What is frank dehydration?

What is frank dehydration?

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On Wikipedia article about Urine specific gravity we can read:

A specific gravity greater than 1.035 is consistent with frank dehydration.

What is frank dehydration? How it is different than regular dehydration?

"Frank dehydration" is not really a regular medical term. You can suspect this by using Google search with "frank dehydration" in quotes and site:gov (only 3 websites showing up) and site:edu (2 websites) operators.

The term "frank dehydration" as an informal term can refer to "obvious," "actual," "test-confirmed" dehydration as opposed to feeling dehydrated or thirsty.

Tests to confirm dehydration include a combination of the body exam (dry mouth, prolonged skin turgor, decreased body weight), urine tests (dark urine, increased urine specific gravity, decreased urination frequency and 24-hour urine volume) and blood tests (increased sodium levels - hypernatremia).


Diprosopus (Greek: διπρόσωπος , "two-faced", from δι- , di-, "two" and πρόσωπον , prósopon [neuter], "face", "person" with Latin ending), also known as craniofacial duplication (cranio- from Greek κρανίον , "skull", the other parts Latin), is an extremely rare congenital disorder whereby parts (accessories) or all of the face are duplicated on the head. [1] [2] [3] [4] [5] [6]


The Frank-Starling mechanism occurs as the result of the length-tension relationship observed in striated muscle, including for example skeletal muscles, arthropod muscle [4] and cardiac (heart) muscle. [5] [6] [7] As a muscle fiber is stretched, active tension is created by altering the overlap of thick and thin filaments. The greatest isometric active tension is developed when a muscle is at its optimal length. In most relaxed skeletal muscle fibers, passive elastic properties maintain the muscle fibers length near optimal, as determined usually by the fixed distance between the attachment points of tendons to the bones (or the exoskeleton of arthropods) at either end of the muscle. In contrast, the relaxed sarcomere length of cardiac muscle cells, in a resting ventricle, is lower than the optimal length for contraction. [1] There is no bone to fix sarcomere length in the heart (of any animal) so sarcomere length is very variable and depends directly upon blood filling and thereby expanding the heart chambers. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in a normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For longer sarcomere lengths, this is the result of there being less overlap of the thin and thick filaments [8] [9] [10] for shorter sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. [11] [7] An increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length. [1]

The stretching of the muscle fibers augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils, [12] causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. Specifically, the sensitivity of troponin for binding Ca 2+ increases and there is an increased release of Ca 2+ from the sarcoplasmic reticulum. In addition, there is a decrease in the spacing between thick and thin filaments, when a cardiac muscle fiber is stretched, allowing an increased number of cross-bridges to form. [1] The force that any single cardiac muscle fiber generates is related to the sarcomere length at the time of muscle cell activation by calcium. The stretch on the individual fibers, caused by ventricular filling, determines the sarcomere length of the fibres. Therefore the force (pressure) generated by the cardiac muscle fibres is related to the end-diastolic volume of the left and right ventricles as determined by complexities of the force-sarcomere length relationship. [11] [7] [6]

Due to the intrinsic property of myocardium that is responsible for the Frank-Starling mechanism, the heart can automatically accommodate an increase in venous return, at any heart rate. [1] [10] The mechanism is of functional importance because it serves to adapt left ventricular output to right ventricular output. [3] If this mechanism did not exist and the right and left cardiac outputs were not equivalent, blood would accumulate in the pulmonary circulation (were the right ventricle producing more output than the left) or the systemic circulation (were the left ventricle producing more output than the right). [1] [13]

Premature ventricular contraction Edit

Premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction occurs at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Due to the Frank–Starling mechanism, the next ventricular contraction is more forceful, leading to the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline. [13]

Diastolic dysfunction – heart failure Edit

Diastolic dysfunction is associated with a reduced compliance, or increased stiffness, of the ventricle wall. This reduced compliance results in an inadequate filling of the ventricle and a decrease in the end-diastolic volume. The decreased end-diastolic volume then leads to a reduction in stroke volume because of the Frank-Starling mechanism. [1]

The Frank–Starling law is named after the two physiologists, Otto Frank and Ernest Henry Starling. However, neither Frank nor Starling was the first to describe the relationship between the end-diastolic volume and the regulation of cardiac output. [5] The first formulation of the law was theorized by the Italian physiologist Dario Maestrini, who on December 13, 1914, started the first of 19 experiments that led him to formulate the "legge del cuore" . [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [ excessive citations ]

Otto Frank's contributions are derived from his 1895 experiments on frog hearts. In order to relate the work of the heart to skeletal muscle mechanics, Frank observed changes in diastolic pressure with varying volumes of the frog ventricle. His data was analyzed on a pressure-volume diagram, which resulted in his description of peak isovolumic pressure and its effects on ventricular volume. [5]

Starling experimented on intact mammalian hearts, such as from dogs, to understand why variations in arterial pressure, heart rate, and temperature do not affect the relatively constant cardiac output. [5] More than 30 years before the development of the sliding filament model of muscle contraction and the understanding of the relationship between active tension and sarcomere length, Starling hypothesized in 1914, "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Starling used a volume-pressure diagram to construct a length-tension diagram from his data. Starling's data and associated diagrams, provided evidence that the length of the muscle fibers, and resulting tension, altered the systolic pressure. [27]

Born to Charles Jr. and Mary Matthews Just on August 14, 1883. His father and grandfather, Charles Sr., were builders. When Ernest was four years old, both his father and grandfather died (the former of alcoholism). [1] Just's mother became the sole supporter of Just, his younger brother, and his younger sister. Mary Matthews Just, taught at an African-American school in Charleston to support her family. During the summer, she worked in the phosphate mines on James Island. Noticing that there was much vacant land near the island, Mary persuaded several black families to move there to farm. The town they founded, now incorporated in the West Ashley area of Charleston, was eventually named Maryville in her honor. [2]

When Just was young, he became severely sick for six weeks with typhoid. Once the fever passed, he had a hard time recuperating, and his memory had been greatly affected. He had previously learned to read and write, but now had to relearn. His mother had been very sympathetic in teaching him, but after a while she gave up. [3]

Hoping Just would become a teacher, at the age of 13 his mother sent him to the "Colored Normal Industrial Agricultural and Mechanical College of South Carolina", the only 1890 land grant school for the education of Negros in South Carolina, later known as South Carolina State University in Orangeburg, South Carolina. Believing that schools for blacks in the south were inferior, Just and his mother thought it better for him to go north. At the age of 16, Just enrolled at the Meriden, New Hampshire, college-preparatory high school Kimball Union Academy. During Just's second year at Kimball, he returned home for a visit only to learn that his mother had been buried an hour before he arrived. [3] Despite this hardship, Just completed the four-year program in only three years and graduated in 1903 with the highest grades in his class. [4]

