This is called a process of alteration of the set point in a feedback loop. Changes can be made in a group of body organ systems in order to maintain a set point in another system. This is called acclimatization. This occurs, for instance, when an animal migrates to a higher altitude than it is accustomed to.
In order to adjust to the lower oxygen levels at the new altitude, the body increases the number of red blood cells circulating in the blood to ensure adequate oxygen delivery to the tissues. Another example of acclimatization is animals that have seasonal changes in their coats: a heavier coat in the winter ensures adequate heat retention, and a light coat in summer assists in keeping body temperature from rising to harmful levels.
Feedback mechanisms can be understood in terms of driving a race car along a track: watch a short video lesson on positive and negative feedback loops. Body temperature affects body activities. Generally, as body temperature rises, enzyme activity rises as well.
For every ten degree centigrade rise in temperature, enzyme activity doubles, up to a point. Body proteins, including enzymes, begin to denature and lose their function with high heat around 50 o C for mammals.
Enzyme activity will decrease by half for every ten degree centigrade drop in temperature, to the point of freezing, with a few exceptions. Some fish can withstand freezing solid and return to normal with thawing. Watch this Discovery Channel video on thermoregulation to see illustrations of this process in a variety of animals.
Animals can be divided into two groups: some maintain a constant body temperature in the face of differing environmental temperatures, while others have a body temperature that is the same as their environment and thus varies with the environment.
Animals that do not control their body temperature are ectotherms. This group has been called cold-blooded, but the term may not apply to an animal in the desert with a very warm body temperature.
In contrast to ectotherms, which rely on external temperatures to set their body temperatures, poikilotherms are animals with constantly varying internal temperatures. An animal that maintains a constant body temperature in the face of environmental changes is called a homeotherm. Endotherms are animals that rely on internal sources for body temperature but which can exhibit extremes in temperature.
These animals are able to maintain a level of activity at cooler temperature, which an ectotherm cannot due to differing enzyme levels of activity. Heat can be exchanged between an animal and its environment through four mechanisms: radiation, evaporation, convection, and conduction. Heat comes from the sun in this manner and radiates from dry skin the same way. Heat can be removed with liquid from a surface during evaporation.
This occurs when a mammal sweats. Convection currents of air remove heat from the surface of dry skin as the air passes over it. Heat will be conducted from one surface to another during direct contact with the surfaces, such as an animal resting on a warm rock. Figure 3. Heat can be exchanged by four mechanisms: a radiation, b evaporation, c convection, or d conduction.
Animals conserve or dissipate heat in a variety of ways. In certain climates, endothermic animals have some form of insulation, such as fur, fat, feathers, or some combination thereof. Animals with thick fur or feathers create an insulating layer of air between their skin and internal organs.
Polar bears and seals live and swim in a subfreezing environment and yet maintain a constant, warm, body temperature. The arctic fox, for example, uses its fluffy tail as extra insulation when it curls up to sleep in cold weather. Poikilotherms, with their lower metabolic rates, can feed less and are therefore more likely to be able to live in resource-poor environments Grigg et al.
Are there limits to the thermoregulatory abilities of animals in the face of climate change Kearney et al. Both homeotherms and poikilotherms have remarkable adaptations for living in environments that pose temperature challenges. But these adaptations for variable but predictable thermal conditions may not be able to compensate for climate change. For example, late summer steelhead salmon Oncorhynchus mykiss migration is now only possible by fish that are able to access cooler thermal refugia during their runs.
Climate change may uniformly increase water temperature and reduce recruitment Keefer et al. Species that are distributed along areas with a wide range of temperature extremes may have populations that show plasticity in thermoregulatory behavior. For example, Lehmer et al. The reduced activity in the hibernating population may be the result of unusually dry and cold conditions experienced in this portion of the range of the species.
Plasticity in thermoregulatory behavior is also evident from populations of grasshoppers Samietz et al. However, an "ecological trap" occurs when a behavior that is adaptive in one context, such as thermoregulation, has a negative consequence in a different context, such as reproduction.
Steelhead salmon that tary too long in thermal refugia may exceed their energy reserves necessary for a long migration Keefer et al. In sockeye salmon Oncorhynchus nerka , the high temperature extremes of their altered environments force them to select habitats where they become more vulnerable to predation and less likely to reproduce.
