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1.7: Equilibrium vs. Homeostasis - Biology

1.7: Equilibrium vs. Homeostasis - Biology



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Chemical Reactions

Chemical reactions occur when two or more atoms bond together to form molecules or when bonded atoms are broken apart. The substances that "go in" to a chemical reaction are called the reactants (by convention these are usually listed on the left side of a chemical equation), and the substances found that "come out" of the reaction are known as the products (by convention these are usually found on the right side of a chemical equation). An arrow linking the reactants and products is typically drawn between them to indicate the direction of the chemical reaction. By convention, for reactions in which the net flow is in a particular direction, we draw a single-headed arrow.

[ce{2 H2O2 -> 2 H2O + O2}]

Note:

Practice: Identify the reactants and products of the reaction involving hydrogen peroxide above.

Note:

Possible discussion: When we write H2O2 to represent the molecule hydrogen peroxide it is a model representing an actual molecule. What information about the molecule is immediately communicated by this molecular formula? That is, what do you know about the molecule just by looking at the term H2O2?

What information is not explicitly communicated about this molecule by looking only at the formula?

Some chemical reactions, such as the one shown above, proceed mostly in one direction. However, all reactions are technically proceeding in both directions- individual molecules may be heading "backward", but the bulk flow of the reaction described above is from left to right. In a chemistry experiment we often dump a reagent or two into a test tube, allow them to react, and then come back later and see what we've got. Often the reactants are rapidly turned into products, but as the concentration of products builds up, the reverse reaction will start to occur also. When a certain relative balance between reactants and products occurs, one in which the rate of the reverse reaction (the frequency of product molecules becoming reactants)— matches the rate of the forward reaction, we reach a state called equilibrium. Some chemical reactions proceed strongly in in one direction until virtually everything become Product, at equilibrium- these are sometimes, perhaps a little loosely, referred to as "irreversible" reactions. Other reactions reach equilibrium when the relative concentration of product to reactant is relatively low. As we'll discuss later, the balance between products and reactants at equilibrium depends on the difference between them in the potential energy associated with their molecular structure.

Note:

Use of vocabulary: You may have realized that the terms "reactants" and "products" are relative to the direction of the reaction. If you have a reaction that is reversible, though, the products of running the reaction in one direction become the reactants of the reverse reaction. You can label the same compound with two different terms. That can be a bit confusing. So, what is one to do in such cases? The answer is that if you want to use the terms "reactants" and "products" you must be clear about the direction of reaction that you are referring to.

Let's look at an example of a reversible reaction in biology. In human blood, excess hydrogen ions (H+) bind to bicarbonate ions (HCO3-) forming an equilibrium state with carbonic acid (H2CO3). This reaction is readily reversible. If carbonic acid were added to this system, some of it would be converted to bicarbonate and hydrogen ions as the chemical system approached equilibrium.

[ce{HCO3^{-} + H^{+} -> H2CO3 }]

The examples above examine "idealized" chemical systems as they might occur in a test-tube (a closed system). In biological systems, however, equilibrium for a single reaction is rarely obtained as it might be in the lab. In biological systems reactions do not occur in isolation. In some cases (for example, the detoxification of a poison by the liver), the concentrations of the reactants and/or products are changing. In others, the concentration of products and reactants is held at a constant value (steady state), but this value is not necessarily at equilibrium. In this class, we'll encounter many example of "biochemical pathways", in which a product of one reaction becomes a reactant for another reaction i.e., ...A -> B -> C -> D... As we'll discover, just as your body maintains its temperature at a level that is not in equilibrium with the air around you, and living things maintain the concentrations of various metabolites at ideal relative concentrations tuned to make reactions "go" in the direction that required. This ability of living things to maintain many aspects of metabolism, temperature, pH, and dissolved gas levels within a relatively narrow, often nonequilibrium range is referred to as homeostasis.

In a previous reading ("Matter and Energy") we discussed the concept of Gibbs free energy- the energy that can be derived from a chemical reaction. We'll see soon how Life harvests and stores this energy. For now, let's discuss the two most relevant components (for Biologists) that contribute to our consideration of whether a reaction will a) proceed as written (in the direction of our arrow) and b) produce energy that Life might possibly use to perform work (such as moving a muscle, or building a complex molecule). Both a and b will be always true at the same time, as reactions only proceed spontaneously from a state of higher to a state of lower potential energy (in other words, ∆G is a negative number). Life may not always be prepared to harvest that potential energy difference, however.

Many things affect the ∆G (change in free energy) of a reaction, but fortunately for us, as students of biology, we can choose to ignore most of them, because Life exists within fairly narrow range of temperature, pressure, and pH. The most important variables for us will be the intrinsic structures (the inherent potential energy) of the molecules, and their relative concentrations. These variables are summarized in the equation:

[∆G = ∆G^{o'} + RTln Q]

where Q is the ratio of concentration of products divided by the concentration of reactants. For example, if A -> B, then Q is simply [B]/[A]. If the reaction is instead 2A -> B, then you need include both molecules of A, so Q = [B]/[A]2. If, in a different example, A breaks down to form B and C, Q would be [B][C]/[A]. Again, luckily for us, we will be discussing fairly steady-state concentrations. While the cell is processing A into B, A is being replaced from upstream chemical reactions, and B is being broken down by downstream reactions. We'll see that Life has tricks for regulating the flow of metabolites, and for stopping that flow (by stopping the production of upstream chemicals) when the biochemical pathway is not required.

