Christopher Minson is an expert in human cardiovascular health, thermoregulation, and exercise physiology. He is the Kenneth and Kenda Singer Professor of Human Physiology. Dr. Minson has received funding from numerous funding agencies including the NIH, American Heart Association, and the Department of Defense. His research is focused on how the blood vessels, heart, and nervous system regulate blood pressure and blood flow in humans. One line of research investigates how humans adapt to extreme heat. Current work is directed towards understanding how chronic heat therapy can be used to improve cardiovascular health of people with spinal cord injuries. A second line of research investigates how natural and synthetic forms of estrogen and progesterone impact cardiovascular health and blood pressure regulation in women. His teaching emphases are in the areas of cardiovascular and environmental physiology. He also serves as a consultant to professional athletes, sports teams, and industry partners.
Areas of Expertise (4)
Media Appearances (11)
Triple digits? Done properly, training in intense heat can have advantages
Cronkite News Arizona PBS
Before the 2008 Summer Olympics in Beijing, Oregon professor Christopher Minson trained Olympic hopeful and marathon runner Dathan Ritzenhein. Minson, a thermoregulation physicist, implemented heat acclimation training into Ritzenhein’s training regimen to help him adjust to the hot climate he would encounter in Beijing...
Can You Handle the Heat
Essex Local Magazines
Here are the magic numbers you need to know to maximize your heat acclimation:
101. The number of degrees Fahrenheit you need to elevate your core body temperature during training sessions, says Minson.
60. The number of minutes you want to have that elevated core temperature maintained during your heat training to make sure that you’re truly getting the heat acclimation benefits, says Minson.
5 to 10. The number of days you need to train in the heat. “To really heat acclimate the way we’re talking about, someone has to really go out and exercise in the heat for five to ten days, with pretty significant exposure at times,” Minson says. Just be sure to follow warm-weather precautions to keep from overly stressing your body...
Could a Cooling Wristband Be The Answer To Athletes Who Struggle with the Heat?
It’s impossible for us to exercise without having a rise in our core body temperature,” said Dr. Christopher Minson, a professor at the University of Oregon’s Department of Human Physiology who specializes in the body’s thermoregulatory system. “When we do exercise, a large part of the energy cost of exercise actually turns into heat. And that heat has to be dissipated. Some of that heat rise is very important for the exercise response, but when the body temperature gets too high, then it can actually impede performance. That impacts things such as sustainable power as well as certainly, perception of effort will be higher when someone’s hotter.”
Your Body in Extreme Heat
Whenever you exert yourself physically, blood flow to non-essential organs, like your gut, is reduced, says Christopher Minson, a professor of physiology at the University of Oregon. “This is only exacerbated in hot conditions,” he says, “when blood is being sent to your skin in order to cool.” (You can experience this phenomenon by feeling your belly after a hard effort—chances are it will be cool to the touch.)
The result is that your gut, which is normally rich with blood, is put under significant duress and its function declines. “It becomes harder to digest and absorb nutrients and the chances of nausea and general GI-distress rise dramatically.”
The Surprising Benefits of Training in the Heat
When performed safely, however, heat training can have extraordinary effects. This phenomena fascinates Chris Minson, a professor of human physiology at the University of Oregon, who studies heat acclimation responses in athletes. According to his research, heat training can expand blood plasma volume, but Minson says there also seem to be inexplicable changes to the heart’s left ventricle, which helps to increase oxygen delivery to the muscles. In addition, he says that athletes who train in warm temperatures generally get better at regulating heat by sweating earlier, as Salazar did, or developing a colder resting body temperature.
Heat Acclimation with Chris Minson PhD
Science of Ultra Podcast
Learn how to prepare for performance in the heat and how heat acclimation can actually improve your performance in moderate temperatures.
How Heat Kills
Hot weather alone is not dangerous, said Chris Minson, an environmental physiologist at the University of Oregon, Eugene. Instead, it's a combination of hot temperatures, high humidity, and often preexisting health conditions that can push a person's core body temperature to reach the danger zone of 104 F. At that point, the nervous system goes haywire, the heart experiences excessive stress, and organ systems begin to fail...
Dear Science: Why Am I Always Cold Indoors?
Washington Post online
Even the time of year can change the temperature at which you feel cold. Christopher Minson, an expert in human thermo-regulation, pointed out that the body makes a number of physiological adjustments in response to long periods of heat. The proportion of plasma (liquid) in our blood gets boosted, we sweat sooner and in larger quantities, and the number of heat-shock proteins — which manage the body's response to stressful conditions — increases. It takes time to scale back this "heat acclimation" at the end of the summer; that's why a 60-degree day in springtime seems gloriously pleasant, while the same temperature in mid-September will send you running for a sweater.