Just went on to graduate magna cum laude from Dartmouth College in Hanover, New Hampshire. [5] There, Just developed an interest in biology after learning about fertilization and egg development. [6] Just won special honors in zoology, and distinguished himself in botany, history, and sociology as well. He was also honored as a Rufus Choate scholar for two years and was elected to Phi Beta Kappa. [4] Just was also a candidate to deliver a commencement speech, but was not chosen because the faculty "decided it would be a faux pas to allow the only black in the graduating class to address the crowd of parents, alumni, and benefactors. It would have made too glaring the fact, that Just had won just about every prize imaginable." [3] Including, honors in botany, sociology, and history. [6]

On June 12, 1912, he married Ethel Highwarden, who taught German at Howard University. They had three children: Margaret, Highwarden, and Maribel. The two divorced in 1939. [6] That same year, Just married Hedwig Schnetzler, who was a philosophy student he met in Berlin. [6]

In 1940, Just was imprisoned by German Nazis, but was easily released thanks to the help of his wife's father. [6]

On November 17, 1911, Ernest Just and three Howard University students (Edgar Amos Love, Oscar James Cooper, and Frank Coleman), established the Omega Psi Phi fraternity on the campus of Howard. Love, Cooper, and Coleman had approached Just about establishing the first black fraternity on campus. Howard's faculty and administration initially opposed the idea of establishing the fraternity, fearing that it could pose a political threat to Howard's white administration. However, Just worked to mediate the controversy and, despite the initial doubts, Omega Psi Phi, Alpha Chapter, was chartered on Howard's campus on December 15, 1911. Omega Psi Phi was incorporated under the laws of the District of Columbia on October 28, 1914. [1]

When he graduated from Dartmouth, Just faced the same problems all black college graduates of his time did: no matter how brilliant they were or how high their grades were, it was almost impossible for black people to become faculty members at white colleges or universities. Just took what seemed to be the best choice available to him and accepted a teaching position at historically black Howard University in Washington, D.C. In 1907, Just first began teaching rhetoric and English, fields somewhat removed from his specialty. By 1909, however, he was teaching not only English but also Biology. [7] In 1910, he was put in charge of a newly formed biology department by Howard's president, Wilbur P. Thirkield and, in 1912, he became head of the new Department of Zoology, a position he held until his death in 1941. Not long after beginning his appointment at Howard, Just was introduced to Frank R. Lillie, the head of the Department of Zoology at the University of Chicago. Lillie, who was also director of the Marine Biological Laboratory (MBL) at Woods Hole, Massachusetts, invited Just to spend the summer of 1909 as his research assistant at the MBL. During this time and later, Just's experiments focused mainly on the eggs of marine invertebrates. He investigated the fertilization reaction and the breeding habits of species such as Platynereis megalops, Nereis limbata, and Arbacia punctulata. For the next 20 or so years, Just spent every summer but one at the MBL.

While at the MBL, Just learned to handle marine invertebrate eggs and embryos with skill and understanding, and soon his expertise was in great demand by both junior and senior researchers alike. [8] In 1915, Just took a leave of absence from Howard to enroll in an advanced academic program at the University of Chicago. That same year, Just, who was gaining a national reputation as an outstanding young scientist, was the first recipient of the NAACP's Spingarn Medal, which he received on February 12, 1915. The medal recognized his scientific achievements and his “foremost service to his race." [3] He began his graduate training with coursework at the MBL: in 1909 and 1910 he took courses in invertebrate zoology and embryology, respectively, there. His coursework continued in-residence at the University of Chicago. His duties at Howard delayed the completion of his coursework and his receipt of the Ph.D. degree. [8] However, in June 1916, Just received his degree in zoology, with a thesis on the mechanics of fertilization. Just thereby became one of only a handful of blacks who had gained the doctoral degree from a major university. By the time he received his doctorate from Chicago, he had already published several research articles, both as a single author and a co-author with Lillie. [7] During his tenure at Woods Hole, Just rose from student apprentice to internationally respected scientist. A careful and meticulous experimentalist, he was regarded as "a genius in the design of experiments." [9] He had explored other areas including: experimental parthenogenesis, cell division, hydration, dehydration in cells, UV carcinogenic radiation on cells, and physiology of development. [6]

Just, however, became frustrated because he could not obtain an appointment at a major American university. He wanted a position that would provide a steady income and allow him to spend more time with his research. Just's scientific career involved a constant struggle for an opportunity for research, "the breath of his life". He was condemned by racism to remain attached to Howard, an institution that could not give full opportunity to ambitions such as the ones Just had. [8] In 1929, Just traveled to Naples, Italy, where he conducted experiments at the prestigious zoological station "Anton Dohrn". Then, in 1930, he became the first American to be invited to the Kaiser Wilhelm Institute in Berlin-Dahlem, Germany, where several Nobel Prize winners carried out research. Altogether from his first trip in 1929 to his last in 1938, Just made ten or more visits to Europe to pursue research. It was during this time, that Just co-authored on a research paper with a few other scientists, called, "General Cytology," which Scientists treated him like a celebrity and encouraged him to extend his theory on the ectoplasm to other species. [8] Just enjoyed working in Europe because he did not face as much discrimination there in comparison to the U.S. and when he did encounter racism, it invariably came from Americans. [3] Beginning in 1933, when the Nazis began to take the control of the country, Just ceased his work in Germany. He later moved his European-based studies to Paris and to the marine laboratory at the French fishing village of Roscoff, located on the English channel.

