Lower body negative pressure (LBNP) is a unique method as it induces blood shift from upper (above the iliac crest) to lower body compartments without other effects induced by a change from supine to upright such as altered stimulus patterns in otolithic receptors or full orthostatic weight loading on the lower extremities. It has been employed as an experimental tool for decades to study hemodynamic and neurohormonal responses following central hypovolemia. Deconditioning of bed rest or spaceﬂight is another topic where LBNP has been used both as an investigative as well as a cardiovascular training tool.
LBNP reduces venous return to the heart by causing blood pooling in the lower parts of the body (with the demarca-tion between “upper” and “lower” body depending on seal location). The resulting central hypovolemia leads to hypo-tensive activation of arterial and cardiopulmonary barore-ﬂexes that initiates neurohumoral-mediated increases in heart rate and vasoconstriction (1, 305), which assists in a compensatory effort to maintain adequate arterial pressure and cerebral perfusion. An overview of mechanical and physiological effects of LBNP are shown in FIGURE 1. The effects of LBNP cessation, on the other hand, are similar to those that follow a Valsalva maneuver: blood moves to the thorax, leading to a transient increase in blood pressure and a decrease in heart rate.
LBNP elicits reproducible reﬂexive hemodynamic and cardiovascular control responses, similar to those following increased G load (e.g., increases in heart rate and total peripheral resistance), which ensure a compensatory effort to maintain blood pressure and cerebral perfusion.
2.Cerebral blood ﬂow and LBNP
LBNP is commonly used as a means to study cardiovascular reﬂex responses to central hypovolemia. Typical cardiovascular effects induced by LBNP are best illustrated by the classic data published more than three decades ago by Blomqvist and Stone and presented here as FIGURE 2.
3.Effects of LBNP on pulmonary function
The application of LBNP causes a shift of the diaphragm in the caudal direction, pulmonary hypoperfusion, and in-crease in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and functional residual capacity without alterations in pulmonary compliance. These functional changes are explained by a reduced thoracic blood volume due to the translocation of ﬂuid from the thorax to the lower body, subsequently allowing for more air to be moved faster without the impedance caused by circulating pulmonary blood volume. The notion that blood in the lung reduces FVC and FEV1.0 is further sup-ported by the relationship of larger increases in FVC and FEV1.0 during LBNP in subjects with larger lung volumes that allow a greater absolute shift in blood to or from the thorax. Finally, the absence of change in lung compliance provides evidence that the increases in FVC and FEV1.0 during LBNP result from changes in thoracic blood volume rather than mechanical properties of the lungs themselves.
4.Autonomic system and LBNP
Compensatory responses associated with the control of car-diac output and peripheral vascular resistance during the reduction in central blood volume and hypotension induced by LBNP are under the control of parasympathetic (cardiac vagal) and sympathetic activity. These compensatory mechanisms work in concert through autonomically mediated baroreﬂexes to maintain global tissue oxygenation through the regulation of systemic (arterial) perfusion pressure.
LBNP has led to a greater understanding of the compensa-tory hormonal responses to central hypovolemia. These in-clude rapid elevations of plasma epinephrine and norepi-nephrine and, after a 10- to 20-min delay, renin-angiotensin system activation with elevated plasma renin activity, an-giotensin II, and aldosterone.
In a study conducted to compare the effects of LBNP at 40 mmHg with the effects of central hypovolemia in-duced by standing on respiratory mechanics (24), two notable differences were observed: functional residual capacity (FRC) and peak intra-abdominal pressure (IAP) both increased with standing but not during LBNP (FIGURE 6).