VPHY 101 Module 3: Muscle Physiology Notes PDF

VPHY 101 MODULE 3: MUSCLE PHYSIOLOGY CATEGORIZATION OF MUSCLE Sarcomere – an area between two Z lines (functional unit of a muscle) BASIC STRUCTURES OF MUSCLES...

VPHY 101 MODULE 3: MUSCLE PHYSIOLOGY CATEGORIZATION OF MUSCLE Sarcomere – an area between two Z lines (functional unit of a muscle) BASIC STRUCTURES OF MUSCLES H zone – the lighter are in the middle of A band where thin filaments do not reach Muscle M line – made up of supporting proteins, extends vertically down the  A highly organized microfilament-based structure middle of the A band within the center of H zone  A specialized cell that contracts to pull an external structure or squeeze a fluid  Can produce a force that can be transmitted over a considerable distance and can generate large and often rapid movements  Largest group of tissue in the body (most vertebrates)  40% of the body weight of human males SKELETAL MUSCLE  32% of the body weight of human females  25% of the body weight of hummingbirds STRUCTURE OF SKELETAL MUSCLE  Can shorten and develop tension from highly developed microfilament system – enable them to produce force and do work  Converts the chemical energy of ATP into mechanical energy that can act on the environment in response to electrical signal 3 TYPES OF MUSCLES LEVELS OF ORGANIZATION IN A SKELETAL MUSCLE  Skeletal  Cardiac  Smooth WHAT CAN CONTRACTION OF MUSCLES DO? FIGURE 8-2 Levels of organization in a skeletal muscle. Note in the cross section of a myofi bril in part (c) that each thick fi lament is surrounded by six thin fi laments, and each thin fi lament is surrounded by three thick fi laments. Also note only a  Purposeful locomotory movement small portion of titin (which spans the whole sarcomere) is shown.  Manipulation of external objects  Propulsion of contents  Emptying of contents of certain organs - Urination MYOFIBRIL - Emptying of bile  Production of heat as a metabolic by-product - Thermoregulation  Production of sound TERMINOLOGIES A band – consist of a stacked set of thick filaments with a portion of thin filament that overlap on both ends of the thick filaments I band – consist of remaining portion of the thin filaments that do not project into the A band Z line – a flat cytoskeletal disc a line visible in the middle of each I band STRUCTURE OF MYOSIN FILAMENT thin fi lament is two chains of spherical actin molecules that are twisted together. SKELETAL VS SMOOTH VS CARDIAC MUSCLES Troponin molecules (which consist of three small, spherical subunits) and threadlike tropomyosin molecules are arranged to form a ribbon that lies alongside SIMILARITY the groove of the actin helix and physically covers the binding sites on actin molecules for attachment with myosin cross bridges. (The thin fi laments shown  both have specialized contractile apparatus (thin and thick here are not drawn in proportion to the thick fi laments in Figure 8-4. Thick fi filaments) laments are two to three times larger in diameter than thin fi laments.)  needs calcium for contraction  directly uses ATP as energy source of cross- bridge cycling DIFFERENCES  structure and organization of fibers  mechanism of excitation and contraction  distinction in contractile response FIGURE 8-4 Structure of myosin molecules and their organization within a thick fi lament. (a) Each myosin molecule consists of two identical, golf-club-shaped subunits with their tails intertwined and with globular heads each containing an DIFFERENCE BETWEEN SMOOTH AND SKELETAL MUSCLE ANATOMY actin-binding site and a myosin ATPase site, projecting out at one end. (b) A thick fi lament is made up of myosin molecules lying lengthwise parallel to one another. Half are oriented in one direction and half in the opposite direction. The globular heads, which protrude at regular intervals along the thick fi lament, form the cross bridges. COMPOSITION OF THIN FILAMENT FIGURE 8-7 Changes in banding patt ern during shortening. During muscle contraction, each sarcomere shortens as the thin fi laments slide closer together between the thick fi laments so that the Z lines are pulled closer together. The width of the A bands does not change as a muscle fiber shortens, but the I bands and H zones become shorter. FIGURE 8-5 Composition of a thin fi lament. The main structural component of a ROLES OF CALCIUM SKELETAL MUSCLE CELLS  striated and voluntary  large, cylindrical, multinucleated (syncytium)  lies in all skeletal muscles  extends in full length of skeletal muscles  with numerous myofibrils  with t – tubules  with sarcoplasmic reticulum SMOOTH MUSCLE CELLS  small and unstriated  Elongated, spindle-shaped, with single nucleus  Lie in the walls of hollow organs and tubes  Contraction exerts pressure on and regulates the SMOOTH MUSCLE CELLS CLASSIFICATION  forward movement of contents of hollow organs  and tubes  Phasic or Tonic  Does