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Object Suboptimal recovery following repair of major peripheral nerves has been partially attributed to denervation atrophy. Administration of anabolic steroids in conjunction with neurotization may improve functional recovery of chronically denervated muscle. The purpose of this study was to evaluate the effect of the administration of nandrolone on muscle recovery following prolonged denervation in a rat model. Methods Eight groups of female Sprague-Dawley rats (15 rats per group, 120 in all) were divided into 3- or 6-month denervated hind limb and sham surgery groups and, then, nandrolone treatment groups and sham treatment groups. Evaluation of treatment effects included nerve conduction, force of contraction, comparative morphology, histology (of muscle fibers), protein electrophoresis (for muscle fiber grouping), and immunohistochemical evaluation. Results Although a positive trend was noted, neither reinnervated nor normal muscle showed a statistically significant increase in peak muscle force following nandrolone treatment. Indirect measures, including muscle mass (weight and diameter), muscle cell size, muscle fiber type, and satellite cell counts, all failed to support significant anabolic effect. Conclusions There does not seem to be a functional benefit from nandrolone treatment following reinnervation of either mild or moderately atrophic muscle (related to prolonged denervation) in a rodent model.

This chapter unifies the forces that cause charged solutes to move in solution. Fick’s law indicates that the flux is proportional to the negative of the concentration gradient. The electrical force on charged solutes is proportional to the negative of the electrical gradient. It is possible to define an electrochemical gradient so that the overall force on the charged particles is proportional to the negative of the electrochemical gradient. The equation for the electrochemical gradient is thus justified. It is further shown that the electrochemical gradient is the Gibbs free energy per mole. The sign of the free energy change is shown to indicate the direction of the completed reaction: all reactions must have a negative free energy change. The free energy of ATP hydrolysis is then discussed. The relationship between the standard free energy change and the equilibrium constant is discussed. How to calculate the free energy of ATP hydrolysis under different conditions is shown.

This chapter presents various problem sets related to airway resistance and alveolar gas exchange, which include the approximate area for gas exchange, assuming that the alveoli are spheres, the typical diameter of an alveolus being 0.3 mm, and the number of alveoli in the lungs being 300 х 10 6 ; and the calculation of the overall airway resistance if the airflow is about 0.5 L s –1 and the pressure driving airflow is about 1 mmHg.

This chapter begins with a description of the anatomic location of the hypothalamus and pituitary gland, drawing distinctions between the adenohypophysis, or anterior pituitary, and the neurohypophysis, or posterior pituitary. It describes the secretions of the posterior pituitary, ADH and oxytocin, their stimuli for secretion and their main physiological functions. It then discusses the overall plan of anterior pituitary hormone secretion under the control of releasing factors released by neurons into the portal circulation of the anterior pituitary. These releasing factors are discussed. Only one system—growth hormone—is described in detail in the rest of the chapter, because the other systems are described in their own chapters. The control of growth hormone secretion is described, as well as its mode of action on peripheral tissues.

This chapter begins with a description of the rate of CO 2 production and O 2 consumption and its ratio, the respiratory quotient. This differs from the respiratory exchange ratio only transiently. The physical principles that govern gas exchange (partial pressure, Henry’s law, vapor pressure of water and solubility) are discussed. All gases and solubilities are expressed in volumes at STPD conditions. Gases move passively across the lungs in which flow is proportional to the area of exchange, inversely proportional to the thickness of the barrier, proportional to the solubility, diffusion coefficient in the membrane, and proportional to the partial pressure difference across the membrane. The diffusing capacity is the flow per unit pressure. It increases during exercise as blood perfuses more areas of the lungs. The alveolar ventilation equation and alveolar gas equation are derived, which allow calculation of alveolar gas composition. The anatomic dead space and physiological dead space are discussed. The ventilation–perfusion ratio is discussed.