R is a constant, and we'll essentially treat T (temperature) as one too, though this is a bit lazy on our part, as Life can be found living in a range from just below freezing to well above boiling (see thermophiles). Note that the ∆G˚' refers to the difference in inherent energy due to the structure of the reactants and products, at biologically standard conditions (which are not the same as the standard conditions employed by chemists.). These conditions are: pH 7.0, 1 atm pressure, an aqueous environment, and 25˚C. Note water, while often a product or reactant, is not included in our calculation of Q. The presence of plenty of liquid water is assumed as part of standard conditions and is already taken care of in our ∆G˚' term in the equation written above.

Practice:

1) Remember that the natural log of (ln) values greater than one is a positive number, while the natural log of values less than 1 is a negative number (see graph below). Knowing this, what is the effect on the ∆G of the reaction A -> B when the concentration of B is greater than the concentration of A? How would this affect the cell's ability harvest energy from a reaction, in comparison to a situation in which [A] = [B]?

2) As we will see when we study respiration, Life can harvest energy simply by allowing molecules to move from a high concentration compartment to a low concentration compartment. This energy is derived purely from the decrease in concentration- there is no change in chemical bonds. How is this negative ∆G related to the equation above?

Y = ln(X)


Why Homeostasis Is Important In Living Organisms?

H omeostasis: During the study of life, one of the most important attribute to be aware of is the concept of internal balance or homeostasis.

But what exactly is homeostasis, how does it occur, and why is it important in living organisms?

Find out the answers to these questions below.


What is Hemostasis

Hemostasis refers to the arrest of the escape of blood from the circulation system in animals. The blood can escape from the circulation system either naturally by clot formation or vessel spasm or artificially by compression or ligation. During hemostasis, the blood flow is slowed down and a clot is formed to prevent the blood loss. The hemostasis changes blood from a liquid to a gelatinous state.

Steps Involved in Hemostasis

Three steps are involved in the hemostasis that occurs in a rapid sequence

The ceasing of the blood flow initiates the tissue repair.

Figure 1: Hemostasis Steps

The main steps involved in hemostasis are shown in figure 1.

Vascular spasm (Vasoconstriction)

Vascular spasm refers to the narrowing of blood vessels to reduce the blood flow during injury while clot formation. It is mediated by the contraction of the smooth muscles lining a blood vessel. An injury to a vascular smooth muscle triggers the vasoconstriction response. The injured endothelial cells secrete signaling molecules to activate platelets such as thromboxane A2. The intense contraction of the blood vessels increases the blood pressure of the affected, large blood vessels. In small blood vessels, it brings the internal walls of the vessels together, stopping the blood flow completely.

Formation of a Platelet Plug

The formation of a platelet plug is the beginning of the blood clot formation. Platelet adherence, activation, and aggregation are the three steps of the formation of the platelet plug.

Platelet Adherence

The exposed subendothelial collagen releases von Willebrand Factor (VWF) during the injury, allowing the platelets to form adhesive filaments. These filaments facilitate the adherence of the platelets with the subendothelial collagen.

Platelet Activation

The binding of the subendothelial collagen to the receptors of the adhered platelets activates them. The activated platelets release various chemicals including ADP and VWF, allowing more platelets to bind to the adhered platelets.

Platelet Aggregation

During platelet aggregation, new platelets aggregate with the barrier to form the plug. The VWF serves as the glue between platelets themselves and platelets and the subendothelial collagen. The aggregation of platelets is shown in figure 2.

Figure 2: Platelet Aggregation

The small wounds will be completely covered with the platelet plug. But if the wound is large enough to flow the blood out from the vessel, a fibrin mesh is produced by the coagulation cascade, preventing the bleeding. Thus, the formation of the platelet plug is referred to as the primary hemostasis while the coagulation cascade is referred to as the secondary hemostasis.

Blood Clotting

Blood clotting is the process by which a blood clot is formed by coagulation in order to prevent further bleeding during the injury. It occurs through a series of reactions known as the coagulation cascade. The three pathways involved in the blood clotting are the intrinsic (contact) pathway, extrinsic (tissue factor) pathway, and the common pathway. Both intrinsic and extrinsic pathway feed into the common pathway.

Intrinsic Pathway

The intrinsic pathway is induced by the contact of the negatively-charged molecules such as lipids or molecules from bacteria. It finally activates the factor X in the common pathway.

Extrinsic Pathway

The extrinsic pathway releases thrombin that cleaves fibrinogen into fibrin. The fibrin is a component of the coagulation cascade, which aids the blood vessel repair. This pathway is initiated by the release of tissue factor III by the damages tissues, activating factor X to convert prothrombin into thrombin.

Common Pathway

The prothrombin is converted into thrombin by the activated factor X by either of the above two pathways. The ultimate formation of fibrin forms the mesh, strengthening the platelet plug.


Homeostatic control

To maintain homeostasis, communication within the body is essential. The image below is an example of how a homeostatic control system works. Here is a brief explanation:

  1. Stimulus– produces a change to a variable (the factor being regulated).
  2. Receptor– detects the change. The receptor monitors the environment and responds to change (stimuli).
  3. Input– information travels along the (afferent) pathway to the control center. The control center determines the appropriate response and course of action.
  4. Output– information sent from the control center travels down the (efferent) pathway to the effector.
  5. Response– a response from the effector balances out the original stimulus to maintain homeostasis.

Interactions among the elements of a homeostatic control system maintain stable internal conditions by using positive and negative feedback mechanisms.

Think of it as an extremely complex balancing act. Here’s a few more definitions you may want to know.

Afferent pathways– carry nerve impulses into the central nervous system. For instance, if you felt scorching heat on your hand, the message would travel through afferent pathways to your central nervous system.

Efferent pathways– carry nerve impulses away from the central nervous system to effectors (muscles, glands).

