Adaptive Functioning and Sleep Quality: Associations in Young Children with Congenital Heart Disease.

Congenital heart disease (CHD) is one of today's leading birth anomalies. Children with CHD are at risk for adaptive functioning challenges. Sleep difficulties are also common in children with CHD. Indeed, sleep-disordered breathing, a common type of sleep dysfunction, is associated with increased mortality for infants with CHD. The present study examined the associations between adaptive functioning and sleep quality (i.e., duration and disruptions) in children with CHD (n = 23) compared to healthy children (n = 38). Results demonstrated associations between mean hours slept and overall adaptive functioning in the CHD group r(21) = .57, p = .005 but not in the healthy group. The CHD group demonstrated lower levels of adaptive functioning in the Conceptual, t(59) = 2.12, p = .039, Cohen's d = 0.53 and Practical, t(59) = 2.22, p = .030, Cohen's d = 0.55 domains, and overall adaptive functioning (i.e., General Adaptive Composite) nearing statistical significance in comparison to the healthy group, t(59) = 2.00, p = .051, Cohen's d = 0.51. The CHD group also demonstrated greater time awake at night, t(56) = 2.19, p = .033, Cohen's d = 0.58 and a greater instance of parent-caregiver reported snoring, χ2 (1, N = 60) = 5.25, p = .022, V = .296 than the healthy group. Further exploration of the association between adaptive functioning and sleep quality in those with CHD is required to inform clinical practice guidelines.

Elevated sympathetic-mediated vasoconstriction at rest but intact functional sympatholysis during exercise in heart failure with reduced ejection fraction.

Patients with heart failure with reduced ejection fraction (HFrEF) have exaggerated sympathoexcitation and impaired peripheral vascular conductance. Evidence demonstrating consequent impaired functional sympatholysis is limited in HFrEF. This study aimed to determine the magnitude of reduced limb vascular conductance during sympathoexcitation and whether functional sympatholysis would abolish such reductions in HFrEF. Twenty patients with HFrEF and 22 age-matched controls performed the cold pressor test (CPT) [left foot 2-min in -0.5 (1)°C water] alone and with right handgrip exercise (EX + CPT). Right forearm vascular conductance (FVC), forearm blood flow (FBF), and mean arterial pressure (MAP) were measured. Patients with HFrEF had greater decreases in %ΔFVC and %ΔFBF during CPT (both P < 0.0001) but not EX + CPT (P = 0.449, P = 0.199) compared with controls, respectively. %ΔFVC and %ΔFBF decreased from CPT to EX + CPT in patients with HFrEF (both P < 0.0001) and controls (P = 0.018, P = 0.015), respectively. MAP increased during CPT and EX + CPT in both groups (all P < 0.0001). MAP was greater in controls than in patients with HFrEF during EX + CPT (P = 0.025) but not CPT (P = 0.209). In conclusion, acute sympathoexcitation caused exaggerated peripheral vasoconstriction and reduced peripheral blood flow in patients with HFrEF. Handgrip exercise abolished sympathoexcitatory-mediated peripheral vasoconstriction and normalized peripheral blood flow in patients with HFrEF. These novel data reveal intact functional sympatholysis in the upper limb and suggest that exercise-mediated, local control of blood flow is preserved when cardiac limitations that are cardinal to HFrEF are evaded with dynamic handgrip exercise.NEW & NOTEWORTHY Patients with HFrEF demonstrate impaired peripheral blood flow regulation, evidenced by heightened peripheral vasoconstriction that reduces limb blood flow in response to physiological sympathoexcitation (cold pressor test). Despite evidence of exaggerated sympathetic vasoconstriction, patients with HFrEF demonstrate a normal hyperemic response to moderate-intensity handgrip exercise. Most importantly, acute, simultaneous handgrip exercise restores normal limb vasomotor control and vascular conductance during acute sympathoexcitation (cold pressor test), suggesting intact functional sympatholysis in patients with HFrEF.

Cerebral sympatholysis: experiments on in vivo cerebrovascular regulation and ex vivo cerebral vasomotor control.