This chapter analyzes the sources and sinks of ATP during muscle contractions. The rate of ATP consumption depends on the intensity of activity, whereas the amount of ATP consumed depends on the intensity and its duration. Individual muscle fibers are either on or off, but total muscle activity depends on the recruitment and frequency of activation. The duty cycle is the fraction of time activated. The relative speed and amount of ATP regenerated through creatine phosphokinase, or glycolysis, or oxidative phosphorylation, is discussed. The source and fate of lactic acid during strenuous activity, and the meaning of “anaerobic threshold,” are discussed. The cause of fatigue in intense, short duration and submaximal intensity but long durations is discussed. The recruitment of satellite cells during hypertrophy during training is also discussed.

The chapter begins with discussing the energetics of food and the Atwater factors discovered by direct calorimetry. The use of indirect calorimetry to determine the use of fats, proteins, and carbohydrates for energy is then dealt with, introducing the concept of energy equivalence of O 2 . The components of metabolic rate are then looked at. Regulation of food intake is then discussed, using the early notions of a “satiety center” and “feeding center,” since supplanted by a more complex picture of multiple centers and a more diffuse regulation of food intake. The notion of short-term and long-term satiety signals is introduced. An integrated picture of food intake regulation is attempted, combining gastrointestinal and humoral short-term signals and long-term signals of body adiposity. The role of nervous efferents in adjusting energy expenditure is included.

The chapter begins with an overview, showing how the regulation of water permeability of the distal nephron, combined with the osmotic gradient established in the kidney interstitium, allows the kidney to concentrate or dilute the urine. It then shows how the kidney establishes this osmotic gradient by using the counter-current flow of the loop of Henle and collecting ducts, and the spatial separation of transport mechanisms, to make a gradient greater than that achievable by the transport mechanisms themselves. The essential role of the vasa recta is discussed. The contribution of urea to the osmotic gradient in the inner medulla is explained. The function of ADH in allowing the contribution of urea is also discussed. The mechanism of osmotic diuresis is explained.

Publisher Summary This chapter presents various problem sets related to gas transport and pH disturbances, which include the calculation of the concentrations of [H2PO4–1] and [HPO4–2] at pH 7.4 if the total phosphate concentration is 1 mM for the phosphate buffer system; and the total CO2 content of arterial blood assuming an arterial pH of 7.4.

Air that enters the respiratory system is first conditioned: it is filtered, warmed, and humidified by the tracheobronchial tree before the air arrives at the parts of the tree than exchange gas. Gas flow in the respiratory system is governed by pressure differences, and these are driven by expansion or compression of the volume of the lungs. During restful breathing, the diaphragm provides the force for expansion, while expiration is passive and requires no muscles. The external intercostals aid inspiration. The abdominal muscles and internal intercostals aid forceful expiration. Muscles move the chest wall and not the lungs, but the lungs follow because the thin fluid in the pleura paste the lungs to the chest wall. The lungs have a compliance that is produced by elastic fibers and by surface tension. The surface tension is reduced by surfactant, whose lack in newborns causes respiratory distress syndrome. The surfactant helps stabilize alveoli size, keeps the alveoli dry, and reduces the work of breathing. The chest wall acts like a spring: at low volumes it recoils to a higher volume; at high volumes it recoils to a smaller volume. The lungs always tend to collapse. Put together, the balance of lung collapse and chest expansion is the FRC—the functional residual capacity.

The chapter begins with comparing the filtered load of materials with the amount excreted and shows that in some cases all of the filtered load is reabsorbed, and in others it is added to by secretion. It introduces renal titration and considers the titration of inulin, glucose, phosphate, and PAH. It defines the transport maximum for either reabsorption or secretion and shows how the interpretation of the clearance depends on the renal handling of the material. It shows how the endogenous creatinine clearance approximates the GFR. The chapter then discusses the TF/ P ratio. The TF/ P ratio for inulin marks the reabsorption of water because inulin is filtered but not reabsorbed or secreted; The double ratio (TF/ P ) x /(TF/ P ) inulin marks reabsorption or filtration processes. The rest of the chapter discusses the mechanisms of reabsorption of glucose, amino acids, phosphate, bicarbonate, water, salt, urea, and proteins.

