Body Heat
According to the U.S. Department of Energy, in 1997, the
The laws of physics form the foundation for all of science.
Just as
The Surface Law also has an impact on the ultimate variable: longevity. Mice and other small rodents live on the order of a few years; dogs about 10 years; elephants on the order of decades. The high surface-to-volume ratio of small mammals leads to a fast-paced life and, inevitably, to early burnout, while, elephants lumber along at a much slower pace. The Etruscan shrew, at three grams one of the smallest mammals (and at 12-18 months one of the shortest lived), possesses a heart that races along at over 1,000 beats each minute, compared to 600 for a mouse, 150 for a dog, and only 30 for an elephant. Interestingly, the reciprocal relation between longevity and pace of life balances out so that the heart of threws, mice, dogs, and elephants all beat approximately 800 million times during the very different lives of these species. (Humans reach that number of heartbeat on only twenty-five years, but our allotment of beats, like the size of our brains, is relatively greater for our body size than those of our mammalian cousins.) (p. 38)
Why do you and I regulate our body temperature at approximately 37ēC (98.6ēF) and not 34ēC or 40ēC? It is no coincidence that this is the body temperature of our parents and grandparents; thus it is quite obvious that our body temperature is an inherited characteristic. But what is the mechanism of this inheritance? It could be that there are genes that govern the development of body temperature in our species; this is what we usually think of when we think of inherited characteristics.
But is it possible that our species-typical body temperature of approximately 37ēC derives from the fact that our mothers not only share their genes with us but also provide a secure and comfortable developmental environment whose temperature is regulated at 37ēC throughout a 400,000 minutes of gestation? (p. 82)
I believe 37ē is the result of natural selection. Too high a temperature, the energy cost is too high. Too low temperature, the movement will be too slow. We have to prove it with precise internal physiological measures and external movement measures among different species or groups of species.
The testes of mammals, especially placental mammals like rats, rams, and humans, have special thermal needs. The abdominal temperature of mammals is higher than the ideal temperature for the production of healthy, viable sperm; moreover, high temperature in the testes can result in genetic mutations and testicular damage. Therefore, as regulation of a high body temperature evolves, it became advantageous for some animals to find a new home for the testes outside the abdominal cavity. Hence the evolution of the scrotum.
The scrotum is a highly sophisticated thermoregulatory device by which testicular temperature is maintained 2-9 ēC below body temperature, depending on the species and thermal environment.(p. 95)
How can birds, which have higher temperature than mammals, protect their sperms?
As just described, a ram with an artificially warmed scrotum begins to pant to drive down body temperature. But what happens when despite this panting and decreased body temperature, scrotal temperature is unaffected because the scrotum is encased in a warm chamber? Interestingly, the ram continues panting as long as its scrotum is overheated, even if its body temperature decreases more than 2 ēC. It appears that the rams more committed to maintaining the temperature of its testes than to maintaining its deep body temperature. (p. 96)
It matters because the eyes and brain work better when they are stable and warm: as general rule, the neurons that make up the eyes and brain fire faster and require less time to recover between firing when they are warm. In other words, the integrative systems of the nervous system are highly dependent on temperature. (p. 97)
Birds live on the thermal precipice: they have the highest body and brain temperature of all animals, often exceeding 40 ēC at rest. Why? Birds (the ones that fly) strike a balance between two needs. First, they need to be pre-warmed at all times so that instantaneous flight is possible, if necessary. As we have seen in insects, flight requires warmed muscles --- and many birds have evolved very high body temperatures. Second, they need to protect their brains from heat damage, which begins at temperature above 41 ēC. Therefore, birds face the challenge of maintaining high muscle temperatures without incurring brain damage. Moreover, because brain tissue is more sensitive to overheating than muscle and other types of tissue, keeping the brain cool allows birds to fly for longer periods than would otherwise possible. (p. 101)
It seems the upper limit of animal
temperature is constrained by brain. What is the exact reason brain cannot
evolve a higher temperature tolerance?
In heavy exercises, we often experience sweating in the head. It used to puzzle me a lot because it was the legs do the work. Why head sweating? Now I understand. It is the head that is most vulnerable to overheating.
We have come a long way in our understanding of how animals produce, control, and distribute heat. As we saw in Chapter 4, animals have not only one but many body temperatures, each with its own functional significance. We saw that different animals protect the temperature of different parts of the body --- thoracic temperature in moths, testicular temperature in mammals, eye and brain temperature in fish, brain temperature in mammals and birds. The lesson was that if one wants to make meaningful statements about thermoregulation in any given species, one must put some thought into the functional relevance of the temperature that is measured. (p. 118)
This could be why it is difficult to master Chinese medicine. One has to target the change the temperature of one area without affect the temperature of other areas.