Homeostatic Processes for Thermoregulation. Physiological Ecology Introduction. Physiological Optima and Critical Limits. Avian Egg Coloration and Visual Ecology. The Ecology of Photosynthetic Pathways. Global Treeline Position. Allometry: The Study of Biological Scaling. Extreme Cold Hardiness in Ectotherms.
Plant-Soil Interactions: Nutrient Uptake. Water Uptake and Transport in Vascular Plants. Citation: Akin, J. Nature Education Knowledge 3 10 Aa Aa Aa. Types of Thermoregulation. Figure 1.
Comparison of body temperature response by ectotherm i. Thermoneutral Zone. Figure 2. The effect of changing ambient temperature on metabolic rate in mice above and below the thermoneutral zone. Figure 3. Figure 4. For various shapes, surface area to volume is highest for the smallest length dimensions. Control of Thermoregulation. Both the nervous and endocrine systems control thermoregulatory physiology.
Many poikilotherms exhibit periodicity in behavioral thermoregulation; they actively thermoregulate during the day and passively conform during the night Kiefer et al. Ellis et al. The hormone melatonin produced by the pineal gland is implicated in temperature regulation in many ectotherms Lutterschmidt et al. The "thermostat" for vertebrates resides in the hypothalamus of the brain, which triggers physiological responses to ambient temperatures above and below set points Cabanac Life in Extreme Temperatures.
When the options of migration and metabolic adjustments are not feasible, resident homeotherms are capable of withstanding extreme temperatures. Reindeer Rangifer tarandus are notable in remaining active in extremely cold oC environments, even having young during the height of the winter.
Their thick fur helps with insulation, while regional heterothermy conserves heat in the body core. In addition, their thermoneutral zone extends much further into lower temperatures than in other vertebrates.
Indeed, the metabolic rate of a reindeer in winter pelage is lower than that of a reindeer in the summer Soppela et al. The opposite problem is faced by large mammals, such as camels and oryxes, that need to withstand extreme heat but be diurnally active. Like reindeer, camels also have thick fur, but this insulation is to prevent ambient heat from the atmosphere entering the body from convection and radiation. Camels and oryxes become hyperthermic with a body temperature as high as 41 o C during the heat of the day to reduce the gradient for heat entry into their body Ostrowski et al.
References and Recommended Reading Cabanac, M. Adjustable set point: To honor Harold T. Journal of Applied Physiology , — Cannon, B. Nonshivering thermogenesis and its adequate measurement in metabolic studies. Journal of Experimental Biology , — Cannon, W.
The Wisdom of the Body. New York, NY: W. This is due to the body automatically readjusting itself to a lower metabolic set-point to allow it to survive with its lower supply of energy. Exercise can change this effect by increasing the metabolic demand. Yet another good example of a negative feedback mechanism is body temperature control. The hypothalamus, which monitors body temperature, is capable of determining even the slightest variations in body temperature.
Response to such variation could be stimulation of glands that produce sweat to reduce the temperature, or signaling various muscles to shiver to increase body temperature. Many diseases involve disturbances in homeostasis.
For example, as the organism ages, the efficiency in the control of systems becomes reduced due to the loss of receptors. The inefficiencies gradually result in an unstable internal environment that increases the risk of illness, leading to the physical changes associated with aging [ 2 ].
Certain homeostatic imbalances, such as a high core body temperature, a high concentration of salt in the blood, or a low concentration of oxygen, can generate homeostatic reactions such as warmth, thirst, or breathlessness, which motivate behavior aimed at restoring homeostasis [ 35 ].
There is a fundamental epistemologic cart and horse problem in Evolution Theory—the perspective on the life cycle. As Waddington suggests in the quote above, it is necessary to see the entire process of life as a continuum in order to understand the underlying evolutionary principles involved. The first paper published on the cellular approach to vertebrate evolution [ 26 ] reduced both lung evolution and physiology to its cellular, mechanistic level, which allowed examination of ontogeny and phylogeny across space and time as one continuous process, i.
In retrospect, that was an important breakthrough because it demonstrated the fallacy in looking at ontogeny and phylogeny as independent of one another, as would seem to be the case when looked at from the perspective of their present forms.
But by looking at the process from its cell-molecular mechanistic basis, one can see it longitudinally as a continuous process of adaptation, largely to atmospheric oxygen, accommodating the metabolic demand for vertebrate evolution. Perhaps Haeckel overstated the case in his zeal to identify the basis for evolution, but by inferring that the two processes have common properties, he provided an important insight to the mechanism of evolution, begging the question as to what underlies Ontogeny and Phylogeny.