Just authored two books, Basic Methods for Experiments on Eggs of Marine Animals (1939) and The Biology of the Cell Surface (1939), and he also published at least seventy papers in the areas of cytology, fertilization and early embryonic development. [10] He discovered what is known as the fast block to polyspermy he further elucidated the slow block, which had been discovered by Fol in the 1870s and he showed that the adhesive properties of the cells of the early embryo are surface phenomena exquisitely dependent on developmental stage. [11] He believed that the conditions used for experiments in the laboratory should closely match those in nature in this sense, he can be considered to have been an early ecological developmental biologist. [12] His work on experimental parthenogenesis informed Johannes Holtfreter's concept of "autoinduction" [13] which, in turn, has broadly influenced modern evolutionary and developmental biology. [14] His investigation of the movement of water into and out of living egg cells (all the while maintaining their full developmental potential) gave insights into internal cellular structure that is now being more fully elucidated using powerful biophysical tools and computational methods. [15] [16] [17] [18] These experiments anticipated the non-invasive imaging of live cells that is being developed today. Although Just's experimental work showed an important role for the cell surface and the layer below it, the "ectoplasm," in development, it was largely and unfortunately ignored. [3] [19] This was true even with respect to scientists who emphasized the cell surface in their work. It was especially true of the Americans with the Europeans, he fared somewhat better. [8]

At the outbreak of World War II, Just was working at the Station Biologique in Roscoff, researching the paper that would become Unsolved Problems of General Biology. Although the French government requested foreigners to evacuate the country, Just remained to complete his work. In 1940, Germany invaded France, and Just was briefly imprisoned in a prisoner-of-war camp. With the help of the family of his second wife, a German citizen, he was rescued by the U.S. State Department and he returned to his home country in September 1940. However, Just had been very ill for months prior to his encampment and his condition deteriorated in prison and on the journey back to the U.S. In the fall of 1941, he was diagnosed with pancreatic cancer and died shortly thereafter. [20]

Just was the subject of the 1983 biography Black Apollo of Science: The Life of Ernest Everett Just by Kenneth R. Manning. The book received the 1983 Pfizer Award and was a finalist for the 1984 Pulitzer Prize for Biography or Autobiography. [21] [22] In 1996, the U.S. Postal Service issued a commemorative stamp honoring Just. [23]

Beginning in 2000, the Medical University of South Carolina has hosted the annual Ernest E. Just Symposium to encourage non-white students to pursue careers in biomedical sciences and health professions. [24] In 2008, a National Science Foundation-funded symposium honoring Just and his scientific work was held on the campus of Howard University, where he was a faculty member from 1907 until his death in 1941. Many of the speakers at the symposium contributed papers to a special issue of the journal Molecular Reproduction and Development dedicated to Just that was published in 2009. Since 1994 the American Society for Cell Biology has given an award [25] and hosted a lecture in Just's name. At least two of the institutions with which Just was associated have established prizes or symposia in his name: The University of Chicago, where Just received his PhD (in zoology, in 1916), and Dartmouth College, where he received his undergraduate degree. In 2013, an international symposium honoring Just was held at the Stazione Zoologica Anton Dohrn in Naples, Italy, where Just had worked starting in 1929. [26] [27] [28] [29]

In 2002, scholar Molefi Kete Asante included Just on his list of the 100 Greatest African Americans. [30] A children's book about Just, titled The Vast Wonder of the World: Biologist Ernest Everett Just, written by Mélina Mangal and illustrated by Luisa Uribe, was published by Millbrook Press in November 2018.

Top Five Problems with Current Origin-of-Life Theories

Last summer I published a list of the “Top Ten Problems with Darwinian Evolution.” Since that time, some readers have requested a list of major problems with theories seeking to explain the chemical origin of life. There are numerous problems, but here’s my list of the top 5:

Problem 1: No Viable Mechanism to Generate a Primordial Soup.
According to conventional thinking among origin-of-life theorists, life arose via unguided chemical reactions on the early Earth some 3 to 4 billion years ago. Most theorists believe that there were many steps involved in the origin of life, but the very first step would have involved the production of a primordial soup — a water-based sea of simple organic molecules — out of which life arose. While the existence of this “soup” has been accepted as unquestioned fact for decades, this first step in most origin-of-life theories faces numerous scientific difficulties.

In 1953, a graduate student at the University of Chicago named Stanley Miller, along with his faculty advisor Harold Urey, performed experiments hoping to produce the building blocks of life under natural conditions on the early Earth. 1 These “Miller-Urey experiments” intended to simulate lightning striking the gasses in the early Earth’s atmosphere. After running the experiments and letting the chemical products sit for a period of time, Miller discovered that amino acids — the building blocks of proteins — had been produced.

For decades, these experiments have been hailed as a demonstration that the “building blocks” of life could have arisen under natural, realistic Earthlike conditions, 2 corroborating the primordial soup hypothesis. However, it has also been known for decades that the Earth’s early atmosphere was fundamentally different from the gasses used by Miller and Urey.

The atmosphere used in the Miller-Urey experiments was primarily composed of reducing gasses like methane, ammonia, and high levels of hydrogen. Geochemists now believe that the atmosphere of the early Earth did not contain appreciable amounts of these components. UC Santa Cruz origin-of-life theorist David Deamer explains in the journal Microbiology & Molecular Biology Reviews:

This optimistic picture began to change in the late 1970s, when it became increasingly clear that the early atmosphere was probably volcanic in origin and composition, composed largely of carbon dioxide and nitrogen rather than the mixture of reducing gases assumed by the Miller-Urey model. Carbon dioxide does not support the rich array of synthetic pathways leading to possible monomers… 3

Likewise, an article in the journal Science stated: “Miller and Urey relied on a ‘reducing’ atmosphere, a condition in which molecules are fat with hydrogen atoms. As Miller showed later, he could not make organics in an ‘oxidizing’ atmosphere.” 4 The article put it bluntly: “the early atmosphere looked nothing like the Miller-Urey situation.” 5 Consistent with this, geological studies have not uncovered evidence that a primordial soup once existed. 6

There are good reasons why the Earth’s early atmosphere did not contain high concentrations of methane, ammonia, or other reducing gasses. The Earth’s early atmosphere is thought to have been produced by outgassing from volcanoes, and the composition of those volcanic gasses is related to the chemical properties of the Earth’s inner mantle. Geochemical studies have found that the chemical properties of the Earth’s mantle would have been the same in the past as they are today. 7 But today, volcanic gasses do not contain methane or ammonia, and are not reducing.

A paper in Earth and Planetary Science Letters found that the chemical properties of the Earth’s interior have been essentially constant over Earth’s history, leading to the conclusion that “Life may have found its origins in other environments or by other mechanisms.” 8 So strong is the evidence against pre-biotic synthesis of life’s building blocks that in 1990 the Space Studies Board of the National Research Council recommended that origin-of-life investigators undertake a “reexamination of biological monomer synthesis under primitive Earthlike environments, as revealed in current models of the early Earth.” 9

Because of these difficulties, some leading theorists have abandoned the Miller-Urey experiment and the “primordial soup” theory. In 2010, University College London biochemist Nick Lane stated that the primordial soup theory “doesn’t hold water” and is “past its expiration date.” 10 Instead, he proposes that life arose in undersea hydrothermal vents. But both the hydrothermal vent and primordial soup hypotheses face another major problem.