not extend the full length of a muscle  Multi-unit or Single-unit  Arrange in sheets  Neurogenic or Myogenic  Has three types of filaments - thick myosin filaments (longer than skeletal m) - thin actin filaments with tropomyosin only PHASIC VS TONIC - filaments of intermediate size (not contractile) Phasic – contracts in burst (hollow organs) triggered by the action  Do not form myofibril potential of the cytosolic contractions (e.g. digestive tract)  Not arranged in sarcomere  No banding, hence, the name smooth Tonic – partially contracted at all times (arterioles), this state of partial  No Z lines but have dense bodies (positioned throughout the contraction is called a tone. This type of muscle has a relatively low smooth muscle and attached to internal surface of the resting potential of -55mV to -40mV plasma membrane MULTI-UNIT OR SINGLE-UNIT Multi-unit is neurogenic – contractile activity is nerve-produce and phasic-contracting only when stimulated (walls of large blood vessels, large airways of the lung, muscle of the eye, iris of the eye, base of hair follicles) Single-unit (visceral smooth muscle) – become excited and contract as a single unit (functional syncytium)-presence of gap junctions 1. Multiunit a) Each muscle fiber is innervated separately b) Contracts only receive stimuli c) Can contract independent of each other d) Exist in bundles CARDIAC MUSCLE CELLS Examples:  Found only in the heart 1. Ciliary body  Has three major types: 2. Iris of the eye - Atrial 3. Arrector pili of muscle of skin hair 4. Walls of large blood vessels - Ventricular 5. Large airways to lungs - Excitatory and conductive muscle fibers 6. Muscles of the eye  Has intercalated disc 7. Base of hair follicles  Striated with thick and thin filaments  Thin filament has troponin and tropomyosin  Abundant mitochondria and myoglobin 2. Single-unit (visceral)  Has T-tubules  Self-excitable, display spontaneous electrical activity-do not  With moderately well-developed sarcoplasmic reticulum maintain a constant resting potential, myogenic  Calcium enters the cytosol both from ECF (voltage gated - Pacemaker potentials dihydropyridine receptor) and sarcoplasmic reticulum  Has pacemaker activity - Slow – wave potentials  Interconnected with gap junctions that enhance the spread of action potential throughout the heart  Innervated by autonomic NS  Influenced by hormones and local factors  Output is graded by controlling contraction frequency and modulating mechanical output of each cell  Fibers are joined together in a branching network  Action potential has much longer duration before repolarizing a) Large amount of muscle fibers b) Cell membranes are adherent with each other at multiple points MOLECULAR BASIS OF MUSCLE CONTRACTION (force of one fiber can be transferred to the next) c) Gap junctions that allow ions to flow freely from one muscle fiber to NEUROMUSCULAR JUNCTION the next.  a motor unit is consist of a motor neuron and muscle fibers that it innervates Examples: 1. Digestive tract  a motor axon is a myelinated one 2. Uterus  1 axon can terminate into many motor end plate 3. Ureters  the largest motor unit in which one supply many muscle fibers can be found in the limbs and the postural muscles  the smallest motor units in which one axon may supply one or only a few muscle fibers can be found in association with eye movements   the end bulb of each terminal branch makes contact with an SARCOPLASMIC RETICULUM individual muscle fiber at specialized area called the neuromuscular junction - a modified endoplasmic reticulum  it occurs at the approximate midpoint of the muscle fiber - important in turning the muscle on and off  the terminal branch of the axon does not actually make - consist of fine network of interconnected tubules contact with a muscle fiber, but is separated from it by gap surrounding is myofibril like a mesh sleeve junction approximately 50 nm wide which is known as synaptic cleft - it is not continuous  at the end plate of a motor neuron, there is the - the more sarcoplasmic reticulum, the more calcium pumps neurotransmitter acetylcholine, which is stored in the - located in between each A-bond and I-bond membrane-bound vesicle within the terminal branch of the axon  the NMJ functions as an amplifier for the spinal or cranial motor neuron action potential  sodium ions will propagate the action potential by opening and closing the calcium and sodium channels. FIGURE 8-10 Relationship between dihydropyridine receptors on the T tubule and ryanodine receptors (Ca2+-release channels) on the adjacent lateral sacs of the sarcoplasmic reticulum. FIGURE 8-9 The T tubules and sarcoplasmic reticulum in relationship to the myofi brils. The transverse (T) tubules are membranous, perpendicular extensions of the surface membrane that dip deep into the muscle fi ber at the junctions between the A and I bands of the myofi