This chapter begins with an overview of the structure of the gastrointestinal system from mouth to anus, naming the major structural features. It then discusses chewing, naming the major muscles and their actions involved in chewing. It next discusses the function of saliva. The mechanism of secretion of saliva is discussed along with its control by parasympathetic and sympathetic nerves. Central connections regulating salivary secretion are mentioned. Swallowing is then discussed, from the mechanical events involved in this complicated program to its nervous control. The esophageal phase of swallowing is covered, including both primary peristalsis resulting from the swallowing program and secondary peristalsis resulting from distension of the esophagus. The function of the upper and lower esophageal sphincters is explored.

This chapter describes passive transport using a microporous model or a lipid bilayer model of biological membranes. The derived equations define a permeability for either type of membrane as the transmembrane flux divided by the concentration difference across the membrane. This chapter considers facilitated diffusion that produces a saturable flux across the membrane with concentration. It discusses the mechanism of action of ionophores and voltage- and ligand-gated channels.

This chapter considers how fats and proteins make ATP. It begins with a discussion of the mobilization of depot fat by hormone-sensitive lipase. It discusses how fatty acids are transported into the mitochondria and give rise to a lot of acetyl CoA and NADH and FADH 2 through beta oxidation. It then traces the synthesis of ATP both from the beta oxidation and the complete oxidation of the acetyl CoA through the TCA cycle. It also considers the use of amino acids either to generate acetyl CoA (for the ketogenic amino acids) or glycolytic or TCA intermediates for the glucogenic amino acids. It categorizes all of the amino acids as either ketogenic, glucogenic, or both. At the end, the chapter shows how the amino acids are used to generate urea as a final end product of amino acid metabolism.

Publisher Summary This chapter presents various problem sets related to neuromuscular transmission, muscle force, and energetics, which include the overlap between the thick and thin filaments when the sarcomere length is 2.8 μm; the fraction of the force generators on the thick filament that do not overlap with the thin filament when the sarcomere length is 2.8 μm; and the amount of adenosine triphosphate (ATP) split by the SERCA pumps to return activating Ca2+ to the SR per g tissue, if the troponin C (TnC) binds 2 Ca2+.

Since respiration requires muscular activity, its control must ultimately be neural. This neural control has voluntary and involuntary components. The diaphragm is controlled by the phrenic nerve, which originates from C3–C5 vertebrae; the external and internal intercostals are controlled by spinal nerves in the thoracic cord; the abdominal muscles are controlled by spinal nerves in the lumbar cord. Respiratory control goes through centers in the brain stem, the pons and medulla, including the pontine respiratory group and dorsal and ventral respiratory groups of the medulla. Sensory information reaches these groups over the vagus and glossopharyngeal nerves. Sensory information includes stretch, P aCO 2 P aCO 2 , P aO 2 P aO 2 , and pH. Central chemoreceptors in the dorsal medulla also sense P aCO 2 P aCO 2 and pH. The DRG provides inspiratory drive, the VRG both inspiratory and expiratory drives. Peripheral chemoreceptors increase firing with decreased pH, increased P aCO 2 P aCO 2 , and decreased P aO 2 P aO 2 . Increased activity of the peripheral chemoreceptors increases ventilatory drive. Compensation for hypercapnia, hypoxia, and metabolic acidosis is discussed.

This chapter considers the different types of smooth muscle and how they generate force. Smooth muscle is classified as tonic or phasic and exhibits various patterns of electrical and mechanical activities. Some have electromechanical coupling, others pharmacomechanical coupling. The difference in contractile elements between smooth and skeletal muscles is described. Since smooth muscle contraction is largely controlled through cytosolic [Ca2+], the sources and sinks for cytosolic Ca2+, and their regulation, are discussed. The consequence of activation through Ca2+ activation of myosin light chain kinase (MLCK) is also discussed. The role of myosin light chain phosphatase (MLCP) is also discussed. The role of other pathways, such as RhoA kinase and alpha or beta adrenergic mechanisms, is also discussed. The role of NO is also covered.