Problem 2: Forming Polymers Requires Dehydration Synthesis
Assume for a moment that there was some way to produce simple organic molecules on the early Earth. Perhaps they did form a “primordial soup,” or perhaps these molecules arose near some hydrothermal vent. Either way, origin-of-life theorists must then explain how amino acids or other key organic molecules linked up to form long chains (polymers) like proteins (or RNA).

Chemically speaking, however, the last place you’d want to link amino acids into chains would be a vast water-based environment like the “primordial soup” or underwater near a hydrothermal vent. As the National Academy of Sciences acknowledges, “Two amino acids do not spontaneously join in water. Rather, the opposite reaction is thermodynamically favored.” 11 In other words, water breaks down protein chains into amino acids (or other constituents), making it very difficult to produce proteins (or other polymers) in the primordial soup.

Problem 3: RNA World Hypothesis Lacks Confirming Evidence
Let’s assume, again, that a primordial sea filled with life’s building blocks did exist on the early Earth, and somehow it formed proteins and other complex organic molecules. Origin-of-life theorists believe that the next step in the origin of life is that — entirely by chance — more and more complex molecules formed until some began to self-replicate. From there, they believe Darwinian natural selection took over, favoring those molecules which were better able to make copies. Eventually, they assume, it became inevitable that these molecules would evolve complex machinery — like that used in today’s genetic code — to survive and reproduce.

Have modern theorists explained how this crucial bridge from inert nonliving chemicals to self-replicating molecular systems took place? Not at all. In fact, even Stanley Miller readily admitted the difficulty of explaining this in Discover Magazine:

Even Miller throws up his hands at certain aspects of it. The first step, making the monomers, that’s easy. We understand it pretty well. But then you have to make the first self-replicating polymers. That’s very easy, he says, the sarcasm fairly dripping. Just like it’s easy to make money in the stock market — all you have to do is buy low and sell high. He laughs. Nobody knows how it’s done. 12

The most prominent hypothesis for the origin of the first life is called the “RNA world.” In living cells, genetic information is carried by DNA, and most cellular functions are performed by proteins. However, RNA is capable of both carrying genetic information and catalyzing some biochemical reactions. As a result, some theorists postulate the first life might have used RNA alone to fulfill all these functions.

But there are many problems with this hypothesis.

For one, the first RNA molecules would have to arise by unguided, non-biological chemical processes. But RNA is not known to assemble without the help of a skilled laboratory chemist intelligently guiding the process. New York University chemist Robert Shapiro critiqued the efforts of those who tried to make RNA in the lab, stating: “The flaw is in the logic — that this experimental control by researchers in a modern laboratory could have been available on the early Earth.” 13

Second, while RNA has been shown to perform many roles in the cell, there is no evidence that it could perform all the necessary cellular functions currently carried out by proteins. 14

Third, the RNA world hypothesis can’t explain the origin of genetic information.

RNA world advocates suggest that if the first self-replicating life was based upon RNA, it would have required a molecule between 200 and 300 nucleotides in length. 15 However, there are no known chemical or physical laws that dictate the order of those nucleotides. 16 To explain the ordering of nucleotides in the first self-replicating RNA molecule, materialists must rely on sheer chance. But the odds of specifying, say, 250 nucleotides in an RNA molecule by chance is about 1 in 10 150 — below the “universal probability bound,” a term characterizing events whose occurrence is at least remotely possible within the history of the universe. 17 Shapiro puts the problem this way:

The sudden appearance of a large self-copying molecule such as RNA was exceedingly improbable. … [The probability] is so vanishingly small that its happening even once anywhere in the visible universe would count as a piece of exceptional good luck. 18

Fourth — and most fundamentally — the RNA world hypothesis can’t explain the origin of the genetic code itself. In order to evolve into the DNA/protein-based life that exists today, the RNA world would need to evolve the ability to convert genetic information into proteins. However, this process of transcription and translation requires a large suite of proteins and molecular machines — which themselves are encoded by genetic information.

All of this poses a chicken-and-egg problem, where essential enzymes and molecular machines are needed to perform the very task that constructs them.

Problem 4: Unguided Chemical Processes Cannot Explain the Origin of the Genetic Code.
To appreciate this problem, consider the origin of the first DVD and DVD player. DVDs are rich in information, but without the machinery of a DVD player to read the disk, process its information, and convert it into a picture and sound, the disk would be useless. But what if the instructions for building the first DVD player were only found encoded on a DVD? You could never play the DVD to learn how to build a DVD player. So how did the first disk and DVD player system arise? The answer is obvious: a goal-directed process — intelligent design — is required to produce both the player and the disk.

In living cells, information-carrying molecules (such as DNA or RNA) are like the DVD, and the cellular machinery that reads that information and converts it into proteins is like the DVD player. As in the DVD analogy, genetic information can never be converted into proteins without the proper machinery. Yet in cells, the machines required for processing the genetic information in RNA or DNA are encoded by those same genetic molecules — they perform and direct the very task that builds them.

This system cannot exist unless both the genetic information and transcription/translation machinery are present at the same time, and unless both speak the same language. Not long after the workings of the genetic code were first uncovered, biologist Frank Salisbury explained the problem in a paper in American Biology Teacher:

It’s nice to talk about replicating DNA molecules arising in a soupy sea, but in modern cells this replication requires the presence of suitable enzymes. … [T]he link between DNA and the enzyme is a highly complex one, involving RNA and an enzyme for its synthesis on a DNA template ribosomes enzymes to activate the amino acids and transfer-RNA molecules. … How, in the absence of the final enzyme, could selection act upon DNA and all the mechanisms for replicating it? It’s as though everything must happen at once: the entire system must come into being as one unit, or it is worthless. There may well be ways out of this dilemma, but I don’t see them at the moment. 19

The same problem confronts modern RNA world researchers, and it remains unsolved. As two theorists observed in a 2004 article in Cell Biology International:

The nucleotide sequence is also meaningless without a conceptual translative scheme and physical “hardware” capabilities. Ribosomes, tRNAs, aminoacyl tRNA synthetases, and amino acids are all hardware components of the Shannon message “receiver.” But the instructions for this machinery is itself coded in DNA and executed by protein “workers” produced by that machinery. Without the machinery and protein workers, the message cannot be received and understood. And without genetic instruction, the machinery cannot be assembled. 20