brils. The sarcoplasmic reticulum is a fi ne, membranous network that runs longitudinally and surrounds each myofi bril, with separate segments encircling each A band and I band. The ends of each segment are expanded to form lateral sacs that lie next to the adjacent T tubules. T – TUBULES AND SARCOPLASMIC RETICULUM (inside myofiber) RECEPTORS IN T TUBULES AND SARCOPLASMIC RETICULUM T – TUBULES FOOT PROTEIN /Calcium released channel/ryanodine receptors (SPR) - located at the A-bond of the mammalian and reptilian muscle, and the z- disk of the amphibian muscle - composed of four protein molecules which is located in the - these surface membrane dips deeply into the large muscle lateral sac of the sacoplasmic reticulum fiber to form a transverse tubule DIHYDROPYRIDINE RECEPTORS (T-tubules) - it runs perpendicularly from the surface of the muscle cell membrane into the center proportion of the muscle fiber - it would let a dihydropyridine drag bind to it - has 4 units of protein (these two are complementary with each other) - when the muscle relaxes, the h zone is longer. When the muscle contracts, the h zone becomes shorter  width of the A bands does not change as a muscle fiber shortens, but the I bands CROSS – BRIDGE CYCLE and H zones become shorter. USES OF ATP IN MUSCLE CONTRACTION  Indirect energy provider for power stroke  Detachment of cross bridging  Active transport of calcium SOURCE OF ATP  Phosphagen  Oxidative phosphorylation  Glycolysis FIGURE 8-7 Changes in banding patt ern during shortening. During muscle contraction, each sarcomere shortens as the thin fi laments slide closer together between the thick fi laments so that the Z lines are pulled closer together. The METABOLIC PATHWAYS PRODUCING ATP drawn to scale but is exaggerated. Note that the resting potential of a skeletal  Stop contracting after 30s of oxygen deprivation muscle fiber is –90 mV, compared to a resting potential of –70 mV in a neuron.  Has numerous lipid droplets FACTORS AFFECTING MUSCLE CONTRACTION  Gap junction in intercalated disks  Action potential spreads from fiber to fiber allowing  Neuromuscular block depolarization to spread in the entire heart  - Hypocalcemia  Muscle relaxants - Curare - Succinylcholine MECHANISM OF MUSCLE CONTRACTION  A muscle is composed of a tendon from end to end  a muscle is innervated by a motor neuron, which gives it signal to a particular muscle via neuromuscular junction  neuromuscular junction is where acetyl- chlorine is released  Acetyl-choline would trigger a muscle potential in the muscle fibers which lead to muscle contraction  the signal or action potential would travel from the muscular junction down to the depth of a muscle into its muscle fibers  muscle fibers are consist of many myofibril  each muscle fiber is composed of hundreds of myofibril  myofibril is composed of units or segments of sarcomere  sarcomere has may segments which are the m-line, z-line, a- band, I-bond EXCITATION-CONTRACTION COUPLING OF CARDIAC MUSCLE  One thick filament is composed of 6 thin filaments  during muscle contraction, the sarcomere would contracts or  Mechanism by which the action potential causes the gets shorter due to the cross-bridging of the myocin (main myofibrils of muscle to contract molecule of the thick filament) and the actine (major  Autorhythmic cells or pacemaker cells (SA node) molecule of the thin filaments)  Have T-tubules  Moderately-developed SR  2 sources of calcium CARDIAC MUSCLE PHJYSIOLOGY  Found only in the heart MUSCLE ADAPTATIONS  Striated  Form functional syncytium  Most adaptive tissue in animal body  Intercalated discs  Hypertrophy – increase in individual muscle fiber size  Reliant to aerobic metabolism  Hyperplasia – increase in the number of muscle fibers  Atrophy – decrease in the size of muscle that happens when a body part has been immobilized for a period of time and the muscles become smaller MORPHOLOGICAL DIFFERENCES  Energy source is mitochondria (40%) FIGURE 8-13 Relationship of an action  Uni nucleated each potential to the resultant muscle twitch. The duration of the action potential is not MUSCLE DISORDER (similar to the stretching spring) as a result of sarcomere shortening brought about by cross-bridge cycling.  Tetanus – bacterial disease caused by a potent neurotoxin The number of fibers contracting within a vertebrate depends on elaborated by the organism Chlostridium tetan. The extent of motor unit recruitment neurotoxin reaches the CNS that prohibits the release of inhibtory transmitter glycin 1. One motor neuron innervates a number of muscle fibers,  Exertional rhabdomyolysis – a specific disease of horses but each vertebrate muscle fiber is supplied by only one characterized by a suddenly develop muscle pain or motor neuron. cramping of the hindlimbs 2. Motor unit  Milk fever – a paralysis and a loss of consciousness which 3. Motor unit recruitment leads to comma in dairy cows that recently calved. Caused by sudden drop of calcium of hypocalcaemia associated with the onset of lactation and is most common in high- The frequency of stimulation can influence the tension developed by producing dairy cows skeletal muscle fiber  Eclampsia – K9 pwelpelar tetani is an acute condition usually seen at peak lactation 2-3 weeks after whelping. 