This chapter describes active transport in terms of the energetics of transport, using the electrochemical potential of the transported material on both sides of the membrane, and the free energy of ATP hydrolysis. The free energy change for sodium, potassium, or calcium entry is calculated for resting cardiomyocytes that have a resting membrane potential. These free energy changes are then used to calculate the overall free energy for the sodium–calcium exchanger or for the sodium–potassium pump. These calculations illustrate thermodynamic coupling between energy-yielding processes and energy-consuming processes. The mechanism of the Na,K-ATPase is considered. Examples of primary and secondary active transport are given.

This chapter shows how the resting membrane potential derives from relative conductances of all permeable ions. It does this by first considering hypothetical membranes that are permeable to single ions. The membrane in each of these cases is the equilibrium potential, and its magnitude is determined by the Nernst equation. The Nernst equation is derived from Fick’s law in the presence of a potential or from thermodynamics. The equilibrium potential is calculated for Na + , K + , and Cl − . How these individual ions determine the resting membrane potential is clarified by deriving the Goldman–Hodgkin–Katz current equation by integrating the Nernst–Planck electrodiffusion equation. The dependence of ionic currents on membrane potential is used to introduce slope and chord conductance, and this is used to derive the chord conductance equation for resting membrane potential. The chapter ends with the conventions for potential and current flow.

This chapter describes how the action potential moves along axons and how the velocity of this movement depends on the size and myelination of the axon. The velocity of action potential propagation depends solely on the time required to reach threshold at points distant from excitation. This occurs through passive or electrotonic spread of current. This chapter introduces the cable properties of nerves as the determinant of action potential propagation. The cable properties are the space or length constant and the time constant. These vary with transmembrane resistance, the membrane capacitance, and the axial resistance. Transmembrane resistance is increased proportionate to myelination, and membrane capacitance is lowered with increasing myelination. Axial resistance varies with the inverse of the cross-sectional area. Formulas for the length constant and time constant are derived. This chapter ends with a discussion of saltatory conduction.

This chapter begins with an overview of membrane structure and function: membranes separate compartments and consist of a lipid bilayer core in which proteins are embedded. It then details the chemical nature of the lipid component of biological membranes, considering the relative proportion of phospholipids, cardiolipins, and cholesterol, and then discussing the components of phospholipids. The amphipathic character of lipids is discussed. The energetics of surfaces is discussed, particularly the surface tension as energy per unit area or force per unit length, and how lipids at the air–water interface reduce surface tension. This is given as a rationale for the minimum energy configuration of lipid bilayers in aqueous media. The motion of lipids within the bilayer is discussed, and how proteins are inserted into membranes is also discussed. The mechanism of synthesis of secreted proteins is described.

This chapter provides a tour or overview of the main structural features of cells. It starts by recognizing the tasks that each cell must accomplish: catalysis, transport, signal transduction, surface recognition, movement, proliferation, and control. It then discusses cell membranes and their function in transport of nutrients into the cell and wastes out of the cell, and its role in signal transduction and surface recognition. It describes the cytosol and its approximate electrolyte composition. It then describes the cytoskeleton, composed of microtubules, actin filaments, intermediate filaments, and myosin filaments. Microtubule-associated transport is described. This chapter describes the nuclear membrane and its pore complexes, and then goes on to describe the ribosomes and endoplasmic reticulum and Golgi apparatus, where proteins are made and modified posttranslationally. The mitochondrion is then described. Lysosomes, peroxisomes, and proteasomes are also described. Lastly, the specialized regions of the cell membrane that attach to other cells are described.

This chapter presents various problem sets related to kinetics and diffusion such as the molecular weight of glucose when its empirical formula is C 6 H 12 O 6 ; the formula weight of magnesium chloride having a formula of MgCl 2 .6H 2 O; and the amount of MgCl 2 .6H 2 O required to make 1 L of 0.1 MgCl 2 solution.