Whatever that property is, it has allowed vertebrates to adapt to a changing oxygen environment over eons, somehow mediated through the processes of embryogenesis. The most logical mechanism that transcends such diverse scales of adaptation is homeostasis. And the recapitulation of phylogeny may act to constrain evolutionary changes that are internally consistent with homeostatic control at key stages of embryologic development.
That, in turn, raises the question as to what homeostasis has evolved in support of? It has been suggested [ 2 ] that reduced entropy is the driving force behind evolution, a property of life that requires homeostatic control to be sustained and perpetuated. Reducing evolution to homeostasis offers a fundamental mechanistic insight to the origin and causal nature of this process.
It is no longer random mutation and Natural Selection, but adaptation of the internal environment of the organism to the external environment of the physical world in service to homeostasis.
Ultimately, Selection facilitates the homeostatically-determined change resulting from the interaction between the organism and the environment. Polyploid embryos had fewer but larger cells, which had no effect on tissue or body size. For example, kidney duct size remained unaffected by the reduced number of epithelial cells surrounding it. Fankhauser then questioned what the real determinant of form and organization is. Yet, if one hypothesizes that homeostasis is the underlying selection pressure for solute exchange over the surface area of the kidney duct, the absence of overall structural change now makes sense.
We must begin thinking along cellular-molecular lines regarding evolution if we are to make advances in Biology and Medicine, or we will languish as the Alchemists did until Chemistry, the Periodic Table and Quantum Theory finally set us on the road to predictive Physics. Downward Causation describes a causal relationship from higher levels of a system to lower-level components of that system. For example, mental events acting to cause physical events. The term was coined in by the philosopher and social scientist Donald T.
Campbell [ 39 ]. He concludes from this approach that there is no privileged level of selection in biological systems. As a result, for example, Noble [ 40 ] concludes that teleologically there is no privileged level of causality in biological systems.
However there is, but it can only be seen by running the tape forward from unicellular state to unicellular state over the entire course of the life cycle of the organism. Our laboratory has been studying the effect of maternal nicotine exposure on the transgenerational inheritance of the asthma phenotype [ 45 ]. Nicotine induces specific epigenetic changes in both the upper airway of the lung and the gonads of the offspring for at least three generations.
This is the first experimental evidence for true epigenetic transgenerational inheritance. These findings beg the question as to the level of selection because newly-acquired epigenetic mutations only affect the offspring, not the adults. Downward Causation. Teleologically, there is no privileged level of causality in biological systems.
Seen as a vectorial product of these forces Figure 2 , evolution would be propelled horizontally from generation to generation, constantly gaining information from the environment in the process. Evolution as Cell-Cell Signaling. Perhaps the reason why we go through the life cycle from zygote to zygote is to acquire epigenetically-heritable information from the environment and selectively integrate it into our genome.
Homeostasis is integral to morphogenesis, since the growth factor signaling mechanisms of embryogenesis become homeostatic mechanisms in the offspring [ 47 ]. As such, they also can discriminate between adaptive and maladaptive genetic mutations that affect homeostasis, either indirectly through the developmental process, or directly through the regulatory mechanisms of physiology.
Embryonic growth and development are determined by paracrine growth factor-receptor signaling, forming the spatio-temporal patterns that provide the form and function of tissues and organs [ 48 ].
The lung is the most extensively characterized organ because of its critical importance to survival at the time of birth in humans. In order to generate an efficient diffusible surface for gas exchange, the lung endoderm grows and differentiates to form the conducting airways and alveoli interfaced with a complementary vascular system. The key genes involved in lung development are highly conserved across phylogeny at least as far back as the swim bladder of physostomous fish [ 49 ].
The soluble growth factors secreted by lung mesoderm are a complete inducer of lung morphogenesis [ 48 ], first observed by Clifford Grobstein [ 50 ]. Duplication of specific genes is well known to have occurred during the vertebrate water-land transition. The amplification of these specific genes was not merely fortuitous, as the literature would have us believe [ 57 ]; they were essential for either adapting to land or becoming extinct [ 58 , 59 ].
Why they duplicated is answered by thinking of them in the physiologic contexts of their functions in lung breathing, neuroendocrine stress, and metabolism. How these genetic changes occurred is speculative, but would have occurred as a result of microvascular shear stress causing remodeling of these specific tissues and organs, as follows. As one reads the Evolutionary Biology literature, observations of pre-adaptations, or exaptations, come up recurrently.
