P.C.E. de Groot
Radboud University Nijmegen Medical Centre
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Publication
Featured researches published by P.C.E. de Groot.
The Journal of Physiology | 2008
Miriam Kooijman; Dick H. J. Thijssen; P.C.E. de Groot; Michiel W. P. Bleeker; H.J.M. van Kuppevelt; Daniel J. Green; Gerard A. Rongen; Paul Smits; Maria T. E. Hopman
Flow‐mediated dilatation (FMD) of the brachial and radial arteries is an important research tool for assessment of endothelial function in vivo, and is nitric oxide (NO) dependent. The leg skeletal muscle vascular bed is an important territory for studies in exercise physiology. However, the role of endothelial NO in the FMD response of lower limb arteries has never been investigated. The purpose of this study was to examine the contribution of NO to FMD in the superficial femoral artery in healthy subjects. Since physical inactivity may affect endothelial function, and therefore NO availability, spinal cord‐injured (SCI) individuals were included as a model of extreme deconditioning. In eight healthy men (34 ± 13 years) and six SCI individuals (37 ± 10 years), the 5 min FMD response in the superficial femoral artery was assessed by echo‐Doppler, both during infusion of saline and during infusion of the NO synthase blocker NG‐monomethyl‐l‐arginine (l‐NMMA). In a subset of the controls (n= 6), the 10 min FMD response was also examined using the same procedure. The 5 min FMD response in controls (4.2 ± 0.3%) was significantly diminished during l‐NMMA infusion (1.0 ± 0.2%, P < 0.001). In SCI, l‐NMMA also significantly decreased the FMD response (from 8.2 ± 0.4% during saline to 2.4 ± 0.5% during l‐NMMA infusion). The hyperaemic flow response during the first 45 s after cuff deflation was lower in both groups during infusion of l‐NMMA, but the effect of l‐NMMA on FMD persisted in both groups after correction for the shear stress stimulus. The 10 min FMD was not affected by l‐NMMA (saline: 5.4 ± 1.6%, l‐NMMA: 5.6 ± 1.5%). Superficial femoral artery FMD in response to distal arterial occlusion for a period of 5 min is predominantly mediated by NO in healthy men and in the extremely deconditioned legs of SCI individuals.
Experimental Physiology | 2005
Mark Rakobowchuk; C.L. McGowan; P.C.E. de Groot; D. Bruinsma; Joseph W. Hartman; Stuart M. Phillips; Maureen J. MacDonald
The effect of resistance training on arterial stiffening is controversial. We tested the hypothesis that resistance training would not alter central arterial compliance. Young healthy men (age, 23 ± 3.9 (mean ±s.e.m.) years; n= 28,) were whole‐body resistance trained five times a week for 12 weeks, using a rotating 3‐day split‐body routine. Resting brachial blood pressure (BP), carotid pulse pressure, carotid cross‐sectional compliance (CSC), carotid initima–media thickness (IMT) and left ventricular dimensions were evaluated before beginning exercise (PRE), after 6 weeks of exercise (MID) and at the end of 12 weeks of exercise (POST). CSC was measured using the pressure‐sonography method. Results indicate reductions in brachial (61.1 ± 1.4 versus 57.6 ± 1.2 mmHg; P < 0.01) and carotid pulse pressure (52.2 ± 1.9 versus 46.8 ± 2.0 mmHg; P < 0.01) PRE to POST. In contrast, carotid CSC, β‐stiffness index, IMT and cardiac dimensions were unchanged. In young men, central arterial compliance is unaltered with 12 weeks of resistance training and the mechanisms responsible for cardiac hypertrophy and reduced arterial compliance are either not inherent to all resistance‐training programmes or may require a prolonged stimulus.
Acta Physiologica | 2007
Dick H. J. Thijssen; P.C.E. de Groot; Paul Smits; Maria T. E. Hopman
Aim: Because age‐related changes in the large conduit arteries (increased wall thickness, and attenuated arterial compliance and endothelial function) are associated with cardiovascular pathology, prevention is of paramount importance. The effects of endurance training (i.e. walking or cycling) in older humans are assessed in cross‐sectional studies, examining the brachial and carotid arteries (supplying non‐trained areas). The purpose of this study was to assess the effects of 8‐week endurance training in older men on conduit artery characteristics in the trained and non‐trained vascular beds.
Journal of Applied Physiology | 2008
Dick H. J. Thijssen; Miriam Kooijman; P.C.E. de Groot; Michiel W. P. Bleeker; Paul Smits; Daniel J. Green; Maria T. E. Hopman
Extreme inactivity of the legs in spinal cord-injured (SCI) individuals does not result in an impairment of the superficial femoral artery flow-mediated dilation (FMD). To gain insight into the underlying mechanism, the present study examined nitric oxide (NO) responsiveness of vascular smooth muscles in controls and SCI subjects. In eight healthy men (34 +/- 13 yr) and six SCI subjects (37 +/- 10 yr), superficial femoral artery FMD response was assessed by echo Doppler. Subsequently, infusion of incremental dosages of sodium nitroprusside (SNP) was used to assess NO responsiveness. Peak diameter was examined on a second day after 13 min of arterial occlusion in combination with sublingual administration of nitroglycerine. Resting and peak superficial femoral artery diameter in SCI subjects were smaller than in controls (P < 0.001). The FMD response in controls (4.2 +/- 0.9%) was lower than in SCI subjects (8.2 +/- 0.9%, P < 0.001), but not after correcting for area under the curve for shear rate (P = 0.35). When expressed as relative change from baseline, SCI subjects demonstrate a significantly larger diameter increase compared with controls at each dose of SNP. However, when expressed as a relative increase within the range of diameter changes [baseline (0%) - peak diameter (100%)], both groups demonstrate similar changes in response to SNP. Changes in diameter during SNP infusion and FMD response are larger in SCI subjects compared with controls. When these results are corrected, superficial femoral artery FMD and NO sensitivity in SCI subjects are not different from those in controls. This illustrates the importance of appropriate data presentation and suggests that, subsequent to structural inward remodeling of conduit arteries as a consequence of extreme physical inactivity, arterial function is normalized.
Heart | 2010
P.C.E. de Groot; Dick H. J. Thijssen; Maria T. E. Hopman
To the editor: With great interest, we read the articles of a recent issue of Heart addressing the important role of abdominal obesity in relation to cardiovascular risk and the metabolic syndrome.1 2 The metabolic syndrome, considered the ailment of the 20th century, emerges from clustering and interactions of multiple cardiovascular risk factors affecting a large proportion of the population. The presence of the metabolic syndrome in children is of particular interest given the rapid and alarming increase in prevalence in the past …
Journal of Applied Physiology | 2005
Mark Rakobowchuk; C.L. McGowan; P.C.E. de Groot; Joseph W. Hartman; Stuart M. Phillips; Maureen J. MacDonald
Physical Therapy | 2006
W. ter Woerds; P.C.E. de Groot; D. van Kuppevelt; Maria T. E. Hopman
Journal of Applied Physiology | 2004
M. W. P. Bleeker; P.C.E. de Groot; James A. Pawelczyk; Maria T. E. Hopman; Benjamin D. Levine
Heart | 2010
P.C.E. de Groot; Dick H. J. Thijssen; Maria T. E. Hopman
Journal of Applied Physiology | 2009
P.C.E. de Groot; Maria T. E. Hopman