The feeling of heat would travel through an afferent pathway to the central nervous system. It would then interact with the effector and travel down the efferent pathway, eventually making the person remove their hand from the scorching heat.

Negative feedback mechanisms

Almost all homeostatic control mechanisms are negative feedback mechanisms. These mechanisms change the variable back to its original state or “ideal value”.

A good example of a negative feedback mechanism is a home thermostat (heating system). The thermostat contains the receptor (thermometer) and control center. If the heating system is set at 70 degrees Fahrenheit, the heat (effector) is turned on if the temperature drops below 70 degrees Fahrenheit. After the heater heats the house to 70 degrees Fahrenheit, it shuts off effectively maintaining the ideal temperature.

The control of blood sugar (glucose) by insulin is another good example of a negative feedback mechanism. When blood sugar rises, receptors in the body sense a change . In turn, the control center (pancreas) secretes insulin into the blood effectively lowering blood sugar levels. Once blood sugar levels reach homeostasis, the pancreas stops releasing insulin. Not everyone has such an effective system however, so some people have to have a little help from herbal sources like cannabis when it comes to keeping their insulin-regulated. If you think something might be wrong with your blood sugar levels, take a look at https://www.budbuddies.ca/5-strongest-marijuana-strains-of-2019/.

These are just two examples of negative feedback mechanisms within our body, there are 100’s, can you think of a few more?

Another good example of a positive feedback mechanism is blood clotting. Once a vessel is damaged, platelets start to cling to the injured site and release chemicals that attract more platelets. The platelets continue to pile up and release chemicals until a clot is formed.

Just remember that positive feedback mechanisms enhance the original stimulus and negative feedback mechanisms inhibit it.


Homeostasis, Allostasis and the Application of Engineering Control Theory

The adoption of engineering concepts and terminology by the life sciences and their application to physiological regulation (Wiener, 1948) caused changes in prevailing perceptions of homeostasis that have led to unfortunate contemporary misconceptions. Physiological negative feedback loops were soon described from this perspective, and control theory became firmly entrenched in biological explanations (Mrosovsky, 1990). Thus, physiological negative feedback loops were commonly described as including a reference signal or set point against which the value of the regulated variable is compared. When the value of the regulated variable aligns with the set point, effectors are not recruited. Thus, when a discrepancy occurs between the actual and the idealized set value, it is described as creating an error signal. The error signal activates an effector that moves the regulated variable back toward the value of the set point. As the corrective effector responses take effect, countering the effect of the perturbation, the regulated variable begins to return toward set point values and the deviation (error signal) is reduced.

It is usually assumed that the magnitude of corrective effector responses that are elicited is proportional to the magnitude of the error signal (called proportional control). Thus, as effector mechanisms move the regulated variable back toward reference levels, despite the continued presence of the disturbance, the error signal consequently diminishes and the compensatory responses wane in parallel. Accordingly, the regulated variable returns to close to reference levels.

This somewhat mechanical view of negative feedback resulted in the frequent incorporation of a set point as an explicit or implicit component of homeostasis. Thus, a stable set point or reference signal as used in engineering became linked to homeostatic models of physiological regulation, and while some argue that this analogy can be useful, others argued that it can also be misleading (Berridge, 2004 Gordon, 2001 Kanosue et al., 2010 Werner, 2010). For example, the Commission for Thermal Physiology (2001, p. 266�) of the International Union of Physiological Sciences noted that the use of the term set point for temperature regulation “has evoked much confusion, as it has been used for different phenomena …[including]…. a central reference signal (which obviously does not exist explicitly in the thermoregulatory system).”

In physiology, the term set point is used metaphorically to indicate that a regulatory system operates 𠆊s if’ there was an engineering type of set point or reference signal (Hardy, 1965) i.e., a set point is a hypothetical construct that is inferred by assessing whether an animal defends a given value of one or another variable using behavioral and/or physiological responses. When the regulated variable is at a value where all effectors are at minimal or basal levels of activity, this would be considered the null point or null zone and would correspond to what is metaphorically considered as the set point.

Furthermore, rather than being ‘set,’ these set points are often adjustable and can be altered by diverse naturalistic factors (e.g. circadian and seasonal changes, maturation, hormonal status, nutrition, stress) (Hammel, 1970 Satinoff, 2005). Common examples of regulation with an adjustable set point include the increased and well-defended level of body temperature (fever) when an individual has an infection and the increase in otherwise well-regulated body fat stores as some species prepare for migration or hibernation. Mrosovsky’s (1990) thoughtful monograph on this topic defines changes in the level of the variable around which regulation occurs as rheostasis. As an aside, it should be noted that 25 years prior to Sterling and Eyer’s (1988) assertion that allostatic regulation was needed because homeostasis is limited to having an invariant set point, others had already modified the model of homeostatic regulation to include an adjustable set point (Hammel, 1965, 1970 Hammel et al., 1963).

Investigation and consideration of thermoregulation has led to the development of several physiologically plausible neuronal models that endow the homeostatic system with the 𠆊s if’ appearance of a set point (Bligh, 1972, 1998, 2006 Boulant, 1981, 2000, 2006 Hammel, 1965 Hammel, Jackson, Stolwijk, Hardy, & Strømme, 1963 Wyndham & Atkins, 1968). An important dictum of these homeostatic models was that the sensory input from diverse thermal receptors located in the skin and throughout the body converges on an integrated neural circuit in the central nervous system so that elicitation of effector activity can be centrally coordinated. It was argued that if there were no central coordination, opposing effectors could operate concurrently and in competition with one another. For example, Bligh (1998) argued that a general principle of homeostatic regulation is that the activities of two effectors with opposite influences on the regulated variable are not concurrently active.