Problem 5: No Workable Model for the Origin of Life
Despite decades of work, origin-of-life theorists are at a loss to explain how this system arose. In 2007, Harvard chemist George Whitesides was given the Priestley Medal, the highest award of the American Chemical Society. During his acceptance speech, he offered this stark analysis, reprinted in the respected journal Chemical and Engineering News:

The Origin of Life. This problem is one of the big ones in science. It begins to place life, and us, in the universe. Most chemists believe, as do I, that life emerged spontaneously from mixtures of molecules in the prebiotic Earth. How? I have no idea. 21

Many other authors have made similar comments. Massimo Pigliucci states: “[I]t has to be true that we really don’t have a clue how life originated on Earth by natural means.” 22 Or as science writer Gregg Easterbrook wrote in Wired, “What creates life out of the inanimate compounds that make up living things? No one knows. How were the first organisms assembled? Nature hasn’t given us the slightest hint. If anything, the mystery has deepened over time.” 23

Likewise, the aforementioned article in Cell Biology International concludes: “New approaches to investigating the origin of the genetic code are required. The constraints of historical science are such that the origin of life may never be understood.” 24 That is, they may never be understood unless scientists are willing to consider goal-directed scientific explanations like intelligent design.


Dehydration refers to a loss of total body water producing hypertonicity. Unfortunately, the word dehydration is often used interchangeably with volume depletion, which refers to something different, a deficit in extracellular fluid volume. The distinction between these two conditions is important as the type of fluids used for therapy and their rate of administration differs for each. Hypertonicity is the primary pathophysiologic feature of water deficiency and is preferred terminology over the now careless use of dehydration. Here we examine a patient with hyperglycemic hypertonic nonketosis (HHNK) to illustrate the concepts of volume depletion and hypertonicity and their role in designing rational fluid therapy.

Dehydration Synthesis GIZMO&colon Student Exploration&colon Dehydration Synthesis&period 100&percnt Correct Exam Content&period

Name&colon C Date&colon June 23&comma 2020 Student Exploration&colon Dehydration Synthesis Vocabulary&colon carbohydrate&comma chemical formula&comma dehydration synthesis&comma disaccharide&comma glucose&comma hydrolysis&comma monosacch aride&comma polysaccha ride&comma valence Prior Knowledge Questions &lparDo these BEFORE using the Gizmo&period&rpar 1&period If you exercise on a hot day&comma you need to worry about dehydration&period In this context&comma what do you think dehydration means&quest 2&period Astronauts and backpackers often bring dehydrated food&period What do you think dehydrated food is&quest Gizmo Warm-up What do rice&comma potatoes&comma and sugar have in common&quest They are all foods rich in carbohydrates&period Carbohydrates are an important energy source for your body&period The basic building block of most carbohydrate compounds is the molecule glucose&period Using the Dehydration Synthesis Gizmo&trade&comma you will learn about the structure of a glucose molecule and how glucose molecules can be joined together to make larger carbohydrate molecules&period 1&period Look at the chemical formula for glucose&period How many carbon &lparC&rpar&comma hydrogen &lparH&rpar&comma and oxygen &lparO&rpar atoms are found in a molecule of glucose&quest C&colon 2&period Turn on Show chemical structure&period Each black sphere represents a carbon&comma hydrogen&comma or oxygen atom&period The lines connecting the spheres represent chemical bonds&period A&period How many black spheres are in the diagram&quest How does this relate to the number of carbon&comma hydrogen&comma and oxygen atoms in the chemical formula for glucose&quest B&period Activity A&colon Build a glucose molecule Get the Gizmo ready&colon &bull Introduction&colon Goal&colon Construct a molecule of glucose&period 1&period Identify&colon A&period What is the valence of oxygen&quest B&period What is the valence of hydrogen&quest 2&period Build a model&colon Use the carbon&comma oxygen&comma and hydrogen atoms from the Atoms box 3&period Make a diagram&colon Congratulations&comma you have completed a molecule of glucose 4&period Explain&colon How did the valence of each element help you determine the structure of the glucose molecule&quest 5&period Make connections&colon Carbon forms the backbone of every major type of biological molecule&comma including carbohydrates&comma fats&comma proteins&comma and nucleic acids&period How does carbon&rsquos high valence relate to its ability to form these large and complex biomolecules&quest Activity B&colon Dehydration synthesis Get the Gizmo ready&colon &bull Select the DEHYDRATION tab&period Question&colon What occurs when two glucose molecules bond&quest 1&period Infer&colon What do you think the prefixes mono- and di- mean&quest Mono-&colon 2&period Predict&colon Turn on Show description&period Drag both glucose molecules into the building region&period Observe the highlighted region&period What do you think will happen to the atoms in this region when the glucose molecules bond&quest I predict that they will combine&period 3&period Run Gizmo&colon Click Continue and watch the animation&period A&period What happened&quest B&period What was removed from the glucose molecules when they bonded to form maltose&quest 4&period Infer&colon Based on what you have seen&comma create a balanced equation for the dehydration synthesis reaction&period &lparRecall that the formula for glucose is C6H12O6&period&rpar You will have to determine the formula of maltose yourself&period Turn on Show current formula&solequation to check your answer&period 5&period Summarize&colon Use what you have observed to explain what occurs during a dehydration synthesis reaction 6&period Apply&colon A trisaccharide is a carbohydrate made of three monosaccharides&period What do you think would be the chemical formula of a trisaccharide made of three bonded glucose molecules&quest Activity C&colon Hydrolysis Get the Gizmo ready&colon &bull Select the Hydrolysis tab&period &bull Turn on Show description and Show current formula&solequation&period Introduction&colon Carbohydrates made up of three or more bonded monosaccharides are known as polysaccharides&period In a reaction known as hydrolysis&comma your body breaks down polysaccharides into individual monosaccharides that can be used by your cells for energy&period Question&colon What occurs when polysaccharides break up into monosaccharides&quest 1&period Predict&colon Examine the polysaccharide in the building region and its chemical formula&period A&period How many monosaccharides can form if this polysaccharide breaks up&quest I B&period Recall the formula of glucose is C6H12O6&period How many carbon&comma oxygen&comma and hydrogen atoms will you need for three glucose molecules&quest C&period What must be added to the polysaccharide in the Gizmo to get three glucose molecules&quest 2&period Observe&colon Turn off Show current formula&solequation&period Drag a water molecule into the building region&period Click Continue&period What happened&quest 3&period Infer&colon Create a balanced equation for the hydrolysis reaction that just occurred&period Turn on Show current formula&solequation to check your answer&period 4&period Observe&colon Turn off Show current formula&solequation&period Drag the second water molecule into the building region&period Click Continue&period What happened&quest 5&period Activity C &lparcontinued from previous page&rpar 6&period Summarize&colon Now create a balanced equation for that shows the entire hydrolysis reaction&period &lparIn other words&comma the equation should show how the polysaccharide broke up into three separate glucose molecules&period&rpar Turn on Show current formula&solequation 7&period Compare&colon How do hydrolysis reactions compare to dehydration synthesis reactions&quest 8&period Apply&colon Amylose is a polysaccharide made from the synthesis of four glucose molecules&period A&period How many water molecules are produced when amylose forms&quest B&period What do you think is the chemical formula for amylose&quest C&period How many water molecules would be needed to break amylase down into four glucose molecules&quest 9&period Extend your thinking&colon Hydrolysis of the carbohydrates you eat begins in your mouth as you chew&period How do you think this process might be affected if a person&rsquos salivary glands were unable to produce saliva&comma which is mostly composed of water&quest Show Less Show Less

