Abstract

We tested the hypothesis that 10 days of endurance training (ET) would enhance stroke volume (SV) during peak exercise and increase the inotropic response to β-adrenergic stimulation. Ten subjects (26±2 yrs; mean± SE) trained on a cycle ergometer for 10 consecutive days. At peak exercise, ET increased VO2 (2.54±0.29 to 2.80±0.32 l/min, p<0.001), cardiac output (18.3±1.3 to 20.5±1.7 l/min, p<0.001), and stroke volume (97±7 to 112±9 ml/b, p<0.001). Blood volume increased with ET (4659±330 to 4951±401 ml, p<0.01). Left ventricular (LV) size and function were assessed with 2-D echocardiography. Data were collected before (baseline) and after 1.0 mg injection of atropine, and during 4 continuous doses of dobutamine. LV end-diastolic diameter (EDD) at baseline increased with ET (48.5±2.1 to 50.6±1.5 mm, p<0.02), while LV wall thicknesses were unchanged. LV contractile performance was assessed by relating fractional shortening (FS) to the estimated end-systolic wall stress (σES). ET increased the slope of the FS-σES relationship (-0.55±0.9 to-0.89±0.14, p<0.03), indicative of enhanced systolic function withβ-adrenergic stimulation. Further, the increase in FS (9.6±2.7 to 14.1±1.5%, p<0.05) was greater at a given change in LVEDD (pre: 0.3±0.3 mm, post: 0.3±0.4 mm) during dobutamine. The change in the slope of the FS-σES relationship correlated with increases in both cardiac output (R = -0.71, p<0.05) and stroke volume (R = -0.70, p<0.05). These data show that even 10 days of ET induces adaptations consistent with enhanced inotropic response to β-adrenergic stimulation, and this improvement is associated with increases in cardiac output and stroke volume during peak exercise.

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