Lower Body Negative Pressure: Physiological Effects, Applications, and Implementation.

This review presents lower body negative pressure (LBNP) as a unique tool to investigate the physiology of integrated systemic compensatory responses to altered hemodynamic patterns during conditions of central hypovolemia in humans. An early review published in Physiological Reviews over 40 yr ago (Wolthuis et al. Physiol Rev 54: 566-595, 1974) focused on the use of LBNP as a tool to study effects of central hypovolemia, while more than a decade ago a review appeared that focused on LBNP as a model of hemorrhagic shock (Cooke et al. J Appl Physiol (1985) 96: 1249-1261, 2004). Since then there has been a great deal of new research that has applied LBNP to investigate complex physiological responses to a variety of challenges including orthostasis, hemorrhage, and other important stressors seen in humans such as microgravity encountered during spaceflight. The LBNP stimulus has provided novel insights into the physiology underlying areas such as intolerance to reduced central blood volume, sex differences concerning blood pressure regulation, autonomic dysfunctions, adaptations to exercise training, and effects of space flight. Furthermore, approaching cardiovascular assessment using prediction models for orthostatic capacity in healthy populations, derived from LBNP tolerance protocols, has provided important insights into the mechanisms of orthostatic hypotension and central hypovolemia, especially in some patient populations as well as in healthy subjects. This review also presents a concise discussion of mathematical modeling regarding compensatory responses induced by LBNP. Given the diverse applications of LBNP, it is to be expected that new and innovative applications of LBNP will be developed to explore the complex physiological mechanisms that underline health and disease.

Poststroke alterations in heart rate variability during orthostatic challenge.

Older adults following recovery from ischemic stroke have a higher incidence of orthostatic hypotension, syncope, and fall risk, which may be related to impaired autonomic responses limiting the ability to maintain cerebral blood flow. Thus, we investigated cerebrovascular and cardiovascular regulation in 23 adults ≥55 years of age, 10 diagnosed with ischemic stroke, and 13 age-matched healthy controls when sitting at rest and upon standing to compare differences of autonomic variables at ∼7 months (218 ±â€Š41 days) poststroke.Arterial blood pressure via finger plethysmography, muscle-pump baroreflex via electromyography, heart rate variability via 3-lead ECG, and cerebral blood flow velocity via transcranial Doppler were analyzed while sitting for 5 minutes and then during quiet standing for 5 minutes.From the seated to standing position, the stroke group had significantly greater decline in the low frequency component of heart rate variability (164 [79] vs 25 [162] ms; P = 0.043). All other cardiovascular parameters and assessments of autonomic function were not significantly different between the two groups.Our findings support the hypothesis of continued autonomic dysfunction after recovery from ischemic stroke, with potential attenuation of the cardiovascular response to standing. However, further investigation is required to determine the mechanisms underlying the increased risk of orthostatic hypotension, syncope, and falls poststroke.

Physiological responses of ultraendurance athletes and nonathletes during an attempt to summit Denali.

OBJECTIVE: To compare altitude responses of 2 ultraendurance athletes and 2 nonathletes during a 2-week expedition on Denali (Mount McKinley). METHODS: The severity of acute mountain sickness (AMS) symptoms (Lake Louise AMS guidelines) and pulmonary function parameters (forced vital capacity, forced expiratory volume in 1 second, peak expiratory flow) as well as resting heart rate and arterial oxygen saturation measurements were taken during the climb. Baseline measurements were made at 375 m, and field tests were performed at altitudes of 2200 m, 2400 m, 3000 m, 3400 m, 4100 m, 4300 m, and 10 m. RESULTS: Nonathletes reported moderate AMS symptoms at altitudes up to and including 3000 m, whereas ultraendurance athletes reported moderate AMS symptoms at altitudes above 3000 m. Considerable daily variation existed in pulmonary function measures within and between groups; however, the largest shift from baseline and between groups occurred at 3000 m where ultraendurance athletes had increased and nonathletes had decreased peak expiratory flow and forced vital capacity. Resting heart rate increased and arterial oxygen saturation decreased with altitude. CONCLUSIONS: Highly aerobically fit individuals may be more susceptible to delayed and more prolonged onset of AMS than are moderately fit individuals. Pulmonary function, although highly variable, also may be dissimilar between these groups.