Mental fatigue was associated with increased power in frontal theta (θ) and parietal alpha (α) EEG rhythms. A statistical classifier can use these effects to model EEG-fatigue relationships accurately. Participants (n = 22) solved math problems on a computer until either they felt exhausted or 3 h had elapsed. Pre-and post-task mood scales showed that fatigue increased and energy decreased. Mean response times rose from 6.7 s to 7.9 s but accuracy did not change significantly. Mean power spectral densities or PSDs of θ and α bands rose by 29% and 44%, respectively. A kernel partial least squares classifier trained to classify PSD coefficients (1-18 Hz) of single 13-s EEG segments from alert or fatigued task periods was 91% to 100% accurate. For EEG segments from other task periods, the classifier outputs tracked the time course of the development of mental fatigue. By this measure, most subjects became substantially fatigued after 60 min of task performance. However, the trajectories of individual classifier outputs showed that EEG signs of developing fatigue were present in all subjects after 15-30 minutes of task performance. The results show that EEG can track the development of mental fatigue over time with accurate updates on a time scale a short as 13 seconds. In addition, the results agree with the notion that growing mental fatigue produces a shift away from executive and attention networks to default mode and is accompanied by a shift in alpha frequency to the lower alpha band.

Variants of postural tachycardia syndrome (POTS) are associated with increased ["high-flow" POTS (HFP)], decreased ["low-flow" POTS (LFP)], and normal ["normal-flow" POTS (NFP)] blood flow measured in the lower extremities while subjects were in the supine position. We propose that postural tachycardia is related to thoracic hypovolemia during orthostasis but that the patterns of peripheral blood flow relate to different mechanisms for thoracic hypovolemia. We studied 37 POTS patients aged 14-21 yr: 14 LFP, 15 NFP, and 8 HFP patients and 12 healthy control subjects. Peripheral blood flow was measured in the supine position by venous occlusion strain-gauge plethysmography of the forearm and calf to subgroup patients. Using indocyanine green techniques, we showed decreased cardiac index (CI) and increased total peripheral resistance (TPR) in LFP, increased CI and decreased TPR in HFP, and unchanged CI and TPR in NFP while subjects were supine compared with control subjects. Blood volume tended to be decreased in LFP compared with control subjects. We used impedance plethysmography to assess regional blood volume redistribution during upright tilt. Thoracic blood volume decreased, whereas splanchnic, pelvic, and leg blood volumes increased, for all subjects during orthostasis but were markedly lower than control for all POTS groups. Splanchnic volume was increased in NFP and LFP. Pelvic blood volume was increased in HFP only. Calf volume was increased above control in HFP and LFP. The results support the hypothesis of (at least) three pathophysiologic variants of POTS distinguished by peripheral blood flow related to characteristic changes in regional circulations. The data demonstrate enhanced thoracic hypovolemia during upright tilt and confirm that POTS is related to inadequate cardiac venous return during orthostasis.

Previous investigations have allowed for stratification of patients with postural tachycardia syndrome (POTS) on the basis of peripheral blood flow. One such subset, comprising "normal-flow POTS" patients, is characterized by normal peripheral resistance and blood volume in the supine position but thoracic hypovolemia and splanchnic blood pooling in the upright position. We studied 32 consecutive 14- to 22-yr-old POTS patients comprising 13 with low-flow POTS, 14 with normal-flow POTS, and 5 with high-flow POTS and 12 comparably aged healthy volunteers. We measured changes in impedance plethysmographic (IPG) indexes of blood volume and blood flow within thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations in the supine posture and during incremental tilt to 20 degrees, 35 degrees, and 70 degrees. We validated IPG measures of thoracic and splanchnic blood flow against indocyanine green dye-dilution measurements. We validated IPG leg blood flow against venous occlusion plethysmography. Control subjects developed progressive vasoconstriction with incremental tilt. Splanchnic blood flow was increased in the supine position in normal-flow POTS, despite marked peripheral vasoconstriction, and did not change during incremental tilt, producing progressive splanchnic hypervolemia. Absolute hypovolemia was present in low-flow POTS, all supine flows and volumes were reduced, there was no vasoconstriction with tilt in all segments, and segmental volumes tended to increase uniformly throughout tilt. Lower body (pelvic and leg) flows were increased in high-flow POTS at all angles, with consequent lower body hypervolemia during tilt. Our main finding is selective and maintained orthostatic splanchnic vasodilation in normal-flow POTS, despite marked peripheral vasoconstriction in these same patients. Local splanchnic vasoregulatory factors may counteract vasoconstriction and venoconstriction in these patients. Lower body vasoconstriction in high-flow POTS was abnormal, and vasoconstriction in low-flow POTS was sustained at initially elevated supine levels.