The transport of O 2 as dissolved O 2 is small because the solubility of O 2 is small. Most O 2 is bound to hemoglobin. The oxygen saturation curve is shown, along with the Hill equation to fit the data to an equation. Oxygen binds to hemoglobin in the lungs, nearly saturating it, and desorbs in the tissue but only partially deoxygenating the blood. Oxygen delivery to the tissues is calculated as the cardiac output times the arteriovenous difference in total oxygen content of the blood. The oxygen consumption calculated from the respiratory rate times the difference in oxygen content of inspired and expired air match. The oxygen gradients to the tissues are discussed. Temperature, decreased pH, increased P CO 2 P CO 2 P CO 2 P CO 2 , and increased 2,3-diphosphoglycerate all shift the O 2 saturation curve to the right. CO 2 is carried as dissolved CO 2 (10%), HCO 3 − (85%), and as carbaminohemoglobin (5%).

Overall calcium and phosphorus balance is considered, listing the estimated daily sources and sinks for each. Their interaction via the solubility product of calcium phosphate is discussed. PTH is introduced as the first calcitropic hormone; it is secreted in response to hypocalcemia and has direct effects on bone and kidney, and indirect effects on the intestine through activation of vitamin D. Calcitonin and its effects described, but no known diseases due to deficiencies or excess of CT secretion are known. Vitamin D structure and synthesis are discussed, along with its activation by successive hydroxylation reactions in the liver and kidney. The fact that vitamin D is not a vitamin is explored. The physiological regulation of its activation in the kidney by PTH and low plasma [phosphate] is discussed.

This chapter discusses the general principles underlying protein structure. It begins with the chemical structures of the 20 amino acids, grouping them as acidic, basic, polar, or nonpolar. It describes what is meant by hydrophobic and how one could measure hydrophobicity. The peptide bond is discussed. The four levels of protein structure are discussed: primary, secondary, tertiary, and quaternary. The importance of hydrogen bonds, hydrophilic/hydrophobic interactions, steric hindrance, and electrostatic interactions is discussed. The use of posttranslational modifications to stabilize protein structure is discussed, including acetylation, methylation, hydroxylation, gamma carboxylation, glycosylation, myristoylation, and phosphorylation. What makes proteins stick in membranes is particularly discussed.

This chapter summarizes the core principles of human physiology. It begins with the definition of human physiology as “the integrated study of the normal function of the human body.” It discusses reductionism, the explanation of a system on the basis of its parts, and contrasts this to holism, in which the behavior of the parts is altered by their context within the whole. The core principles include: (1) cells are the functional unit of life; (2) physiological systems seek homeostasis; (3) causal mechanisms within the body obey physical and chemical laws; (4) our bodies are the product of evolution of prior forms; (5) our bodies transform matter and energy into body materials and physiological work; (6) the function of body parts follows their form; (7) coordinated control of body systems requires signaling at all levels of organization; (8) control systems use negative feedback, anticipatory or feed-forward control, or developmental or threshold control; and (9) physiology is quantitative.

Spirometers can measure three of four lung volumes, inspiratory reserve volume, tidal volume, expiratory reserve volume, but cannot measure residual volume. Four lung capacities are also defined: inspiratory capacity, vital capacity, functional residual capacity, and the total lung capacity. Pulmonary ventilation is the product of tidal volume and respiratory frequency. The maximum voluntary ventilation is the maximum air that can be moved per minute. Spirometry also provides a measure of airway resistance by use of the forced expiratory volume test. The clinical spirogram presents the forced vital capacity differently. In laminar flow, pressure necessary to drive flow increases linearly with the flow. In turbulent flow, pressure increases with the square of the flow. The Reynolds number is used to estimate whether flow is laminar or turbulent. Airway resistance also increases inversely with lung volume because stretch of the lungs opens airways. Dynamic compression limits flow at high expiratory effort.

This chapter begins with a review of gastric emptying into the intestine and the intestine’s role in regulating gastric emptying. It then discusses the intrinsic innervation of the small intestine, consisting of the interstitial cells of Cajal, the myenteric plexus, and the submucosal plexus. How these components regulate local responses, including secretion and activity of longitudinal and circular muscles, is discussed. The extrinsic innervation through the sympathetic and parasympathetic nervous system is described. The pattern of motility including segmentation, peristalsis, migrating motor complex or migrating myoelectric complex, and reverse peristalsis is mentioned. Neuronal control of peristalsis is discussed. Motility of the large intestine is then discussed, beginning with its patterns. The various motility reflexes in the gut are then described, including receptive relaxation, gastric accommodation, enterogastric inhibitory reflex; gastrocolic reflex; ileal brake; gastroileal reflex; the various reflexes between ileum and transverse colon; and rectoanal inhibitory reflex. This chapter ends with a description of the neural control of vomiting.

