BIOS 252 MIDTERM EXAM STUDY GUIDE – ANATOMY AND PHYSIOLOGY, Exams of Animal Anatomy and Physiology

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BIOS 252 MIDTERM EXAM STUDY GUIDE –

ANATOMY AND PHYSIOLOGY

Chapter 11 Muscles ● Muscle cells: cell specialized for the function of movement. A device for converting the chemical energy of ATP into mechanical energy of movement ● The functions of Muscles 0 Muscle function include: movement, stability, control of openings, heat production, and glycemic control ● Movement: 0 Move from place to place; move body parts; move body contents in breathing, circulation, and digestion ○ In communication: speech, writing, facial expression and other nonverbral communications ● Stability 0 Maintain posture by preventing unwanted movements ○ Antigravity muscles: prevent us from falling over ○ Stabilize joints by maintaining tension ● Control of openings and passageways 0 Sphincters: internal muscular rings that control the movement of food, blood, and other materials within body ● Heat Production by skeletal muscles 0 As much as 85% of our body heat ● Glycemic Control 0 Muscles absorb and store glucose which helps regulate blood sugar concentration within normal ranges Structural and Functional Organization of Muscles ● About 600 human skeletal muscles ● Constitutes about half of our body weight ● Three kinds of muscle tissue 0 Skeletal, cardiac, smooth ● Specialized for one major purpose

0 Converting the chemical energy in ATP into the mechanical energy of motion ● Myology: the study of the muscular system Universal Characteristics of Muscle ● Excitability (responsiveness) 0 To chemical signals, stretch, and electrical changes across the plasma membrane. All living things have this property but muscle and nerve cells to the highest degree ● Conductivity ○ Muscle cells produce more than a local effect. Local electrical excitation sets off a wave of excitation that travels along the muscle fiber and initiates processes leading to contraction ● Contractility ○ Shortens when stimulated. This enables them to pull on bones and other organs to create movement ● Extensibility ○ Capable of being stretched between contractions. Most cells rupture if they are stretched. Muscle cells can stretch 3x their contracted length ● Elasticity 0 Returns to its original rest length after being stretched. If they didn't have this elastic recoil, resting muscles would be too slack Skeletal Muscle Tissue: ● Skeletal muscle: defined as voluntary, striated muscle that is usually attached to one or more bone. ● Made of muscle fibers- because of their length, skeletal muscle cells are usually called muscle fibers or myofibers- long thin cells (up to 30 cm) ● Most skeletal muscles attach to bone ● Contains multiple nuclei adjacent to the plasma membrane ● Striations: altering dark and light transverse bands-reflecting overlapping arrangement of their contractile proteins ● Voluntary: conscious control over skeletal muscles; involuntary (not usually under conscious control) and they are never attached to bones ● Skeletal muscle is composed not only of muscular tissue, but also of fibrous connective tissue: the endomysium, that surrounds each muscle fiber. The perimysium that bundles muscle fibers together into fascicles. And the epimysium that encloses the entire muscle. These connective tissues are continuous with collagen fibers of tendons and

those in turn with the collagen of the bone matrix. When a muscle fiber contracts it pulls on these collagen fibers and typically moves a bone. ● Collagen is neither excitable not contractile, but it is extensible and elastic. When a muscle lengthens (extension of a joint) collagenous component resist excessive stretching and protect the muscle from injury. ● When the muscle relaxes, elastic recoil of collagen may help return the muscle to its resting length and keep it from becoming too laccid. Cardiac and smooth muscle have special structure and physiological properties in common with each other, but different from those of skeletal muscle. There are related to their distinctive functions. Any of the 3 types of muscle cells can be called myocytes,. This term is preferable to muscle fiber for smooth and cardiac muscle because these 2 types of cells do not have the long fibrous shape of skeletal muscle cells. They are relatively short and have one or two nuclei. Cardiac muscle cells are also called cardiomyocytes. Cardiac and smooth muscles are involuntary muscle tissues, not usually subject to our conscious control. They receive no innervation from somatic motor neurons, but cardiac muscle and some smooth muscle receive nerves from the sympathetic and parasympathetic divisions of the ANS Cardiac Muscle Tissue ● Limited to the heart where it functions to pump blood ● Cardiomyocytes are branched, shorter than skeletal muscle fibers ● Contains one centrally located nucleus ● Intercalated discs join cadiomyocutes end to end 0 Provide electrical and mechanical connection (gap junctions allow them to stimulate their neighbor) ● Striated and involuntary (not under conscious control) ● Autorhythmic ● Use aerobic respiration Smooth Muscle Tissue ● Made of fusiform myocytes lacking striations 0 Cells are relatively short and have one central nucleus ● Involuntary function ● Smooth muscle doesnt form organs in itstelf but forms layers in the walls of large organs ○ Most visceral muscles-making up part of walls of hollow organs

