Pendergast DR, Olszowka A, Farhi LE. Cardiovascular and pulmonary responses to increased acceleration forces during rest and exercise. Aviat Space Environ Med 2012; 83:488–95.
Background:
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.
Methods:
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.
Results:
CO (-1.53 L · min−1/+Gz), stroke volume (−30 ml/+Gz, SV), and pulmonary diffusing capacity (−3.42 ml · mmHg−1/+Gz, DLCO)
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 · min−1/+Gz,
VE) 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.
Discussion:
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.