Thus, these neuronal models were designed so that sensory information indicating a challenge to the regulated variable not only provides an excitatory input that activates corrective effector responses, but also provides inhibitory input to the opposing effectors. Bligh (1998) described this as being analogous to the reciprocal cross-inhibition system described by Sherrington (1906) that prevents opposing flexor and extensor muscles from contracting concurrently. This proposed design feature prevents the uneconomical concurrent activation of opposing effectors while defending thermal stability, and it fits with the observation that opposing effectors are not found to be concurrently active (e.g., shivering to increase heat production while simultaneously sweating or panting to increase heat loss).

These models were also able to account for an adjustable set point (Hammel, 1965, 1970 Hammel et al., 1963) by allowing additional signals from other systems to influence the elicitation and magnitude of corrective effector responses at the thermoregulatory coordinating interface in the central nervous system (CNS). This additional design feature allowed the level of the set point to be adjustable while maintaining the key feature of homeostatic regulation that detects challenges to, or deviations of, regulated variables and triggers appropriate effector responses to stabilize the variable. While much of this work was based on the thermoregulatory system, these principles are considered to be general and relevant to understanding other homeostatically regulated systems as well (Bligh, 1998, 2006 Boulant, 2006 Cabanac, 2006). Further, although succumbing to the lure of control theory terminology, all of these models of homeostasis nonetheless recognized that physiological regulation has movable set points.

A model provided by Gordon (2009) provides an excellent example that illustrates how thermoregulation is viewed within this sort of homeostatic framework. He points out that an interpretational complexity arises in studies of homeostasis because an observed change in a regulated variable can result either from an environmental disturbance that forces the variable away from its defended value (e.g., entering into a warm room) or else from a rheostatic adjustment of the set point value that causes effectors to move the variable toward a new level (e.g., a bacterial infection eliciting fever).

Gordon (1983, 2005, 2009) refers to changes in a regulated variable that reflect a deviation away from a defended level as being 𠆏orced’ while changes in a variable that are due to a rheostatic adjustment of the defended value are termed ‘regulated.’ Gordon proposed that forced and regulated changes could be distinguished by inference because behavioral and physiological homeostatic effectors are activated to oppose or compensate for a forced change whereas effector mechanisms act in the opposite direction to facilitate a change that is regulated because of a rheostatic set point adjustment. This is consistent with the commonly accepted attribute of homeostasis discussed above that behavioral and autonomic effectors work in concert to defend the set point (e.g., Bligh, 1998 Cabanac, 2006). Gordon’s model ( Figure 1 ) illustrates the coordination of behavioral and autonomic effectors in moving the measured value of the regulated variable toward the target value of an adjustable set point.

“Summary of behavioral and autonomic responses of a homeotherm when subjected to manipulation of body and set-point temperature. Graphs on the left represent the relationship between the set point (dashed line) and core temperature (solid line).” [This figure and figure legend are reprinted with permission (Gordon, 2009, p. 894).]

Figure 1 depicts a homeostatic thermoregulatory model that employs adjustable set points and coordinated effector activity. The left column illustrates the relationship between the regulated variable of core temperature (solid line) and the hypothetical centrally determined set point (dashed line). The middle column illustrates how the behavioral effector in a thermal gradient (i.e., the animal’s actively moving to a warmer or cooler end of the gradient) defends the set point, and the third column illustrates how autonomic effectors defend the set point [i.e., metabolism (heat production effectors), skin blood flow (heat loss effectors), evaporation (e.g., heat-loss effectors of sweating, panting, saliva spreading), and piloerection (heat loss effectors).]

In the top row, core temperature is depicted as having the variability that would typically be observed in the null zone and when the effectors are all functioning at the most energetically efficient or basal levels to maintain normothermia. Measured changes in core temperature (Rows 2𠄵) illustrate how behavioral and autonomic effectors act in coordination to defend the set point by correcting the discrepancy between the set point and the actual core temperature. It is important to note that in Gordon’s model, both behavioral and autonomic patterns of responses are either collectively warming or collectively cooling the body, consistent with the requirements of a homeostatic model that uses an adjustable set point. Further, and also consistent with homeostasis, the five patterns of autonomic and behavioral effector activity depicted are the only ones possible i.e., concurrent activation of opposing effectors is prohibited. If concurrent activation of opposing effectors did occur, it would require a different, non-homeostatic model of regulation.

The necessity of a central integrator for physiological regulation

A key aspect of most models of regulation is the premise that the central nervous system (CNS) contains an integrator/controller that coordinates responses with regard to each regulated variable’s set point, and how best to cope with the magnitude of ongoing or potential perturbations. In 1986, Smullin [as discussed by Bligh (1998)], constructed a functional physical model of thermoregulation to test the theoretical validity of the neuronal implementation of an adjustable set point and central integrator for homeostatic thermoregulation and that prevented concurrent activation of competing effectors. Experiments using this model demonstrated that efficient regulation could be achieved using a physiologically tenable design.

Models of thermoregulation such as this were designed to resolve concerns arising from the use of engineering principles to explain physiological temperature regulation i.e., they were designed to function in a way that was compatible with the current understanding of how homeostasis was thought to operate. That said, many concerns about this approach to understanding physiological regulation have been raised (Werner, 2010). Yates (1996) argued that engineered physical models “… illustrate nothing about biology because programmers are ghosts in those machines, and it is the designer’s intentionality, not that of the machine, that is observed” (p. 683). Yates further states that the �ilure of models based on machines that do work or process information to explain homeostasis has provoked an intellectual crisis in science” (p. 683). While this position may sound extreme, it emphasizes that demonstrating that a biologically plausible system can be designed to achieve a pre-conceived homeostatic outcome does not provide evidence that such an approach actually exists in physiology. The value of such models is that they provide a well-described hypothesis that is suitable for testing. The important point is that whereas much theorizing can occur about how a physiological system could be designed and constructed to appear as if control theory concepts are applicable, they lack biological validity in and of themselves.

