We examined left ventricular (LV) function before, during and following prolonged exercise (EX) in 12 healthy middle-aged men (mean±sem: age=43.5±1.9; VO_2max =51.7±1.5 ml^.kg^-1.min^-1). Subjects cycled for 120 minutes at 65%VO_2max(75% of maximal heart rate}. 2-D echocardiography (ECHO was used 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. RESULTS: 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 s^-1 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 versus 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 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 L throughout EX. Following 30 min of recovery, LV longitudinal strain was depressed relative to baseline (-23.20±0.87% to -19.57±1.21%, p<0.01). Following 30 min of recovery, LV longitudinal strain was depressed relative to baseline (-23.20±0.87% to -19.57±1.21%, p<0.01). CONCLUSION: 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 in spite of 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.