Determinants of fast marathon performance: low basal sympathetic drive, enhanced postcompetition vasodilatation and preserved cardiac performance after competition.

OBJECTIVE: To test the hypothesis that enhanced postexercise vasodilatation is related to sympathetic drive to resistance vessels and to fast marathon performance. DESIGN: Prospective field study before and after running a marathon. PARTICIPANTS: 51 healthy amateur runners who volunteered to participate. The fastest competitor finished fourth, the slowest 1290 th out of 1324 participants. INTERVENTIONS: None. MAIN OUTCOME MEASUREMENTS: Competition time, beat-to-beat blood pressure by the vascular unloading technique, oscillometric blood pressure, beat-to-beat stroke volume by impedance cardiography, total peripheral resistance changes calculated from blood pressure and stroke volume changes, sympathetic modulation of vasomotor tone and parasympathetic modulation of sinus node function by spectral analysis of blood pressure and heart rate variability, baroreceptor reflex sensitivity by the sequence method. RESULTS: Slow performers, in contrast to fast performers, exhibited a higher 0.1 Hz band of diastolic blood pressure variability before the competition (0.1 Hz BPV) (40.0 (SD 2.39) vs 54.9 (2.47), p<0.001), diminished vasodilatation (-11.3 (4.78) vs -29.4 (3.23), p<0.01) and a decrease in stroke index (-14.9 (3.55) vs +0.9 (3.37), p<0.001) in response to the race. Single and multiple regression analyses further corroborated the findings. CONCLUSIONS: Fast performance in the marathon is associated with low sympathetic modulation of vasomotor tone, maintained stroke index postcompetition and enhanced exercise-induced vasodilatation. We postulate that maintaining a low level of sympathetic modulation to resistance vessels during the course of training may indicate its appropriateness, thus enabling fast performance by optimal postexercise vasodilatation and by prevention of postcompetition cardiac dysfunction. This will have to be tested in future longitudinal studies.

beta-2 Adrenergic receptor variants affect resting blood pressure and agonist-induced vasodilation in young adult Caucasians.

Recent evidence suggests that the prodownregulatory Gly16 allele of the beta-2 adrenergic receptor (beta-2 AR) is associated with essential hypertension in African Caribbeans. To further investigate the effect of the glycine (Gly)16 and arginine (Arg)16 beta-2 AR variants on hemodynamics, we investigated the agonist-mediated in vivo vasodilation in normotensive Austrian Caucasians and analyzed the results with respect to the Gly16/Arg16 polymorphism. Fifty-seven normotensive men, 20 to 32 years of age with body mass index of 18.7 to 29.9 kg/m2, were genotyped for the Arg16/Gly16 beta-2 AR alleles. All 15 Gly16/Gly16 subjects, all 12 Arg16/Arg/16 subjects, and 27 of 30 heterozygous subjects underwent hemodynamic measurements while supine after an overnight fast. The observers were unaware of the subjects' genotypes. The subjects received a graded infusion of the selective beta-2 AR agonist salbutamol (0.07, 0.14, and 0.21 microgram/kg per minute, respectively), each dose over 8 minutes. Stroke volume and blood pressure were determined continuously by means of impedance cardiography and oscillometry, respectively. The last 4 minutes of each infusion were evaluated statistically. Basal mean blood pressure was higher in the Gly16/Gly16 subjects compared with Arg16/Arg16 subjects (mean+/-SD: 81.6+/-6.14 versus 75.2+/-4.93 mm Hg, P<0.01). Homozygous Gly16 subjects showed a significantly decreased vasodilation during the first dose of salbutamol infusion compared with Arg16/Arg16 subjects (Deltatotal peripheral resistance index -17.9+/-14.4 versus -30. 6+/-8.3%, P<0.01) despite increased sympathetic counterregulation in the Arg16/Arg16 group (Deltaheart rate +16.9+/-7.0% versus +8.6+/-7. 0%, P<0.01; Deltacardiac index +39.5+/-18.5% versus 21.4+/-18.8%, P<0.05). Our results provide additional evidence that the Gly16/Arg16 alleles of the beta-2 AR are intimately related to blood pressure regulation and deserve further studies in the pathogenesis of essential hypertension.

A software package for non-invasive, real-time beat-to-beat monitoring of stroke volume, blood pressure, total peripheral resistance and for assessment of autonomic function.

The goal of the present study was to develop and evaluate algorithms for non-invasive, real-time, beat-to-beat monitoring of stroke index (SI), blood pressure (BP) and total peripheral resistance index (TPRI) which has a menu-driven interface, suitable for routine use by unskilled staff. In addition, it was our aim to include a meta-analysis for the evaluation of autonomic function derived from the above haemodynamic data. This includes spectral analysis of heart rate (HR), BP, SI and TPRI and the automatic calculation of baroreceptor reflex sensitivity. Impedance cardiography was used for beat-to-beat SI determination, Finapres corrected by an oscillometric blood pressure measurement (Dinamap) on the upper arm for beat-to-beat BP measurement. We demonstrate noise free recordings during physiological (head up tilt) and pharmacological intervention (alpha 1-, beta 2-adrenoreceptor agonists, insulin induced hypoglycemia). The newly developed software should prove valuable for physiological, pharmacological and clinical studies.