The function of the stomach to store food, grind it, and release it slowly into the stomach is reviewed. The functional regions of the stomach—fundus, body, and antrum—are discussed. Receptive relaxation and gastric accommodation of the fundus are described, and the mechanisms that bring these about. The cardiac pacemaker is described. Gastric motility is discussed along with gastric emptying and the enterogastric inhibitory reflex and the function of GI hormones cholecystokinin and secretin. The migrating motility complex or migrating myoelectric complex during the interdigestive period is described. Stomach secretions are considered, beginning with a description of the secretory glands and cells. Secretion of mucus by neck cells, pepsinogen by chief cells, and HCl and intrinsic factor by parietal cells is discussed. The mechanism of acid secretion is covered and its regulation by nerves, hormones, and paracrine substances such as histamine.

This chapter describes the general relation between forces and flows in physiological systems. It draws an analogy between heat flow driven by a temperature gradient, charge flow (current) driven by a potential gradient, diffusive flow driven by a concentration gradient, and fluid flow driven by a pressure gradient. In all cases, flow is downhill along the gradient. It shows how conservation of matter leads to the continuity equation. All these flows also can store that which flows—heat, charge, chemicals, and volume—and draws analogy in their capacitances. The chapter then focuses on pressure-driven flow and derives conversion of the common pressure units. The chapter introduces Poiseuille’s law for laminar flow through narrow tubes and introduces the idea of viscosity. The chapter ends with a derivation of the Law of Laplace for spheres and cylinders.

This chapter begins with an overview of the exocrine and endocrine functions of the pancreas. The four classes of exocrine secretion are listed: proteolytic, lipolytic, amylolytic, and nucleolytic enzymes. The composition of these classes and their activation is discussed, in particular with regard to prevention of the pancreas digesting itself and stimulation of secretion through cholecystokinin and parasympathetic stimulation. The fluid secretion by the pancreatic ducts is then discussed. The importance of the CFTR is emphasized, along with its regulation through secretin. The role of bicarbonate in neutralizing stomach acid is discussed. The conduits of the bile are then discussed. The components of the bile are discussed, with description of the mechanisms through which bile is secreted. Secretion by the biliary ducts is akin to that by the pancreatic ducts. This chapter describes primary bile acids and secondary bile acids and the enterohepatic circulation of the bile salts.

Publisher Summary This chapter presents various problem sets related to fluid volumes, glomerular filtration, and clearance, which include the amount of filtration coefficient and its magnitude when the average glomerular capillary pressure is about 55 mmHg, plasma oncotic pressure is about 28 mmHg, the hydrostatic pressure within Bowman's space is 20 mmHg, ultrafiltrate oncotic pressure is 0 mmHg, the glomerular filtration rate (GFR) is 120 mL min21, and each kidney weighs 125 g; the lean body mass of a person weighing 105 kg and having total body water of 48 L; and the calculation of the percentage of body fat in excess of the lean body mass when the person weighs 105 kg and has total body water of 48 L.

This chapter points out that muscles are slaves to the nerves and that motor neuron activity ultimately controls muscle activity. Motor neurons are activated by the integration of multiple inputs from multiple sources. Stimulatory connections produce EPSPs—excitatory postsynaptic potentials; inhibitory connections produce IPSPs—inhibitory postsynaptic potentials. This chapter discusses the time and space evolution of EPSPs and IPSPs, and describes spatial summation and temporal summation. Neuromuscular transmission is then described. Excitation–contraction coupling involving the sarcolemma, T-tubule, and sarcoplasmic reticulum is then described. The turn-on of muscle contraction through Ca 2+ transients begun by Ca 2+ release from the SR through the activation of the ryanodine receptor is discussed. Activation of muscle contraction by Ca 2+ binding to troponin C and subsequent removal of activator Ca 2+ by reuptake into the SR mediated by the SERCA pump are discussed.

