title: Left ventricular contractile function is preserved during prolonged exercise in middle-aged men.
abstract: We examined left ventricular (LV) performance before, during, and following prolonged exercise (EX) in 12 healthy middle-aged men [means +/- SE: age = 43.5 +/- 1.9 yr; maximal O(2) uptake (Vo(2max)) = 51.7 +/- 1.5 ml.kg(-1).min(-1)]. Subjects cycled for 120 min at 65% Vo(2max) (75% of maximal heart rate). Two-dimensional echocardiography (ECHO) to determine tissue-Doppler longitudinal myocardial strain and strain rate, LV ejection fraction (EF), end-diastolic (EDV), end-systolic (ESV), and stroke volume (SV) at baseline and after 5, 30, and 120 min of EX and following 30 min of recovery. In addition, hematocrit and plasma norepinephrine (NE) were measured. From baseline to 5 min of EX, there were significant increases in LV longitudinal strain (-23.20 +/- 0.87 to -27.63 +/- 1.07%; P < 0.01), strain rate (-1.50 +/- 0.15 to -2.08 +/- 0.14 s(-1); P < 0.01), and EF (56.3 +/- 2.2 to 77.1 +/- 1.0%; P < 0.05) with continued increases by both at 30 min of exercise vs. SV, EDV, and ESV, which remained constant. After 120 min of EX, HR and NE increased further with reductions in SV, cardiac output, and systolic blood pressure without changes in strain or strain rate. EDV decreased after 120 min of EX (-9.2- vs. 30-min value; P = 0.05) along with a hemoconcentration (baseline = 41.3 +/- 1.0 vs. EX = 45.1 +/- 1.2%; P < 0001) and significant reduction in body mass despite a mean fluid consumption of 1.8 +/- 0.2 liters throughout EX. After 30 min of recovery, LV longitudinal strain was depressed relative to baseline (-23.20 +/- 0.87 to -19.57 +/- 1.21%; P < 0.01). The reduction in LV SV during prolonged EX occurred without changes in the LV contractile state and is likely secondary to reduced LV preload. A reduction in LV contractility despite a reduced afterload following exercise may be due to factors unique to the recovery period and do not appear to contribute to a reduction in SV during prolonged exercise.
authors.affiliation: University of Toronto, Toronto, Ontario, Canada M5S 2W6. jack.goodman@utoronto.ca
authors.forename: Jack M
authors.initials: JM
authors.lastname: Goodman
authors.forename: Gian-Marco
authors.initials: GM
authors.lastname: Busato
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Frey
authors.forename: Zion
authors.initials: Z
authors.lastname: Sasson
mesh_terms: D000328:Adult; D001794:Blood Pressure; D002302:Cardiac Output; D015150:Echocardiography, Doppler; D015444:Exercise; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006400:Hematocrit; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption; D020127:Recovery of Function; D013318:Stroke Volume; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D009638:Norepinephrine