Perhaps that is an artifactual consequence of looking at the process of evolution from its ends instead of its means. A priori, if one follows pre-adaptation to its logical extension, it would terminate in the unicellular state, which is the origin of metazoans, using ontogenetic and phylogenetic principles. However, moving in a prograde direction, by thinking about the evolutionary adaptations in the context of the ever-changing environment, the causal relationships become clear, as has previously been shown for the evolution of the lung [ 10 ]—by regressing the genes that have determined structure and function during lung ontogeny and phylogeny against major epochs in the environment-ocean salinity, the drying-up of the oceans, fluctuations in atmospheric oxygen-expressed as Cartesian Coordinates Figure 3 , one can see the adaptive mechanisms of internal selection due to physical forces, mediated by physiologic stress, starting with the advent of the peroxisome as balancing selection for calcium dyshomeostasis [ 60 ].
The lung is the optimal example, or cipher, for such evolutionary changes in vertebrate visceral physiology because of the powerful positive selection pressure for its evolution during the water-land transition—there were no alternatives, it was either adapt for air breathing or die. Extrinsic and intrinsic selection pressures for the genes of lung phylogeny and ontogeny. The effects of the extrinsic factors salinity, land nutrients, and oxygen on the x-axis on genes that determine the phylogeny and ontogeny of the mammalian lung alternate sequentially with the intrinsic genetic factors y-axis , highlighted by the squares and circles, respectively.
But PTHrP signaling is also important for air breathing and for the skin as a barrier [ 56 ], both of which were also necessary for terrestrial adaptation. Experimentally, if you delete the PTHrP gene from a developing mouse, it causes developmental deficits in the lung no alveoli , bone failure to calcify , and skin immature barrier [ 56 ], consistent with all of the aforementioned phenotypes.
The literature would lead us think that these gene duplications occurred by chance alone [ 57 ], but these genetic mutations are not considered within their ecologic and biologic contexts. The physiologic stresses incurred by the transitioning from water to land-air breathing, increased gravitational force, loss of water and electrolytes- were enormous. Vascular shear would have been greatest within those specific microvascular beds on which that transition was dependent-lung, bone, kidney-generating Radical Oxygen Species known to cause gene mutations and duplications in the process [ 62 ].
Genetic remodeling of the alveolar bed for stretch-regulated PTHrP signaling would have had dual physiologic adaptational advantages Figure 4 , initially by stimulating alveolar surfactant production [ 63 ], relieving the inevitable episodic stress of alveolar insufficiency, resulting in hypoxia during the process of evolution. That would have been followed by PTHrP acting both to generate more alveoli [ 63 ], and as a potent vasodilator [ 64 ] accommodating the concomitant increase in alveolar microvascular blood flow.
Physiologic Adaptation. The blue arrows on the far left signify how evolved traits refer back to their antecedents, or are exapted. That new physiologic trait may have evolved as a result of the coevolution of PTHrP signaling in the anterior pituitary [ 66 ], and in the adrenal cortex [ 67 ], increasing ACTH and glucocorticoid production, respectively, in adaptation to terrestrial physiologic stress.
The resultant increased responsiveness to physiologic stress by the Pituitary-Adrenal Axis PAA would have amplified adrenalin production, since the corticoids produced in the adrenal cortex pass through the adrenal medulla, where they physiologically stimulate the rate-limiting step in adrenalin production, Catechol-O-Methyltransferase, or COMT [ 68 ]. Moreover, the increased PTHrP flowing through the medulla may actually have promoted the formation of more vascular arcades in the mammalian adrenal medulla [ 69 ], since PTHrP is angiogenic [ 70 ].
Terrestrial adaptation mediated by the PAA may have been brought on by the episodic pulmonary insufficiencies that inevitably would have occurred during the step-wise morphogenetic processes of lung evolution in adaptation to land, causing intermittent periods of hypoxia, the most potent physiologic agonist for the stress reaction. It should be emphasized that all of these pre-adapted physiologic traits were recruited in service to optimized air breathing, and ultimately were selected for by the concerted effects of internal selection and natural selection.
Interestingly, the glucocorticoid receptor also evolved from the mineralocorticoid receptor during this same window of time due to two gene mutations [ 8 ]. This should not be surprising, since the expanding surface area of the lung evolved in tandem with the heart, from the one-chambered Annelid worm heart, to the two-chambered fish heart, to the three-chambered frog heart, to the four-chambered mammalian heart [ 73 ].