No seasonal pattern was found in total swimbladder weight, sonic muscle weight, or spinal sonic motor nucleus neuron soma size of the oyster toadfish Opsanus tau, indicating that additional nonsteroidal factors are also involved in the development of the toadfish sonic neuromuscular system.

The amount of cardiac sarcoplasmic reticulum in rat hearts was estimated by comparing marker activities in the isolated SR fraction with their activities in the homogenate. Four distinguishable markers were measured: the oxalate-supported rate of calcium uptake, the calcium oxalate capacity, 3 H-ryanodine binding and the thapsigargin equivalents. The calcium uptake rate and capacity and thapsigargin equivalents were determined in the presence and absence of SR Ca 2+ channel blockade with high concentrations of ryanodine. All of these activities are believed to be located only in the SR. However, the calculation of the heart content of SR was somewhat different for the four markers. The calcium uptake rate gave 8.4 mg SR protein per g tissue in the absence of ryanodine, and 9.6 mg per g in its presence; calcium oxalate capacity gave similar numbers, 9.9 mg per g in the absence of ryanodine and 8.0 mg per g in its presence. The thapsigargin titration gave similar equivalent with or without ryanodine, indicating that the homogenate contained about 8.0 mg of SR per g tissue. Using 3 H-ranodine binding as a marker, the cardiac content of SR was calculated to be 16.7 mg per g. These differences are attributed to the non-ideal behavior of these markers. Some of the Ca 2+ uptake activity is not thapsigargin sensitive, and some of the 3 H-ryanodine binding does not fractionate with the SR Ca 2+ uptake activity.

The sonic muscle of the oyster toadfish, Opsanus tau, can produce unfused contractions at 300Hz. Electron microscopy shows a great abundance of the Sarcoplasmic reticulum (SR) in this muscle, but no functional characterization of the capabilities of this SR has been reported. We measured the oxalate-supported Ca2+ uptake rate and capacities of homogenates of toadfish sonic muscle and rat extensor digitorum longus (EDL) muscle, and estimated the number of pump units by titration with thapsigargin, a high-affinity, specific inhibitor of the SR Ca-ATPase. The Ca2+ uptake rate averaged 70.9±9.5 mol min−1 per g tissue for the toad fish sonic muscle, and 73.5±3.7 mol min−1 g−1 for rat EDL. The capacity for Ca2+-oxalate uptake was 161±20 mol g−1 and 33±2 mol g−1 for toadfish sonic muscle and rat EDL, respectively. Thus, the rates of Ca2+ uptake were similar in the two muscles, but the toadfish sonic muscle had about five times the capacity of the rat EDL. The number of pumps as estimated by thapsigargin titration was 68±4 nmol of Ca-ATPase per g tissue in the toadfish, and 42±5 nmol Ca-ATPase per g tissue in the rat EDL. The turnover number, defined as the Ca2+ uptake divided by the number of pumps, was 1065±150 min−1 for toadfish and 1786±230 min−1 for rat EDL (p

Suboptimal recovery following repair of major peripheral nerves has been partially attributed to denervation atrophy. Administration of anabolic steroids in conjunction with neurotization may improve functional recovery of chronically denervated muscle. The purpose of this study was to evaluate the effect of the administration of nandrolone on muscle recovery following prolonged denervation in a rat model.Eight groups of female Sprague-Dawley rats (15 rats per group, 120 in all) were divided into 3- or 6-month denervated hind limb and sham surgery groups and, then, nandrolone treatment groups and sham treatment groups. Evaluation of treatment effects included nerve conduction, force of contraction, comparative morphology, histology (of muscle fibers), protein electrophoresis (for muscle fiber grouping), and immunohistochemical evaluation.Although a positive trend was noted, neither reinnervated nor normal muscle showed a statistically significant increase in peak muscle force following nandrolone treatment. Indirect measures, including muscle mass (weight and diameter), muscle cell size, muscle fiber type, and satellite cell counts, all failed to support significant anabolic effect.There does not seem to be a functional benefit from nandrolone treatment following reinnervation of either mild or moderately atrophic muscle (related to prolonged denervation) in a rodent model.