In 1978, Satinoff challenged the widely accepted belief that thermoregulation depends on a central neural integrator. Citing findings by Carlisle and Ingram (1973), she argued that a single central integrator is unlikely to exist because when temperatures in the spinal cord and hypothalamus were manipulated in different directions, opposing effector responses were concurrently elicited. In accord with the standard view of homeostasis, Satinoff (1978) recognized that this was anomalous because “in a normal animal in a hot or cold environment, one would never see such opposing behaviors” (p. 20).

Nonetheless, in light of these experimental findings of concurrently active opposing effector responses, Satinoff concluded that the model of thermoregulation must be modified to include separate integrators for each individual thermosensor-effector loop, rather than having a single overall central integrator. In her model, temperature regulation would be the arithmetic sum of activity in whichever thermoactive sensor-effector loops were turned on at any point of time, whether pushing temperature in the same or different directions. Satinoff’s (1978) analysis began a movement away from the traditional homeostatic conceptualization of thermoregulation as being a unified model with a single central controller to achieve effector coordination. The current view of the thermoregulatory system’s structure and function was well described by Romanovsky (2007b), and it is much different than the traditional, unified homeostatic model outlined above that incorporates engineering control theory.

In point of fact, many contemporary models have abandoned the concept of a coordinated central controller. Mammalian body temperature regulation is thought to have evolved utilizing multiple thermoeffector loops, each with its own independent central control (McAllen, Tanaka, Ootsuka, & McKinley, 2010). From that perspective, the structure and function of complex regulatory systems, including thermoregulation, are considered to have been created through evolutionary ‘tinkering’ (Jacob, 1977). As Jacob eloquently described, 𠇎volution does not produce novelties from scratch. It works on what already exists, either transforming a system to give it new function or combining several systems to produce a more elaborate one” (p. 1164) …. “… living organisms are historical structures: literally creations of history. They represent, not a perfect product of engineering, but a patchwork of odd sets pieced together when and where opportunities arose” (p. 1166). It follows from this that the thermoregulatory system is not organized in the way that an engineer might ideally design (e.g., McAllen et al., 2010). This view contrasts sharply with the model Bligh (1998) designed that was intended to provide a biologically feasible method for coordinating effectors so as to prevent concurrent opposing effector activation and to provide the functional attributes of an adjustable set point, both of which were believed to be integral to homeostasis. Kanosue and colleagues (2010) present a contemporary homeostatic model of the thermoregulatory system that fits the data and that has no reference signal (or set point), no error signal and no overall coordinator for the thermoeffectors.

As reviewed by others (McAllen et al., 2010 Romanovsky, 2007b), there has been reluctance to broad acceptance of the view that thermoregulation occurs via independent control circuits without central coordination. McAllen and colleagues (2010) described the problem succinctly, suggesting that the reluctance stems from the fact that thermal regulatory mechanisms 𠆊ppear’ to function seamlessly together as a precisely coordinated control system seeking a set point. Despite this appearance, Romanovsky (2007a, 2007b) explains that the apparent coordination of thermoeffectors typically observed does not require or imply a common central coordinator as had been previously proposed, but instead can result from the common influence of the regulated variable (core temperature) acting at the sensor of each independent thermoeffector loop. For example, as a thermoeffector’s activity alters core temperature, the newly altered level of core temperature necessarily influences the activation/cessation of other thermoeffector mechanisms, each according to its own thresholds. While this example is based on thermoregulation, Romanovsky (2007b) makes the important point that the principles are relevant and apply to physiological regulation for other regulated variables.

A regulatory system consisting of diverse sensor-effector circuits that operate independently has significant implications for how set points are understood in homeostatic regulation. Without a unified control system in the CNS to coordinate effector activity in defense of a common set point, regulation instead results from the sum of influences of each independent effector’s action. Each effector loop has its own threshold that determines its individual activity, and thus each effector may be described as having its own ‘set point’ reflecting the sum of the individual thresholds of the activated sensory neurons (Kobayashi, Okazawa, Hori, Matsumura, & Hosokawa, 2006 Romanovsky, 2007b Werner, 2010). A thermoeffector loop provides an illustrative example (e.g., Kobayashi et al., 2006 Romanovsky, 2007b Tajino et al., 2011). If a cold temperature exceeds the activation threshold of a receptor located on the sensory neuron of a thermoeffector loop, the sensory neuron changes its basal firing rate in accord with stimulus intensity and sends its signal via a neural circuit to a thermoeffector which will respond if it receives sufficient inputs (Tajino et al., 2011).

Figure 2 depicts a single regulatory sensor-effector loop. This view of a sensor-effector loop allows for integration of afferent information as well as for modulatory influences from other inputs to that circuit. However, individual thermoeffector loops are largely independent from one another, and there is not a central controller that receives all of the relevant afferent signals from the thermoeffectors in order to coordinate the effector activity. Kobayashi and colleagues (2006) suggest describing the sensory neuron as a 𠆌omparator’ rather than simply a sensor. This is because the decision about whether a neural signal is generated is determined by the activation threshold of the receptors on that sensory neuron.

Schematic representation of a single regulatory sensor - effector loop. Although the sensory cell is depicted in the periphery, they also exist within the CNS. The activation threshold of the receptor on the primary sensory neuron is triggered when the quantity of the physical stimulus is sufficient. Note: all such loops involve the CNS and are multi-synaptic.