Whether cerebral sympathetic-mediated vasomotor control can be modulated by local brain activity remains unknown. This study tested the hypothesis that the application or removal of a cognitive task during a cold pressor test (CPT) would attenuate and restore decreases in cerebrovascular conductance (CVC), respectively. Middle cerebral artery blood velocity (transcranial Doppler) and mean arterial pressure (finger photoplethysmography) were examined in healthy adults (n = 16; 8 females and 8 males) who completed a control CPT, followed by a CPT coupled with a cognitive task administered either 1) 30 s after the onset of the CPT and for the duration of the CPT or 2) at the onset of the CPT and terminated 30 s before the end of the CPT (condition order was counterbalanced). The major finding was that the CPT decreased the index of CVC, and such decreases were abolished when a cognitive task was completed concurrently and restored when the cognitive task was removed. As a secondary experiment, vasomotor interactions between sympathetic transduction pathways (α1-adrenergic and Y1-peptidergic) and compounds implicated in cerebral blood flow control [adenosine, and adenosine triphosphate (ATP)] were explored in isolated porcine cerebral arteries (wire myography). The data reveal α1-receptor agonism potentiated vasorelaxation modestly in response to adenosine, and preexposure to ATP attenuated contractile responses to α1-agonism. Overall, the data suggest a cognitive task attenuates decreases in CVC during sympathoexcitation, possibly related to an interaction between purinergic and α1-adrenergic signaling pathways.NEW & NOTEWORTHY The present study demonstrates that the cerebrovascular conductance index decreases during sympathoexcitation and this response can be positively and negatively modulated by the application or withdrawal of a nonexercise cognitive task. Furthermore, isolated vessel experiments reveal that cerebral α1-adrenergic agonism potentiates adenosine-mediated vasorelaxation and ATP attenuates α1-adrenergic-mediated vasocontraction.

Augmented sympathoexcitation slows postexercise heart rate recovery.

Slow heart rate recovery following exercise may be influenced by persistent sympathoexcitation. This study examined 1) the effect of muscle metaboreflex activation (MMA) on heart rate recovery following dynamic exercise; and 2) whether the effect of MMA on heart rate recovery is reversible by reducing sympathoexcitation [baroreflex activation via phenylephrine (PE)] in canines. Twenty-two young adults completed control and MMA protocols during cycle ergometry at 110% ventilatory threshold with 5 min recovery. Heart rate recovery kinetics [tau (τ), amplitude, end-exercise, and end-recovery heart rate] and root mean square of successive differences (RMSSD) were measured. Five chronically instrumented canines completed control, MMA (50%-60% imposed reduction in hindlimb blood flow), and MMA with end-exercise PE infusion (MMA + PE) protocols during moderate exercise (6.4 km·h-1) and 3 min recovery. Heart rate recovery kinetics and MAP were measured. MAP increased during MMA versus control in canines (P < 0.001). Heart rate recovery τ was slower during MMA versus control in humans (17% slower; P = 0.011) and canines (150% slower; P = 0.002). Heart rate recovery τ was faster during MMA + PE versus MMA (40% faster; P = 0.034) and was similar to control in canines (P = 0.426). Amplitude, end-exercise, and end-recovery heart rate were similar between conditions in humans (all P ≥ 0.122) and in canines (all P ≥ 0.084). MMA decreased RMSSD in early recovery (P = 0.004). MMA-induced sympathoexcitation slows heart rate recovery and this effect is markedly attenuated with PE. Therefore, elevated sympathoexcitation via MMA impairs heart rate recovery and inhibition of this stimulus normalizes, in part, heart rate recovery.NEW & NOTEWORTHY Augmented sympathoexcitation, via muscle metaboreflex activation, functionally slows heart rate recovery in both young healthy adults and chronically instrumented canines. Furthermore, elevated sympathoexcitation corresponded with lower parasympathetic activity, as assessed by heart rate variability, during the first 3 min of recovery. Finally, sympathoinhibition, via phenylephrine infusion, normalizes heart rate recovery during muscle metaboreflex activation.

Muscle metaboreflex control of left ventricular systolic function in heart failure with reduced ejection fraction.