1. Frequency stimulation Restlessness with subsequent changes including mild 2. Length of the fiber at the onset of contractions tremors, twitching, muscle spasm, stiffness, and ataxia 3. Extent of fatigue  Dark cutters – or dark cutting beef is a description of cuts of 4. Thickness of the fiber beer that do not bloom or brighten when they are exposed to air when marketed in a display case. This represents a financial loss to the meat industry. Caused are link to pre- FIGURE 8-17 Length–tension relationship. Maximal tetanic contraction can be harvest of live animals prior to slaughter and the depletion achieved when a muscle fiber is at its optimal length (lo) before the onset of of muscle glycogen, which makes the pH more alkaline contraction, because this is the point of optimal overlap of thick-fi lament cross bridges and thin-fi lament cross-bridge binding sites (point A). The percentage of maximal tetanic contraction that can be achieved decreases when the muscle fiber is longer or shorter than lo before contraction. When it is longer, fewer thin- SKELETAL MUSCLE MECHANICS fi lament binding sites are accessible for binding with thick-fi lament cross bridges because the thin fi laments are pulled out from between the thick fi laments CONTRACTION OF THE WHOLE MUSCLE: MAJOR PROBLEMS (points B and C). When the fiber is shorter, fewer thin-fi lament binding sites are exposed to thickfi lament cross bridges because the thin fi laments overlap (point 1. Precise control D). Also, further shortening and tension development are impeded as the thick fi 2. Diverse motions laments become forced against the Z lines (point D). In the body, the resting muscle length is at lo. Furthermore, because of restrictions imposed by skeletal 3. Fundamental limits attachments, muscles cannot vary beyond 30% of their lo in either direction (the 4. Too slow sarcomere me FIGURE 8-16 Twitch summation and tetanus range screened in light green). At the outer limits of this range, muscles still can achieve about 50% of their maximal tetanic contraction. MUSCLE ORGANS 1. Covered by a sheath of connective tissue Isotonic and isometric contraction 2. Tendons attach muscle to bones 1. Work 2. Force 3. Load CONTRACTION OF A WHOLE MUSCLE ORGAN CAN BE OF VARYING STRENGTH 1. All or none contraction FIGURE 8-18 Relationship between the 2. The number of fibers contracting within a muscle contractile component and the series-elastic component in transmitting muscle 3. The tension developed by contracting muscle fiber tension to bone. Muscle tension is transmitted to the bone by means of the stretching and tightening of the muscle’s elastic connective tissue and tendon  CHARACTERISTICS OF SKELETAL MUSCLE FIBERS FIGURE 8-23 Motor control (shown for a human). Arrows imply influence, whether excitatory or inhibitory; connections are not necessarily direct but may involve interneurons. MUSCLE RECEPTORS FIGURE 8-19 Load–velocity relationship in concentric contractions. The velocity of shortening decreases as the load increases. FIGURE 8-20 Lever systems of muscles, bones, and joints. Note that the lever ratio (length of the power arm to length of the load arm) is 1:7 (5 cm:35 cm), which amplifies the distance and velocity of movement seven times (distance moved by the muscle [extent of shortening] = 1 cm, distance moved by the hand = 7 cm, velocity of muscle shortening = 1 cm/unit of time, hand velocity = 7 cm/unit of time), but at the expense of the muscle having to exert seven times the force of the load (muscle force = 35 kg, load = 5 kg). MUSCLE SPINDLE FUNCTION PUMPING MECHANISMS systemic circulation and pumps it into the pulmonary circulation. The left side of the heart receives O2-rich blood from the pulmonary circulation and pumps it  Flagella (sponges) (e.g. sea urchin) into the systemic circulation. (b) Note the parallel pathways of blood flow  Extrinsic muscle/skeletal pumps (cuneus ungulae or frog in through the systemic organs. (The relative volume of blood flowing through each organ is not drawn to scale.) (c) Note that the left ventricular wall is much thicker horses) – wherein fluids are moved in motion by some than the right wall. muscle or elements that are not part of the circulatory system itself (starfish)  Peristaltic (tubular) muscle pumps – occurs when muscles in the walls of the vessels contract in a moving wave that pushes fluid infront of it (e.g earthworms)  Chamber muscle pump – more familiar form of hearts which consist of chambers of muscles to