Recent studies have indicated that plantar-based vibration may be an effective approach for the prevention and treatment of osteoporosis. We addressed the hypothesis of whether the plantar vibration operated by way of the skeletal muscle pump, resulting in enhanced blood and fluid flow to the lower body. We combined plantar stimulation with upright tilt table testing in 18 women aged 46-63 yr. We used strain-gauge plethysmography to measure calf blood flow, venous capacitance, and the microvascular filtration relation, as well as impedance plethysmography to examine changes in leg, splanchnic, and thoracic blood flow while supine at a 35 degrees upright tilt. A vibrating platform was placed on the footboard of a tilt table, and measurements were made at 0, 15, and 45 Hz with an amplitude of 0.2 g point to point, presented in random order. Impedance-measured supine blood flows were significantly (P = 0.05) increased in the calf (30%), pelvic (26%), and thoracic regions (20%) by plantar vibration at 45 Hz. Moreover, the 25-35% decreases in calf and pelvic blood flows associated with upright tilt were reversed by plantar vibration, and the decrease in thoracic blood flow was significantly attenuated. Strain-gauge measurements showed an attenuation of upright calf blood flow. In addition, the microvascular filtration relation was shifted with vibration, producing a pronounced increase in the threshold for edema, P(i), due to enhanced lymphatic flow. Supine values for P(i) increased from 24 +/- 2 mmHg at 0 Hz to 27 +/- 3 mmHg at 15 Hz, and finally to 31 +/- 2 mmHg at 45 Hz (P < 0.01). Upright values for P(i) increased from 25 +/- 3 mmHg at 0 Hz, to 28 +/- 4 mmHg at 15 Hz, and finally to 35 +/- 4 mmHg at 45 Hz. The results suggest that plantar vibration serves to significantly enhance peripheral and systemic blood flow, peripheral lymphatic flow, and venous drainage, which may account for the apparent ability of such stimuli to influence bone mass.

Postural tachycardia syndrome (POTS) is defined by orthostatic intolerance associated with abnormal upright tachycardia. Some patients have defective peripheral vasoconstriction and increased calf blood flow. Others have increased peripheral arterial resistance and decreased blood flow. In 14 POTS patients (13-19 yr) evenly subdivided among low-flow POTS (LFP) and high-flow POTS (HFP) we tested the hypothesis that myogenic, venoarteriolar, and reactive hyperemic responses are abnormal. We used venous occlusion plethysmography to measure calf venous pressure and blood flow in the supine position and when the calf was lowered by 40 cm to evoke myogenic and venoarteriolar responses and during venous hypertension by 40-mmHg occlusion to evoke the venoarteriolar response. We measured calf reactive hyperemia with plethysmography and cutaneous laser-Doppler flowmetry. Baseline blood flow in LFP was reduced compared with HFP and control subjects (0.8 +/- 0.2 vs. 4.4 +/- 0.5 and 2.7 +/- 0.4 ml.min-1.100 ml-1) but increased during leg lowering (1.2 +/- 0.5 ml.min-1. 100 ml-1) while decreasing in the others. Baseline peripheral arterial resistance was increased in LFP and decreased in HFP compared with control subjects (39 +/- 13 vs. 15 +/- 3 and 22 +/- 5 mmHg.ml-1. 100 ml. min) but decreased to 29 +/- 13 mmHg.ml-1.100 ml. min in LFP during venous hypertension. Resistance increased in the other groups. Maximum calf hyperemic flow and cutaneous flow were similar in all subjects. The duration of hyperemic blood flow was curtailed in LFP compared with either control or HFP subjects (plethysmographic time constant = 20 +/- 2 vs. 29 +/- 4 and 28 +/- 4 s; cutaneous time constant = 60 +/- 25 vs. 149 +/- 53 s in controls). Local blood flow regulation in low-flow POTS is impaired.

Increased blood pressure (BP) and heart rate during exercise characterizes the exercise pressor reflex. When evoked by static handgrip, mechanoreceptors and metaboreceptors produce regional changes in blood volume and blood flow, which are incompletely characterized in humans. We studied 16 healthy subjects aged 20-27 yr using segmental impedance plethysmography validated against dye dilution and venous occlusion plethysmography to noninvasively measure changes in regional blood volumes and blood flows. Static handgrip while in supine position was performed for 2 min without postexercise ischemia. Measurements of heart rate and BP variability and coherence analyses were used to examine baroreflex-mediated autonomic effects. During handgrip exercise, systolic BP increased from 120 +/- 10 to 148 +/- 14 mmHg, whereas heart rate increased from 60 +/- 8 to 82 +/- 12 beats/min. Heart rate variability decreased, whereas BP variability increased, and transfer function amplitude was reduced from 18 +/- 2 to 8 +/- 2 ms/mmHg at low frequencies of approximately 0.1 Hz. This was associated with marked reduction of coherence between BP and heart rate (from 0.76 +/- 0.10 to 0.26 +/- 0.05) indicative of uncoupling of heart rate regulation by the baroreflex. Cardiac output increased by approximately 18% with a 4.5% increase in central blood volume and an 8.5% increase in total peripheral resistance, suggesting increased cardiac preload and contractility. Splanchnic blood volume decreased reciprocally with smaller decreases in pelvic and leg volumes, increased splanchnic, pelvic and calf peripheral resistance, and evidence for splanchnic venoconstriction. We conclude that the exercise pressor reflex is associated with reduced baroreflex cardiovagal regulation and driven by increased cardiac output related to enhanced preload, cardiac contractility, and splanchnic blood mobilization.

