Cardiovascular and pulmonary responses to increased acceleration forces during rest and exercise

Background: The reduced cardiac output (CO) secondary to increased acceleration forces (+G_z) has applicability to daily life and pathophysiology. Increased +G_z and reduced CO affect the lung, resulting in reduced oxygen transport. A variety of studies have examined tolerance to high +G_z. Methods: The present study examines the effect of +1 to +3 G_z on steady-state cardiopulmonary variables at rest and while exercising at + 2 G_z and + 3 G_z. This study also looks at the deterioration of steadystate cardiopulmonary variables with sustained increased +G_z and after de-training in eight male centrifuge trained subjects. Results: CO (-1.53 L· min^-1/+G_z), stroke volume (-30 ml/+G_z, SV), and pulmonary diffusing capacity (-3.42 ml· mmHg^-1/+G_z, DL_CO) decreased linearly with increased +G_z at rest while heart rate (23 bpm/+G_z, HR), total peripheral resistance (0.0095 TPRU/G_z, TPR), mean arterial pressure (13.2 mmHg/ +G_z, MAP), and ventilation (4.13 L·z min^-1/+G_z, V_E) increased linearly. During graded exercise, CO and SV increased less at +2 G_z and +3 G_z while MAP and V E increased more. Failure to endure increased +G_z and the effects of de-training were primarily due to the inability to regulate MAP. Discussion: The incremental increase in increased +G_z from 1 to 3 resulted in increased MAP, which was accomplished by increasing TPR sufficiently so as to offset the reduced CO. The effects of increased +G_z and reduced CO compromised lung function and oxygen transport (-18-30%), thus compromising exercise capacity. The failure to regulate MAP at lower increased +G_z levels resulted in intolerance to higher increased +G_z.