squeeze the fluid in and out (e.g. arthropods, mollusk, & all vertebrates) Vertebrate systemic hearts evolved from two-chambered to fourchambered hear  Pulmonary circulation – pumps blood to lungs  Systemic circulation – pumps blood throughout the entire body Avian and mammalian hearts: dual pumps  Right and left separate pumps  4 chambers  2 Atria (upper) and 2 ventricles (lower)  heart valves 2 AV’s and 2 semilunars MODULE 4: CARDIAC PHYSIOLOGY CARDIOVASCULAR SYSTEM COMPONENTS  Pump – move the fluid, called hearts (cardio)  Vessels – carry fluids between the pump and body tissues (vascular)  Fluid – carries transported molecules and cells: blood or hemolymph (hemo/emia) a. Automacity of the heart b. Coordinated spread of excitation and conduction in the heart c. Nueral control of the conductive system of the heart FIGURE 9-18 Blood flow through and pump action of the mammalian heart. (a) d. Components of the excitatory and conductive system of the The arrows indicate the direction of blood flow. To illustrate the direction of blood flow through the heart, all of the heart valves are shown open, which is FIGURE 9-20 Heart valves. Eversion of the AV valves is prevented by tension on heart (describe) never the case. The right side of the heart receives O2-poor blood from the the valve leaflets exerted by the chordae tendineae when the papillary muscles contract. When the semilunar valves are swept closed, their upturned edges fi t FIGURE 9-21 Organization of mammalian cardiac muscle fibers. Bundles of together in a deep, leakproof seam that prevents valve eversion. cardiac muscle fibers are arranged spirally around the ventricle. Adjacent cardiac muscle cells are joined end to end by intercalated discs, which contain two types of specialized junctions: desmosomes, which act as spot rivets mechanically holding the cells together, and gap junctions, which permit action potentials to spread from one cell to adjacent cells. HEARTS ELECTRICAL ACTIVITY - contraction of the cardiac muscle cells bring about ejection of blood which is triggered by action potential  Action potentials - sweep across the muscle cell membrane  Autorhythmic cells/pacemakers (myogenic) Conditions associated with cardiac pumping: - which do not contract, instead, are specialized for repeatively initiating the action potentials  Edema in broiler chicken responsible for the cotraction of the contractile  Brisket disease in cattle and horses cells - -hearts that have pacemaker cells are called myogenic VERTEBRATE HEART WALLS ARE COMPOSED PRIMARILY OF SPIRALLY ARRANGED CARDIAC MUSCLE FIBERS INTERCONNECTED BY - - ensure blood or hemolin flow even if there is severe neural trauma INTERCALATED DISC - myogenic insect hearts are largely under the 1. Desmosomes – are type of adhering junctions that control of external neural stimuli mechanically holds cells together under high mechanical stress 2. Gap junctions – are channels that allows action potentials PACEMAKER CELLS to spread from one cardiac cell to the next Layers: - Have channels that cyclically move them to “firing” threshold 1. Myocardium - bulk of the vertebrate heart wall - composed - Has a role in origin and spread of a heartbeat of bundles of interlazing bundles of muscle fibers arranged spirally around the heart circumference - thus, when the - Cardiac pacemakers do not have a stable resting potential. Instead, their membrane potential slowly depolarizes or ventricular muscle contracts, the diameter of the ventricular drifts between action potential until threshold is rich chamber is reduced while the apex is simultaneously pulled upward toward the top of the heart in a rotating manner. This ringing effects efficiently exerts pressure on the blood within the chambers and directs it upward to the arteries PACEMAKER POTENTIAL AND ACTION POTENTIAL IN AUTORHYTHMIC that exit the ventricles. CELLS 2. Endocardium - middle layer lined with endophileal layer 3. Epicardium - Thin outer-shaped layer  Net Sodium entry (HCN) – found only in the cardiac pacemaker cells and some neurons)  Passive outward flux of potassium - slowly close at negative potential which gradually diminishes the positive outflow of potassium ions down their concentration gradient   Increased Calcium entry - occurs in the second half of the THE SPREAD OF CARDIAC EXCITATION IS THE ACTION POTENTIAL OF CONTRACTILE CARDIAC MUSCLE CELLS pacemaker potential SHOWS A CHARACTERISTIC PLATEAU COORDINATED TO ENSURE EFFICIENT PUMPING  Completion of atrial excitation and contraction before onset of ventricular contraction  Coordinated cardiac muscle fiber excitation to accomplish efficient pumping  Coordination of atria and ventricles in pair so both members contract simultaneously  Atrial excitation  Transmission between atria and ventricles  Excitation of ventricle - Bundle of His - Purkinje fibers SPREAD OF CARDIAC EXCITATION FIGURE 9-24 