Cardiovascular consequences of skeletal muscle impairments in breast cancer

Breast cancer survivors suffer from disproportionate cardiovascular disease risk compared to age-matched controls. Beyond direct cardiotoxic effects due to treatments such as chemotherapy and radiation, breast-cancer-related reductions in skeletal muscle mass, quality and oxidative capacity may further contribute to cardiovascular disease risk in this population by limiting the ability to engage in aerobic exercise—a known promoter of cardiovascular health. Indeed, 20%–30% decreases in peak oxygen consumption are commonly observed in breast cancer survivors, which are indicative of exercise intolerance. Thus, breast-cancer-related skeletal muscle damage may reduce exercise-based opportunities for cardiovascular disease risk reduction. Resistance training is a potential strategy to improve skeletal muscle health in this population, which in turn may enhance the capacity to engage in aerobic exercise and reduce cardiovascular disease risk

Endothelium function dependence of acute changes in pulse wave velocity and flow-mediated slowing

Flow-mediated slowing (FMS), defined as the minimum pulse wave velocity (PWVmin) during reactive hyperemia, is potentially a simple, user-objective test for examining endothelial function. The purpose of the current study was to determine the effects of a known endothelial dysfunction protocol on arm PWV and PWVmin. Complete data were successfully collected in 22 out of 23 healthy adults (23.8 years [SD 4.1], 16 F, 22.8 kg/m2 [SD 2.8]). Local endothelial dysfunction was induced by increasing retrograde shear stress in the upper arm, through inflation of a distal (forearm) tourniquet to 75 mmHg, for 30 min. Pre- and post-endothelial dysfunction, PWV was measured followed by simultaneous assessment of PWVmin and flow-mediated dilation (FMD). PWV was measured between the upper arm and wrist using an oscillometric device, and brachial FMD using ultrasound. FMD (%) and PWVmin (m/s) were calculated as the maximum increase in diameter and minimum PWV during reactive hyperemia, respectively. Endothelial dysfunction resulted in a large effect size (ES) decrease in FMD (∆ = −3.10%; 95% CI: –4.15, –2.05; ES = −1.3), and a moderate increase in PWV (∆ = 0.38 m/s; 95% CI: 0.07, 0.69; ES = 0.5) and PWVmin (∆ = 0.16 m/s; 95% CI: 0.05, 0.28; ES = 0.6). There was a large intra-individual (pre- vs post-endothelial dysfunction) association between FMD and PWVmin (r = −0.61; 95% CI: –0.82, –0.24). In conclusion, acute change in PWV and PWVmin are at least partially driven by changes in endothelial function

Cardiovascular Consequences of Skeletal Muscle Impairments in Breast Cancer

Breast cancer survivors suffer from disproportionate cardiovascular disease risk compared to age-matched controls. Beyond direct cardiotoxic effects due to treatments such as chemotherapy and radiation, breast-cancer-related reductions in skeletal muscle mass, quality and oxidative capacity may further contribute to cardiovascular disease risk in this population by limiting the ability to engage in aerobic exercise—a known promoter of cardiovascular health. Indeed, 20–30% decreases in peak oxygen consumption are commonly observed in breast cancer survivors, which are indicative of exercise intolerance. Thus, breast-cancer-related skeletal muscle damage may reduce exercise-based opportunities for cardiovascular disease risk reduction. Resistance training is a potential strategy to improve skeletal muscle health in this population, which in turn may enhance the capacity to engage in aerobic exercise and reduce cardiovascular disease risk

The effect of acute exercise on pre-prandial ghrelin levels in healthy adults: A systematic review and meta-analysis