D.C.’s Humidity Can Break or Build You Up
Christopher Minson, a physiologist at the University of Oregon and Lorenzo’s graduate school advisor, is currently studying overdressing, the non-D.C. man’s humidity. By wearing additional layers, you block the evaporative cooling effect. Many athletes use this technique to prep for hot weather races. (Maegan Krifchin, of Silver Spring, did this ahead of her seventh place finish in this year’s steamy Olympic Trials marathon.)...
How to Get Your Body Used to Working Out in Hot Weather
Sports Illustrated online
Dr. Michael Joyner: Chris, can you briefly summarize the 140 character insights you shared with Steve on Twitter about how to get ready for a hot Boston with only a week to go?
Dr. Chris Minson: One of Steve’s concerns was about the wind, with an expected tailwind of about 10 mph. At his planned pace of 2:35, he was concerned there would be little to no cooling benefit on a day that was warmer than where he had been training in Chicago. So I suggested that a couple easy runs in a hot room over the few days before the race could help. Steve needed to keep it easy; get hot and watch his hydration status. I also suggested that overdressing might help and that he consider adding one more layer to get body temp up. The other important point was in terms of fluid replacement: in the short run leading up to a race, don’t change from what you’ve been doing as it’s too risky for GI problems. Steve subsequently reported that very few runners seemed to be acclimated well to the heat, and that the pack he was running with diminished quickly after the first 8-12 miles.
How Does Aging Affect Athletic Performance?
I remember the moment a few years ago while watching TV when I realized that if I were riding in the Tour de France, at age 42 I’d be the oldest person in the race. It hit me that my dream of racing in cycling’s biggest event was over…it was not going to happen.
Not that I’d been competing, let alone training seriously, on the bike for a number of years.
Or that not even in my “prime” years for competitive cycling would I have been good enough. It’s just that now I had an excuse…. I was too old, too far past my prime years...
PURPOSE: To investigate whether a five-day cycling training block in the heat (35°C) in Australian rules footballers was superior to exercising at the same relative intensity in cool conditions (15°C) for improving intermittent running performance in a cool environment (
Cyclooxygenase (COX) contributes to the regulation of cutaneous vasodilatation and sweating; however, the mechanism(s) underpinning this response remain unresolved. We hypothesized that prostacyclin (a COX-derived product) may directly mediate cutaneous vasodilatation and sweating through nitric oxide synthase (NOS) and calcium-activated potassium (KCa) channels in young adults. However, these responses would be diminished in older adults because ageing attenuates COX-dependent cutaneous vasodilatation and sweating. In young (25 ± 4 years) and older (60 ± 6 years) males (nine per group), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites: (i) control; (ii) 10 mm NG -nitro-l-arginine (l-NNA), a non-specific NOS inhibitor; (iii) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blocker; and (iv) 10 mm l-NNA + 50 mm TEA. All four sites were coadministered with prostacyclin in an incremental manner (0.04, 0.4, 4, 40 and 400 μm each for 25 min). Prostacyclin-induced increases in CVC were similar between groups (all concentrations, P > 0.05). l-NNA and TEA, as well as their combination, lowered CVC in young males at all prostacyclin concentrations (P ≤ 0.05), with the exception of l-NNA at 0.04 μm (P > 0.05). In older males, CVC during prostacyclin administration was not influenced by l-NNA (all concentrations), TEA (4-400 μm) or their combination (400 μm) (P > 0.05). No effect on sweat rate was observed in either group (all concentrations, P > 0.05). We conclude that, although prostacyclin does not mediate sweating, it modulates cutaneous vasodilatation to a similar extent in young and older males. Furthermore, although NOS and KCa channels contribute to the prostacyclin-induced cutaneous vasodilatation in young males, these contributions are diminished in older males.