Action potential in mammalian contractile cardiac muscle cells. The action potential in cardiac contractile cells differs considerably from the action potential in cardiac autorhythmic cells (compare with Figure 9-22). The rapid FIGURE 9-22 Pacemaker activity of mammalian cardiac autorhythmic cells. The rising phase of the action potential in contractile cells is the result of Na+ entry first half of the pacemaker potential (1) is the result of simultaneous opening of on opening of fast Na+ channels at threshold. The early, brief repolarization after the funny (f or HCN) channels, which permit inward Na+ current, and closure of the potential reaches its peak is because of limited K+ efflux on opening of the K+ channels, which reduce outward K+ current. The second half of the FIGURE 9-23 Specialized conduction system of the mammalian heart and spread transient K+ channels, coupled with inactivation of the Na+ channels. The pacemaker potential (2) is the result of opening of T-type Ca2+ channels. Once of cardiac excitation. An action potential initiated at the SA node first spreads prolonged plateau phase is the result of slow Ca2+ entry on opening of L-type threshold is reached (green dashed line), the action potential rise (3) results from throughout both atria. Its spread is facilitated by two specialized atrial Ca2+ channels, coupled with reduced K+ efflux on closure of several types of K+ opening of L-type Ca2+ channels; the falling phase (4) results from the opening of conduction pathways, the interatrial and internodal pathways. The AV node is the channels. The rapid falling phase is the result of K+ efflux on opening of ordinary K+ channels. only point where an action potential can spread from the atria to the ventricles. voltage-gated K+ channels, as in other excitable cells. Resting potential is From the AV node, the action potential spreads rapidly throughout the ventricles, maintained by opening of leaky K+ channels. SPECIALIZED, NONCONTRACTILE CARDIAC CELLS OF AUTOMATICITY hastened by a specialized ventricular conduction system consisting of the bundle of His and Purkinje fibers.  SA node - normal pacemaker of vertebrate heart (right atrial wall) fastest rate 90-100 action potentials - small specialized region in the right atrial wall in reptiles, birds, and mammals, and amphibians. The equivalent of the SA nodes lies in the wall of the sinus vinusus  AV node (base of right atrium) - a small bundle of specialized cardiac muscle cells located at the base of the right atrium near the septum CARDIAC MUSCLE HAS LONG REFRACTORY PERIOD WHICH PREVENTS be detected using electrons on the skin. It can also be ECG measurements TETANUS detected by internally implanted devices  Conducted on humans and animals to diagnose heart Normal vertebrae ECG – exhibits 3 distinct waves problems Ex. P wave with no subsequent QRST events (a skipped  P wave (atrial depolarization) beat) is called AV block –damaged of conduction fibers.. A  QRS complex (ventricular depolarization) healthy horse does not have a skip beat.  T wave (ventricular repolarization)  Part of physiological monitoring during studies of behavior and effects of temperature, drugs, stress, exercise 1. The firing of the SA nodes does not generate electrical activity to reach the surface of the body. So, no wave is recorded for SA nodal depolarization. Therefore, the first recorded wave when the impulse cross the atria. 2. The P-wave is much smaller than the QRX complex because the atria FIGURE 9-25 Relationship of an action potential and the refractory period to the have a much smaller muscle mass than the ventricles, thus, generate duration of the contractile response in cardiac muscle. less electrical activity. ECG / EKG / Electrocardiogram ECG IN BASELINE - recording of electrical currents/electrical activity induced by  PR segment (AV nodal delay) body fluids by the cardiac impulse that reaches the body surface detected by recording electrodes on the skin (limbs) - This delay is between the interval of time and the end of the P wave and the onset of the QRS and or/chest wave - a complex recording representing the sum of electrical  ST segment (plateau phase of action potential of cardiac activity spreading throughout all of the hearts ,muscle cells contractile cells) during depolarization - when the ventricles are completely depolarized, - remember that ECG is a recording of that proportion of the and cardiac contractile cells are undergoing the electrical activity induced in the body fluid by the cardiac plateau phase of their action potential before impulse that reaches the surface of the body they repolarize. The ST segment is the interval - not a recording of the actual electrical activity of the heart between the QRS complex and the T wave - generated by cardiac muscle during depolarization and  TP interval (heart completely at rest) repolarization