Background Ghrelin is a gut hormone with numerous physiological effects, including the regulation of energy balance, insulin sensitivity, vascular health, and body composition. Acylated (AG) and des-acylated (DAG) ghrelin constitute approximately 22 % and 78 % of total plasma ghrelin (TG), respectively. Alterations in the TG concentration and the AG/DAG ratio may be implicated in conditions involving energy imbalances and insulin resistant states (e.g., metabolic syndrome or Type 2 diabetes mellitus). Exercise is a therapeutic option that can potentially optimize ghrelin levels. Understanding the precise intensity and dose of exercise to optimize ghrelin levels may lead to targeted interventions to restore metabolic regulation in obesity and other clinical conditions. Objective To perform a systematic review and meta-analysis on the effects of acute exercise on pre-prandial levels of TG, AG, and DAG in healthy adults and to determine if sample demographics or exercise doses moderate such effects. Methods Electronic databases (PubMed, Medline, SPORTDiscus, Web of Science, and Google Scholar) were searched with articles published through August 2020. The following criteria was determined a priori for article inclusion: (i) the study was a randomized controlled trial (RCT),(ii) exercise was an acute bout, (iii) the exercise bout for the intervention group(s)/condition was structured, (iv) the control group/condition received no exercise, (v) participants were adults age 18 or older, (vi) ghrelin was sampled through blood, (vii) there was at least one baseline measure and one post-exercise measure of ghrelin, (viii) there were at least 3 timepoints where ghrelin was measured while participants were fasted to allow for pre-prandial total area-under-the-curve (AUCtotal) calculation, (ix) participants were healthy with no overt disease, (x) interventions were carried out without any environmental manipulations. Standardized mean difference (SMD) with 95 % confidence intervals were calculated using the restricted maximum likelihood estimation Moderator analyses to determine whether the overall pooled effect was influenced by: sex, ghrelin form, method of ghrelin analysis, age, body mass index, body fat percentage, fitness, intensity of exercise bout, duration of exercise bout, energy expenditure, and length of AUCtotal data. Results The analysis included 24 studies that consisted of 52 trials, n = 504 (age 27.0 (8.8) years, BMI 24.7 (2.7) kg/m2) and measured AG (n = 38 trials), DAG (n = 7), and TG (n = 7). The overall model indicated that exercise lowered ghrelin levels compared to control (no exercise); (SMD=-0.44, p < 0.001), and exercise intensity exhibited an inverse relationship with ghrelin levels (regression coefficient (ß)=-0.016, p = 0.04). There was no significant difference by ghrelin form (p = 0.18). Discussion Acute exercise significantly lowers plasma ghrelin levels, with higher intensity exercise associated with greater ghrelin suppression. The majority of studies applied a moderate intensity exercise bout and measured AG, with limited data on DAG. This exercise dose may be clinically significant in individuals with metabolic dysregulation and energy imbalance as a therapy to optimize AG levels. More work is needed to compare moderate and high intensity exercise and the ghrelin response in clinical populations

The effects of acute exposure to prolonged sitting, with and without interruption, on peripheral blood pressure among adults: A systematic review and meta-analysis

Background: Previous reviews have shown that exposure to acute prolonged sitting can have detrimental effects on several cardiovascular and cardiometabolic health markers. However, to date there has been no synthesis of peripheral blood pressure data (including systolic [SBP], diastolic [DBP], and mean arterial pressure [MAP]), an important and translatable marker of cardiovascular health. Similarly, no previous study has consolidated the effects of sitting interruptions on peripheral blood pressure. Objectives: (1) To assess the effect of exposure to acute prolonged sitting on peripheral blood pressure, and (2) to determine the efficacy of sitting interruption strategies as a means of offsetting any negative effects. Subgroup analyses by age and interruption modality were performed to explore heterogeneity. Data Sources: Electronic databases (PubMed, Web of Science, and SportDiscus) were searched from inception to March 2021. Reference lists of eligible studies and relevant reviews were also screened. Study Selection: Inclusion criteria for objective (1) were: (i) peripheral blood pressure was assessed non-invasively in the upper limb pre- and post-sitting; (ii) studies were either randomised controlled, randomised crossover, or quasi-experimental pre- versus post-test trials; (iii) the sitting period was >1 hour; (iv) pre- and post-sitting measures were performed in the same posture; (v) participants were adults (>18 years), free of autonomic or neuromuscular dysfunction. Additional criteria for objective (2) were: (i) the interruption strategy was during the sitting period; (ii) there was an uninterrupted sitting control condition; (iii) the interruption strategy must have involved participants actively moving their upper or lower limbs. Appraisal and synthesis methods: 9763 articles were identified, of which 32 met inclusion criteria for objective (1). Of those articles, 22 met inclusion criteria for objective (2). Weighted mean difference (WMD), 95% confidence intervals (95% CI), and standardised mean difference (SMD) were calculated for all trials using inverse variance heterogeneity meta-analysis modelling. SMD was used to determine the magnitude of effect, where <0.2, 0.2, 0.5, and 0.8 were defined as trivial, small, moderate, and large, respectively. Results: (1) Prolonged uninterrupted sitting resulted in trivial and small significant increases in SBP (WMD=3.2 mmHg, 95% CI:0.6 to 5.8, SMD=0.14) and MAP (WMD=3.3 mmHg, 95% CI:2.2 to 4.4, SMD=0.37), respectively, and a non-significant trivial increase in DBP. Subgroup analyses indicated that the increases in SBP and MAP were more pronounced in younger age groups. (2) Interrupting bouts of prolonged sitting resulted in significantly lower SBP (WMD=-4.4 3mmHg, 95% CI:-7.4 to -1.5, SMD=0.26) and DBP (WMD=-2.4 mmHg, 95% CI:-4.5 to -0.3, SMD=0.19) compared to control conditions, particularly when using aerobic interruption strategies. Conclusions: Exposure to acute prolonged uninterrupted sitting results in significant increases in SBP and MAP, particularly in younger age groups. Regularly interrupting bouts of prolonged sitting, particularly with aerobic interruption strategies may reduce negative effects