● Myocutes are small allowing for fine control of such tissues and organs as a single hair, the iris of the eye, and the tiniest arteries. ● Not always innervated but when it is, the nerve supply is autonomic. ● Varicosite- periodic swellings along its length. Contains synaptic vesicles from which it releases neurotransmitters. Norepinephrine form sympathetic and ach from parasympathetic Organization of Skeletal Muscle ● Muscle fiber (Cell) 0 Endomysium: Thin sleeve of loose connective tissue around each fiber ○ Allows room for capillaries and nerve fibers ○ Provides chemical environment for muscle fiber ● Fascicles: bundles of muscle fibers wrapped together 0 Perimysium: Thicker layer of connective tissue that wraps fascicles ○ Carries nerves, blood vessels, and stretch receptors ● Whole Muscle 0 Epimysium: fibrous sheath surrounding entire muscle ○ Outer surface grades into fascia; inner surface projections form perimysium ● Fascia: a sheet of connective tissue that separates neighboring muscles of muscle groups from each other and the subcutaneous tissue Structure of a Skeletal Muscle Fiber ● Sarcolemma: plasma membrane of a muscle fiber ● Sarcoplasm: cytoplasm of a muscle fiber occupied by 0 Myofibrils: long protein cords occupying most of the sarcoplasm ○ Glycogen: carbohydrate stored to provide energy for exercise ○ Myoglobin: red oxygen binding pigment; provides some oxygen needed for muscle activity ● Multiple Nuclei: flattened nuclei pressed against the inside of the sarcolemma.This multinuclear condition results from the embryonic development of muscle fiber- several stem cells called myoblasts fuse to produce each fiber. With each myoblast contributing one muscleus. Some myoblast remain unspecialized satellite cells between the muscle fiber and endomysium. These play an important role in the regeneration of damaged skeletal muscle ● Mitochondria: packed into spaces between myofibrils ● Sarcoplasmic Reticulum: smooth ER that forms a network around each myofibril 0 Terminal cisterns: dilated end sacs of ST which cross the muscle fiber from one side to another

○ Acts as a calcium reservoir; it releases calcium through channels to activate contraction ● T Tubules: tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side ● Triad: a T tubule and two terminal cisterns associated with it Muscle contraction requires a lot of calcium ions. A high concentration of calcium in the cytosol is letal- it can react with phosphate ions and create calcium phosphate crystals, and can trigger cell death by apoptosis. At rest the muscle stores its calcium in the sarcoplasmic reticulum, safely bound to a protein called calsequestrin. In a resting muscle fiber, calcium is about 10,ooox as concentrated in the SR as it is in the cytosol. When the cell is stimulated ion gates in the SR open and calcium floods into the cytosol to activate contraction. The T tubule signals the SR when to release these calcium burs Myofilaments: long portotein cords hat fill most of the muscle cell. Each myofibril is a bundle of parallel protein microfilaments called myofilaments. There are 3 kinds of myofilaments Molecular Structure of Thick Filaments ● Thick filaments (1): made of several hundred myosin molecules 0 Each molecule shaped like a golf club