What you should know about dehydration

Dehydration occurs when more water and fluids leave the body than enter it. Even low levels of dehydration can cause headaches, lethargy, and constipation.

The human body is roughly 75 percent water. Without this water, it cannot survive. Water is found inside cells, within blood vessels, and between cells.

A sophisticated water management system keeps our water levels balanced, and our thirst mechanism tells us when we need to increase fluid intake.

Although water is constantly lost throughout the day as we breathe, sweat, urinate, and defecate, we can replenish the water in our body by drinking fluids. The body can also move water around to areas where it is needed most if dehydration begins to occur.

Most occurrences of dehydration can be easily reversed by increasing fluid intake, but severe cases of dehydration require immediate medical attention.

Dehydration is easy to remedy but can be serious if left unchecked.

The first symptoms of dehydration include thirst, darker urine, and decreased urine production. In fact, urine color is one of the best indicators of a person’s hydration level – clear urine means you are well hydrated and darker urine means you are dehydrated.

However, it is important to note that, particularly in older adults, dehydration can occur without thirst. This is why it is important to drink more water when ill, or during hotter weather.

As the condition progresses to moderate dehydration, symptoms include:

Severe dehydration (loss of 10-15 percent of the body’s water) may be characterized by extreme versions of the symptoms above as well as:

  • lack of sweating
  • sunken eyes
  • shriveled and dry skin
  • low blood pressure
  • increased heart rate
  • delirium
  • unconsciousness

Symptoms in children

  • in babies – a sunken fontanel (soft spot on the top of the head)
  • dry tongue and mouth
  • irritable
  • no tears when crying
  • sunken cheeks and/or eyes
  • no wet diaper for 3 or more hours

The basic causes of dehydration are not taking in enough water, losing too much water, or a combination of both.

Sometimes, it is not possible to consume enough fluids because we are too busy, lack the facilities or strength to drink, or are in an area without potable water (while hiking or camping, for example). Additional causes of dehydration include:

Diarrhea – the most common cause of dehydration and related deaths. The large intestine absorbs water from food matter, and diarrhea prevents this from happening. The body excretes too much water, leading to dehydration.

Vomiting – leads to a loss of fluids and makes it difficult to replace water by drinking it.

Sweating – the body’s cooling mechanism releases a significant amount of water. Hot and humid weather and vigorous physical activity can further increase fluid loss from sweating. Similarly, a fever can cause an increase in sweating and may dehydrate the patient, especially if there is also diarrhea and vomiting.

Diabetes – high blood sugar levels cause increased urination and fluid loss. Tips for handling summer heat for people with diabetes.

Frequent urination – usually caused by uncontrolled diabetes, but also can be due to alcohol and medications such as diuretics, antihistamines, blood pressure medications, and antipsychotics.

Burns – blood vessels can become damaged, causing fluid to leak into the surrounding tissues.

Although dehydration can happen to anyone, some people are at a greater risk. Those at most risk include:

Older adults commonly become dehydrated.

  • People at higher altitudes.
  • Athletes, especially those in endurance events, such as marathons, triathlons, and cycling tournaments. Dehydration can undermine performance in sports, as this article explains.
  • People with chronic illnesses, such as diabetes, kidney disease, cystic fibrosis, alcoholism, and adrenal gland disorders.
  • Infants and children – most commonly due to diarrhea and vomiting.

Dehydration in older adults is also common sometimes this occurs because they drink less water so that they do not need to get up for the toilet as often. There are also changes in the brain meaning that thirst does not always occur.

If dehydration is not checked, it can lead to serious complications these can include:

Low blood volume – less blood produces a drop in blood pressure and a reduction in the amount of oxygen reaching tissues this can be life threatening.

Seizures – due to an imbalance of electrolytes.

Kidney problems – including kidney stones, urinary tract infections, and eventually kidney failure.

Heat injury – ranging from mild cramps to heat exhaustion or even heat stroke.

A doctor will use both physical and mental exams to diagnose dehydration. A patient presenting symptoms such as disorientation, low blood pressure, rapid heartbeat, fever, lack of sweat, and inelastic skin will usually be considered dehydrated.

Blood tests are often employed to test kidney function and to check sodium, potassium, and other electrolyte levels. Electrolytes are chemicals that regulate hydration in the body and are crucial for nerve and muscle function. A urine analysis will provide very useful information to help diagnose dehydration. In a dehydrated person, urine will be darker in color and more concentrated – containing a certain level of compounds called ketones.

To diagnose dehydration in infants, doctors usually check for a sunken soft spot on the skull. They may also look for a loss of sweat and certain muscle tone characteristics.

Dehydration must be treated by replenishing the fluid level in the body. This can be done by consuming clear fluids such as water, clear broths, frozen water or ice pops, or sports drinks (such as Gatorade). Some dehydration patients, however, will require intravenous fluids in order to rehydrate. People who are dehydrated should avoid drinks containing caffeine such as coffee, tea, and sodas.

Underlying conditions that are causing dehydration should also be treated with the appropriate medication. This may include medication available to purchase over-the-counter or online, such as anti-diarrhea medicines, anti-emetics (stop vomiting), and anti-fever medicines.

Prevention is really the most important treatment for dehydration. Consuming plenty of fluids and foods that have high water content (such as fruits and vegetables) should be enough for most people to prevent dehydration.

People should be cautious about doing activities during extreme heat or the hottest part of the day, and anyone who is exercising should make replenishing fluids a priority.

