title: Enhanced beta-adrenergic-mediated cardiovascular responses in endurance athletes.
abstract: To determine whether the adaptive increase in left ventricular systolic function in the trained state is mediated by enhanced responses to beta-adrenergic stimulation, we studied eight male endurance athletes [age 27 +/- 1.8 yr; maximal O2 uptake (VO2max) 60 +/- 0.9 (SE) ml x kg-1 x min-1] and eight sedentary men (age 27 +/- 1.4 yr; VO2max 43.1 +/- 1.7 ml x kg-1 x min-1). Left ventricular function was evaluated with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile in the basal state, after parasympathetic blockade by atropine, and during infusion of dobutamine. Cardiac output and stroke volume, determined with the acetylene rebreathing technique, during maximal exercise were significantly higher in the endurance athletes than in the sedentary men (28.9 +/- 1.7 vs. 23 +/- 1.23 1/min, P = 0.019, and 162 +/- 12 vs. 125 +/- 7 ml/min, P = 0.029). Endurance athletes showed physiological volume overload-left ventricular hypertrophy and greater enhancements of left ventricular systolic function and filling dynamics in response to dobutamine than did the sedentary men as reflected in 1) a steeper slope of the fractional shortening-end-systolic wall stress relationship (-0.986 +/- 0.16 vs. -0.508 +/- 0.054, P = 0.014, athletes vs. controls) and 2) a higher early-to-late transmitral diastolic Doppler velocity ratio (2.14 +/- 0.14 vs. 1.74 +/- 0.12, P = 0.016) at a comparable heart rate. Although endurance athletes had a significantly greater inotropic response to dobutamine, they demonstrated a markedly attenuated chronotropic response to beta1-adrenergic stimulation compared with sedentary subjects. Our findings suggest that, even with a blunted chronotropic response, endurance-trained young men show an augmented inotropic response to a beta1-adrenergic agonist that, along with physiological volume overload hypertrophy and increased diastolic filling, can contribute to a larger stroke volume during maximal exercise in the trained state.
authors.affiliation: Section of Applied Physiology, and Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: M G
authors.initials: MG
authors.lastname: Hopkins
authors.forename: R J
authors.initials: RJ
authors.lastname: Spina
authors.forename: A A
authors.initials: AA
authors.lastname: Ehsani
mesh_terms: D058665:Adrenergic beta-1 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000328:Adult; D001823:Body Composition / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D004280:Dobutamine / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D010807:Physical Endurance / Q000502:physiology*; D010809:Physical Fitness; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D058665:Adrenergic beta-1 Receptor Agonists; D000318:Adrenergic beta-Agonists; D018727:Muscarinic Antagonists; D011943:Receptors, Adrenergic, beta; D004280:Dobutamine