We propose to prevent the cardiac atrophy and orthostatic intolerance associated with prolonged bed rest using rowing ergometry/resistance training with aggressive volume loading on the day of testing. We hypothesize that prevention of cardiac atrophy will forestall cardiovascular deconditioning, leading to preserved exercise capacity and orthostatic tolerance. Twenty-four healthy subjects, ages 20 –55, were enrolled with 8 randomized to training (EX), 8 with training and volume loading (VOL), and 8 as sedentary (SED) controls. Testing included maximal upright exercise, orthostatic tolerance via graded lower body negative pressure (LBNP), cardiac MRI, as well as invasive cardiac pressure-volume measurements, performed at baseline and at the end of 5 weeks of 6° head down bedrest. Upright exercise capacity was preserved with training as measured by peak workrate and VO2max (EX/VOL: pre 195±46W, 34±7 ml/kg/min; post 202±42W, 33±4 ml/kg/min) but deteriorated in SED group (pre 171±55W, 34±8 ml/kg/min; post 145±51W, 27±7 ml/kg/min). MRI derived mass (% change: +6.3±9.9% EX/VOL vs. −5.5±3.7% SED) was increased by training. Exercise training appears to preserve LV chamber compliance (stiffness constants: EX/VOL: pre= 0.035±0.021, post = 0.036±0.029; SED: pre= 0.020±0.011, post = 0.028±0.007). Training also preserves hemodynamic variables measured at −40mmHg of LBNP, including stroke volume (EX: pre 44±12; post 38±9 ml, VOL: pre 49±30; post 45±29 ml, SED: pre 35±5; post 24±8 ml ). These preliminary data support our hypothesis that an optimized training program consisting of dynamic and resistance exercise can prevent part of the multisystem atrophy and orthostatic intolerance associated with prolonged bed rest. This defines a specific countermeasure that is practical, safe, and effective against the cardiovascular, muscle and bone deconditioning associated with prolonged bed rest. This information is relevant not only for astronauts exposed to long duration spaceflight, but also for patients with chronic reductions in physical activity, and those with disease processes that alter cardiac stiffness such as obesity, hypertension, heart failure or ischemic heart disease, plus normal aging and osteoporosis.
This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).
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