Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

This study sought to determine the independent influence of hypoxia on thermoregulatory responses to exercise in compensable and uncompensable hot conditions. Eight participants completed three experimental trials of cycling in either normoxia (21% O2) or hypoxia (13% O2) in order to manipulate relative exercise intensity (%VO2peak), since VO2peak was reduced by ~30% in hypoxia. When trials were matched for %VO2peak, changes in core temperature and local sweat rates (LSR) were significantly lower in the hypoxic trial as a result of a lower rate of metabolic heat production (Hprod) in order to maintain a similar %VO2peak compared to normoxia. However, when Hprod was fixed between normoxic and hypoxic trials the systematic differences in core temperature and LSR were eliminated. Conversely, at a fixed Hprod skin blood flow (SkBF) was greater in hypoxia compared to normoxia by ~40%. Despite improvements in SkBF, the potential for maximum heat loss was unaffected during an incremental humidity ramp protocol, resulting in no difference between normoxia and hypoxia in the critical ambient vapour pressures at which core temperature inflected upwards. These data further demonstrate, using a within-subjects design, that metabolic heat production, irrespective of large differences in %VO2peak, determines thermoregulatory responses during exercise. Furthermore, this study suggests that the influence of large differences in skin blood flow on heat dissipation may be lesser than previously thought.

Studies that have investigated the effects of L-arginine supplementation on blood flow to the uterus have not determined the optimal time of supplementation. No research has been conducted on nitrite concentration in the placenta and blood of mares supplemented with L-arginine. L-arginine is a precursor of NO and therefore, should increase nitrite production both in blood as well as in expelled placenta. Presence of nitrites would also be indicative of increased angiogenesis. No studies have addressed placental efficiency in mares supplemented L-arginine. Placental efficiency is vital for production of a healthy foal. Therefore, to address these short-comings the objectives of this study were to supplement pregnant mares with L-arginine on effects of supplementation at differing time points on blood flow to the uterus, nitrite concentration in blood and placenta, and placental efficiency.

Melatonin is a strong antioxidant that has previously been observed to increase uteroplacental blood flow and increase postnatal calf growth when supplemented during gestation. The objective of the current study was to examine the effects of melatonin implants on uterine blood flow and subsequent offspring growth. Commercial beef heifers and cows were artificially inseminated and assigned to one of two treatment groups supplemented with (MEL) or without (CON) melatonin from days 180 to 240 of gestation. Total uterine artery blood flow was increased in MEL- versus CON-treated cattle. Fetal and birth weight were not different between treatments. However, at castration, body weight was increased in calves from MEL-treated dams compared with CON-treated dams. Further research on placental vascularization and the mechanism in which melatonin impacts angiogenic factors is necessary to understand the relationship between melatonin and compensatory growth that occurs in postnatal offspring.

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This work represents the next step in the ongoing development of a system to noninvasively estimate blood perfusion using thermal methods. A combination thermocouple/thermopile sensor records heat flux and temperature measurements on the tissue of interest (in this case skin) for a given period of time. These data, in combination with other experimental parameters, are read into a computer program that compares them to a biothermal finite difference model of the system. The program uses an iterative process incorporating Gauss Minimization to adjust parameters in the biothermal model until the predicted system behavior satisfactorily approximates the real world data. The result is an estimation of blood perfusion in the tissue being measured, as well as an estimate of the thermal contact resistance between the probe and tissue. The system is tested on human forearms, canine legs during laparoscopic spay surgery, and on a canine medial saphenous fasciocutaneous free tissue flap model. Experimental measurements, especially those performed on the tissue flap model, show distinct correlation between blood perfusion and bioprobe output. This research demonstrates the accuracy of the biothermal model and the parameter estimation technique, as well as the usability of the system in a clinical setting. / Master of Science

The purpose of the study was to investigate the effects of hypoxia responses during moderate- and severe-intensity exercise performed to exhaustion. Nine healthy university students, five men, and four women (mean ± SD, age, 23 ± 1 y; height 167 ± 8 cm; weight 73 ± 7 kg) performed a cycle ergometer test in normoxia and hypoxia conditions. Cardiorespiratory, metabolic, and perceptual responses were measured during moderate-intensity and during severe-intensity exercise. During moderate-intensity exercise, hypoxia exaggerates the cardiorespiratory and ventilatory responses and delays the attainment of the steady state VO2 kinetics. However, during severe-intensity exercise, compensatory responses were not adequate, oxygen demand was slightly increased and VO2 max was reduced in hypoxia affecting the overall performance. Therefore, the greater reliance on the anaerobic pathways could have a serious implication on the performance of the exercise over a wide range of intensities.

Master of Science / Department of Kinesiology / Thomas Barstow / Previously in our laboratory, capillary blood flow (QCAP) kinetics were found to be significantly slower than femoral artery (QFA) kinetics following the onset of knee extension exercise. If the increase in QCAP does not follow a similar time course to QFA, blood must be flowing into the leg but not to the working muscle. One possible explanation for this discrepancy is that blood flow also increases to the nonworking lower leg muscles. Purpose: To determine if cuffing below the knee alters the kinetics of QFA and QCAP during knee extension exercise, and provide insight into the potential mechanisms controlling the rapid increase in QFA. Methods: Subjects performed a ramp max test to determine the work rate at which gas exchange threshold (GET) occurred. At least four constant work rate trials in each condition were conducted at work rates eliciting ~80% GET. Trials were performed with and without below knee occlusion. Pulmonary gas exchange, near-infrared spectroscopy, QFA and mean arterial pressure (MAP) measurements were taken. Muscle oxygen uptake (VO2m) and deoxy[hemoglobin + myoglobin] were used to estimate QCAP. Conductance (C) was calculated (QFA/MAP) and the percent change from baseline at 60s into exercise was calculated to indicate a time course of change. Results: There was no significant difference between the uncuffed and cuffed conditions (P>0.05). The mean response times (MRT) of QFA were 18.7 ± 14.2s (uncuffed) and 24.6 ± 14.9s (cuffed). QCAP MRTs were 51.8 ± 23.4s (uncuffed) and 56.7 ± 23.2s (cuffed), which were not significantly different from the time constants (τ) of VO2m (39.7 ± 23.2s (uncuffed) and 46.3 ± 24.1s (cuffed)). However, the MRT of QFA was significantly faster (P<0.05) than the MRT of QCAP and τVO2m. τVO2m and MRT QCAP were significantly correlated. The QFA and C percent increase from baseline at 60s were significantly different from MAP but not from each other. Conclusion: Cuffing below the knee did not significantly change the kinetics of QFA, QCAP or VO2m. Estimated QCAP kinetics tracked VO2m following exercise onset, while changes in QFA appeared to be primarily driven by an increase in C, not an increase in MAP.