spread into the tissues surrounding the heart - when the heart muscle is completely at rest, the and that are conducted into body fluids ventricular filling is taking place. After the T wave - electrical currents generated from cardiac muscles during and before the next P wave is called the TP depolarization and repolarization, they would spread into interval the tissues surrounding the heart. A small of these electrical activities would actually reach the body surface. These can HEART MECHANICS AND CARDIAC CYCLE Hearts alternately contract in systole to empty and relax in diastole to fill. In vertebrates, the atria and ventricle goes through separate cycles of systole and diastole. Contraction occurs as the spread of excitation, which started by the pacemaker across the heart, whereas relaxation follows subsequent repolarization of the musculature. During early ventricular diastole, the atrium is also in diastole. The ventricular volume slowly continue to rise even before the atrial contraction take place. However in late ventricular diastole, the SA node reaches threshold and fire, so the depolarization impulse spreads throughout the atria, this is the P wave in the ECG. Triggering atrial contraction which causes a rise in the electrical control of the mammalian heart. CARDIAC CYCLE  Systole – contraction and emptying  Diastole – relaxation and filling  CARDIAC OUTPUTS (C.O.) AND ITS CONTROL CHANGES IN CARDIAC OUTPUT DURING ACTIVITY CARDIAC OUTPUT - a product of heart rate and stroke volume - cardiac output should be per minute, and the heart rate is beats/minute, and the stroke volume is vol pump/beat or stroke - the values vary tremendously with activity state of an individual animal - Heart rate = Larger animals < small animals - Stroke volume = larger animals > small animals Heart rate – how fast the heart beats in bpm Stroke volume – how much volume it pumps per beat or volume Heart rate is determined primarily by antagonistic regulation of pumped per beat or stroke autonomic influences on the SA node C.O. (per minute) = heart rate X stroke volume  Sympathetic (Stimulates cAMP) - fight or flight CARDIAC OUTPUTS ACROSS THE ANIMAL KINGDOM - supply the atria including the SA and AV nodes, and like the vagus nerve, it richly innervates the ventricles as well in order to boost cardiac output  Parasympathetic NS (Inhibits cAMP) - the rest and digest - the vagus nerve primary supplies the atrium, especially the SA and AV nodes in order to reduce cardiac output Effect of Parasympathetic Stimulation  Acetylcholine - it enhance the potassium permeability because Acetylcholine hyper polarizes the sinoatrial node FIGURE 9-27 Mammalian cardiac cycle. This graph depicts various events that occur concurrently during the cardiac cycle. Follow each horizontal strip across to membrane. And because more potassium leaves see the changes that take place in the electrocardiogram; aortic, ventricular, and than normal, it makes it even more negative atrial pressures; ventricular volume; and heart sounds throughout the cycle. Late  Decrease heart rate diastole, one full systole and diastole (one full cardiac cycle), and another systole  Decreases excitability of the AV node are shown for the left side of the heart. Follow each vertical strip downward to – prolonging transmission of impulses see what happens simultaneously with each of these factors during each phase of to the ventricles even longer than the the cardiac cycle. See the text (pp. 412 and 414) for a detailed explanation of the usual AV nodal delay circled numbers. The sketches of the heart illustrate the flow of O2-poor (dark blue) and O2- rich (bright red) blood in and out of the ventricles during the  Shortens AP cardiac cycle. Effect of Sympathetic Stimulation ultimately leads to a heartbeat, increased parasympathetic activity decreases the heart rate, whereas increased sympathetic activity increases the heart rate. Norepinephrine  Increases heart rate – through its effect on the cyclic AMP which raises the influx of sodium and calcium. It permits a greater frequency of action potentials and correspondingly more rapid heartrate.  Reduces the AV nodal delay – by increasing conduction velocity, and by enhancing the slow inward calcium current  Speeds up the spread of action potential – throughout the specialized conduction pathways  Increases contractile strength – of the atrial and ventricular contractiles, both have which have numerous sympathetic nerve endings so that the heart beats more forcefully and squeezes out more blood CONTROL OF HEART RATE  Vagus nerve  Cardiac sympathetic nerve  Brain stem  Epinephrine – a hormone that is secreted to the blood and into the adrenal medulla on STROKE VOLUME FIGURE 9-29 Control of cardiac output. Cardiac output equals heart rate times stroke volume. Heart rate in turn is increased by sympathetic activity and  Venous return decreased by parasympathetic activity, while stroke volume is increased by sympathetic activity and higher venous return.  