Effect of live-fire training on ventricular-vascular coupling.

INTRODUCTION: Cardiovascular events are a leading cause of firefighter duty-related death, with the greatest risk occurring during or shortly after fire suppression activity. Increased cardiovascular risk potentially manifests from detrimental changes in ventricular function, vascular load, and their interaction, described as ventricular-vascular coupling. PURPOSE: To determine the effect of live-fire training on ventricular-vascular coupling. METHODS: Sixty-eight male (28 [Formula: see text] 7 years, 26.9 [Formula: see text] 3.9 kg/m2) and fifteen female (36 [Formula: see text] 8 years, 24.3 [Formula: see text] 3.9 kg/m2) firefighters completed hemodynamic and cardiac measures before and after 3 h of intermittent live-fire training. Left ventricular function was assessed as ejection fraction (EF) and ventricular elastance (ELV: end systolic pressure [ESP]/end systolic volume) via echocardiography and applanation tonometry-estimated ESP. Vascular load was assessed as arterial elastance (EA: ESP/stroke volume [SV]). Ventricular-vascular coupling (VVC) was quantified as the ratio of EA to ELV and indexed to body surface area (EAI, ELVI). RESULTS: Following firefighting EF decreased (p < 0.01) with no change in ELVI (p = 0.34). SV decreased (p < 0.01) with no change in ESP (p = 0.09), driving a significant increase in EAI (p < 0.01). These changes resulted in a significant increase in the VVC ratio (p < 0.01). CONCLUSION: The findings suggest that firefighting does not alter ventricular elastance but increases arterial elastance in healthy firefighters, resulting in a mismatch between ventricular and vascular systems. This increase in ventricular-vascular coupling ratio and concomitant reduction in ventricular systolic function may contribute to increased cardiovascular risk following live firefighting.

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.

Impact of acute changes in blood pressure and arterial stiffness on cerebral pulsatile haemodynamics in young and middle-aged adults.

NEW FINDINGS: What is the central question of this study? Does cerebrovascular pulsatility respond differently to acute increases in arterial stiffness in middle-aged compared with young adults? What is the main finding and its importance? Compared with young adults, middle-aged adults exhibited similar changes in cerebral pulsatile damping despite attenuated changes in carotid diameter and cerebrovascular pulsatility during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness. ABSTRACT: Acute manipulation of arterial stiffness through interventions that increase sympathetic activity might provoke cerebral pulsatility and damping and reveal whether cerebrovascular haemodynamics respond differently to transient elevations in arterial stiffness in middle-aged compared with young adults. We compared cerebral pulsatility and damping in middle-aged versus young adults during two different sympathetic interventions [cold pressor test (CP) and lower-body negative pressure (LBNP)] that increase arterial stiffness acutely. Cerebrovascular haemodynamics were assessed in 15 middle-aged (54 ± 7 years old; 11 female) and 15 sex-matched young adults (25 ± 4 years old) at rest and during the CP test (4 min, 6.4 ± 0.8°C) and LBNP (6 min, -20 mmHg). Mean blood pressure was measured continuously via finger photoplethysmography. Carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness were measured via tonometry and ultrasound. Blood velocity pulsatility index (PI) was measured at the middle cerebral (MCA) and common carotid artery (CCA) using Doppler, with pulsatile damping calculated as CCA PI divided by MCA PI. Increases in cfPWV were driven by changes in mean pressure during CP but not during LBNP in both groups (P < 0.05). Pulsatile damping decreased in both groups (P < 0.05) despite reductions in MCA PI and greater carotid dilatation during CP in young compared with middle-aged adults (P < 0.05). Pressure-independent increases in cfPWV during LBNP did not alter pulsatile damping but decreased MCA PI in both young and middle-aged adults (P < 0.05). These data suggest that changes in carotid diameter and cerebrovascular pulsatility differ between young and middle-aged adults despite similar changes in cerebral pulsatile damping during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness.

An early appointment to outpatient cardiac rehabilitation at hospital discharge improves attendance at orientation: a randomized, single-blind, controlled trial.