Since the elderly and very young are most at risk of being dehydrated, special attention should be given to them to make sure they are receiving enough fluids.

How does dehydration cause low blood pressure?

I am not sure why this topic is getting downvoted, because that's actually a good question that took quite a bit of scientific research in physiology to find out the answer to.

Part of what we describe as extracellular fluid space is within your blood in the shape of blood plasma (blood plasma is a subset of extracellular fluid). this means that dehydration, i.e. depletion of fluid volume in the extracellular fluid space, has an immediate effect on the fluid volume of your blood.

Your heart is a very clever organ when it comes to organizing pumping blood volume - it has an entire autonomous mechanism of regulating stroke output. An important thing to point out is that your heart consists of functionally 2 seperate pumps: one half of the heart (the right) pumps into the small circulation of your lungs, the other half (left) pumps into the large circulation of your body. Both pumps must pump exactly the same amount of blood volume per time unit. If they don't, fluid will accumulate in either portion of the body before the heart half (right side is weaker -> blood will accumulate as body edema, left half is weaker -> blood will accumulate as lung edema. among other symptoms of course, this is only generalization). For example, if your left heart would pump 5 liters per minute into the body, but your right heart pumps 5.5 liters per minute, you would accumulate 0.5 liters of blood per minute in your lungs. Now imagine what happens if that instance is prolonged for 10 minutes, and by the knowledge that the human body contains 5 liters of blood total, we would have accumulated the entirety of your blood in your lung's blood vessels. Of course your circulation can still draw liquid from other sources of the extracellular fluid space (like from tissues), but this is still enormously excessive! This is why there needed to be a way to coordinate the input and output volumes of each half of the heart.

The solution to this situation is a behavior that has practical consequences like the one you asked about, and is described as the so called Frank-Starling mechanism. Basically, the heart is not a static pump that will pump a specified amount of volume independent of how much blood volume is arriving, but it's a dynamic pump that will output exactly as much blood volume as is arriving during the diastole (the blood refilling stage of the heart rhythm cycle). If the veins give the heart 5 liters per minute, the heart (or its respective half) will pump 5 liters per minute. If it receives 10 liters, it will pump 10 liters. If it receives 4 liters it will pump 4 liters. The exact mechanisms are not fully understood, but we know it depends on how "stretched" the inner walls of the ventricles are from the blood volume on the inside, which affects how sensitive heart muscle cells are to electric input and how strong the muscle cells are able to contract, thereby creating a stronger ejection force to get the additional volume out. More volume, more stretching, more contraction. (despite common assumption, this has less to do with the overlap of actin-myosin filaments like in skeletal muscles than with other stretch sensing mechanisms, but I think this is getting a bit too technical) This also has the consequence that since the muscle cells exhibit stronger contraction, the pressure with which the heart pumps increases. The blood volume that is responsible for stretching the ventricle during diastole is called the preload.

Naturally, during dehydration the opposite phenomenon occurs. You have a lower fluid volume (which has an immediate consequence on the blood filling of your veins because they have the "capacity" to hold a lot of blood), thereby your heart can only receive a lower amount of blood. Because of the reduced preload the heart muscle cells contract with a weaker force, which in turn has the consequence that blood pressure is reduced (which is primarily generated by the strength of the output volume/time).

Note that the body has several mechanisms to prevent and compensate this, and blood pressure is reduced when these mechanisms fail in comparison to the magnitude of the fluid balance problem. Namely, we have something called the baroreceptor reflex: in the aortic arc and the carotid arteries (arteries that are in very close proximity to the left heart - not a coincidence), we have sensors that sense blood pressure called baroreceptors. Low blood pressure is signaled to the medulla oblongata (brain stem), where the signal is coordinated to stimulate the "activating" portion of the vegetative nervous system, the sympathetic nervous system, and inhibit the "relaxing" portion of the vegetative nervous system, the parasympathetic nervous system. The consequence is that the heart is commanded to beat harder and faster independently from the frank-starling mechanism (which is why most dehydrated people also have a really high heart rate), and the arteries (especially arterioles) are commanded to contract in order to build up resistance, which increases blood pressure. The other important mechanism is the renin-angiotensin-aldosterone-system (RAAS): The kidneys sense the fluid status of the body by evaluating the salinity and fluid contents of preprocessed urine (and a complex network of vegetative nerves signaling the sensations of other fluid volume and salinity sensing organs have a large input effect as well), which causes them to secrete a hormone-like enzyme called renin that activates another prohormone called angiotensinogen to angiotensin I, which is again converted by the ACE (angiotensin conversion enzyme) to the actual hormone angiotensin II. Angiotensin II stimulates the secretion of aldosterone (another hormone that stimulates salt and water reabsorption in the kidneys, thereby counteracting the dehydration directly) from the adrenal gland, while angiotensin II also has an immediate effect on the contraction of blood vessels (in the body periphery they're constricted to increase blood pressure similar to the baroreceptor reflex), among other things. There are a plethora of other mechanisms concerning the compensation of fluid balance itself instead of the cardiovascular consequences, but I feel like it's not subject of the topic, so it's best left out.

The Cardiovascular System

Erika J. Eliason , Katja Anttila , in Fish Physiology , 2017

1.4.1 Acute Responses

Cardiac stroke volume ( VS, volume of blood pumped per heart beat) is much less responsive to changes in temperature in comparison with fH. Resting VS has been reported to be insensitive to acute temperature increases in several fish species ( Fig. 2 ): lingcod ( Stevens et al., 1972 ) rainbow trout ( Gamperl et al., 2011 Petersen et al., 2011 ) Chinook salmon ( Clark et al., 2008 ) sockeye salmon ( Steinhausen et al., 2008 ) Atlantic salmon and Arctic char ( Penney et al., 2014 ) spiny dogfish ( Sandblom et al., 2009 ) European sea bass ( Wang et al., 2014 ) and European perch ( Ekström et al., 2016a ). However, studies have also reported moderate decreases in resting VS with warming temperatures: P. bernacchii ( Axelsson et al., 1992 ) P. borchgrevinki ( Franklin et al., 2007 ) M. scorpioides and M. scorpius ( Gräns et al., 2013 ) Asian swamp eel ( Lefevre et al., 2016 ) rainbow trout ( Brodeur et al., 2001 Sandblom and Axelsson, 2007 ) sockeye salmon ( Eliason et al., 2013 ) and European perch ( Sandblom et al., 2016a ). Finally, one study with rainbow trout found a minor, but significant, increase in resting VS (by 14%) during an acute temperature increase ( Keen and Gamperl, 2012 ), and both Gollock et al. (2006) and Ekström et al. (2014) found no change in resting VS during acute warming until fish approached their CTmax at which time VS increased significantly, concomitant with a reduction in fH. Collectively, these studies show that that VS does not normally increase greatly with an acute increase in temperature.