■ Two chains intertwined to form a shaft-like tail ■ Double globular head ○ Heads directed outward in a helical array around the bundle ■ Heads on one half of the thick filament angle to the left, while head on other half angle to the right ■ Bare zone with no heads in the middle Molecular Structure of Thin Filaments (2) ● Composed primarily of two intertwined strands of a protein called Fibrous (F) Actin 0 Each F Actin is like a beaded necklace-String of globular (G) actin subunits each with an active site that can bind to head of myosin molecule ● Thin filaments also have 40-60 molecules of another protein called Tropomyosin. When a muscle fiber is relaxed, each tropomyosin blocks the active site of six or 7 G actins and prevents myosin from binding to them. Each tropomyosin molecule in turn has a smaller calcium-binding protein called troponin, bound to it ● Troponin Molecule: Small, calcium-binding protein on each tropomyosin molecule ● Elastic Filaments (3) : 0 made of a huge springy protein called titin. ○ They run through the core of each thick filament and anchor it to a structure called Z discs, at one end, and M line at the other. ○ Titin stabilizes the thick filaments, center it between the thin filaments, prevents overstretching and recoils like a spring after a muscle is stretched

Sarcomere ● The myofilaments, along with several other proteins, are organized into a series of repeating structures called sarcomeres. A sarcomere is the functional contractile unit of a muscle fiber 0 Segment from Z disc to Z disc ● The striations visible in skeletal and cardiac muscle are the result of precise organization of myosin and actin within the sarcomere ● A band: dark “A” stands for anisotropic 0 Darkest part is where thick filaments overlap a hexagonal array of thin filaments ○ H band: not as dark; middle of A band; thick filaments only ○ M line: Middle of H band ● I Band: light; “I” stands for isotropic 0 The way the bands reflect polarized light ○ Z disc: provides anchorage for thin filaments and elastic filaments ■ Bisects I band

● Muscle cells shorten because their individual sarcomeres shorten 0 Z disc (z lines) are pulled closer together as thick and thin filaments slide past each other ● Neither thick or thin filaments change length during shortening 0 Only the amount of overlap changes ● During shortening, dystrophin and linking proteins also ull on extracellular proteins ○ Transfers pull to extracellular tissue The Nerve- Muscle Relationship ● Skeletal muscle never contracts unless stimulated by a nerve ● If nerve connections are severed or poisoned, a muscle is paraluzed 0 Denervation atrophy: shrinkage of paralyzed muscle when nerve remains disconnected

Motor Units ● Somatic motor neurons 0 Nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles ● Somatic motor fibers: their axons that lead to the skeletal muscle ● Each nerve fiber branches out to a number of muscle fibers ● Each muscle fiber is supplied by only one motor neuron ● Motor unit: one nerve fiber and all the muscle fibers innervated by it Muscle fibers of one motor unit ● Dispersed throughout muscle ● Contract in unison ● Produce weak contraction over wide area ● Provide ability to sustain long-term contraction as a motor units take turns contracting ● Effective contraction usually requires contraction of several motor units at once ● Average motor unit contains 200 muscle fibers ● Small motor units-fine degree of control 0 Three to siz muscle fibers per neuron ○ Eye and hand muscles ● Large motor units- more strength than control 0 Powerful contraction supplied by large motor units with hundreds of fibers ○ Gastrocnemius of calf has 1,00 muscle fibers per neuron Neuromuscular Junction ● Synapse: point where a nerve fiber meets its target cell ● Neuromuscular junction (NMJ): when target cell is a muscle fiber ● Each terminal branch of the nerve fiber within the NMJ forms separate synapse with the muscle fiber ● One nerve fiber stimulates the muscle fiber at several points within the NMJ 0 Axon terminal: swollen end of nerve fiber ○ Contains synaptic vesicles with acetylcholine (ACh)

○ Synaptic cleft: gap between axon terminal and sarcolemma ○ Schwann cell envelopes and isolates NMJ ● Nerve impulse causes synaptic vesicles to undergo exocytosis releasing Ach into synaptic cleft ● Muscle cell has millions of ACh receptors-proteins incorporated into its membrane 0 Junctional folds of sarcolemma beneath axon terminal increases surface area holding ACh receptors. The muscle nuclei beneath the folds are specifically dedicated to the synthesis of ACh receptors and other proteins of the sarcolemma. ■ Lack of receptors causes weakness in myasthenia gravis ● The entire neuromuscular junction is enclosed in a basal lamina. ● Basal Lamina: thin layer of collagen and glycoprotein separating schwann cell and muscle from surrounding connective tissues 0 Contains acetylcholinesterase (AchE) that breaks down ACh, allowing for relaxation Electrically Excitable cells ● Muscle and nerve cells are regarded as electrically excitable cells because their plasma membranes exhibit voltage changes in response to stimulation. The study of the electrical activity of cells, called electrophysiology, is a key to understanding nerve activity and muscle contraction. ● The electrical activity of cells hinges on differences in the concentration of ions in the intracellular fluid (ICF) and extracellular fluid (ECF) adjacent to the plasma membrane.

