Tag: Vienna Brunt

Presenter: Kaitlin Livingston

Mentors: Christopher Minson and Vienna Brunt, Human Physiology

Poster: 44

Major: Human Physiology 

Repeated bouts of exercise in the heat are known to decrease resting body core temperature (Tc), mean arterial pressure (MAP) and resting heart rate (HR). Although exercise in the heat produces these cardiovascular changes, it is currently unknown whether passive chronic heating provides the same benefits. Our research sought to examine the effects of passive chronic heating on resting Tc, MAP, and HR. Five sedentary, college-aged subjects (4 females, 1 male) were assigned to an 8-week hot water immersion program (4-5 sessions/week). Subjects were submerged to the clavicle in 40.5°C water until a rectal temperature (Tre) of 38.5°C was reached. Subjects maintained a Tre between 38.5-39.0°C during an hour of partial immersion. HR and Tre were measured with a HR monitor and rectal thermistor both at rest and at 5-minute intervals during the heat stress. MAP was measured on another day with brachial auscultation after ≥20 minutes of supine rest. Both resting MAP (81±1 vs. 76±2 mmHg, p=0.02) and resting Tre (37.4±0.5 vs. 36.8±0.4°C, p=0.03) decreased after 8 weeks of passive heat stress with no change in resting HR (63±5 vs. 63±6 beats/min, p=0.26). Chronic passive heat stress reduces resting MAP and Tre similarly to what is observed with exercise heat in the heat. This suggests that chronic passive heat stress could be used to benefit cardiovascular health similarly to exercise in the heat.

Presenter: Andrew Jeckell

Mentors: Christopher Minson and Vienna Brunt, Human Physiology

Poster: 31

Major: Post-baccalaureate 

Reactive hyperemia is a transient increase in blood flow that occurs following a period of ischemia (e.g. arterial occlusion) and is indicative of microvascular health. Regular exercise is a critical preventive measure in maintaining reactive hyperemia; however, consistent exercise is difficult or impossible for some people. Recent evidence suggests chronic passive heat therapy (CHT) may result in improvements to cardiovascular health similar to exercise. To examine the effects of 8 weeks of CHT on forearm post-occlusive reactive hyperemia, six healthy university students (21 ± 1 years) underwent hot water immersion 4-5 times per week to maintained rectal temperature of 38.5°C
for 1 hour per session. Before and after 8 weeks of CHT, brachial artery blood flow was measured via Doppler ultrasonography for 3 minutes following a 5-minute forearm arterial occlusion. Data presented as mean ± SE vascular conductance (VC, blood flow divided by mean arterial pressure). In preliminary subjects, change in peak VC from baseline, indicating structural microvascular changes, increased following CHT from 1.77 ± 0.24 to 2.26 ± 0.20 ml/ min/mmHg (p = 0.09). Area-under-the-curve of the hyperemic response, indicating functional changes, increased from 59.7 ± 9.0 to 111.9 ± 13.0 sec.ml/min/mmHg (p = 0.11). CHT appears to produce structural and functional microvasculature changes comparable to that of exercise, and could potentially serve as an alternative method for improving cardiovascular health.

Presenter: Taylor Eymann

Mentors: Christopher Minson and Vienna Brunt, Human Physiology

Poster: 21

Major: Human Physiology

Vascular dysfunction, often caused by deficient nitric oxide (NO) production, is present in the majority of cardiovascular disease and is first detectible in the microcirculation. Heat stress can increase NO production via
heat shock protein expression. Therefore chronic passive heat therapy (CHT) may improve microvascular health
and lower cardiovascular risk. The cutaneous circulation is easily accessible and represents overall microvascular health. PURPOSE: To observe the effects of 8wks of CHT on cutaneous NO-dependent dilation. METHODS: Seven healthy, sedentary subjects were immersed in either 40.5°C (N=5; CHT) or 36.5°C (N=2; sham group) water for 90min 4-5 times per week for 8 weeks. Before and after the 8wks, two intradermal microdialysis fibers were inserted into the forearm and infused with lactated Ringer’s solution (control) and a nitric oxide synthase competitive inhibitor (L-NNA), to inhibit NO synthase. Increased skin blood flow responding to local skin heating to 39°C, which is a test of microvascular health, was measured at each site using laser-Doppler flowmetry. NO-dependent dilation, calculated as the difference between control and L-NNA sites, was expressed as percent maximal cutaneous vascular conductance (%CVCmax; flow/mean arterial pressure). RESULTS: CHT increased NO-dependent dilation from 27±4 to 36±5%CVCmax (p<0.05). No improvement was observed in sham subjects. CONCLUSION: Our findings suggest heat therapy increases NO production and vasodilation in the human microcirculation. Continued exposure to passive heat may lower cardiovascular risk.