Background-The mechanisms of simple faint remain elusive. We propose that postural fainting is related to excessive thoracic hypovolemia and splanchnic hypervolemia during orthostasis compared with healthy subjects. Methods and Results-We studied 34 patients 12 to 22 years old referred for multiple episodes of postural faint and 11 healthy subjects. Subjects were studied in the supine position and during upright tilt to 70°for 30 minutes and subgrouped into Sϩ, historical fainters who fainted during testing (nϭ24); SϪ, historical fainters who did not faint during testing (nϭ10); and control subjects. Supine venous occlusion plethysmography showed no differences between blood flows of the forearm and calf in Sϩ, SϪ, or control. Cardiac index, total peripheral resistance, and blood volume were not different. Using impedance plethysmography, we assessed blood redistribution during upright tilt. This demonstrated decreased thoracic blood volume and increased splanchnic, pelvic, and leg blood volumes for all subjects. However, thoracic blood volume was decreased in Sϩ compared with control volume, correlating well with the maximum upright heart rate. Splanchnic volume was decreased in the Sϩ and SϪ groups, correlating with the change in thoracic blood volume. Pelvic and leg volume changes were similar for all groups and uncorrelated to thoracic blood volume. Conclusions-Enhanced

Taneja I, Moran C, Medow MS, Glover JL, Montgomery LD, Stewart JM. Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume. Am J Physiol Heart Circ Physiol 292: H1420 -H1426, 2007. First published November 3, 2006; doi:10.1152/ajpheart.01096.2006.-Upright posture and lower body negative pressure (LBNP) both induce reductions in central blood volume. However, regional circulatory responses to postural changes and LBNP may differ. Therefore, we studied regional blood flow and blood volume changes in 10 healthy subjects undergoing graded lower-body negative pressure (Ϫ10 to Ϫ50 mmHg) and 8 subjects undergoing incremental head-up tilt (HUT; 20°, 40°, and 70°) on separate days. We continuously measured blood pressure (BP), heart rate, and regional blood volumes and blood flows in the thoracic, splanchnic, pelvic, and leg segments by impedance plethysmography and calculated regional arterial resistances. Neither LBNP nor HUT altered systolic BP, whereas pulse pressure decreased significantly. Blood flow decreased in all segments, whereas peripheral resistances uniformly and significantly increased with both HUT and LBNP. Thoracic volume decreased while pelvic and leg volumes increased with HUT and LBNP. However, splanchnic volume changes were directionally opposite with stepwise decreases in splanchnic volume with LBNP and stepwise increases in splanchnic volume during HUT. Splanchnic emptying in LBNP models regional vascular changes during hemorrhage. Splanchnic filling may limit the ability of the splanchnic bed to respond to thoracic hypovolemia during upright posture.vasoconstriction; splanchnic; blood volume; orthostatic stress; hemorrhage STANDING TRANSLOCATES BLOOD from the central thoracic circulation to the dependent regional circulations, producing ϳ20% reduction in cardiac output. The decrease in cardiac output comprises a 40% decrease in stroke volume associated with reflex tachycardia, increased peripheral resistance, and a generally maintained systolic blood pressure (SBP) with somewhat reduced pulse pressure (PP) while quietly standing (35). Changes in circulatory physiology during head-up tilt (HUT) are said to resemble the changes observed during hypovolemia caused by dehydration or hemorrhage (39, 41).Lower body negative pressure (LBNP; see Refs. 44 -46) has been used as a reversible simulation for hemorrhage (8,30). LBNP has also been used to model orthostatic stress (7) because many of the changes of neurovascular physiology resemble changes during standing or HUT (31). Thus, for example, both HUT and LBNP produce central hypovolemia and comparable unloading of the cardiopulmonary and arterial baroreceptors (9, 19). However, gravitational differences in regional vascular properties have also been noted (21, 24). Thus recent work by Cooke et al. (8) and el Bedawi and Hainsworth (12) has demonstrated that, although LBNP physiology most closely resembles the physiology of acute hemorrhage, it may be incomplete as a model for orthostatic stress, which must prod...