Note that this narrow definition of a set point is quite different from the commonly held belief that there is an integrated central set point that serves to coordinate the action of all of the thermoregulatory system’s different effectors with the goal of defending a common specified value (Romanovsky, 2007b). Instead, the stabilized level of a regulated variable is better conceived as a �lance point’ that reflects the summed action of all of the influences on that variable (Romanovsky, 2007b Werner, 2010 Kanosue et al, 2010). The point is that whereas in common parlance the term set point refers to a hypothetically optimal level of a parameter that is monitored, maintained and defended (e.g., 37° C for body temperature), in actuality body temperature is the consequence of multiple individual and independent thermoeffector loops, each with its own threshold (or ‘set point’) for activation, whose collective activity results in a value that reflects the current conditions and for which there is no central integrator that coordinates effector activity. Figure 3 depicts a balance point model of homeostasis that yields a pattern of effector activity that appears as if it might be the result of purposeful coordination by a central command center but instead occurs without monitoring the magnitude of a presumed regulated variable, without using a comparator to evaluate the regulated value relative to a set point value in order to generate an error signal, and in fact without any central coordination of effector activity.

Schematic describing how a homeostatic model explains thermoregulatory effector activity when body temperature (Tcore) is comparably elevated due to being in a high ambient temperature or an infection-induced fever. Panel A. Schematic depicting how the activity of multiple independent sensor-effector loops contributes to the balance point of a regulated variable. Panel B. Two different patterns of effector activity (adjusted for basal activity levels during normothermia) that result from five different thermo-effector loops. When ambient temperature is high, cooling responses are activated during a fever, warming responses are activated. As in Gordon’s homeostatic model (see Fig. 1 ), the same pattern of coordinated effector activity occurs to move Tcore in the same direction, but this approach does not measure the value of the regulated variable and compare it to a set-point value.

This view of homeostasis clarifies how to interpret the term ‘regulated variable.’ There is not a unified, integrated control system that is constantly calculating and monitoring the value of an assumed regulated variable. Rather, what is considered to be the regulated variable reflects the scientific community’s current understanding of the functional outcome of a regulatory system (e.g., defense of core temperature, body adiposity or blood glucose). The term provides an organizational construct to categorize the regulatory function of multiple effectors acting at once, and the consequent value that is attained reflects not a set point and rather a balancing or settling point. Therapeutic strategies would not be intended to target a non-existent central representation of a regulated variable, but would instead shift the balance point of a regulated variable via targeted alterations in effector loop activity.

It should be noted that the suggestion that a term such as balance point or settling point be used in the context of homeostatic regulation is not new (Berridge, 2004 Booth, 2008 Hardy, 1965 Romanovsky, 2007b Wirtshafter & Davis, 1977). Kanosue and colleagues (2010) point out that it is cumbersome for �lance point’ theory to describe homeostatic processes, because the notion that core temperature is determined as the balance of active and passive processes lacks a clear delineation of regulation. For example, in the case of fever versus exposure to excessive ambient heat, both situations can result in an elevated balance point for core temperature. Those studying physiological regulation are interested in understanding how the effector responses differ in these situations (see different patterns of effector activity for an elevation in core temperature in Figures 1 and ​ and3). 3 ). However, simply knowing that the level of the balance point has increased is uninformative about underlying effector activity. Thus, additional clarification is needed to describe the influence of the regulatory effectors on the regulated variable in these different situations. 1

Another problem hinders the adoption of terminology that correctly describes the current view of homeostatic regulation. Traditional views of homeostasis based on characteristics of engineered controllers have been so influential that the concepts are deeply entrenched in science and medicine. Thus, the use of terms like reference signal, set point, error signal, and the belief in the existence a single central coordinator for each regulatory system, are commonplace. In the field of thermoregulation, Romanovsky (2007b) states that “… in the minds of biologists, physicians, and students, the term set point is strongly, perhaps inseparably associated with the reference signal of a unified thermoregulatory system” (p. R43). We agree, and believe that the constraints imposed by this commonly held misunderstanding of homeostasis may be an impediment to achieving a deeper understanding of physiological regulation.

As a final point on the evolution of homeostatic concepts, all of the same points can be made about allostasis. Allostasis has its roots set firmly in homeostasis, and the same control theory terms and models are commonly used to explain allostatic regulation. In fact, two of the most fundamental features of allostasis are that it has an adjustable rather than an invariant ‘set point’ and that regulatory responses are coordinated by a �ntral controller.’ Based on contemporary views of regulation, and the discussion above, we believe that a balance-point model should be applied to both homeostasis and allostasis.


Positive Feedback Loop

A positive feedback loop maintains the direction of the stimulus, possibly accelerating it. Few examples of positive feedback loops exist in animal bodies, but one is found in the cascade of chemical reactions that result in blood clotting, or coagulation. As one clotting factor is activated, it activates the next factor in sequence until a fibrin clot is achieved. The direction is maintained, not changed, so this is positive feedback. Another example of positive feedback is uterine contractions during childbirth, as illustrated in Figure 2. The hormone oxytocin, made by the endocrine system, stimulates the contraction of the uterus. This produces pain sensed by the nervous system. Instead of lowering the oxytocin and causing the pain to subside, more oxytocin is produced until the contractions are powerful enough to produce childbirth.

Art Connection

State whether each of the following processes is regulated by a positive feedback loop or a negative feedback loop.

  1. A person feels satiated after eating a large meal.
  2. The blood has plenty of red blood cells. As a result, erythropoietin, a hormone that stimulates the production of new red blood cells, is no longer released from the kidney.