BACKGROUND: Outpatient cardiac rehabilitation (CR) decreases mortality rates but is underutilized. Current median time from hospital discharge to enrollment is 35 days. We hypothesized that an appointment within 10 days would improve attendance at CR orientation. METHODS AND RESULTS: At hospital discharge, 148 patients with a nonsurgical qualifying diagnosis for CR were randomized to receive a CR orientation appointment either within 10 days (early) or at 35 days (standard). The primary end point was attendance at CR orientation. Secondary outcome measures were attendance at ≥1 exercise session, the total number of exercise sessions attended, completion of CR, and change in exercise training workload while in CR. Average age was 60±12 years; 56% of participants were male and 49% were black, with balanced baseline characteristics between groups. Median time (95% confidence interval) to orientation was 8.5 (7-13) versus 42 (35 to NA [not applicable]) days for the early and standard appointment groups, respectively (P<0.001). Attendance rates at the orientation session were 77% (57/74) versus 59% (44/74) in the early and standard appointment groups, respectively, which demonstrates a significant 18% absolute and 56% relative improvement (relative risk, 1.56; 95% confidence interval, 1.03-2.37; P=0.022). The number needed to treat was 5.7. There was no difference (P>0.05) in any of the secondary outcome measures, but statistical power for these end points was low. Safety analysis demonstrated no difference between groups in CR-related adverse events. CONCLUSIONS: Early appointments for CR significantly improve attendance at orientation. This simple technique could potentially increase initial CR participation nationwide. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01596036.

Vascular function in multiple sclerosis: Systematic review with meta-analysis.

BACKGROUND: Vascular comorbidities are prevalent in persons with multiple sclerosis (MS), yet less is known about underlying vascular function (VF). We performed a systematic review with meta-analysis of studies that compared VF in persons with MS and healthy controls and examined factors that may moderate the difference in vascular outcomes between groups. METHODS: We conducted a systematic search using PubMed/MEDLINE, CINAHL, and Embase from inception through March 2024. The search identified studies that included comparisons of VF between MS and controls on a range of function and structure outcomes (e.g., pulse wave velocity, augmentation index, arterial diameter, intima-media thickness, flow-mediated dilation). Effect sizes were calculated as standardized mean differences (SMD) using Hedge's g with a positive effect indicating worse VF in MS than controls. The meta-analysis involved a multilevel random effects model with follow-up moderator analyses. RESULTS: Fourteen studies met the inclusion criteria and yielded 49 effect sizes for meta-analysis. The MS subjects (N = 614) were predominantly female (72.0 %), with mean ages ranging from 29.9 to 54.4 years. There was a moderate difference in VF between persons with MS and healthy controls (SMD [95 % CI] = 0.56 [0.08, 1.03]; p = 0.02), and the effects were heterogenous (Q48=634.5, p < 0.01; I2=94.39 %). There was a greater difference in arterial stiffness between MS and controls (0.78 [0.21, 1.36], p = 0.008), but not in other arterial structure or function outcomes (p > 0.05). No significant moderators were detected (p > 0.05). CONCLUSIONS: The cumulative evidence supports that persons with MS have worse VF, notably greater arterial stiffness, than healthy controls. Such findings support future research on the cause, consequences, and management of arterial stiffness among persons with MS.

Alcohol Consumption: A New Risk Factor for Arterial Stiffness?

The relationship between alcohol consumption and cardiovascular disease risk is complex. Low-to-moderate daily alcohol consumption (1-2 drinks/day) is associated with reduced risk, whereas greater amounts of alcohol consumption and a "binge" pattern of drinking are associated with increased cardiovascular risk and mortality. Arterial stiffness may help explain the complex relationship. This integrated review summarizes data from studies examining the associations between alcohol consumption and pulse wave velocity, a gold standard measure of arterial stiffness. We also briefly review the concept and methodology of pulse wave velocity measurement as well as the mechanisms of alcohol-induced arterial stiffening. Findings among the different studies reviewed were inconsistent with methodological challenges related to alcohol use assessment. While making specific conclusions regarding this relationship is tenuous; the data suggest that excessive alcohol consumption or a binge drinking pattern is associated with increased arterial stiffness.

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.

Physical activity and peak oxygen consumption are associated with walking in multiple sclerosis.

INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system with a prevalence of nearly 1 million adults in the United States. MS results in declines in physical activity and peak oxygen consumption that might be independently associated with declines in walking performance. Therefore our purpose was to evaluate the association between physical activity and peak oxygen consumption with walking performance in individuals with MS. METHODS: Fifty individuals with MS between the ages of 18-70 yrs. (Female: 38; 46  ±  12 yrs.; BMI: 28.5  ±  6.4; EDSS: 3.3 [IQR: 2.5-4]) performed a maximal incremental cycle test to assess peak oxygen consumption (VO2peak), and wore an accelerometer for one week to measure moderate-to-vigorous physical activity (MVPA). Subjects further completed a timed 25-foot walk test (T25FW) and 6-minute walk (6MW) to measure walking performance. RESULTS: MVPA and VO2peak were correlated with 6MW and T25FW (p < 0.05). When combined in multivariate regression analyses, VO2peak and MVPA were both significant contributors of T25FW speed and 6MW, but after controlling for sex and age, MVPA was the only significant contributor (ß = 0.32 and ß = 0.44, respectively). CONCLUSION: Both higher MVPA and VO2peak were associated with better walking performance and in a combined model physical activity, but not peak oxygen consumption, remained an independent contributor to walking performance in individuals with MS. These results suggest that improving MVPA is a potential target for interventions to improve walking performance in persons with MS.

Greater improvement in cardiorespiratory fitness using higher-intensity interval training in the standard cardiac rehabilitation setting.

PURPOSE: We tested the hypothesis that higher-intensity interval training (HIIT) could be deployed into a standard cardiac rehabilitation (CR) setting and would result in a greater increase in cardiorespiratory fitness (ie, peak oxygen uptake, (·)VO2) versus moderate-intensity continuous training (MCT). METHODS: Thirty-nine patients participating in a standard phase 2 CR program were randomized to HIIT or MCT; 15 patients and 13 patients in the HIIT and MCT groups, respectively, completed CR and baseline and followup cardiopulmonary exercise testing. RESULTS: No patients in either study group experienced an event that required hospitalization during or within 3 hours after exercise. The changes in resting heart rate and blood pressure at followup testing were similar for both HIIT and MCT. (·)VO2 at ventilatory-derived anaerobic threshold increased more (P < .05) with HIIT (3.0 ± 2.8 mL·kg⁻¹·min⁻¹) versus MCT (0.7 ± 2.2 mL·kg⁻¹·min⁻¹). During followup testing, submaximal heart rate at the end of stage 2 of the exercise test was significantly lower within both the HIIT and MCT groups, with no difference noted between groups. Peak (·)VO2 improved more after CR in patients in HIIT versus MCT (3.6 ± 3.1 mL·kg⁻¹·min⁻¹ vs 1.7 ± 1.7 mL·kg⁻¹·min⁻¹; P < .05). CONCLUSIONS: Among patients with stable coronary heart disease on evidence-based therapy, HIIT was successfully integrated into a standard CR setting and, when compared to MCT, resulted in greater improvement in peak exercise capacity and submaximal endurance.

Clinical role of exercise training in the management of patients with chronic heart failure.

Prior exercise research and the recently completed HF-ACTION (Heart Failure and A Controlled Trial Investigating Outcomes of Exercise Training) trial indicate that regular exercise represents an effective therapy in the management of patients with stable chronic heart failure (HF) due to left ventricular systolic dysfunction. This review summarizes the results from these studies and provides a guide for prescribing exercise. Regular aerobic-type exercise training improves exercise capacity; does not worsen and may, in fact, mildly improve cardiac function; and partially improves other physiological abnormalities that develop because of chronic HF (eg, autonomic and skeletal muscle function). Regular exercise is safe, improves health status, and modestly reduces ( approximately 15%) combined risk for cardiovascular death or HF-related hospitalization. Even greater physiological and clinical benefits appear likely in patients with HF who adhere to a higher volume of exercise (eg, 6 MET-hr per week). The exercise regimen should include an aerobic-type activity performed at least 30 minutes, 5 or more days per week, and at an intensity approximating 55% to 80% of heart rate reserve. Resistance training should be considered for patients who first demonstrate they are able to tolerate aerobic exercise training. Common to other interventions that also rely on human behavior, long-term adherence to exercise in patients with HF remains a challenge and requires additional research to determine strategies aimed at improving compliance. Areas of needed research include identifying which patient subgroup(s) benefits the most and determination of the optimal intensity, duration, and frequency of exercise needed to maximize clinical benefits and attenuate fatigue.