Association Between Arterial Stiffness and Measures of Autonomic Dysfunction in People With Chronic Kidney Disease.

Background: Autonomic nervous system (ANS) dysfunction and vascular stiffness increase cardiovascular risk in people with chronic kidney disease (CKD). Chronic elevations in sympathetic activity can lead to increased arterial stiffness; however, the relationship between these variables is unknown in CKD. Objective: To explore the association between measures of autonomic function and arterial stiffness in patients with moderate-to-severe CKD. Methods: This study was a prespecified secondary analysis of a randomized controlled trial. This included the following measures: 24-hour ambulatory blood pressure (BP), carotid-femoral and carotid-radial pulse wave velocity (PWV), and postexercise heart rate recovery (HRR). We used mixed effect linear regression models with Bayesian information criteria (BIC) to assess the contribution of ANS measurements. Results: Forty-four patients were included in the analysis. Mean carotid-femoral and carotid-radial PWV were 7.12 m/s (95% CI 6.13, 8.12) and 8.51 m/s (7.90, 9.11), respectively. Mean systolic dipping, calculated as percentage change in mean systolic readings from day to night, was 10.0% (95% CI 7.79, 12.18). Systolic dipping was independently associated with carotid-radial PWV, MD -0.09 m/s (95% CI -0.15, -0.02) and had the lowest BIC. Conclusions: Systolic dipping was associated with carotid-radial PWV in people with moderate-to-severe CKD; however, there was no association with carotid-femoral PWV. Systolic dipping may be a feasible surrogate of ANS function, as the association with carotid-radial PWV was consistent with the minimal clinically important difference (MCID). Future studies are needed to define the relationship between ANS function, arterial stiffness, and CV events over time in people with CKD.

Contexte: Le dysfonctionnement du système nerveux autonome (SNA) et la rigidité artérielle augmentent le risque d'événements cardiovasculaires chez les personnes atteintes d'insuffisance rénale chronique (IRC). Les élévations chroniques de l'activité sympathique peuvent accroître la rigidité artérielle, mais on ne connaît pas le lien entre ces variables en contexte d'IRC. Objectif: Explorer l'association entre les mesures de la fonction autonome et la rigidité artérielle chez les patients atteints d'IRC modérée ou grave. Méthodologie: Cette étude était l'analyze secondaire prédéfinie d'un essai contrôlé randomisé. Mesures incluses: le suivi de la pression artérielle (PA) ambulatoire sur 24 heures, la vitesse de l'onde de pouls (VOP) carotido-fémorale et carotido-radiale, et la récupération de la fréquence cardiaque (HRR­Heart Rate Recovery) après l'effort. Nous avons eu recours à des modèles de régression linéaire à effets mixtes avec critères d'information bayésiens (BIC ­ Bayesian Information Criteria) pour évaluer la contribution des mesures du SNA. Résultats: Quarante-quatre patients sont inclus dans l'analyze. La valeur moyenne des VOP carotido-fémorale et carotido-radiale était respectivement de 7,12 m/s (IC 95 %: 6,13 à 8,12) et de 8,51 m/s (IC 95 %: 7,90 à 9,11). La chute systolique moyenne, calculée en pourcentage de variation entre les valeurs systoliques moyennes du jour et de la nuit, était de 10,0 % (IC 95 %: 7,79 à 12,18). La chute systolique a été indépendamment associée à la VOP carotido-radiale, avec un écart moyen de -0,09 m/s (IC 95 %: -0,15 à -0,02) et a présenté les plus faibles BIC. Conclusion: La chute systolique a été associée à la VOP carotido-radiale chez les personnes atteintes d'IRC modérée ou grave, mais aucune association n'a été observée avec la VOP carotido-fémorale. La chute systolique pourrait être un substitut de la fonction du SNA, car l'association avec la VOP carotido-radiale était cohérente avec la différence minimale cliniquement importante (DMCI). D'autres études sont nécessaires pour mieux définir la relation entre la fonction du SNA, la rigidité artérielle et les événements cardiovasculaires au fil du temps chez les personnes atteintes d'IRC.

Physical Activity in Renal Disease and the Effect on Hypertension: A Randomized Controlled Trial.