Heart failure with reduced ejection fraction (HFrEF) exhibits exaggerated sympathoexcitation and altered cardiac and vascular responses to muscle metaboreflex activation (MMA). However, left ventricular (LV) responses to MMA are not well studied in patients with HFrEF. The purpose of this study was to examine LV function during MMA using cardiac magnetic resonance imaging (MRI) in patients with HFrEF. Thirteen patients with HFrEF and 18 healthy age-matched controls underwent cardiac MRI during rest and MMA. MMA protocol included 6 min of isometric handgrip exercise followed by 6-min of brachial postexercise circulatory occlusion. LV stroke volume index (SVi), end-systolic volume index (ESVi), end-diastolic volume index (EDVi), and global longitudinal strain (GLS) were measured by two- and four-chamber cine images. Volumes were indexed to body surface area. Heart rate (via ECG) and brachial mean arterial pressure (MAP) were recorded. Cardiac output and total peripheral resistance (TPR) were calculated. SVi decreased during MMA in HFrEF (P = 0.037) but not in controls (P = 0.392). ESVi (P = 0.007) and heart rate (P < 0.001) increased during MMA in HFrEF but not controls (P ≥ 0.170). TPR (P = 0.021) and MAP (P < 0.001) increased during MMA in both groups. Cardiac output (P = 0.946), EDVi (P = 0.177), and GLS (P = 0.619) were maintained from rest to MMA in both groups. Despite similarly maintained cardiac output, LV strain, and increased TPR in HFrEF and control groups, SVi decreased, and heart rate increased during MMA in patients with HFrEF. These findings suggest an impaired contractility reserve in response to increased TPR during MMA in HFrEF.NEW & NOTEWORTHY Stroke volume decreases and end-systolic volume increases during muscle metaboreflex activation in patients with heart failure with reduced ejection fraction (HFrEF), suggesting impaired contractile reserve during muscle metaboreflex activation in patients with HFrEF. Total peripheral resistance increases similarly during muscle metaboreflex activation in patients with HFrEF compared to controls, indicating normal levels of peripheral vasoconstriction during muscle metaboreflex activation in patients with HFrEF.

Health anxiety and associated constructs in school-age children and adolescents with congenital heart disease and their parents: A children's healthy-heart activity monitoring program in Saskatchewan cohort study.

Youth with congenital heart disease (CHD) have been found to experience higher levels of health anxiety and associated constructs than typically developing peers. The association between youth and parent health anxiety has been explored in typically developing youth but this association remains unknown in youth with CHD. This association was explored using a prospective, cross-sectional study that included 36 school-age children and adolescents with CHD (median age =10.5 years, IQR = 4) and 35 parents (median age = 44 years, IQR = 10.5). Participants completed a demographic form and measures of health anxiety, anxiety sensitivity, intolerance of uncertainty, and anxiety disorder symptom categories (youth) or general anxiety (parent). Associations were observed between child and adolescent panic/agoraphobia symptoms and parent state anxiety (r = .41), child and adolescent intolerance of uncertainty and parent state and trait anxiety (r = .37; r = .46, respectively), and child and adolescent anxiety sensitivity and parent state anxiety (r = .40). No association was observed between health anxiety in children and adolescents and parents nor between child and adolescent health anxiety and parent associated constructs. For parents, associations between health anxiety and all measures of associated constructs of interest were observed. Study findings will facilitate improved understanding of the psychological needs of school-age children and adolescents with CHD.

Left ventricle chest compression improves ETCO2, blood pressure, and cerebral blood velocity in a swine model of cardiac arrest and cardiopulmonary resuscitation.

Introduction: During cardiopulmonary resuscitation (CPR), high quality chest compressions are critical to organ perfusion, especially the brain. Yet, the optimal location for chest compressions is unclear. It was hypothesized that compared with the standard chest compression (SCC) location, left ventricle chest compressions (LVCCs) would result in greater ETCO2, blood pressure (BP), and cerebral blood velocity (CBV) during CPR in swine. Methods: Female Landrace swine (N = 32; 35 ± 2 kg) underwent two mins of untreated asphyxiated cardiac arrest (CA). Thereafter, swine were treated with three 2-min cycles of either SCC or LVCC mechanical basic life support CPR (LUCAS 3). ETCO2 (in-line sampling), BP (arterial catheter line), and CBV (transcranial Doppler) were measured during the pre-CA, untreated-CA, and CPR-treated phases. Results: ETCO2, BP, and CBV were similar between groups at pre- and during untreated-CA (P ≥ 0.188). During CPR, ETCO2 (36 ± 6 versus 24 ± 10 mmHg, P < 0.001), mean arterial BP (MAP; 49 ± 9 versus 37 ± 9 mmHg, P = 0.002), and CBV (11 ± 5 versus 5 ± 2 cm/s, P < 0.001) were significantly greater in the LVCC versus SCC group. Moreover, a greater proportion of animals obtained targets for ETCO2 (ETCO2 ≥ 20 mmHg; 52 % (17/33) versus 100 % (32/32), P < 0.001) and diastolic BP (DBP ≥ 25 mmHg; 82 % (33/40) versus 97 % (48/49), P = 0.020) in the LVCC versus SCC group. Conclusion: Indicators of cardiac output, BP, and cerebral perfusion during CPR were greatest in the LVCC group, suggesting the quality of chest compressions during BLS CPR may be improved by performing compressions over the left ventricle compared to the centre of the chest.

