Bed rest deconditioning leads to physiologic cardiac atrophy which may compromise left ventricular filling during orthostatic stress by reducing diastolic untwisting and suction. To test this hypothesis, myocardial tagged magnetic resonance imaging (MRI) was performed and maximal untwisting rates of the endocardium, midwall, and epicardium were calculated by Harmonic Phase Analysis (HARP) before and after -6° head-down tilt bedrest for 18 days with (N=14) and without exercise (N=10). Left ventricular (LV)mass and LV end-diastolic volume were measured using cine MRI. Exercise subjects cycled on a supine ergometer for 30min, 3x/day at 75% maximal heart rate. After sedentary bedrest there was a significant reduction in max untwisting rates of the midwall (-46.8±14.3 degrees/sec to -35.4±12.4 degrees/sec, P=0.04) where untwisting is most reliably measured, and to a lesser degree of certainty in the endocardium (-50.3±13.8 degrees/sec to -40.1±18.5 degrees/sec, P=0.09); the epicardium was unchanged. In contrast, when exercise was performed in bed, untwisting rates were enhanced at the endocardium (-48.4±20.8 degrees/sec to -72.3±22.3 degrees/ms, P=0.05) and midwall (-39.2±12.2 degrees/sec to -59.0±19.6 degrees/sec, P=0.03). The differential response was significant between groups at the endocardium (interaction P=0.02) and the midwall (interaction P=0.004). LV mass decreased in the sedentary group (156.4±30.3 g to 149.5±27.9 g, P=0.07), but increased slightly in the exercise trained subjects (156.4±34.3g to 162.3±40.5, P=0.16); (interaction P=0.03). We conclude that diastolic untwisting is impaired following sedentary bedrest. However, exercise training in bed can prevent the physiologic cardiac remodeling associated with bedrest and preserve or even enhance diastolic suction.