The ICG contains a greater concentration of negative anions than the ECF does. Especially negatively charged proteins, nucleic acids, and phosphates, which are trapped in the cell and give its interior a net negative charge. ● That means the membrane is polarized. Also contained in the IC is a great excess of potassium ions whereas the ECF contains a great excess of sodium ions. THe electrical events that initiate muscle contraction are driven by the movement of these two cations through the membrane when a muscle or nerve cell is excited ● A difference in electrical charge from one point to another is called an electrical potential or voltage. On the sarcolemma of muscle cell, the voltage is about -90 mV. The negative sign refers to the relatively negative charge on the intracellular side of the membrane. This voltage is called resting membrane potential (RMP). It is maintained by the sodium potassium pump. ● When a nerve or a muscle cell is stimulated ion channels in the plasma membrane open and sodium instantly flows into the cell, driven both by its concentration difference across the membrane and by its attraction to the negative charge of the cell interior- flows down and electrochemical gradient. ● These Na+ cations override the negative charge jus inside the membrane, so the inside of the membrane briefly becomes positive. This is called depolarization of the membrane. Immediately, Na+ channels close and K+ channels open. K+ rushes out of the cell, party because it is repelled by the positive sodium charge, in part because it is more concentrated in the ICF than the ECF- flows down its electrochemical gradient opposite from the sodium movement. The loss of K+ ions from the cell turns the inside of the membrane negative again (repolarization) this quick up and down voltage shift the negative RMP to a positive value and then back to RMP again, is called an action potential. ● Action potentials have a way of perpetuating themselves- an action potential at one point on a plasma membrane causes another one to happen immediately in front of it , which triggers another one a little farther along, and so forth. ● A wave of action potentials spreading along a nerve fiber like this is called a nerve impulse or nerve signal. These travel along the sarcolemma of a muscle fiber Clinical Application: Neuromuscular Toxins and Paralysis ● Toxins that interfere with synaptic function can paralyze the muscles. Cholinesterase inhibitors, bind to AChE and prevent it from degrading ACh. Depending the doe dose, this can prolong the action of ACh and produce spastic paralysis, a state in which the muscles contract and cannot relax; clinically this is called a cholinergic crisis. Another exaple of spastic paralysis is tetanus (lockaw) caused by the toxin of a soil bacterium.

● In the spinal cord a neurotransmitter called glycine normally stops motor neurons from producing unwanted muscle contractions. The tetanus toxin blocks glycine release and thus causes overstimulation and spastic paralysis of the muscles. ● Flaccid paralysis: sis a state in which the muscles are limp and cannot contract. It poses a threat of death by suffocation if it affects the respiratory muscles. Botulism (food poisoning) botulinum toxin blocks ACh release. Used in Botox shots. Excitation of a Muscle Fiber

1. Nerve signal arrives at the axon terminal and opens voltage-gated calcium channels. Calcium ions enter the terminal
2. Calcium stimulates the synaptic vesicles to release acetylcholine (ACh) into the synaptic cleft. One action potential causes exocytosis of about 60 vesicles, and each vesicle releases about 10,000 molecules of ACh
3. ACh diffuses across the synaptic cleft and binds to receptors on the sarcolemma
4. These receptors are ligand-gated ion channels. Two ACh molecules must bind to each receptor to open the channel. When it opens, Na+ flows quickly into the cell and K+ flows out. The voltage on the sarcolemma quickly rises to a less negative value as Na+ enters the cell, then falls back to RMP as K+ exits. This rapid up- and- down fluctuation in voltage at the motor end plate is called end-plate-potential (EPP)

5. Areas of the sarcolemma next to the end plate have voltage-gated ion channels that open in response to the EPP. some of these are specific for Na+ and admit it to the cell, while others are specific for K+ and allow it to leave. These ion movements create an action potential. The muscle fiber is now excited Excitation Contraction-Coupling : refers to events that link action potentials on the sarcolemma to activation of myofilaments preparing them to contract
6. A wave of action potentials spreads from the motor end plate in all directions, like ripples on a pond. When this wave of excitation reaches the T tubules, it continues down them into cell interior
7. Action potentials open voltage-gated ion channels in the T tubules. These are linked to calcium channels in the terminal cisterns of the sarcoplasmic reticulum (SR). Thus,

channels in the SR open and calcium diffuses out of the SR, down its concentration gradient into the cytosol

