Dorfman Todd A, Rosen Boaz D, Perhonen Merja A, Tillery Tommy, McColl Roddy, Peshock Ronald M, Levine Benjamin D
Institute for Exercise and Environmental Medicine, 7232 Greenville Ave., Suite 435, Dallas, TX 75231, USA.
J Appl Physiol (1985). 2008 Apr;104(4):1037-44. doi: 10.1152/japplphysiol.00858.2006. Epub 2008 Jan 31.
Bed rest deconditioning leads to physiological cardiac atrophy, which may compromise left ventricular (LV) 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 degrees head-down tilt bed rest for 18 days with (n = 14) and without exercise training (n = 10). LV mass and LV end-diastolic volume were measured using cine MRI. Exercise subjects cycled on a supine ergometer for 30 min, three times per day at 75% maximal heart rate (HR). After sedentary bed rest, there was a significant reduction in maximal untwisting rates of the midwall (-46.8 +/- 14.3 to -35.4 +/- 12.4 degrees /s; P = 0.04) where untwisting is most reliably measured, and to a lesser degree of certainty in the endocardium (-50.3 +/- 13.8 to -40.1 +/- 18.5 degrees /s; 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 to -72.3 +/- 22.3 degrees /ms; P = 0.05) and midwall (-39.2 +/- 12.2 to -59.0 +/- 19.6 degrees /s; 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 to 149.5 +/- 27.9 g; P = 0.07), but it increased slightly in the exercise-trained subjects (156.4 +/- 34.3 to 162.3 +/- 40.5 g; P = 0.16); (interaction P = 0.03). We conclude that diastolic untwisting is impaired following sedentary bed rest. However, exercise training in bed can prevent the physiological cardiac remodeling associated with bed rest and preserve or even enhance diastolic suction.
卧床休息导致身体机能下降会引起生理性心脏萎缩,这可能会在体位性应激期间通过减少舒张期解旋和抽吸来损害左心室(LV)充盈。为了验证这一假设,在18天-6度头低位卧床休息前后,对有运动训练组(n = 14)和无运动训练组(n = 10)进行了心肌标记磁共振成像(MRI),并通过谐波相位分析(HARP)计算心内膜、心肌中层和心外膜的最大解旋速率。使用电影MRI测量左心室质量和左心室舒张末期容积。运动组受试者在仰卧测力计上以最大心率(HR)的75%每天骑行3次,每次30分钟。卧床休息后,心肌中层的最大解旋速率显著降低(从-46.8±14.3降至-35.4±12.4度/秒;P = 0.04),此处解旋测量最为可靠,心内膜的降低程度较小(从-50.3±13.8降至-40.1±18.5度/秒;P = 0.09);心外膜无变化。相比之下,当在床上进行运动时,心内膜(从-48.4±20.8降至-72.3±22.3度/毫秒;P = 0.05)和心肌中层(从-39.2±12.2降至-59.0±19.6度/秒;P = 0.03)的解旋速率增加。两组在心内膜(交互作用P = 0.02)和心肌中层(交互作用P = 0.004)的差异反应显著。久坐组的左心室质量下降(从156.4±30.3降至149.5±27.9克;P = 0.07),但在运动训练组中略有增加(从156.4±34.3增至162.3±40.5克;P = 0.16);(交互作用P = 0.03)。我们得出结论,久坐卧床休息后舒张期解旋受损。然而,床上运动训练可以防止与卧床休息相关的生理性心脏重塑,并保留甚至增强舒张期抽吸。