Pulse Wave Velocity Assessments Derived From Photoplethymography: Reliability And Agreement With A Referent Device [abstract only]

PURPOSE: Pulse wave velocity (PWV) is a common measure of arterial stiffness. Photoplethysmography (PPG) permits continuous measurement of PWV at multiple arterial segments simultaneously. The purpose of this study was to determine whether a simple, non-invasive PPG PWV method agrees with a referent measure, and to determine whether a posture-mediated change in PPG PWV agrees with change in the referent. METHODS: PPG, with electrocardiogram, measured heart-toe (htPWV) and heart-finger (hfPWV) PWV. Referent measurements were carotid-ankle PWV (caPWV) and carotid-wrist PWV (cwPWV) determined using the Vicorder device. In 30 adults (24.6 ± 4.8 y, body mass index 25.2 ± 5.9 kg/m2, 18 F), three measurements were made: i) two baseline measurements and ii) one measurement 5 minutes after a modified head-up tilt test (mHUTT, 78°). Baseline measurements were used to calculate measurement reliability via intraclass coefficient correlation (ICC). Mixed-models were used to calculate between-measure (overall agreement between PPG and referent), and between-condition (change in PPG versus change in referent) agreement between devices. RESULTS: All measures were reliable (ICC > 0.75). For hfPWV there was strong (ICC 0.7–0.9) between-measure agreement (ICC: 0.78, 95%CI: 0.67 – 0.85), but negligible (ICC < 0.2) and non-significant between-condition agreement (ICC: 0.10, 95%CI: 0.12 – 0.31). The lack of between-condition agreement may be attributable to the non-change in hfPWV and cwPWV with mHUTT. For htPWV, there was moderate (ICC 0.4–0.7) between-measure agreement (ICC:0.51, 95%CI: 0.32 – 0.65) and very strong between-condition agreement (ICC: 0.90, 95%CI: 0.85 – 0.94). CONCLUSION: PPG can be used to continuously measure PWV at multiple arterial segments with acceptable reliability and agreement with a referent

Title: The aortic-femoral stiffness gradient and cardiovascular risk in older adults.

Background: The aortic-femoral arterial stiffness gradient (afSG), calculated as the ratio of lower limb pulse wave velocity (PWV) to central (aortic) PWV, is a promising tool for assessing cardiovascular disease (CVD) risk; but whether it predicts incident CVD is unknown. Methods: We examined the association of the afSG measures carotid-femoral stiffness gradient (cfSG, femoral-ankle PWV divided by carotid-femoral PWV) and the heart-femoral stiffness gradient (hfSG, femoral ankle PWV divided by heart-femoral PWV), as well as PWV, with incident CVD (coronary disease, stroke, and heart failure) and all-cause mortality among 3,109 participants of the Atherosclerosis Risk in Communities Study cohort (Age: 75±5 years; cfPWV:11.5±3.0 m/s), free of CVD. Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results: Over a median 7.4-year follow-up, there were 322 cases of incident CVD and 410 deaths. In fully adjusted models, only top quartiles of cfSG (quartile 4: HR 1.43,95%CI 1.03-1.97 and quartile 3: HR 1.49,95%CI 1.08-2.05) and hfSG (quartile 4: HR 1.77,95%CI 1.27-2.48 and quartile 3: HR 1.41,95%CI 1.00-2.00) were significantly associated with a greater risk of incident CVD. Only high aortic stiffness in combination with low lower-limb stiffness was significantly associated with incident CVD (HR 1.46, 95%CI 1.06-2.02) compared to the referent low aortic stiffness and high lower-limb stiffness. No PWVs were significantly associated with incident CVD. No exposures were associated with all-cause mortality. Conclusions: The afSG may enhance CVD risk assessment in older adults in whom the predictive capacity of traditional risk factors and PWV are attenuated