Cerebral haemodynamics during arrhythmia in health, ischaemic heart disease and heart failure with reduced ejection fraction, and in a preclinical swine model.

Ventricular arrhythmias are associated with neurological impairment and could represent a source of cerebral hypoperfusion. In the present study, data from healthy individuals (n = 11), patients with ischaemic heart disease (IHD; ejection fraction >40%; n = 9) and patients with heart failure with reduced ejection fraction (HFrEF; EF = 31 (5)%, n = 11), as well as data from swine surgeries, where spontaneous ventricular arrhythmias were observed during cerebrovascular examination (transcranial Doppler ultrasound in humans and laser Doppler in swine) were analysed retrospectively to investigate the effect of arrhythmia on cerebral microvascular haemodynamics. A subset of participants also completed the Montreal Cognitive Assessment (MoCA). Middle cerebral artery mean blood velocity (MCAVmean ) decreased during premature ventricular contraction (PVC) in all groups, and data from swine indicate PVCs reduced cerebral microvascular perfusion. Overall MCAVmean was decreased in the HFrEF vs. control group. Further, %∆MCAVmean /%∆mean arterial pressure during the PVC was greater in the HFrEF vs. control group and was correlated with decreased MoCA scores. Subanalysis of HFrEF data revealed that during bigeminy MCAVmean decreased owing to reductions during irregular beats only. During non-sustained ventricular tachycardia, MCAVmean decreased but recovered above baseline upon return to sinus rhythm. Also, haemodynamic perturbations during and following the PVC were greater in the brachial artery vs. the MCA. Therefore, ventricular arrhythmias decreased indices of cerebral perfusion irrespective of IHD or HFrEF. The relative magnitude of arrhythmia-induced haemodynamic perturbations appears to be population specific and arrhythmia type and organ dependent. The cumulative burden of arrhythmia-induced deficits may exacerbate existing cerebral hypoperfusion in HFrEF and contribute to neurological abnormalities in this population. KEY POINTS: Irregular heartbeats are often considered benign in isolation, but individuals who experience them frequently have a higher prevalence of cerebrovascular and/or cognitive associated disorders. How irregular heartbeats affect blood pressure and cerebral haemodynamics in healthy and cardiovascular disease patients, those with and without reduced ejection fraction, remains unknown. Here it was found that in the absence of symptoms associated with irregular heartbeats, such as dizziness or hypotension, single, multiple non-sustained and sustained irregular heartbeats influence cerebral haemodynamics in a population-specific, arrhythmia-type and organ-dependent manner. Relative deficits in the index of cerebral blood flow normalized to relative deficits in blood pressure were greatest in patients with heart failure with reduced ejection and inversely related with cognitive performance. Chronic arrhythmias may exacerbate existing cerebral hypoperfusion in heart failure with reduced ejection fraction, thereby providing a mechanistic link between otherwise benign irregular heartbeats and cognitive dysfunction, independent of embolism.

Autonomic cardiovascular reflex control of hemodynamics during exercise in heart failure with reduced ejection fraction and the effects of exercise training.