8. Calcium binds to the troponin of the thin filaments
9. The troponin-tropomyosin complex changes shape and exposes the active sites on the actin filaments. This makes them available for binding to myosin heads Contraction:muscle fiber develops tension and may shorten. The mechanism of contraction is called the sliding filament theory. It holds that the myofilaments do not become any shorter during contraction, rather the thin filaments slide over the thick ones and pull Z discs behind them, causing each sarcomere as a whole to shorten
10. The myosin head must have an ATP molecule bound to it to initiate contraction, Myosin ATPase, an enzyme in the head, hydrolyzes this ATP into ADP and phosphate (Pi). The energy released by this process activates the head, which “cocks” into an extended, highenergy position. The head temporarily keeps the ADP and Pi bound to it
11. The cocked myosin binds to an exposed active site on the thin filament, forming a crossbridge between the myosin and actin

12. Myosin releases the ADP and Pi and flexes, to a bent, low-energy position, tugging the thin filament along with it. This is called the power stroke. The head remains bound to actin until it binds a new ATP
13. The binding of new ATP to myosin destabilizes the myosin-actin bond, breaking the cross-bridge. THe myosin head now undergoes a recovery stroke. It hydrolyzes the new ATP, recocks (returns to step 10), and attaches to a new active site farther down the thin filament, ready for another powerstroke Relaxation
14. Nerve signals stop arriving at the neuromuscular junction, so the axon terminal stops releasing ACh
15. As ACh dissociates (separates) from its receptor, AChE breaks it down into fragments that cannot stimulate the muscle. The axon terminal reabsorbs these fragments for recycling. All of this happens continually while the muscle is stimulated, too, but when

nerve signals stop, no more ACh is released to replace that which breaks down. Therefore, stimulation of the muscle fiber by ACh ceases

16. Forms excitation through contraction, the SR simultaneously releases and reabsorbs ca2+; but when the nerve fibers stop firing and excitation ceases, ca2+ release also ceases and only its reabsorption continues
17. Owing to reabsorption by the SR, the level of free calcium in the cytosol falls dramatically. Now, when calcium disassociates form troponin, it is not replaced
18. Tropomyosin moves back into the position where it blocks the active sites of the actin filament. Myosin can no longer bind to actin, and the muscle fiber ceases to produce or maintain tension

Rigor Mortis ● Rigor Mortis: hardening of muscles and stiffening of body beginning 3 to 4 hours after death ○ Deteriorating sarcoplasmic reticulum releases Ca+ ○ Deteriorating sarcolemma releases ca+2 to into the cytosol and the deteriorating sarcolemma admits more calcium from the extracellular fluid ○ Ca+2 activates myosin-actin cross-bridging. Once bound to actin myosin cannot release it without first binding to an ATP molecule, and there is not ATP available in a dead body. Thus the thick and thin filaments remain rigidly cross-linked until the myofilaments begin to decay. ○ Muscle contracts, but cannot relax ● Muscle relaxation requires ATP, and ATP production is no longer produced after death ○ Fibers remain contracted until myofilaments begin to decay ● Rigor Mortis peaks about 12 hours after death, then diminishes over the next 48- hours Length-Tension Relationship ● Length-tension relationship: the amount of tension generated by a muscle depends on how stretched or shortened it was before it was stimulated ○ If overly shortened before stimulated, a weak contraction results, as thick filaments just butt against Z discs ○ If too stretched before stimulated, a weak contraction results, as minimal overlap between thick and thin filaments results in minimal cross bridge formation ● Between these 2 extremes is an optimal resting length at which muscles respond. ● Optimum resting length produces greatest force when muscle contracts