What You Need to Know About Metabolism and Homeostasis

The metabolism is comprised of two opposing processes: anabolism and catabolism. Anabolism is a set of synthesis reactions that transform simpler compounds into organic molecules, normally consuming energy. Catabolism is a set of reactions that break down organic molecules into simpler and less complex substances, normally releasing energy. The energy released in catabolism may be used in vital processes of the body, including anabolism.

The Definition of Homeostasis

3. What is homeostasis? What are the sensors, controllers and effectors of homeostasis?

Homeostasis comprises the processes through which the body maintains adequate intra and extracellular conditions so that the metabolism can carry out its normal reactions.

Homeostatic sensors are structures that detect environmental information inside and outside the body. These sensors may be nervous receptor cells, cytoplasmic or membrane proteins or other specialized molecules. Controllers are structures responsible for processing and interpreting information received from the sensors. In general, controllers are specialized regions of the central nervous system. However, they also exist on the molecular level, like in the case of DNA, a molecule that can receive information from proteins to inhibit or boost the expression of certain genes. Effectors are elements commanded by the controllers that have the function of carrying out actions that in fact regulate and maintain the equilibrium of the body, including in muscles, glands, cellular organelles, etc., as well as structures that participate in genetic translation, production of proteins, etc., on the molecular level.

4. How do antagonistic mechanisms produce homeostatic regulation?

The homeostatic maintenance of the body mostly occurs by means of alternating antagonistic compensatory mechanisms. Some of these regulators lower pH while others increase it. Furthermore, there are effectors whose function is to increase body temperature and others that lower it. Likewise, there exist hormones that reduce the level of glucose in the blood, for example, and others that increase the glucose levels. The use of antagonistic mechanisms is an evolutionary strategy to solve the problem of the maintenance of the equilibrium in the body.

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Is homeostasis a type of dynamic equilibrium?

No, homeostasis is not a type of dynamic equilibrium, but the two concepts have similarities.

Homeostasis is the maintenance of a constant internal environment. When a change is made to this environment it restores the environment to its original condition. For example when blood glucose levels rise above a certain threshold the body releases insulin to stimulate the uptake of glucose from the blood into muscle and fat tissue until it falls back into the acceptable range. Homeostasis also regulates other factors such as body temperature and blood pH.

Dynamic equilibrium refers to the extent to which a chemical reaction occurs. Most chemical reactions occur in both directions. Some of the product is reacting to form products and simultaneously some of the product is reacting to form reactants.

#N_2 +3H_2 rightleftharpoons 2NH_3#

The double arrows indicate that the reaction proceeds in both directions. When the rates of forward and back reactions are equal the system is considered to be in equilibrium

For a fuller explanation on dynamic equilibrium click here

Because when a system in equilibrium is altered it moves to partially oppose the change it has some similarities to homeostasis. However there a two key differences. Equilibrium relates to chemical reactions not biological processes, and systems in equilibrium can only partially oppose changes, not restore a change as in homeostasis.


Equilibrium, entropy and homeostasis: A multidisciplinary legacy

Department of Sociology, University of California, Los Angeles, Los Angeles, CA 90024, U.S.A.

Department of Sociology, University of California, Los Angeles, Los Angeles, CA 90024, U.S.A.

Abstract

While the concepts of equilibrium and homeostasis are familiar to sociologists, the companion concept of entropy has only recently received more than a passing glance. This paper reviews the usage of these three concepts in physics, biology, economics and sociology. Each discipline is evaluated according to four dimensions which have received particular attention in equilibrium analysis. These are the use of heuristics, open and closed systems, stable, static and moving equilibrium, and return to equilibrium. The paper concludes that the concept of equilibrium should be used very carefully if at all. Often equilibrium can be replaced by a term such as stability or balance. Homeostasis can be viable concept, as can entropy, which among other things has potential for aiding in the integration of theory and method.


Best Practices in Teaching Homeostasis

Given the centrality of the concept of homeostasis (15, 16), one would expect that both instructional resources and instructors would provide a consistent model of the concept and apply this model to appropriate systems in which variables are sensed and maintained relatively constant.

However, examination of undergraduate textbooks revealed that this is not the case (17). The problems found include, but were not limited to, inconsistent language used to describe the phenomenon and incomplete or inadequate pictorial representations of the model. In addition, texts often define homeostasis early in the narrative but fail to reinforce application of the model when specific regulatory mechanisms are discussed (17).

Furthermore, our work focusing on developing a concept inventory for homeostatic regulation (12, 13) revealed considerable confusion among faculty members regarding the concept. We think this confusion may stem, in part, from the level of faculty uncertainty about the concept and degree of complexity of homeostatic regulatory mechanisms. Our discussion of the sticky points associated with homeostasis is an attempt to suggest potential sources of this confusion and to indicate ways that instructors can work through these difficulties.

How do we ameliorate this situation? We propose five strategies that will help in approaching the problem.

1. Faculty members members should adopt a standard set of terms associated with the model. There is inconsistency within and among textbooks with respect to the names for critical components of the model. We propose the terminology shown in Table 2 to be used when discussing homeostatic regulatory mechanisms.

Table 2. Definitions of terms for homeostasis paper

A glossary of terms used in discussing the core concept of homeostasis. The components of a homeostatically regulated system (Fig. 1) are defined here as are some other terms that occur in teaching this concept.

2. A standard standard pictorial representation of the model should be adopted when initially explaining homeostasis, and it should be used to frame the discussion of the specific system being considered. Figure 1 shows such a diagram.

