) and heart rate variability response to active and passive orthostasis (interaction effect P < 0.05) compared with individuals without ID. Mean arterial pressure (MAP) was higher in individuals with ID at all timepoints. Individuals with ID demonstrated altered hemodynamic and autonomic regulation compared with a sex- and age-matched control group, evidenced by a higher mean arterial pressure and a reduced response in parasympathetic modulation to active and passive orthostasis.NEW & NOTEWORTHY Individuals with ID demonstrated altered hemodynamic and autonomic regulation to the clinical autonomic function tasks standing up and head-up tilt (active and passive orthostasis). Higher resting heart rate and higher MAP throughout the protocol suggest a higher arousal level, and individuals with ID showed a blunted response in parasympathetic modulation. Further research should investigate the relationship of these findings with clinical outcomes.

Hemodynamic Response to Isometric Handgrip Exercise in Adults with Intellectual Disability.

INTRODUCTION: Individuals with intellectual disability (ID) have an increased risk of cardiovascular disease and reduced work capacity, which could partly be explained by alterations to autonomic and hemodynamic regulation. The measurement of heart rate and blood pressure during isometric handgrip (HG) exercise, a sympathoexcitatory stimulus, is a noninvasive method to investigate autonomic and hemodynamic alterations. The purpose of this study was to assess alterations to autonomic and associated hemodynamic regulation between individuals with ID and a matched control group during isometric HG exercise. METHODS: Individuals with ID (n = 13; 31 ± 2 yr, 27.6 ± 7.7 kg·m-2) and without ID (n = 16; 29 ± 7 yr, 24.2 ± 2.8 kg·m-2) performed 2 min of isometric HG exercise at 30% of maximal voluntary contraction (MVC) in the seated position. Blood pressure was averaged for 2 min before, during, and after HG exercise (mean arterial pressure [MAP], systolic blood pressure, and diastolic blood pressure). Heart rate variability, blood pressure variability, and baroreflex sensitivity were calculated from the continuous blood pressure and heart rate recordings. RESULTS: Isometric HG elicited a blunted response in systolic blood pressure, diastolic blood pressure, and MAP among individuals with ID compared with individuals without ID, even after controlling for strength (MAP: rest, HG, recovery; ID: 103 ± 7, 108 ± 9, 103 ± 7; without ID: 102 ± 7, 116 ± 10, 104 ± 10 mm Hg; interaction P < 0.05). Individuals with ID also had an attenuated baroreflex sensitivity response to HG exercise compared with individuals without ID (interaction P = 0.041), but these effects were no longer significant after controlling for maximal voluntary contraction. Indices of heart rate variability and blood pressure variability were not different between groups overall or in response to HG exercise (P > 0.05). CONCLUSIONS: Individuals with ID have a blunted hemodynamic and autonomic response to isometric HG exercise compared with individuals without ID.

Central and Peripheral Postexercise Blood Pressure and Vascular Responses in Young Adults with Obesity.

INTRODUCTION: Adults with obesity are at an increased risk of incident hypertension. Regular aerobic exercise is recommended for the prevention and treatment of hypertension, but whether young adults with obesity exhibit impaired postexercise blood pressure (BP) and vascular responses remains unclear. PURPOSE: We tested the hypothesis that young adults with obesity exhibit attenuated postexercise hypotension (PEH) and postexercise peripheral vasodilation compared with young adults without obesity. METHODS: Thirty-six normotensive adults without and with obesity (11 men and 7 women per group) underwent measurements of brachial and central BP, and leg blood flow (Doppler ultrasound) at baseline and at 30, 60, and 90 min after acute 1-h moderate-intensity cycling. Leg vascular conductance (LVC) was calculated as flow/mean arterial pressure. RESULTS: Both groups exhibited similar brachial and central PEH (peak change from baseline, -2 and -4 mm Hg for brachial and central systolic BPs, respectively, for both groups; time effect, P < 0.05). Both groups also exhibited postexercise peripheral vasodilation, assessed via LVC (time effect, P < 0.05), but its overall magnitude was smaller in young adults with obesity (LVC change from baseline, +47% ± 37%, +29% ± 36%, and +20% ± 29%) compared with young adults without obesity (LVC change from baseline, +88% ± 58%, +59% ± 54%, and +42% ± 51%; group effect, P < 0.05). CONCLUSIONS: Although obesity did not impair PEH after acute moderate-intensity exercise, young adults with obesity exhibited smaller postexercise peripheral vasodilation compared with young adults without obesity. Collectively, these findings have identified evidence for obesity-induced alterations in the peripheral vasculature after exercise.

Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia.

Vasodilatory effects of insulin support the delivery of insulin and glucose to skeletal muscle. Concurrently, insulin exerts central effects that increase sympathetic nervous system activity (SNA), which is required for the acute maintenance of blood pressure (BP). Indeed, in a cohort of young healthy adults, herein we show that intravenous infusion of insulin increases muscle SNA while BP is maintained. We next tested the hypothesis that sympathoexcitation evoked by hyperinsulinemia restrains insulin-stimulated peripheral vasodilation and contributes to sustaining BP. To address this, a separate cohort of participants were subjected to 5-s pulses of neck suction (NS) to simulate carotid hypertension and elicit a reflex-mediated reduction in SNA. NS was conducted before and 60 min following intravenous infusion of insulin. Insulin infusion caused an increase in leg vascular conductance and cardiac output (CO; P < 0.050), with maintenance of BP (P = 0.540). As expected, following NS, decreases in BP were greater in the presence of hyperinsulinemia compared with control (P = 0.045). However, the effect of NS on leg vascular conductance did not differ between insulin and control conditions (P = 0.898). Instead, the greater decreases in BP following NS in the setting of insulin infusion paralleled with greater decreases in CO (P = 0.009). These findings support the idea that during hyperinsulinemia, SNA-mediated increase in CO, rather than restraint of leg vascular conductance, is the principal contributor to the maintenance of BP. Demonstration in isolated arteries that insulin suppresses α-adrenergic vasoconstriction suggests that the observed lack of restraint of leg vascular conductance may be attributed to sympatholytic actions of insulin.NEW & NOTEWORTHY We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.

Aging reduces cerebral blood flow regulation following an acute hypertensive stimulus.

Aging increases arterial stiffness, which has a negative impact on cerebral blood flow (CBF) regulation (decreases CBF and increases CBF pulsatility). The association between arterial stiffness and CBF pulsatility may, in part, explain the relationship between elevated blood pressure (BP) fluctuations and end-organ disease with aging. To understand the mechanisms by which large BP alterations influence cerebral blood flow regulation in both young and old, we examined the effects of age on central and cerebral blood flow regulation following an acute hypertensive stimulus [resistance-exercise (RE)]. Measurements were obtained pre and immediately, 5, and 30 min post-RE in young (n = 35) and older (n = 26) adults. Measurements included cerebral blood velocity (CBv), CBv pulsatility, central pulse-wave velocity (PWV), beta-stiffness index (ß), and carotid blood flow pulsatility. Central hemodynamics and BP were continuously recorded. Mean CBv increased immediately post-RE only in the young and decreased below baseline at 5 min post-RE in both groups (interaction, P < 0.05). Older adults had a greater increase in CBv pulsatility immediately post-RE compared with the young (interaction, P < 0.05). Mean BP was higher and carotid pulsatility was lower in the older group and increased immediately post-RE in both groups (P < 0.05). PWV increased immediately post-RE (P < 0.05). There were no changes in ß. In conclusion, with aging, greater central arterial stiffness leads to a greater transmission of pulsatile blood velocity from the systemic circulation to the cerebral circulation following an acute hypertensive stress.NEW & NOTEWORTHY Reductions in cerebral blood flow and increases in flow pulsatility with aging are associated to cerebrovascular disease; however, little is known about how an acute hypertensive stimulus effects cerebral blood flow regulation in an aged population. Following the hypertensive stimulus, older adults elicit an attenuated increase in cerebral blood velocity and greater transmission of pulsatile velocity to the brain compared with young adults, demonstrating reduced cerebral blood flow regulation to elevated blood pressure responses with aging.