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

The reduced cardiac output (CO) secondary to increased acceleration forces (+Gz) has applicability to daily life and pathophysiology. Increased +Gz and reduced CO affect the lung, resulting in reduced oxygen transport. A variety of studies have examined tolerance to high +Gz.

The present study examines the effect of +1 to +3 Gz on steady-state cardiopulmonary variables at rest and while exercising at +2 Gz and +3 Gz. This study also looks at the deterioration of steady-state cardiopulmonary variables with sustained increased +Gz and after de-training in eight male centrifuge trained subjects.

CO (-1.53 L x min(-1)/+Gz), stroke volume (-30 ml/+Gz, SV), and pulmonary diffusing capacity (-3.42 ml x mmHg(-1)/+Gz, DL(co)) decreased linearly with increased +Gz at rest while heart rate (23 bpm/+Gz, HR), total peripheral resistance (0.0095 TPRU/Gz TPR), mean arterial pressure (13.2 mmHg/+Gz, MAP), and ventilation (4.13 L x min(-1)/+Gz, V(E)) increased linearly. During graded exercise, CO and SV increased less at +2 Gz and +3 Gz while MAP and VE increased more. Failure to endure increased +Gz and the effects of de-training were primarily due to the inability to regulate MAP.

The incremental increase in increased +Gz 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 +Gz and reduced CO compromised lung function and oxygen transport (-18-30%), thus compromising exercise capacity. The failure to regulate MAP at lower increased +Gz levels resulted in intolerance to higher increased +Gz.