○ If the sarcomeres are less than 60% or more than 175% of their optimal length, they develop no tension at all in response to stimulus ○ The nervous system maintains muscle tone (partial contraction) to ensure that resting muscles are near this length Muscle Metabolism ● All muscle contraction depends on ATP, no other energy source can serve in its place. ● ATP supply depends on the availability of: ○ Oxygen and organic energy sources (glucose and fatty acids) ● Two main pathways of ATP synthesis ● Anaerobic Fermentation ○ Enables cells to produce ATP in the absence of oxygen ○ Yields little ATP and lactate, which needs to removed from the muscles and be disposed of by the liver ● Aerobic Respiration ○ Produce far more ATP ○ Does not generate lactate ○ Requires a continual supply of oxygen ○ In resting muscle, most ATP is generated by the aerobic respiration of fatty acids Immediate Energy ● Short intense exercise (100m dash) ○ Oxygen is briefly supplied by myoglobin but is rapidly depleted

○ Until the respiratory and cardiovascular system catch up with the heightened oxygen demand, Muscles meet most ATP demand by borrowing phosphate groups from other molecules and transferring them to ADP ● Two enzyme systems control these phosphate transfers ○ Myokinase: transfers Pi from one ADP to another, converting the latter to ATP that myosin can use ○ Creatine Kinase: obtains Pi from a phosphate-storage molecule creatine phosphate (CP) and gives it to ADP to make ATP. This is a fast acting system that helps to maintain the ATP level while other ATP generating mechanisms are being activated ● Phosphagen system: the combination of ATP and CP which provides nearly all the energy for short burst of activity ○ Enough energy for 6 seconds of sprinting or one minute of brisk walking ○ Amount of ATP in muscle changes very little but the amount of creatine phosphate drops rapidly. ○ Especially important in activities requiring short bursts of maximal effort such as football, baseball, and weight lifting Short-Term Energy ● As the phosphagen system is exhausted, muscles shift to anaerobic fermentation to generate ATP by glycolysis. The point at which this occurs is called Anaerobic threshold/ Lactate threshold because one can begin to detect a rise in blood lactate levels at this time. ○ During the anaerobic phase Muscles obtain glucose from blood and their own stored glycogen and metabolize it to lactate. ○ In the absence of oxygen, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed ○ Converts glucose to lactate ● Anaerobic threshold( lactate threshold): point at which lactate becomes detectable in the blood ● Glycogen-lactate system: the pathway from glycogen to lactate ● Produce enough ATP for 30 to 40 seconds of maximum activity ● Anaerobic fermentation is its final stemp, the conversion of pyruvate to lactate. ○ Playing basketball, running around a baseball diamond, depends heavily on this system Long-Term Energy ● After about 40 seconds, the respiratory and cardiovascular system “ catch up” and deliver oxygen to the muscles fast enough for aerobic respiration to once again meet most of the muscles ATP demand.

● Aerobic respiration produces more ATP per glucose than glycolysis does (typically another another 30 ATP per glucose) ○ Efficient means of meeting the ATP demands of prolonged exercise ○ After 3-4 minutes the rate of oxygen consumption levels off to a steady state where aerobic ATP production keeps pace with demand ○ In exercise lasting more than 10 minutes, over 90% of the ATP is produced aerobically. ○ For 30 minutes energy comes equally from glucose and fatty acids ○ Beyond 30 minutes, depletion of glucose and glycogen causes fatty acids to become the more significant fuel Fatigue and Endurance ● Muscle fatigue: progressive weakness and loss of contractility that results from prolonged use of muscle ● Fatigue in high-intensity exercise is thought to result from: ○ Potassium accumulation- in the T tubules reduces to excitability. Each action potential releases K+ from the sarcoplasm to the extracellular fluid. This lowers the membrane potential (hyperpolarizes) and makes the muscle fiber less excitable. This is especially significant in the T tubules where the low volume of ECF enables the potassium concentration to rise to a high level and interfere with the release of calcium from the SR ○ ADP/Pi Accumulation- The hydrolysis of ATP generates an pool of ADP+ Pi. Excess ADP and Pi slow cross-bridge cycling mechanism of contraction. Free phosphate inhibits calcium release from the SR and decrease force production in myofibrils. ● Fatigue in low- intensity (long duration) exercise is thought to result from: ○ Fuel depletion as glycogen and glucose levels decline leaving less fuel for ATP synthesis. Long distance runners call this “hitting the wall” carbo-load before the race, loading muscles with extra glycogen ○ Electrolyte loss -through sweat can decrease muscle excitability because it alters the ion balance of the ECF ○ Central fatigue- exercising muscles generates ammonia, which is absorbed by the brain and inhibits motor neurons of the cerebrum. FOr this reason, the central nervous system produces less signal output to the skeletal muscles. This is where psychological factors come into play, so as will to persevere and complete a marathon. ● Discredited hypothesis of fatigue: ATP depletion is no longer thought to cause fatigue; the ATP level in fatigued muscle is almost as great as in rested muscle. Lactic acid does not lower pH in the muscle fibers. Liver removes lactate about as fast as the muscle produces

