Purpose: This study aimed to expand our knowledge of the underlying mechanisms of orthostatic tolerance. First, cerebral perfusion was compared with reductions in orthostatic tolerance between normal thermic and heated conditions. The researchers' hypothesized that subjects with the greatest reduction in orthostatic tolerance will experience the largest drop in cerebral blood flow. Additionally, ANG II was measured in order to identify if during passive heating, the elevation in plasma ANG II is negatively correlated with heat-stress induced reductions in orthostatic tolerance. Lastly, orthostatic tolerance changes during the simulated hemorrhage between heat stress and normal thermic conditions will be compared to fitness level, measured by VO2 max. Results and Conclusion: Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P [less than] 0.001); however, the magnitude of reduction did not differ between groups (P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal PCO2 were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P [less than] 0.05 for all). In opposition to the hypotheses, the large differences in tolerance to a simulated hemorrhage during normothermic and heat stress conditions are not solely related to the degree of heat stress-induced reduction in cerebral perfusion. Also, an individual's level of cardiorespiratory capacity (fitness) and/or the degree of heat stress-induced increase in plasma ANG II does not reliably predict the level of reduction in tolerance to a simulated hemorrhage challenge when heat stressed. / text

These studies investigated 1) mechanisms underlying the well-established reduction in orthostatic tolerance (OT) that occurs in humans during heat stress (HS) relative to normothermia (NT) with particular focus on determining factors contributing to the high degree of inter-individual variability in this phenomenon; and 2) influence of obesity on OT, and mechanisms underlying reduced OT, should it exist. In Study #1, OT was assessed during lower body negative pressure (LBNP), and quantified with a cumulative stress index (CSI). Differences in CSI (CSIdiff) between thermal conditions were used to categorize individuals most (LargeDiff) and least (SmallDiff) affected by HS (P<0.001). Cerebral perfusion [indexed as middle cerebral artery blood velocity (MCA Vm̳̳e̳a̳n̳)] was reduced during HS compared to NT (P<0.001); however, the magnitude of reduction did not differ between groups (P=0.51). In the initial stage of LBNP during HS (LBNP20), MCA Vm̳̳e̳a̳n̳ and end-tidal CO₂ (PETC̳O̳₂) were reduced, and heart rate (HR) was higher in the LargeDiff group compared to SmallDiff group (all P<0.05); yet, mean arterial pressure was similar (P=0.23) suggesting impaired mechanisms regulating MCA Vm̳̳e̳a̳n̳ may affect OT. In Study #2, mechanisms of cerebrovascular control were compared in LargeDiff and SmallDiff individuals. Although estimates of cerebral autoregulation (CA) and cerebrovascular reactivity to CO₂ were improved and reduced respectively, during HS compared to NT (all P<0.05), no relationship existed between CA or cerebral reactivity to hypocapnia and CSIdiff (all P>0.05). In Study #3, OT was lower in obese compared to non-obese individuals (P<0.01), and BMI was negatively correlated with CSI (R = -0.47; P < 0.01). HR was elevated at rest and in every level of LBNP (all P<0.05) in obese; yet, peak HR during LBNP was similar between groups (P=0.90). MCA Vm̳̳e̳a̳n̳ and cerebral vascular conductance were similar at rest and during LBNP (both P>0.05), and CA was similar between groups (P>0.05). In summary, a high HR prior to-, and a high HR and reduced MCA Vm̳̳e̳a̳n̳ at the onset of an orthostatic challenge result in reduced OT during HS in healthy individuals; however, reduced OT in obese is related to a higher %peak HR at rest. / text

Corticospinal and intracortical excitability are excitability measures of the central nervous system responsible for motor generation, and are studied for their contribution to fine motor skill execution and learning. Since the need for proper execution of fine motor skills is ever-present and necessary for everyday life, identification of physiological pathways that may disrupt or enhance corticospinal and intracortical excitability is an important research topic. This thesis investigates the effects of baroreceptor unloading on corticospinal and intracortical excitability during various motor tasks. Baroreceptor unloading is a physiological response to common hemodynamic stress (e.g. hypovolemia and orthostasis). The motor tasks investigated are complete muscular relaxation, individual isometric low-force contraction of a muscle, and an isometric co-contraction of a muscle in a joint-stabilizing task. The effects of baroreceptor unloading on corticospinal and intracortical excitability appear to be very task specific. The results are discussed in view of available pharmacological and physiological research, and potential neural pathways for the observed effects are suggested. The overall conclusion is that baroreceptor unloading increases corticospinal excitability and decreases intracortical inhibition in a resting muscle, does not produce any observable effects during individual muscle activity, and decreases corticospinal excitability during joint-stabilizing co-contraction.

Magnetic Resonance Imaging (MRI) was used to determine changes in the size of the Inferior Vena Cava (IVC) as a result of blood pooling induced by lower body negative pressure (LBNP). Images of the IVC of supine human subjects (10 males, 10 females) were obtained under four conditions: 1) steady-state 0 mmHg LBNP, 2) steady-state –35 mmHg LBNP, 3) ramping from 0 to –35 mmHg LBNP, 4) ramping from –35 to 0 mmHg LBNP. Volumes for a given IVC segment were obtained under the first two conditions during both end inspiration and end expiration breath-holds. Inferior Vena Cava widths were measured under all four conditions at the levels of portal entry and portal exit. The IVC volume for men and women combined decreased 41% due to LBNP (p andlt; 1.02 x 10-9). The IVC was 64.4% wider at portal exit than at portal entry in men (p andlt; 0.0003). Lower Body Negative Pressure induced a decrease in men's vena cava width up to 46% at portal exit and up to 62% at portal entry. Supported by NASA EPSCoR WKU 522611 and NIH GCRC MO1 RR262.

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