INTRODUCTION: Exercise is an effective strategy for blood pressure (BP) reduction in the general population, but its efficacy for the management of hypertension in chronic kidney disease (CKD) is not known. We evaluated the difference in 24-h ambulatory systolic BP (SBP) with exercise training in people with moderate to severe CKD. METHODS: Participants with an estimated glomerular filtration rate (eGFR) of 15-44 mL/min per 1.73 m2 and SBP >120 mm Hg were randomized to receive thrice-weekly moderate-intensity aerobic-based exercise over 24 weeks, or usual care. Phase 1 included supervised in-center and home-based sessions for 8 weeks. Phase 2 was 16 weeks of home-based sessions. BP, arterial stiffness, cardiorespiratory fitness, and markers of cardiovascular (CV) risk were analyzed using mixed linear regression. RESULTS: We randomized 44 people; 36% were female, the median age was 69 years, 55% had diabetes, and the median eGFR was 28 mL/min per 1.73 m2. Compared with usual care, there was no significant change in 24-ambulatory SBP at 8 weeks (2.96 mm Hg; 95% confidence interval (CI): -2.56, 8.49) or 24 weeks. Peak oxygen uptake improved by 1.9 mL/kg/min in the exercise group (95% CI: 0.03, 3.79) at 8 weeks with a trend toward higher body mass index 1.84 kg/m2 (95% CI: -0.10, 3.78) and fat free mass, but this was not sustained at 24 weeks. Markers of CV risk were unchanged. CONCLUSIONS: Despite an improvement in peak aerobic capacity and body composition, we did not detect a change in 24-h ambulatory SBP in people with moderate-to-severe CKD.

Physical Activity In Renal Disease (PAIRED) and the effect on hypertension: study protocol for a randomized controlled trial.

BACKGROUND: The prevalence of hypertension among people with chronic kidney disease is high with over 60% of people not attaining recommended targets despite taking multiple medications. Given the health and economic implications of hypertension, additional strategies are needed. Exercise is an effective strategy for reducing blood pressure in the general population; however, it is not known whether exercise would have a comparable benefit in people with moderate to advanced chronic kidney disease and hypertension. METHODS: This is a parallel-arm trial of adults with hypertension (systolic blood pressure greater than 130 mmHg) and an estimated glomerular filtration rate of 15-45 ml/min 1.73 m2. A total of 160 participants will be randomized, with stratification for estimated glomerular filtration rate, to a 24-week, aerobic-based exercise intervention or enhanced usual care. The primary outcome is the difference in 24-h ambulatory systolic blood pressure after 8 weeks of exercise training. Secondary outcomes at 8 and 24 weeks include: other measurements of blood pressure, aortic stiffness (pulse-wave velocity), change in the Defined Daily Dose of anti-hypertensive drugs, medication adherence, markers of cardiovascular risk, physical fitness (cardiopulmonary exercise testing), 7-day accelerometry, quality of life, and adverse events. The effect of exercise on renal function will be evaluated in an exploratory analysis. The intervention is a thrice-weekly, moderate-intensity aerobic exercise supplemented with isometric resistance exercise delivered in two phases. Phase 1: supervised, facility-based, weekly and home-based sessions (8 weeks). Phase 2: home-based sessions (16 weeks). DISCUSSION: To our knowledge, this study is the first trial designed to provide a precise estimate of the effect of exercise on blood pressure in people with moderate to severe CKD and hypertension. The findings from this study should address a significant knowledge gap in hypertension management in CKD and inform the design of a larger study on the effect of exercise on CKD progression. TRIAL REGISTRATION: ClinicalTrials.gov, ID: NCT03551119 . Registered on 11 June 2018.

The Effect of Different Training Loads on the Lung Health of Competitive Youth Swimmers.

Airway hyperresponsiveness (AHR), airway inflammation, and respiratory symptoms are common in competitive swimmers, however it is unclear how volume and intensity of training exacerbate these problems. Thus, our purpose was to measure AHR, inflammation, and respiratory symptoms after low, moderate, and high training loads in swimmers. Competitive youth swimmers (n=8) completed nine weeks of training split into three blocks (Low, Moderate, and High intensity). Spirometry at rest and post-bronchial provocation [Eucapnic Voluntary Hyperpnea (EVH)] and Fractional Exhaled Nitric Oxide (FeNO) were completed at the end of each training block. A weekly self-report questionnaire determined respiratory symptoms. Session Rating of Perceived Exertion (sRPE) quantified internal training loads. Internal load was significantly lower after Moderate training (4840 ± 971 AU) than after High training (5852 ± 737 AU) (p = 0.02, d = 1.17). Pre-EVH FEV1 was significantly decreased after Moderate (4.52 ± 0.69 L) compared to Low (4.74 ± 0.63 L) (p = 0.025, d = 0.326), but not different from High load. Post-EVH FeNO after Moderate training was significantly decreased (9.4 ± 4.9 ppb) compared to Low training (15.4 ± 3.6 ppb) (p = 0.012, r = 0.884). Respiratory symptom frequency was significantly correlated with percent decrease in FEV1 20 minutes post-EVH after Low and Moderate loads (both ρ = -0.71, sig = 0.05), and after High load was significantly correlated with percent decrease in FEV1 at 10 (ρ = -0.74, sig = 0.03), 15 (ρ = -0.91, sig = 0.00), and 20 minutes post (ρ = -0.75, sig = 0.03). In conclusion, Moderate load training resulted in the worst lung health results, suggesting there may be factors other than the total amount of stress within training blocks that influence lung health. Further research is needed to determine the effect of manipulating specific acute training load variables on the lung health of swimmers.