No abstract

Endothelial dysfunction and arterial stiffness are nontraditional risk factors of chronic kidney disease (CKD)-related cardiovascular disease (CVD) that could be targeted with exercise. This study investigated the effect of moderate to vigorous aerobic exercise on vascular function in nondialysis CKD. In this randomized, controlled trial, 36 nondialysis patients with CKD (means ± SE, age: 58 ± 2 yr, estimated glomerular filtration rate: 44 ± 2 ml·min−1·1.73 m−2) were allocated to an exercise training (EXT) or control (CON) arm. The EXT group performed 3 × 45 min of supervised exercise per week at 60–85% heart rate reserve for 12 wk, whereas the CON group received routine care. Outcomes were assessed at 0 and 12 wk. The primary outcome, microvascular function, was assessed via cutaneous vasodilation during local heating measured by laser-Doppler flowmetry coupled with microdialysis. Participants were instrumented with two microdialysis fibers for the delivery of 1) Ringer solution and 2) the superoxide scavenger tempol. Conduit artery function was assessed via brachial artery flow-mediated dilation. Aortic pressure waveforms and pulse wave velocity were acquired with tonometry and oscillometry. Microvascular function improved after EXT ( week 0 vs . week 12, EXT: 87 ± 2% vs. 91 ± 2% and CON: 86 ± 2% vs. 84 ± 3%, P = 0.03). At baseline, pharmacological delivery of tempol improved microvascular function (Ringer solution vs. tempol: 86 ± 1% vs. 90 ± 1%, P = 0.02) but was no longer effective after EXT (91 ± 2% vs. 87 ± 1%, P = 0.2), suggesting that an improved redox balance plays a role in EXT-related improvements. Brachial artery flow-mediated dilation was maintained after EXT (EXT: 2.6 ± 0.4% vs. 3.8 ± 0.8% and CON: 3.5 ± 0.6% vs. 2.3 ± 0.4%, P = 0.02). Central arterial hemodynamics and arterial stiffness were unchanged after EXT. Aerobic exercise improved microvascular function and maintained conduit artery function and should be considered as an adjunct therapy to reduce CVD risk in CKD.

Background Reductions in exercise capacity associated with exercise intolerance augment cardiovascular disease risk and predict mortality in chronic kidney disease. This study utilized cardiopulmonary exercise testing to (a) investigate mechanisms of exercise intolerance; (b) unmask subclinical abnormalities that may precede cardiovascular disease in chronic kidney disease. Design The design of this study was cross-sectional. Methods Cardiopulmonary exercise testing was carried out in 31 Stage 3-4 chronic kidney disease patients (60 ± 11 years; estimated glomerular filtration rate 43 ± 13 ml/min/1.73 m) and 21 matched healthy individuals (healthy controls; 56 ± 5 years; estimated glomerular filtration rate>90 ml/min/1.73 m) on a cycle ergometer with workload increased by 15 W every minute until volitional fatigue. Breath-by-breath respiratory gas analysis was performed with an automated gas analyzer and averaged over 10 s intervals. Results Peak oxygen uptake was reduced in chronic kidney disease compared to healthy controls (17.43 ± 1.03 vs 28 ± 2.05 ml/kg/min; p < 0.01), as was oxygen uptake at the ventilatory threshold (9.44 ± 0.53 vs15.55 ± 1.34 ml/kg/min; p < 0.01). A steeper minute ventilation rate/carbon dioxide production slope (32 ± 0.8 vs 28 ± 1; p < 0.01) and a lower expired carbon dioxide pressure in chronic kidney disease (27 ± 0.6 vs 31 ± 0.9 vs 0.9; p < 0.01) indicated ventilation perfusion mismatching in these patients. The ventilatory cost of oxygen uptake was higher in chronic kidney disease (37 ± 0.8 vs 33 ± 1; p < 0.01). Maximum heart rate (134 ± 5 vs 159 ± 3 bpm) and one-minute heart rate recovery (15 ± 1 vs 20 ± 2 bpm) were reduced in chronic kidney disease ( p < 0.01). Conclusion This study suggests that both central and peripheral limitations likely contribute to reduced exercise capacity in non-dialysis chronic kidney disease. Additionally, cardiopulmonary exercise testing revealed subclinical cardiopulmonary abnormalities in these patients in the absence of overt cardiovascular disease. Cardiopulmonary exercise testing could potentially be a tool for unmasking cardiopulmonary abnormalities preceding cardiovascular disease in chronic kidney disease.

Early return and increased magnitude of wave reflection augments pulsatile load, wastes left ventricular effort, and is associated with cardiovascular events. Acute handgrip (HG) exercise increases surrogate measures of wave reflection such as augmentation index. However, augmentation index does not allow distinguishing between timing vs. magnitude of wave reflection, and is affected by factors other than wave reflection per se. Wave separation analysis decomposes central pressure into relative contributions of forward (Pf) and backward (Pb) pressure wave amplitudes to calculate reflection magnitude (RM=Pb/Pf) and determine the timing of apparent wave reflection return. We tested the hypothesis that acute dynamic and isometric HG exercise increase RM and decrease reflected wave transit time (RWTT). Applanation tonometry was used to record radial artery pressure waveforms in 30 adults (25±4 years) at baseline and during dynamic and isometric HG exercise. Wave separation analysis was performed offline using a physiologic flow wave to derive Pf, Pb, RM, and RWTT. We found that RM increased during dynamic and isometric HG exercise compared to baseline (p=0.04 and p<0.01, respectively; baseline 40±5, dynamic 43±6, isometric 43±7%). Meanwhile, RWTT decreased during dynamic and isometric HG exercise compared to baseline (p=0.03 and p<0.001, respectively; baseline 164±23, dynamic 155±23, isometric 148±20 ms). Moreover, the changes in RM and RWTT were not different between dynamic and isometric HG exercise. The present data suggest wave reflection timing (RWTT) and magnitude (RM) are important factors that contribute to increased central blood pressure during HG exercise.

The GALEX instrument consists of a 50cm normal incidence mirror telescope in combination with a grism, and a dichroic beamsplitter system projecting images onto two detectors simultaneously. The objective of this instrument is to provide sensitive high resolution imaging (3 to 5 arc") of galaxies in two bandpasses (1350 -1800A and 1800 -3000A), with the option of modest resolution spectroscopy. We are currently developing the microchannel plate, delay line, sealed tube detectors for the Galaxy Evolution Explorer' (GALEX) mission to be launched in 2001. The specifications for the two detector systems for GALEX require a large 65mm circular format, with high spatial resolution (<30gm FWHM, 2200 x 2200 resolution elements) and good linearity (±50.tm), <1 event cm2 sec background and counting rates of 1 .25 x i05 events sec . One detector covers the