Ischemia-reperfusion (I/R) injury is a primary cause of poor outcomes following ischemic cardiovascular events. We tested whether acute hot water immersion protects against forearm vascular I/R. Ten (5 male, 5 female) young (23 ± 2 yr), healthy subjects participated in two trials in random order 7-21 days apart, involving: 1) 60 min of seated rest (control), or 2) 60 min of immersion in 40.5°C water (peak rectal temperature: 38.9 ± 0.2°C). I/R was achieved 70 min following each intervention by inflating an upper arm cuff to 250 mmHg for 20 min followed by 20 min of reperfusion. Brachial artery flow-mediated dilation (FMD) and forearm postocclusive reactive hyperemia (RH) were measured as markers of macrovascular and microvascular function at three time points: 1) preintervention, 2) 60 min postintervention, and 3) post-I/R. Neither time control nor hot water immersion alone affected FMD (both, P > 0.99). I/R reduced FMD from 7.4 ± 0.7 to 5.4 ± 0.6% (P = 0.03), and this reduction was prevented following hot water immersion (7.0 ± 0.7 to 7.7 ± 1.0%; P > 0.99). I/R also impaired RH (peak vascular conductance: 2.6 ± 0.5 to 2.0 ± 0.4 ml·min-1·mmHg-1, P = 0.003), resulting in a reduced shear stimulus (SRAUC·10-3: 22.5 ± 2.4 to 16.9 ± 2.4, P = 0.04). The post-I/R reduction in peak RH was prevented by hot water immersion (2.5 ± 0.4 to 2.3 ± 0.4 ml·min-1·mmHg-1; P = 0.33). We observed a decline in brachial artery dilator function post-I/R, which may be (partly) related to damage incurred downstream in the microvasculature, as indicated by impaired RH and shear stimulus. Hot water immersion was protective against reductions in FMD and RH post-I/R, suggesting heat stress induces vascular changes consistent with reducing I/R injury following ischemic events.
The majority of cardiovascular diseases are characterized by disorders of the arteries, predominantly caused by endothelial dysfunction and arterial stiffening. Intermittent hot water immersion ('heat therapy') results in elevations in core temperature and changes in cardiovascular haemodynamics, such as cardiac output and vascular shear stress, that are similar to exercise, and thus may provide an alternative means of improving health which could be utilized by patients with low exercise tolerance and/or capabilities. We sought to comprehensively assess the effects of 8 weeks of heat therapy on biomarkers of vascular function in young, sedentary subjects. Twenty young, sedentary subjects were assigned to participate in 8 weeks (4-5 times per week) of heat therapy (n = 10; immersion in a 40.5°C bath sufficient to maintain rectal temperature ≥ 38.5°C for 60 min per session) or thermoneutral water immersion (n = 10; sham). Eight weeks of heat therapy increased flow-mediated dilatation from 5.6 ± 0.3 to 10.9 ± 1.0% (P < 0.01) and superficial femoral dynamic arterial compliance from 0.06 ± 0.01 to 0.09 ±0.01 mm(2) mmHg(-1) (P = 0.03), and reduced (i.e. improved) aortic pulse wave velocity from 7.1 ± 0.3 to 6.1 ± 0.3 m s(-1) (P = 0.03), carotid intima media thickness from 0.43 ± 0.01 to 0.37 ± 0.01 mm (P < 0.001), and mean arterial blood pressure from 83 ± 1 to 78 ± 2 mmHg (P = 0.02). No changes were observed in the sham group or for carotid arterial compliance, superficial femoral intima media thickness or endothelium-independent dilatation. Heat therapy improved endothelium-dependent dilatation, arterial stiffness, intima media thickness and blood pressure, indicating improved cardiovascular health. These data suggest heat therapy may provide a simple and effective tool for improving cardiovascular health in various populations.
Nitric oxide (NO) increases cutaneous blood flow; however, the underpinning mechanism(s) remains to be elucidated. We hypothesized that the cutaneous blood flow response during intradermal administration of sodium nitroprusside (SNP, a NO donor) is regulated by calcium-activated potassium (KCa) channels and cyclooxygenase (COX) in young adults. We also hypothesized that these contributions are diminished in older adults given that aging can downregulate KCa channels and reduce COX-derived vasodilator prostanoids. In 10 young (23 ± 5 yr) and 10 older (54 ± 4 yr) adults, cutaneous vascular conductance (CVC) was measured at four forearm skin sites infused with 1) Ringer (Control), 2) 50 mM tetraethylammonium (TEA), a nonspecific KCa channel blocker, 3) 10 mM ketorolac, a nonspecific COX inhibitor, or 4) 50 mM TEA + 10 mM ketorolac via intradermal microdialysis. All skin sites were coinfused with incremental doses of SNP (0.005, 0.05, 0.5, 5, and 50 mM each for 25 min). During SNP administration, CVC was similar at the ketorolac site (0.005-50 mM, all P > 0.05) relative to Control, but lower at the TEA and TEA + ketorolac sites (0.005-0.05 mM, all P < 0.05) in young adults. In older adults, ketorolac increased CVC relative to Control during 0.005-0.05 mM SNP administration (all P < 0.05), but this increase was not observed when TEA was coadministered (all P > 0.05). Furthermore, TEA alone did not modulate CVC during any concentration of SNP administration in older adults (all P > 0.05). We show that during low-dose NO administration (e.g., 0.005-0.05 mM), KCa channels contribute to cutaneous blood flow regulation in young adults; however, in older adults, COX inhibition increases cutaneous blood flow through a KCa channel-dependent mechanism.