Extensive experimental evidence from our laboratory has shown the central role of PTHrP in normal lung development [ 3 ], beginning with the embryonic mouse knockout for PTHrP causing impaired lung development due to failure to form alveoli [ 53 ]. In various insult models for lung disease-oxotrauma, barotrauma, infection—we have documented the decrease in PTHrP expression in all of these instances [ 76 ].
Moreover, infants who develop Bronchopulmonary Dysplasia are PTHrP deficient based on measurement of the molecule in bronchoalveolar lavage [ 77 ]. As a consequence, this pathway would have amplified the physiologic stress response by increasing adrenalin production by the adrenal medulla [ 78 ].
This mechanism may have evolved during the water-land transition, wherein the lung would periodically have been unable to generate adequate amounts of oxygen, causing hypoxia. Hypoxia is the most potent physiologic agonist known; by stimulating adrenalin production, which stimulates surfactant secretion, it would have transiently alleviated the atelectatic stress on the lung [ 71 ]. Such a mechanism may refer all the way back to the Cenozoic era , when our common rodent-like ancestor had to be nimble in order to avoid being crushed or eaten by predators.
The key to understanding the interrelationship between homeostasis and embryogenesis lies in recognizing the diachronic nature of the overall mechanism of evolution see Figure 2. During the process of embryogenesis, growth factor signaling determines the structure and function of the offspring. Subsequently, the homeostatic set-point is challenged during postnatal life, overtly being maintained by many of the same signaling principles used for embryogenesis. If the limits of homeostasis are challenged, growth factor signaling mechanisms may revert to their ancestral form in order to sustain the organism, sometimes causing fibrosis as the structural default mode that grants the organism the ability to reproduce under suboptimal physiologic conditions.
Under extreme conditions, such as mass extinctions [ 79 ], or the water-land transition [ 52 ], physiologic stress has caused pragmatic remodeling of organs in order to adapt [ 2 , 3 , 4 ]. Those members of the species best suited to mount such an adaptive strategy pass such homeostatically adaptive genes on to their offspring, generating a heritable phenotype in the process.
When this happens, the feedback loop works to maintain the new setting. An example of this is blood pressure: over time, the normal or set point for blood pressure can increase as a result of continued increases in blood pressure. The body no longer recognizes the elevation as abnormal and no attempt is made to return to the lower set point.
The result is the maintenance of an elevated blood pressure that can have harmful effects on the body. Medication can lower blood pressure and lower the set point in the system to a more healthy level.
This is called a process of alteration of the set point in a feedback loop. Changes can be made in a group of body organ systems in order to maintain a set point in another system. This is called acclimatization. This occurs, for instance, when an animal migrates to a higher altitude than it is accustomed to. In order to adjust to the lower oxygen levels at the new altitude, the body increases the number of red blood cells circulating in the blood to ensure adequate oxygen delivery to the tissues.
Another example of acclimatization is animals that have seasonal changes in their coats: a heavier coat in the winter ensures adequate heat retention, and a light coat in summer assists in keeping body temperature from rising to harmful levels.
Body temperature affects body activities. Generally, as body temperature rises, enzyme activity rises as well. For every ten degree centigrade rise in temperature, enzyme activity doubles, up to a point. Body proteins, including enzymes, begin to denature and lose their function with high heat around 50 o C for mammals. Enzyme activity will decrease by half for every ten degree centigrade drop in temperature, to the point of freezing, with a few exceptions.
Some fish can withstand freezing solid and return to normal with thawing. Watch this Discovery Channel video on thermoregulation to see illustrations of this process in a variety of animals:.
Animals can be divided into two groups: some maintain a constant body temperature in the face of differing environmental temperatures, while others have a body temperature that is the same as their environment and thus varies with the environment. Animals that do not control their body temperature are ectotherms. This group has been called cold-blooded, but the term may not apply to an animal in the desert with a very warm body temperature.
In contrast to ectotherms, which rely on external temperatures to set their body temperatures, poikilotherms are animals with constantly varying internal temperatures. An animal that maintains a constant body temperature in the face of environmental changes is called a homeotherm. Endotherms are animals that rely on internal sources for body temperature but which can exhibit extremes in temperature. These animals are able to maintain a level of activity at cooler temperature, which an ectotherm cannot due to differing enzyme levels of activity.
Heat can be exchanged between an animal and its environment through four mechanisms: radiation, evaporation, convection, and conduction.
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