Fewer studies have assessed the effects of acute increases in temperature on VS in swimming fish. Steinhausen et al. (2008) found that VS was maintained during an acute temperature increase in sockeye salmon swum at 75% of their maximum swimming speed. Similarly, VS was maintained after exhaustive exercise (i.e., a chase) across a 10°C temperature range in three species of Arctic fish (G. tricuspis, M. scorpioides, and M. scorpius) ( Franklin et al., 2013 ). In contrast, VS decreased at high temperatures in continuously swimming yellowfin tuna, maximally swum pink salmon and sockeye salmon, and following exhaustive exercise in P. borchgrevinki and European perch ( Clark et al., 2011 Eliason et al., 2013 Franklin et al., 2007 Korsmeyer et al., 1997 Sandblom et al., 2016a ) ( Figs. 2 and 3 ). Scope for VS was also unaffected by an acute temperature increase in sockeye salmon swum at 75% of their maximum ( Steinhausen et al., 2008 ), but clearly declined at elevated temperatures when this species was swum maximally ( Eliason et al., 2013 and Figs. 2 and 3 ). Acute temperature effects on the scope for VS also differed with acclimation temperature in P. borchgrevinki ( Franklin et al., 2007 ). The scope for VS decreased with acute temperature increases in fish acclimated to − 1°C, while it remained unchanged in fish acclimated to 4°C (note: the scope for VS was zero at all test temperatures for 4°C acclimated fish) ( Franklin et al., 2007 ).

Given that VS can increase more than two-fold during aerobic exercise (e.g., Eliason et al., 2013 Fig. 2 ), it is curious why VS does not generally increase with warming. This could be due to limitations in filling time, filling pressure, and/or contractility ( Sandblom and Axelsson, 2007 ). Studies have repeatedly shown that as contraction frequency increases, the force of contraction decreases (termed the negative force–frequency relationship), and this is exacerbated with acute temperature increases ( Shiels et al., 2002 ). As a result, the heart may not empty as much during contraction ( Gamperl, 2011 ). Another strong possibility is that the heart is unable to increase its blood volume during diastole (i.e., end-diastolic volume), which would limit VS. As fH increases, filling time decreases (e.g., Sandblom and Axelsson, 2007 ), and this would limit the capacity of the heart to fill. In addition, VS is inextricably linked with cardiac filling pressure in fishes. A mere 0.02 kPa increase in filling pressure can double VS ( Farrell et al., 2009 ). If cardiac filling pressure becomes compromised at warm temperatures, or cannot increase to compensate for the decrease in filling time, VS would suffer. However, this does not appear to be the case for most species studied to date. Concurrent with a decrease in VS, central venous blood pressure (PCV) was stable, venous capacitance decreased, and mean circulatory filling pressure increased during an acute moderate temperature increase from 10 to 16°C in resting rainbow trout ( Sandblom and Axelsson, 2007 ). Similarly, central venous blood pressure was maintained and the mean circulatory filling pressure increased (but VS did not change) in resting dogfish acutely warmed from 10 to 16°C ( Sandblom et al., 2009 ). Furthermore, PCV actually increased, while VS was maintained, as temperatures approached upper critical temperatures in resting Chinook salmon ( Clark et al., 2008 ). These studies suggest that cardiac filling pressure is not compromised, or increases, when fishes are exposed to acute increases in temperature.

Systemic vascular resistance (Rsys) has been shown to decrease when fish are exposed to acute increases in temperature ( Clark et al., 2008 Gamperl et al., 2011 Mendonça and Gamperl, 2010 Sandblom et al., 2009 ). In contrast, Sandblom and Axelsson (2007) reported no change in Rsys during acute warming in rainbow trout, though they only tested the fish across a moderate temperature range close to the species’ optimum (10–16°C). Similarly, vascular resistance did not change in the Antarctic fish P. bernacchii during acute warming from 0 to 5°C ( Axelsson et al., 1992 ). A reduction in Rsys with acute warming has been speculated to be associated with increased tissue perfusion to reduce diffusion distances, and thus, enhance tissue oxygen delivery ( Clark et al., 2008 ). However, since the increase in typically outpaces the reduction in Rsys with warming, the heart must generate greater blood pressures to distribute blood to the tissues ( Gamperl, 2011 ). This could further hinder the ability of the heart to increase or maintain VS at high frequencies, especially given the well-documented negative force–frequency relationship ( Shiels et al., 2002 ).

Numerous extrinsic factors (e.g., hormones, paracrine factors) also control the strength and rate of cardiac contraction (e.g., see Chapter 4, Volume 36A: Farrell and Smith, 2017 Chapter 5, Volume 36A: Imbrogno and Cerra, 2017 ), and autonomic nervous control is influenced by temperature (see Sections 1.3.1 and 1.6 ). Alterations in both these influences on cardiac function could lead to negative ionotropic effects, and thus, prevent VS from increasing. On the other hand, cardiac contractility could become compromised at high temperature for many of the same reasons outlined earlier (e.g., the noxious hyperkalemic, acidotic, and/or hypoxic venous blood environment, or a limitation in energy metabolism in the heart (see Sections 1.3.1, 1.7, and 1.9.1 and Chapter 6, Volume 36A: Rodnick and Gesser, 2017 ).

Notably, elevated temperature, per se, does not limit the ability of the heart to increase VS at rest ( Gamperl et al., 2011 ). When resting rainbow trout were acutely warmed to 24°C after zatebradine administration to pharmacologically reduce fH by 50%, routine was maintained by a doubling of VS ( Gamperl et al., 2011 ). Similarly, zatebradine injection in resting rainbow trout prior to a CTmax test significantly reduced fH but remained comparable to control levels via an increase in VS ( Keen and Gamperl, 2012 ). As such, it is possible that central control mechanisms favor an increase in fH over an increase in VS with acute temperature increases ( Gamperl, 2011 ). While the mechanisms preventing VS from increasing during warming may not be resolved (see Keen and Gamperl, 2012 ), the outcome is that VS does not compensate for the commonly observed plateau in maximum fH at high temperature, and thus, cardiac performance has been observed to deteriorate in fish swimming at temperatures approaching upper critical limits (see Section 2.2 and Fig. 3 ).


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