This chapter considers volume flow across a microporous membrane whose pores are very large compared to the solute, or very small, or larger than the solute but not greatly larger. The first case, very large pores, describes pressure-driven flow and equations are derived that express the filtration coefficient, or hydraulic conductivity, of the membrane in terms of the microscopic characteristics of the membrane. When the pore is smaller than the solute, osmosis occurs. The resulting flow is driven by the osmotic pressure which is considered to be produced by a momentum deficit within the pore. In the third case, where the pore is larger but not greatly larger than the solute, a third phenomenological coefficient of the membrane is introduced: the reflection coefficient. The osmotic behavior of red blood cells is used to introduce the concept of isotonic, hypertonic, and hypotonic solutions.

This chapter begins with the definition of an endocrine gland, comparing endocrine signals to autocrine, paracrine, and neurocrine. It then shows how endocrine signals interact with nervous signals for overall physiological control. Hormones are then classified according to structure: modified amino acids, polypeptides, and steroids. The major hormones are listed according to site of release and/or function. The two major types of secretions—released from storage vesicles or as synthesized—are described. Transport in the blood is discussed in a general way and then the idea of the specific receptor is introduced, along with classical plots for the analysis of hormone binding or effect. These plots include the Scatchard plot, titration curve, and Hill plot. The dose–response curve is discussed, along with the idea of up- and downregulation and sensitization or desensitization. Metabolic clearance rate is introduced and its relation to the fractional turnover is derived. Methods for assaying hormones are introduced.

This chapter begins with the mechanism of force generation by cardiac muscle, describing the structure of the cardiomyocytes, their contractile filaments and the organelles that turn them on, and off, and supply them with energy. It distinguishes cardiac muscle from skeletal muscle in terms of its excitation–contraction coupling, long action potential duration that prohibits tetany, and maximal recruitment for every heart beat. Thus, contraction is regulated by recruitment of myofilaments either through the size of the Ca 2+ transient or through regulation of Ca 2+ sensitivity. The mechanism of sympathetic positive ionotropy is described in detail. The force–frequency relation is described. The lusitropic effect is introduced. The mechanism of action of cardiac glycosides is discussed. Finally, the modulation of cardiac force by stretch is described.

This chapter begins with a discussion of the structure of atoms. It describes in general terms electron orbitals and the origin of chemical bonding by sharing electrons in the outer orbitals. The results of these bondings give rise to specific geometric shapes in molecules. The structure of methane, ethane, and ethylene is described. Typical bond energy, length, and angles are described. This chapter defines enthalpy. Various types of isomers are also described. The ionic character of bonds that share electrons unequally is described. The concept of electronegativity is discussed. This chapter describes polar bonds and dipole moments and how these produce intermolecular forces. Other intermolecular forces such as hydrogen bonding and London dispersion forces are also discussed. This chapter ends with a discussion of the dynamic nature of chemical bonds.

This chapter describes how recruitment of which motor neurons with what frequency is the basis of neural control of movement. The lower motor neurons are arranged topologically within the cord, according to myotome and topologically arranged in the ventral horn. The spinal reflexes form a base upon which the motor cortex triggers movement. The somatotopic organization of the motor cortex is described. How motor tasks are initiated, refined and executed is described in terms of the premotor cortex, supplementary motor cortex, somatosensory cortex, and sensory association area. Lesions of these produce apraxia or neglect syndromes. The role of the basal ganglia (caudate nucleus, putamen, internal globus pallidus and external globus pallidus, subthalamic nucleus, and substantia nigra) is discussed, in particular with regard to Parkinsonism. The role of the cerebellum is described. How rotational acceleration and gravity is assessed by hair cells in the ampullary crests of the semicircular canals of the inner ear and in the utricle and saccule is described.