The argument could be made that this diagram may be difficult for undergraduate students to understand. This may be the rationale for presenting the much-simplified diagrams found in most undergraduate texts (17). However, because these simple diagrams do not explicitly include all components of a homeostatic regulatory system (e.g., a set point), they may be a source of the misconceptions discussed as sticky points. As a result, students may not recognize that an essential feature of homeostatic regulatory systems is minimizing an error signal. A simplified representation of the model that includes the critical components of the regulatory system is shown in Fig. 2. Depending on the course content and level of the student, this model can be expanded to add more levels of complexity as are required.

Fig. 2.Simplified representation of a homeostatic regulatory system. Several components shown in Fig. 1 are combined in this representation. The reader should refer to Table 1 to find correspondence between components of physiologically significant homeostatic regulatory systems and this simplified representation. For example, chemosensors in the carotid bodies and aortic body are “sensors,” the brain stem is the “control center,” and the diaphragm and other respiratory muscles are “effectors” in the homeostatic regulatory system for arterial P o 2.

3. Faculty members should introduce the concept of homeostatic regulation early in the course and continue to apply and hence reinforce the model as each new homeostatic system is encountered. It is important to continue to use the standard terminology and visual representation as recommended in the first and second points above. Students tend to neither spontaneously or readily generalize their use of core concepts. It is therefore incumbent on the instructor to create a learning environment where this kind of transfer behavior is promoted. Faculty members can facilitate this by providing multiple opportunities for students to test and refine their understanding of the core concept of homeostatic regulation.

One way to reinforce the broad application of the model of homeostasis and help students demonstrate that they understand any particular homeostatic mechanism is to have them ask (and answer) a series of questions about each of homeostatically regulated systems they encounter (see Table 3). In doing so, they demonstrate that they can determine the essential components of the mental model needed to define the homeostatic system. The effort to thoroughly and accurately answer these questions will help students uncover gaps in their understanding and will reveal uncertainties in the resource information that they are using.

Table 3. Questions students should ask about any homeostatically regulated system

4. Faculty members should use care when they select and explain the physiological examples or analogical models they chose to introduce and illustrate homeostasis in the classroom. In particular, instructors should ensure that the representative examples they use do not introduce additional misconceptions into student thinking. This is especially so when thermoregulation may be considered as an example of homeostatic regulation.

An informal survey of physiology textbooks indicated that thermoregulation is almost universally used as an example of a homeostatic mechanism. The most likely reasons for this selection are that 1) there is an everyday, seemingly easy to understand process involving the regulation of air temperature in room or building (i.e., the operation of a furnace and an air conditioner) and 2) the body's physiological responses are commonly and obviously observable and/or experienced by the learner (sweating, shivering, and changes in skin coloration). However, based on our description of the typical homeostatic regulatory system, there are compelling reasons to recommend that caution be taken if thermoregulation is used as the initial and representative example of homeostasis.

Most concerning, the typical home heating and cooling system operates in a manner that is distinctly different from mechanisms of human thermoregulation. The effectors in most houses, the furnace and air conditioner, operate in a full-on/full-off manner. For example, when the temperature at the thermostat falls below the value that has been dialed in (the set point temperature), the furnace turns on and stays on at maximum output until the temperature returns to the set point value. However, this is not how the human thermoregulatory system functions or how other homeostatic mechanisms operate. One potential consequence of using this model system to illustrate a homeostatic system is the creation of a common student misconception that homeostatic mechanisms operate in an on/off manner (12, 24), a sticky point we have addressed above. Faculty members need to help students overcome this problem area if they chose to use thermoregulation as a representative example of homeostasis.

What alternatives might be recommended? We suggest the automobile cruise control as a helpful nonbiological analog for homeostasis. The use of cruise control is not an uncommon activity for students, and, as we have described previously, the operation of a cruise control is theoretically easy to understand. What about a physiological example to represent homeostasis? A review of Table 1 would suggest the insulin-mediated system for blood glucose regulation during the fed state has much to recommend it. Students are generally familiar with the particulars of the system from either previous coursework or from personal experience. Other systems are likely to be less accessible to the beginning student of physiology.

However, faculty members should be aware that blood glucose regulation is not without its downsides as a representative example of homeostatic regulation. It is not easy to identify or explain the operation of the glucose sensor, the set point, and the controller involved in glucose homeostasis. Furthermore, there is probably no widely understood analog to glucose regulation that can be easily drawn from everyday life. Neither cruise controls, navigation systems on airplanes, autofocuses on cameras or other common, nor everyday examples of servomechanisms fully correspond to the operation of the feedback system involved in regulating blood glucose during the fed state. This points out the tradeoffs that must be made when any particular example or model is adopted to represent homeostatic regulation. Recognizing this, the use of a physiological control system such as glucose regulation during the fed state, where the effectors operate continuously, seems preferable to thermoregulation as a representative example for teaching the concept of homeostatic regulation.

5. When discussing discussing organismal physiology, restrict the use of the term “homeostatic regulation” to mechanisms related to maintaining consistency of the internal environment (i.e., the ECF).

Adopting these five strategies will provide students with a consistent framework for building their own mental models of specific homeostatic mechanisms and will help them recognize the functional similarities among different homeostatic regulatory systems at the organismal level. Because of its widespread application to different systems in organismal biology, homeostasis is one of the most important unifying ideas in physiology (15, 16). To construct a robust and enduring understanding of this concept, students need the proper tools. By giving them a precise and consistent terminology and encouraging them to use a standardized pictorial representation of the homeostatic model, we enable them to build a proper foundation for comprehending homeostatic systems. By making students aware of the potential sources of confusion surrounding the concept of homeostasis, i.e., the sticky points, we help prevent their thinking from becoming misguided or out of square. By doing so, we set the stage for our students to develop an accurate understanding of a wide range of physiological phenomena and to arrive at an integrated sense of the “wisdom of the body.”


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