Heart failure with reduced ejection fraction is associated with increased exercise intolerance, morbidity, and mortality. Importantly, exercise intolerance in heart failure with reduced ejection fraction is a key factor limiting patient quality of life and survival. Exercise intolerance in heart failure with reduced ejection fraction stems from a multi-organ failure to maintain homeostasis at rest and during exercise, including the heart, skeletal muscle, and autonomic nervous system, lending itself to a system constantly trying to "catch-up". Hemodynamic control during exercise is regulated primarily by the autonomic nervous system, whose operation, in turn, is partly regulated via reflexive information from exercise-stimulated receptors throughout the body (e.g., arterial baroreflex, central and peripheral chemoreceptors, and the muscle metabo- and mechanoreflexes). Persons with heart failure with reduced ejection fraction exhibit malfunctioning autonomic reflexes, which lead to exaggerated sympathoexcitation and attenuated parasympathetic tone. Chronic elevation of sympathetic activity is associated with increased morbidity and mortality. In this review, we provide an overview of how each main exercise-related autonomic reflex is changed in heart failure with reduced ejection fraction, and the role of exercise training in attenuating or reversing the counterproductive changes.

Effects of 12-Week Home-based Resistance Training on Peripheral Muscle Oxygenation in Children With Congenital Heart Disease: A CHAMPS Study.

Background: A hallmark feature of children with congenital heart disease (CHD) is exercise intolerance. Whether a home-based resistance training intervention improves muscle oxygenation (as measured by tissue oxygenation index, TOI) and exercise tolerance (V˙O2 reserve) during aerobic exercise in children with CHD compared with healthy children is unknown. Methods: We report findings for 10 children with CHD (female/male: 4/6; mean ± standard deviation age: 13 ± 1 years) and 9 healthy controls (female/male: 5/4; age: 12 ± 3 years). Children with CHD completed a 12-week home-based exercise programme in addition to 6 in-person sessions. Exercise tolerance was assessed with a peak exercise test. Vastus lateralis TOI was continuously sampled during the peak V˙O2 test via near-infrared spectroscopy. Results: There was a medium effect (Cohen's d = 0.67) of exercise training on lowering TOI at peak exercise (pre: 30 ± 16 %total labile signal vs post: 20 ± 13 % total labile signal; P = 0.099). Exercise training had a small effect (Cohen's d = 0.23) on increasing V˙O2 reserve by 1.6 mL/kg/min (pre: 27.2 ± 5.7 mL/kg/min vs post: 29.4 ± 8.8 mL/kg/min; P = 0.382). There was also a small effect (Cohen's d = 0.27) of exercise on peak heart rate (pre: 175 ± 23 beats/min vs post: 169 ± 21 beats/min; P = 0.18). TOI, V˙O2 reserve, and heart rate were generally lower than healthy control participants. Conclusions: Our findings indicate that home-based resistance training may enhance skeletal muscle oxygen extraction (lower TOI) and subsequently V˙O2 reserve in children with CHD.

Contexte: L'une des manifestations caractéristiques de la cardiopathie congénitale chez les enfants est l'intolérance à l'effort. Il n'est pas clair si un entraînement musculaire à la maison permet d'améliorer l'oxygénation musculaire (selon l'indice d'oxygénation tissulaire, ou TOI pour tissue oxygenation index) et la tolérance à l'effort (réserve de consommation d'oxygène [V˙O2]) lors d'un exercice aérobique chez les enfants atteints d'une cardiopathie congénitale, comparativement aux enfants en bonne santé. Méthodologie: Les résultats présentés concernent 10 enfants atteints d'une cardiopathie congénitale (filles/garçons : 4/6; âge moyen ± écart-type : 13 ans ± 1 an) et neuf enfants témoins en bonne santé (filles/garçons : 5/4; âge : 12 ans ± 3 ans). Les enfants atteints d'une cardiopathie congénitale ont participé à un programme d'exercices à la maison de 12 semaines, en plus d'assister en personne à six séances. La tolérance à l'effort a été évaluée au moyen de l'épreuve d'effort maximal. Le TOI du muscle vaste externe a été mesuré de façon continue pendant le test du V˙O2 max par spectroscopie proche infrarouge. Résultats: Le programme d'exercices a entraîné un effet modéré (valeur d de Cohen = 0,67) sur la réduction du TOI au moment de l'effort maximal (pré-entraînement : signal labile total de 30 ± 16 % vs post-entraînement : signal labile total de 20 ± 13 % ; p = 0,099). Le programme d'exercices a eu un effet léger (valeur d de Cohen = 0,23) sur l'augmentation de la réserve de V˙O2, soit de 1,6 ml/kg/min (pré-entraînement : 27,2 ± 5,7 ml/kg/min vs post-entraînement : 29,4 ± 8,8 ml/kg/min; p = 0,382). On a également observé un effet léger (valeur d de Cohen = 0,27) sur la fréquence cardiaque maximale (pré-entraînement : 175 ± 23 battements/minute vs post-entraînement : 169 ± 21 battements/minute; p = 0,18). Le TOI, la réserve de V˙O2 et la fréquence cardiaque étaient généralement inférieurs comparativement aux témoins en bonne santé. Conclusions: Nos résultats montrent qu'un entraînement musculaire à la maison pourrait améliorer la capacité d'extraction de l'oxygène par les muscles squelettiques (TOI inférieur) et ultimement la réserve de V˙O2 chez les enfants atteints d'une cardiopathie congénitale.

