Describe and understand a standard heat acclimatisation procedure in humans
In heat acclimatisation procedures, a subject is placed in a hot room for a certain number of hours each day for a certain number of days in a row. Fun. (Not.)
Describe and understand what physiological changes occurs during the process of heat acclimatisation in humans
In the process of heat acclimatisation, sweat loss increases and contains fewer electrolytes (like sodium). This may be due to the effect of aldosterone on sodium reabsorption. Plasma volume also increases. As someone acclimatises to heat, their heart rate and rectal temperature in the hot environment decrease.
Describe and understand how heat flow is affected by insulation and temperature gradient
Describe and understand the inverse relationship between insulation and thermal conductance
Heat Flow = Temperature Gradient / Insulation
This can also be rearranged to give an equation in terms of conductance (which is the inverse of insulation):
Heat Flow = Temperature Gradient * Conductance
Describe and understand the various components of the heat balance diagram
There are several different curves on the heat balance diagram:
- Deep body temperature: Stays relatively constant at a range of environmental temperatures. Decreases if temperature is too low and increases if temperature is too high.
- Non-evaporative heat loss: Heat loss due to conduction, convection and radiation. Depends on the temperature gradient (if insulation is constant), so heat loss decreases as temperature increases. The slope of the line is not constant- it flattens out in the temperature range between maximum vasoconstriction and maximum vasodilation, before becoming steep again. (Maybe I should draw a diagram, but I really can't be bothered.)
- Heat production: Prior to the point of maximum vasoconstriction, heat production increases with decreasing temperature. After the point of maximum vasoconstriction, the curve flattens out as you are at your basal metabolism rate and can't decrease your heat production further.
- Evaporative heat loss: Heat loss due to sweating and some other factors, such as breathing. Stays relatively flat for a while. Increases slightly between the points of maximum vasoconstriction and maximum vasodilation, before increasing more sharply.
Now for some more terminology! The lower critical temperature is the temperature at which your arteries are maximally vasoconstricted. The upper critical temperature is the temperature at which your arteries are maximally dilated. The thermoneutral zone, also known as the Zone of Vasomotor Adjustment, is located between these two points.
Describe and understand the underlying mechanistic basis of heat stroke
"Heat stroke" is defined as a core body temperature of more than 41°C, but I'm not really sure about the mechanistic basis. I'm assuming that the main idea is that, when the amount of heat you are gaining exceeds the amount you are losing, your body temperature heats up over time until it gets to the point that your body just can't handle it any more (enzymes denature etc.)?
Describe and understand the limits to human heat tolerance
Describe and understand the prescriptive zone, how it is measured and what it means
The "prescriptive zone" is the point at which you can no longer thermoregulate. It is measured by putting subjects in a room with gradually increasing temperature or humidity and then finding the point at which the subjects' temperatures begin to increase. Several factors can influence the prescriptive zone- heat acclimatisation can increase the prescriptive zone, as can wind.
Understand the terms ‘torpor’ and ‘hibernation’
'Torpor' is a state in which heat production and metabolic rate drop. Hibernation is similar to torpor, but occurs for a longer period of time. Torpor is mainly found in small animals, some of which have to produce their own "antifreeze" to prevent their cells from freezing at sub-zero temperatures.
Describe and understand the relationship between surface area and body mass for animals of different sizes
As animals get larger, mass increases faster than surface area. Therefore, smaller animals will tend to have a relatively high surface area, and larger animals will tend to have a relatively low surface area. Since heat loss is proportional to surface area, smaller animals are more likely to struggle in the cold (as they are losing a lot of heat), and larger animals are more likely to struggle in the heat.
Describe the tissue known as brown adipose tissue and its role in non-shivering thermogenesis
Babies are unable to shiver, but they are able to produce heat via brown adipose tissue (a.k.a. "brown fat"). Brown adipose tissue has a lot of mitochondria that are capable of producing heat.
Describe and understand the role of UCP1 in non-shivering thermogenesis
UCP1 (uncoupling protein), also called "thermogenin," is found on the inner mitochondrial membrane in brown fat. UCP1 is essentially a H+ channel. Unlike ATP synthase, which is also an H+ channel, UCP1 does not produce ATP. Instead, UCP1 produces heat.
It was originally thought that adults don't have brown fat. This has been found to be untrue. Some adults do have brown fat, mainly in the supraclavicular and neck regions.
Describe and understand the mechanistic basis of fever, including the role of endogenous pyrogens, and how they operate to alter the thermoregulatory set-point
Fever is usually stimulated by some kind of invading microorganism. Various toxic products of microorganisms, such as lipopolysaccharide, are called exogenous pyrogens as they can stimulate fever. Exogenous pyrogens stimulate phagocytes to make and secrete endogenous pyrogens, such as IL-1β, IL-6, IFNβ, IFNγ and TFNα. It has been suggested that endogenous pyrogens cross the blood-brain barrier at the organism vasculosum of the lamina terminalis (OVLT), which is kind of like a "leakier" part of the blood-brain barrier.
After passing through the OVLT, endogenous pyrogens stimulate phospholipase A2, which cleaves phospholipids to form arachidonic acid. Arachidonic acid is then converted into prostaglandins via cyclooxygenase. (I've described these pathways in more detail here.) One of the more important prostaglandins in fever signalling is prostaglandin E2. Prostaglandin E2 changes the firing rate of cold-sensitive neurons, essentially tricking your body into thinking that it's cold so that thermoregulatory processes can kick in and raise your body temperature.
Interestingly enough, injecting exogenous pyrogen, endogenous pyrogen and prostaglandin E into the hypothalamus can all cause fever. However, the time it takes to cause fever is different. Exogenous pyrogen has the longest latency (i.e. delay before onset of fever), followed by endogenous pyrogen and then prostaglandin E2. In fact, prostaglandin E2 causes fever immediately after injection into the hypothalamus.
What's the point of fever? It's been suggested that fever might play a role in fighting infection. Yay...!
Describe and understand the mechanistic basis for some anti-pyretics
Most anti-pyretics work by blocking either cyclooxygenase or phospholipase A2. Paracetamol and NSAIDs (e.g. ibuprofen) block cyclooxygenase. Steroidal anti-inflammatory drugs (I assume these are just corticosteroids) block phospholipase A2.
Describe and understand how the various components of the heat balance equation change from rest to exercise
If you can't remember from my last post, the heat balance equation is as follows:
S = M ± Cond ± Conv ± Rad ± E - W
During exercise, our metabolic rate (M) increases. Therefore, to stop our temperature from increasing too much, we need to lose heat in some other way (e.g. increasing our evaporative heat loss (E) by sweating).
Describe and understand some of the arguments that the thermoregulatory relies on negative feedback regulation during exercise
During exercise, we make more heat as our metabolic rate increases. In early stages of exercise, our heat loss mechanisms (vasodilation and sweating) are still operating at their resting levels, which is insufficient for the increased metabolism during exercise. Therefore, body temperature rises, stimulating heat loss until heat loss is equal to heat gain. In other words, it's a negative feedback loop. Yay!
Describe and understand the effect of increased thermoregulatory demands on exercise performance
Pretty much all we got up to here is that increased muscle temperature does seem to increase performance, but if muscle temperature increases, body temperature also increases, which isn't necessarily good. There's also a battle between the muscles and the skin- the muscles want blood so they can do their job, and the skin wants blood so it can get rid of the excess heat. Overall, heat tends to reduce exercise performance. I think that's all we got up to in this lecture, so I'll end this post here.
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