it, so it doesn't accumulate in the muscle tissue and has little do with fatigue Fatigue and Endurance ● Maximum oxygen uptake (VO2 max) is a major determinant of one's ability to maintain high-intensity exercise for more than 4-5 minutes ○ Vo2max: the point at which the rate of oxygen consumption plateaus and does not increase further with added workload ■ Proportional to body size ■ Peaks at around age 20 ■ Usually greater in males than females ■ Can be twice as great in trained endurance athletes as in untrained person Excess Postexercise Oxygen Consumption (EPOC) ● EPOC meets a metabolic demand also known as oxygen debt- why you breath heavily for several minutes after strenuous exercise. ● It is the difference between the elevated rate of oxygen consumption following exercise and the usual resting rate ● Needed for the following purposes: ○ To aerobically replenish ATP (some of which helps regenerate CP stores) ○ To replace oxygen reserves on myoglobin ○ To provide oxygen to liver that is busy disposing of lactate ○ To provide oxygen to many cells that have elevated metabolic rates after exercise ● ATP and CP are replenished in the early minutes of heaviest post exercise breathing, and oxygen consumption remains elevated for as much as an hour more as the liver oxidizes lactate ● EPOC can be as much as six times one’s basal oxygen consumption( and last an hour) indicating that anaerobic mechanisms of ATP production during exercise allow 6x as much physical exertion as would have been possible without those mechanisms Physiological Classes of Muscle Fibers ● Fast versus slow-twitch fibers can predominate in certain muscle groups ○ Muscles of the back contract relatively quickly (100 ms to peak tension) whereas muscles that move the eyes contract quickly (8ms to peak tension) ● Slow-twitch, slow oxidative (SO), red or type I fibers ○ Well adapted for endurance; resist fatigue by oxidative ( aerobic) ATP production ○ Important for muscles that maintain posture (e.g. erector spinae of the back, soleus of calf) ○ Fatigue resistance stems from their oxidative mode of ATP production- (aerobic respiration) ○ Oxidative metabolism requires a liveral supply of oxygen and the means to use it efficiently. Therefore, these fibers are surrounded by a dense network of blood capillaries that are rich in mitochondria. And have high concentrations of

myoglobin, the red pigment that facilitates diffusion of oxygen from the blood into the muscle fiber ○ Slow twitch fibers are relatively thin which minimizes the distance that oxygen must diffuse. ○ Slowness of these muscles is due to the sarcoplasmic reticulum that is slow to release and reabsorb calcium. ○ Slow twitch muscles Contain a form of myosin with slow ATPase that is slow in its ATP hydrolysis and cross bridge cycling ○ Grouped in small motor units controlled by small, easily excited motor neurons allowing for precise movements Physiological Classes of Muscle Fibers ● Fast-twitch, fast glycolytic (FG), white, or type llB /llx fibers ○ Fibers are well adapted for quick responses ○ Important for quick and powerful muscles: eye and hand muscles, gastrocnemius of calf and biceps brachii ○ Contains a form of myosin with fast ATPase that hydrolyzes ATP quickly and large SR that releases calcium quickly ○ Utilize glycolysis and anaerobic fermentation for energy- produces ATP quickly but less efficiently than aerobic respiration. TO support this they contain: ■ Abundant glycogen and creatine phosphate- aids in rapidly regenerating ATP ■ They have fewer mitochondria than slow-twitch fibers because thick fibers are stronger and they have no need for especially rapid oxygen delivery to the deepest cytoplasm. ■ Without need for such rapid oxygen uptake they have less myoglobin. Lack of myoglobin gives them pale (white) appearance and why they are sometimes called white fibers. ○ Fibers are thick and strong ○ Grouped in large motor units controlled by larger, less excitable neurons allowing for powerful movements ○ These fibers fatigue more easily. ● Fast twitch, intermediate, or typeIIA fibers ○ Fast twitch but aerobic-fatigue resistant metabolism ○ Known in other animals but rare in humans ● Every muscle contains a mix of fiber types, but one type predominates depending on muscle function ● Fiber type within a muscle differs across individuals