Left Ventricular Dimensions and Diastolic Function Are Different in Throwers, Endurance Athletes, and Sprinters From the World Masters Athletics Championships.

There is controversy whether a lifetime of heavy resistance training, providing pressure-overload, is harmful for left ventricular function. We compared left ventricular dimensions and function in elite Masters athletes involved in throwing events (requiring strength; n = 21, seven females, 60 ± 14 years) to those involved in endurance events (n = 65, 25 females, 59 ± 10 years) and sprinting (n = 68, 21 females, 57 ± 13 years) at the 2018 World Masters Athletic Championships. Left ventricular dimensions and function were assessed with B-mode ultrasound and Doppler. The ratio of left ventricular early diastolic peak filling velocity to peak velocity during atrial contraction (E/A) across the mitral valve and the ratio of E to velocity of the E-wave (E') across the lateral and septal mitral annulus (E/E') were used as indexes of left ventricular diastolic function. Intra-ventricular septal wall thickness was greater in throwers compared to sprinters (11.9 ± 2.2 vs. 10.3 ± 2.3 mm; p = 0.01). Left ventricular end diastolic diameter/body surface area was higher in endurance athletes and sprinters vs. throwers (25.2 ± 3.0, 24.3 ± 3.1, and 22.0 ± 3.1 mm/m2, respectively, p < 0.01). The E/A was higher in endurance athletes and sprinters vs. throwers (1.35 ± 0.40, 1.37 ± 0.43, and 1.05 ± 0.41, respectively; p < 0.01). The E/E' was lower in endurance athletes and sprinters vs. throwers (6.9 ± 1.8, 6.6 ± 1.9, and 8.1 ± 1.9, respectively, p < 0.05). Compared to age-matched historical controls (n > 1,000; E/A = 1.06; E/E' = 7.5), left ventricular diastolic function was not different in throwers, but superior in endurance athletes and sprinters (p < 0.01). Masters throwers have altered left ventricular dimensions and function vs. other athletes, but a lifetime of heavy resistance training does not appear to alter left ventricular function compared to age-matched controls.

Stretching is Superior to Brisk Walking for Reducing Blood Pressure in People With High-Normal Blood Pressure or Stage I Hypertension.

BACKGROUND: Aerobic exercise is recommended for reducing blood pressure; however, recent studies indicate that stretching may also be effective. The authors compared 8 weeks of stretching versus walking exercise in men and women with high-normal blood pressure or stage 1 hypertension (ie, 130/85-159/99 mm Hg). METHODS: Forty men and women (61.6 y) were randomized to a stretching or brisk walking exercise program (30 min/d, 5 d/wk for 8 wk). Blood pressure was assessed during sitting and supine positions and for 24 hours using a portable monitor before and after the training programs. RESULTS: The stretching program elicited greater reductions than the walking program (P < .05) for sitting systolic (146 [9] to 140 [12] vs 139 [9] to 142 [12] mm Hg), supine diastolic (85 [7] to 78 [8] vs 81 [7] to 82 [7] mm Hg), and nighttime diastolic (67 [8] to 65 [10] vs 68 [8] to 73 [12] mm Hg) blood pressures. The stretching program elicited greater reductions than the walking program (P < .05) for mean arterial pressure assessed in sitting (108 [7] to 103 [6] vs 105 [6] vs 105 [8] mm Hg), supine (102 [9] to 96 [9] vs 99 [6] to 99 [7] mm Hg), and at night (86 [9] to 83 [10] vs 88 [9] to 93 [12] mm Hg). CONCLUSIONS: An 8-week stretching program was superior to brisk walking for reducing blood pressure in individuals with high-normal blood pressure or stage 1 hypertension.