Their first problem come from the direct effect that hypothermia has on cardiac functions: as the heart muscle gets progressively colder, both the rapidity and the strength of its contractions diminish. These changes have a significant impact on the pups ability to deliver oxygenated blood to its body. A second problem for the hypothermic pup involves the blood itself. Like many substances (such as fat and motor oil), blood becomes thicker, and more viscous, as it gets colder. And as the blood gets thicker, it becomes harder to pump through the blood vessels. (p. 123)
Klugers next experiment is a classic. He injected iguanas with fever-producing bacteria (this time the bacteria is alive) and then placed the iguanas in homogeneous thermal environments that did not allow for behavioral thermoregulation. Some were housed at a temperature of 42 ēC, the febrile temperature iguanas had selected naturally in the earlier experiment, while others were housed at various temperatures from 34 ēC to 40V. With three days after been affected, nearly all iguanas housed at 34 ēC died, whereas nearly all of those maintained at 42 ēC survived. Iguanas housed at intermediate temperature exhibited intermediate rates of survival. This experiment provides the first convincing demonstration that fever can be beneficial to the host and is not merely a symptom of disease.
When we get a fever, we typically reach for an antipyretic, that is, a drug such as aspirin, ibuprofen (for example, Advil), or acetaminophen (for example, Tylenol) that returns body temperature to normal levels. They underlying principle, we have been taught to believe, is that fever are undesirable and should be treated, just as we might treat headache, the running nose, and the cough that accompany a cold. This negative opinion of fever is relatively recent: many ancient writers, including Hippocrates, considered fever a beneficial bodily response. The view held sway for many centuries, but over the fast few hundred years fever lost its good reputation. Our current, almost reflexive use of antipyretics reflects the widely held view that fever does not benefit the patient. (p. 141)
This shows that the old Chinese way
to treat fever was right. In
This molecule, called interleukin 1 (IL -1), has many known effects, including the generation of fever, the suppression of food intake (a response that is consistent with the admonition to feed a cold; starve a fever), and the activation of the immune cells that help us fight viral and bacterial infections. IL -1 has also been shown to increase sleep, an effect that appears to account for the drowsiness we commonly experience when we are sick. (p. 145)
Increase sleep and reduce food intake are both to save energy for fighting invaders.
It is evident that fever helps an animal fight infection. But if fever is so beneficial, why havent we endotherms --- mammals and birds --- evolved to regulate body temperature at febrile temperature and thereby decrease the ability of pathogens to invade and infect us? Although the answer to this question is not known with certainty, some probable reasons are apparent.
First, we endotherms already devote a great deal of our energy to the regulation of body temperature; if we were to regulate body temperature 2 ēC higher than we do now, our energy consumption would rise approximately 20 percent, a sizable increase that would necessitate significant adjustments in our eating and sleeping habits. Second, constant regulation at higher temperatures would bring us even closer to those temperatures, 41 ēC and above, at which the integrity of body and brain becomes difficult to sustain, and thus would make it even more crucial for animals to ensure protection against overheating. Third, because increase temperature during pregnancy lead to serious developmental disorders in offspring, substantial changes in gene expression during development would be required. And finally, the chronic stimulation of the immune system that would result from a higher regulated body temperature might increase animals susceptibility to autoimmune disease, such as multiple sclerosis and lupus, in which the immune system becomes overactive and attack body tissues as if it were a foreign invader. For these and other reasons, evolving even a small increase in body temperature would have costs as well as benefits for an organism. (p. 149)
Why do we sleep so shallowly and awake so unrefreshed when our bedroom is too hot or too cold? And why does our sleepiness seem to wax and wane like the tides rather than increase continuously over time? As we will see, the answers to these questions have relevance for a number of real life experiences, from camping out in the cold to jet lag. (p. 200)
Our thermoregulatory behavior does not stop when we get into bed and fall asleep. As we cycle through NREM and REM sleep, a cycle tha t human s repeat approximately six times in a normal night, we awake briefly (although we are usually not aware of these awakings), adjust our posture, and kick off or pull up the covers. The sleep period, in other words, is not a time of completely quiet relaxation.
In fact, REM sleep is not a time of relaxation at all. In addition to rapid eye movements, small muscle twitches in the limbs, irregular breathing, and irregular heartbeat, REM sleep is characterized by electrical activity in the cerebral cortex (the outer layer of the brain) that resembles the activity observed in an awake person. (p. 202)
I think irregular breathing and irregular heartbeat is a result of relaxation of regulatory system. It shows that regulation is costly and regulatory system needs rest.
During REM sleep we and other mammals also inhibit our thermoregulatory response to cold and warm stimulation, in effect placing ourselves at the mercy of prevailing thermal environment. For example, when a cat settles down for a nap in an environment that is warm enough to produce panting but not hot enough to prevent slumber, the panting will continue even as the cat descend into NREM sleep. If REM sleep is entered, however, panting ceases, resulting in decreased heat loss and increased body temperature. In humans in a hot environment, sweating is reduced during REM sleep, also resulting in increased body temperature.
Thermoregulatory response to the cold are also inhibited during REM sleep. A cold cat will shiver to maintain body temperature when it is awake, and this shivering will continue during NREM sleep, but shivering will stop if the cat enters REM sleep, resulting in increased heat loss and decreased body temperature. In addition, adult rats inhibit heat production by brown adipose tissue during REM sleep. (P. 203)
So REM sleep is deep sleep, in which regulatory system is at rest. How should we understand heavy sweating during sleep?