○ Some individuals seem genetically predisposed to be sprinters, while others are more suited for endurance In humans, small motor units are composed of relatively small SO muscle fibers and supplied by relatively small but easily excited motor neurons. These motor units are not as strong as large ones but produce more precise movements. Large motor units are composed of larger FG fibers: supplied by larger, less excitable neurons; and produce more power but less fine control. In the multiple motor unit summation discussed earlier, the nervous system recruits small (SO) motor units first, then larger FG motor units only if more strength is needed for a particular task. Muscle composed mainly of SO fiber are called red muscles. And those composed of FG fibers are called white muscles because of the color difference stemming from their difference in myoglobin content. Meat- thighs dark meat composed of fibers adapted to long periods of sanding and breast is white meat composed of fg fibers adapted for short burns of power when the bird is taking flight. Behavior of Whole Muscles ● Myogram: a chart of the timing and strength of a muscles contraction ● Threshold: minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction ● Twitch: a quick cycle of contraction and relaxation when stimulus is at threshold or higher ● Latent Period: very brief delay between stimulus and contraction ○ Time required for excitation, excitation-contraction coupling, and tensing of elastic components of muscle (the force generated during this time is called internal tension) It is not visible on a myogram because there is no shortening of the muscle. ● Contraction phase: time when muscle generates external tension and move a resisting object or load such as a bone or body limbps ○ Force generated can overcome the load and cause movement ● Relaxation phase: time when tension declines to baseline ○ SR reabsorbs ca2+, myosin releases actin and tension decreases ○ Takes longer than contraction (muscles contracts faster than it relaxes) ● Entire twitch duration varies between 7 and 100ms

Contraction Strength of Twitches ● With subthreshold stimuli-no contraction at all ● At threshold intensity and above-twitch produced ● Even if the same voltage is delivered, different stimuli causes twitches varying in strength, because: ○ The muscle’s starting length influences tension generation (length-tension relation) ○ Muscles fatigue after continual use- twitches become weaker as muscles fatigue ○ Vary with temperature of the muscle- warmed up muscle contracts more strongly because enzymes such as the myosin head work more quickly ○ Muscle cells hydration level, affects the spacing between thick and thin filaments and therefore the ability to form myosin-actin cross bridges influences crossbridge formation ○ Increasing the frequency of stimulus delivery increases tension output. Stimuli arriving close together produce stronger twitches than stimuli arriving at longer time intervals The Relationship Between Stimulus Intensity (Voltage) and Muscle Tension ● Muscles must contract with variable strength for different tasks (lifting a glass of champagne versus lifting a barbell) ● Stimulating the nerve with higher voltages produces stronger contraction ○ Higher voltages excite more nerve fibers which stimulate more motor units to contract

○ Recruitment or multiple motor unit (MMU) summation- the process of bringing more motor units into play with stronger stimuli. How the nervous system behaves naturally to produce varying muscle contractions. The neuromuscular system behaves according to the size principle. ○ Size principle: weak stimuli (low voltage) recruit small units, while strong stimuli recruit small and large units for powerful movements. Smaller, less powerul motor units with smaller, slower nerve fibers are activated first. This is good for delicate task and refined movements. If more power is needed then larger motor units with larger, faster nerve fibers are subsequently activated The Relationship Between Stimulus Frequency and Muscle Tension ● High frequency stimulation produces stronger twitches than low frequency stimulation ● When muscle is stimulated at low frequency (5-10 stimulus) it produces an identical twitch for each stimulus and fully recovers between twitches ● Higher frequency stimuli (eg., 20 stimuli/s) produce temporal (wave) summation ○ Each new twitch arrives before the previous twitch is over. It rides on the previous one generating higher tension ○ Only partial relaxation between stimuli resulting in fluttering, incomplete tetanus