Hepatocyte growth factor administration increases bone soluble phosphate and alters bone chemical structure in diabetic hypertensive rats.

Hepatocyte growth factor (HGF) is a novel potential therapy for improving bone health in patients with type II diabetes and hypertension, but its effect on the bone molecular structure is not revealed yet. Here, X-ray absorption near edge structure (XANES) spectroscopy was used to explore the effects elicited by HGF on the bone chemical structure. This study assessed local calcium (Ca) and phosphorus (P) coordination of diabetic hypertensive rat bones, each with and without HGF treatment. Results revealed that HGF has significant effects on Ca and P coordination chemistry as confirmed by presence of more soluble phosphates in the HGT-treated groups. Data indicated that treated bones have a poorly developed phosphate structure as evidenced by drastic drop in post-edge shoulder in P L2,3-edge compared to diabetic hypertensive and diabetic control bone. Presence of soluble Ca and P, products of bone resorption, with HGF treatment suggests unbalanced bone resorption and formation.

A cardiovascular disease risk factor in children with congenital heart disease: unmasking elevated waist circumference - a CHAMPS* study *CHAMPS: Children's Healthy-Heart Activity Monitoring Program in Saskatchewan.

BACKGROUND: Children with congenital heart disease (CHD) have an elevated risk of future cardiovascular disease but the underlying mechanisms are unclear. Abdominal obesity (measured as waist circumference) is a risk factor for adult onset of cardiovascular diseases and is correlated with low physical activity levels, commonly found in children with congenital heart disease. Elevated waist circumference may be a mechanism by which cardiovascular disease risk is elevated in children with CHD. The purpose of this study was to compare waist circumference between children with and without CHD, while considering potential confounders. We hypothesized that children with CHD would have higher measures of waist circumference when controlling for differences in birthweight, lean mass, and physical activity. METHODS: Thirty-two children with CHD (10.9 ± 2.6 years; 12 female) from the Children's Healthy-Heart Activity Monitoring Program in Saskatchewan, and 23 healthy controls (11.7 ± 2.5 years; 10 female) were studied. Waist circumference, physical activity (physical activity questionnaire), body composition (lean mass; dual x-ray absorptiometry), and birthweight were assessed. Analysis of covariance, Mann-Whitney U, and independent sample t-tests were used to assess group differences (p < 0.05). RESULTS: Children with CHD had greater waist circumference than controls, controlling for lean mass, physical activity, birthweight, and sex (F (1, 49) = 4.488, p = 0.039). Physical activity, lean mass, and birthweight were not significantly different between groups (p > 0.05). CONCLUSION: Our findings generate a novel hypothesis-higher waist circumferences in children with CHD compared to age-matched controls, may contribute to an elevated risk of cardiovascular disease.

Health anxiety and associated constructs in children and adolescents with congenital heart disease: A CHAMPS cohort study.

This study explored health anxiety and associated constructs in children and adolescents with congenital heart disease and typically developing children and adolescents. A total of 84 participants (7-16 years) completed measures of health anxiety, intolerance of uncertainty, anxiety sensitivity, and DSM-IV anxiety disorder symptom categories. Results demonstrated that children and adolescents with congenital heart disease experienced significantly higher levels of health anxiety and associated constructs compared to typically developing children and adolescents. Our findings highlight a specific chronic physical health population who may be at risk of clinical levels of health anxiety and related psychopathology and require appropriate intervention.

Pathophysiology of Exercise Intolerance and Its Treatment With Exercise-Based Cardiac Rehabilitation in Heart Failure With Preserved Ejection Fraction.

Heart failure with preserved ejection fraction (HFpEF) is the fastest growing form of heart failure in the United States. The cardinal feature of HFpEF is reduced exercise tolerance (peak oxygen uptake, (Equation is included in full-text article.)O2peak) secondary to impaired cardiac, vascular, and skeletal muscle function. There are currently no evidence-based drug therapies to improve clinical outcomes in patients with HFpEF. In contrast, exercise training is a proven effective intervention for improving (Equation is included in full-text article.)O2peak, aerobic endurance, and quality of life in HFpEF patients. This brief review discusses the pathophysiology of exercise intolerance and the role of exercise training to improve (Equation is included in full-text article.)O2peak in clinically stable HFpEF patients. It also discusses the mechanisms responsible for the exercise training-mediated improvements in (Equation is included in full-text article.)O2peak in HFpEF. Finally, it provides evidence-based exercise prescription guidelines for cardiac rehabilitation specialists to assist them with safely implementing exercise-based cardiac rehabilitation programs for HFpEF patients.

