Cardiac atrophy after bed rest and spaceflight

Cardiac muscle adapts well to changes in loading conditions. For example, l eft ventricular (LV) hypertrophy may be induced physiologically (via exerci se training) or pathologically (via hypertension or valvular heart disease) . If hypertension is treated, LV hypertrophy regresses, suggesting a sensit ivity to LV work. However, whether physical inactivity in nonathletic popul ations causes adaptive changes in LV mass or even frank atrophy is not clea r. We exposed previously sedentary men to 6 (n = 5) and 12 (n = 3) wk of ho rizontal bed rest. LV and right ventricular (RV) mass and end-diastolic vol ume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at l east 6 wk of routine daily activities as controls. In addition, four astron auts were exposed to the complete elimination of hydrostatic gradients duri ng a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 +/- 2.2% (P = 0.005) after 6 wk with an additional atrophy of 7.6 +/- 2.3% in t he subjects who remained in bed for 12 wk; there was no change in LV mass f or the control subjects (153.0 +/- 12.2 vs. 153.4 +/- 12.1 g, P = 0.81). Me an wall thickness decreased (4 +/- 2.5%, P = 0.01) after 6 wk of bed rest a ssociated with the decrease in LV mass, suggesting a physiological remodeli ng with respect to altered load. LV end-diastolic volume decreased by 14 +/ - 1.7% (P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 +/- 2.7% (P = 0. 06) and RV end-diastolic volume by 16 +/- 7.9% (P = 0.06). After spacefligh t, LV mass decreased by 12 +/- 6.9% (P = 0.07). In conclusion, cardiac atro phy occurs during prolonged (6 wk) horizontal bed rest and may also occur a fter short-term spaceflight. We suggest that cardiac atrophy is due to a ph ysiological adaptation to reduced myocardial load and work in real or simul ated microgravity and demonstrates the plasticity of cardiac muscle under d ifferent loading conditions.