Supine cycling plus volume loading prevent cardiovascular deconditioning during bed rest

Abstract

There are two possible mechanisms contributing to the excessive fall of stroke volume (and its contribution to orthostatic intolerance) in the upright position after bed rest or spaceflight: reduced cardiac filling due to hypovolemia and/or a less distensible heart due to cardiac atrophy. We hypothesized that preservation of cardiac mechanical function by exercise training, plus normalization of cardiac filling with volume infusion, would prevent orthostatic intolerance after bed rest. Eighteen men and three women were assigned to 1) exercise countermeasure (n=14) and 2) no exercise countermeasure (n=7) groups during bed rest. Bed rest occurred in the 6 degrees head-down tilt position for 18 days. The exercise regimen was prescribed to compensate for the estimated cardiac work reduction between bed rest and ambulatory periods. At the end of bed rest, the subjects were further divided into two additional groups for post-bed rest testing: 1) volume loading with intravenous dextran to normalize cardiac filling pressure and 2) no volume loading. Dextran infusion was given to half of the exercise group and all of the sedentary group after bed rest, leading ultimately to three groups: 1) exercise plus volume infusion; 2) exercise alone; and 3) volume infusion alone. Exercise training alone preserved left ventricular mass and distensibility as well as upright exercise capacity, but lower body negative pressure (LBNP) tolerance was still depressed. LBNP tolerance was maintained only when exercise training was accompanied by dextran infusion. Dextran infusion alone following bed rest without exercise maintained neither orthostatic tolerance nor upright exercise capacity. We conclude that daily supine cycle exercise sufficient to prevent cardiac atrophy can prevent orthostatic intolerance after bed rest only when combined with plasma volume restoration. This maintenance of orthostatic tolerance was achieved by neither exercise nor dextran infusion alone. Cardiac atrophy and hypovolemia are likely to contribute independently to orthostatic intolerance after bed rest.

Fig. 1.

Detailed study design for 18 days of 6° head-down tilt bed rest and 2 kinds of countermeasures: 1) supine cycle exercise training and 2) intravenous dextran infusion. ExDex (n = 7) and ExNoVol (n = 7) are groups with or without dextran infusion, respectively, after exercise countermeasure (Exercise, n = 14) during bed rest. SedDex (n = 7) is the group with dextran infusion after sedentary bed rest. PCWP, pulmonary capillary wedge pressure.

Fig. 2.

Maximal lower body negative pressure (LBNP) tolerance before (pre) and after (post) head-down tilt bed rest in ExDex, ExNoVol, and SedDex groups.

Fig. 3.

Starling curves before (pre) and after (post) head-down tilt bed rest in ExDex, ExNoVol, and SedDex groups. Shown are mean ± SE group data for stroke volume (SV) at given PCWP. Six data points correspond to 2 degrees of LBNP, 2 baselines, and 2 saline infusions. Dextran infusion groups (ExDex and SedDex) have 7 data points in the post-bed rest results, including another data point from before dextran infusion. Curves were drawn by second-order linear regression based on mean values for each condition.

Fig. 4.

Left ventricular pressure-volume curves before (pre) and after (post) head-down tilt bed rest in ExDex, ExNoVol, and SedDex groups. Shown are mean ± SE group data. Six data points correspond to 2 degrees of LBNP, 2 baselines, and 2 saline infusions. Dextran infusion groups (ExDex and SedDex) have 7 data points in the post-bed rest results, including another data point from before dextran infusion. V₀, V_max, and Stiffness are equilibrium volume, maximum volume, and stiffness constant from the logarithmic model. These indexes are derived from group mean data points and thus differ from the mean of the individual values in Table 3. LVEDV, left ventricular end-diastolic volume.