Effects of heavy-intensity priming exercise on pulmonary oxygen uptake kinetics and muscle oxygenation in heart failure with preserved ejection fraction.

Exercise intolerance is a hallmark feature in heart failure with preserved ejection fraction (HFpEF). Prior heavy exercise ("priming exercise") speeds pulmonary oxygen uptake (V̇o2p) kinetics in older adults through increased muscle oxygen delivery and/or alterations in mitochondrial metabolic activity. We tested the hypothesis that priming exercise would speed V̇o2p on-kinetics in patients with HFpEF because of acute improvements in muscle oxygen delivery. Seven patients with HFpEF performed three bouts of two exercise transitions: MOD1, rest to 4-min moderate-intensity cycling and MOD2, MOD1 preceded by heavy-intensity cycling. V̇o2p, heart rate (HR), total peripheral resistance (TPR), and vastus lateralis tissue oxygenation index (TOI; near-infrared spectroscopy) were measured, interpolated, time-aligned, and averaged. V̇o2p and HR were monoexponentially curve-fitted. TPR and TOI levels were analyzed as repeated measures between pretransition baseline, minimum value, and steady state. Significance was P < 0.05. Time constant (τ; tau) V̇o2p (MOD1 49 ± 16 s) was significantly faster after priming (41 ± 14 s; P = 0.002), and the effective HR τ was slower following priming (41 ± 27 vs. 51 ± 32 s; P = 0.025). TPR in both conditions decreased from baseline to minimum TPR ( P < 0.001), increased from minimum to steady state ( P = 0.041) but remained below baseline throughout ( P = 0.001). Priming increased baseline ( P = 0.003) and minimum TOI ( P = 0.002) and decreased the TOI muscle deoxygenation overshoot ( P = 0.041). Priming may speed the slow V̇o2p on-kinetics in HFpEF and increase muscle oxygen delivery (TOI) at the onset of and throughout exercise. Microvascular muscle oxygen delivery may limit exercise tolerance in HFpEF.

Meta-analysis of Exercise Training on Left Ventricular Ejection Fraction in Heart Failure with Reduced Ejection Fraction: A 10-year Update.

BACKGROUND: The role of exercise training modality to attenuate left ventricular (LV) remodeling in heart failure patients with reduced ejection fraction (HFrEF) remains uncertain. The authors performed a systematic review and meta-analysis of published reports on exercise training (moderate-intensity continuous aerobic, high-intensity interval aerobic, and resistance exercise) and LV remodeling in clinically stable HFrEF patients. METHODS: We searched MEDLINE, Cochrane Central Registry of Controlled Trials, CINAHL, and PubMed (2007 to 2017) for randomized controlled trials of exercise training on resting LV ejection fraction (EF) and end-diastolic and end-systolic volumes in HFrEF patients. RESULTS: 18 trials reported LV ejection fraction (LVEF) data, while 8 and 7 trials reported LV end-diastolic and LV end-systolic volumes, respectively. Overall, moderate-intensity continuous training (MICT) significantly increased LVEF (weighted mean difference, WMD = 3.79%; 95% confidence interval, CI, 2.08 to 5.50%) with no change in LV volumes versus control. In trials ≥6 months duration, MICT significantly improved LVEF (WMD = 6.26%; 95% CI 4.39 to 8.13%) while shorter duration (<6 months) trials modestly increased LVEF (WMD = 2.33%; 95% CI 0.84 to 3.82%). High-intensity interval training (HIIT) significantly increased LVEF compared to control (WMD = 3.70%; 95% CI 1.63 to 5.77%) but was not different than MICT (WMD = 3.17%; 95% CI -0.87 to 7.22%). Resistance training performed alone or combined with aerobic training (MICT or HIIT) did not significantly change LVEF. CONCLUSIONS: In clinically stable HFrEF patients, MICT is an effective therapy to attenuate LV remodeling with the greatest benefits occurring with long-term (≥6 months) training. HIIT performed for 2 to 3 months is superior to control, but not MICT, for improvement of LVEF.