Extrinsic control FIGURE 9-28 Autonomic control of SA node activity and heart rate. (a) Parasympathetic stimulation decreases the rate of SA nodal depolarization so that the membrane reaches threshold more slowly and has fewer action FIGURE 9-30 Intrinsic control of stroke volume (Frank-Starling curve). The potentials, whereas sympathetic stimulation increases the rate of depolarization cardiac muscle fiber’s length, which is determined by the extent of venous filling, of the SA node so that the membrane reaches threshold more rapidly and has is normally less than the optimal length for developing maximal tension. more frequent action potentials. (b) Because each SA node action potential Therefore, an increase in end-diastolic volume (that is, an increase in venous return), by moving the cardiac muscle fiber length closer to optimal length, increases the contractile tension of the fibers on the next systole. A stronger HEART SOUNDS: S1  Increased with fever, anemia, pulmonary hypertension and contraction squeezes out more blood. Thus, as more blood is returned to the hyperthyroidism heart and the end-diastolic volume increases, the heart automatically pumps out  Start of ventricular ejection and begin of QRS complex of  Splitting may occur when semilunar valves close out of a correspondingly larger stroke volume. ECG phase  Closure and tensing of the AV valve  Due to delayed closure of the pulmonic valve  Longer and with lower frequency than S2  Physiologic or Pathologic  Best heard over cardiac apex  PCG recognizes 4 components of the S1  Component 1, Component 2, Component 3, Component 4  First component – contracting ventricular HEART SOUNDS: S3 myocardium, slight AV valve regurgitation at the  Occurs early in diastole near the end of rapid ventricular onset of ventricular systole and coaptation of filling leaflets of the AV valves prior to complete  Sudden tensing of the chordae tendineae, deceleration of closure and distension the filling wave of blood, and vibrations arising from the  Low frequency and amplitude walls of the ventricles  Second and Third component – cause by sudden  Formed a low frequency sound development of tension in closing mitral valve and the tricuspid valve  Higher frequency and amplitude  Fourth component – occurs in the onset of HEART SOUNDS: S4 ventricular ejection and sudden ejection of blood into the great arteries  Occurs early in diastole near the end of rapid ventricular  Low frequency and amplitude filling  Intensity – more intense compared to S2 in dogs but  Sudden tensing of the chordae tendineae, deceleration of reverse in horses the filling wave of blood, and vibrations arising from the HEARTS’ BLOOD SUPPLY?  Lowered with obesity, pericardial pleural effusion, walls of the ventricles  Coronary artery – supplies blood into the heart hypervolemia, pronounced 1st degree AV block,  Formed a low frequency sound  Adenosine – formed from Adenosine triposphate during the diaphragmatic hernia, peritoneal pericardial diaphragmatic cardiac metabolic activity hernia, barrel conformation of the thorax.  Arteriosclerosis – occurs in the artery walls for a variety of  Increased with excitement, after exercise, more vigorous HEART SOUNDS: GALLOP RHYTHM reason, such as: accumulation of cholesterol, following closing and tensing of AV valves, deep thorax, anemia, damage from high blood pressure, & hypertension fever, hypertension, and chronic mitral valve disease  Occurs during tachycardia when S3 and S4 merge into a  Hypertension  Splitting may occur in all species when there is delayed single heart sound  Migrating Salmonid closure of the AV valves  Resembles that of galloping horse  Occasionally heard in animals with severe right or left  Hypertrophic cardiomyopathy and hyperthyroidism in cats bundle branch block HEART SOUNDS  Can be heard through cardiac auscultation HEART SOUNDS: S2  Audible vibrations heard with the use of an stethoscope  Phonocardiogram (graphic recording)  Signals the end of mechanical systole and coincides with the T wave of the ECG  Generated by the closure of the semilunar valves  Shorter higher-pitched sound than S1 HEART SOUNDS: CLASSIFICATION  Intensity  Decreased with pericardial and pleural effusion,  Transient and murmurs diaphragmatic and peritoneal pericardial diaphragmatic  S1 (lub), S2 (dub), S3, S4 hernia, thoracic masses, myocardial failure, and severe chronic mitral valve degeneration  HEART SOUNDS: CARDIAC MURMURS – SYSTOLIC  Aortic stenosis  Pulmonic stenosis  Mitral insufficiency  Tricuspid insufficiency  Interventricular septal defect  Interatrial septal defect  Tetralogy of the Fallot HEART SOUNDS: FUNCTIONAL SYSTOLIC MURMURS  Physiological Figure 39.2 The phonocardiogram (PCG) and electrocardiogram (ECG) from a  Common in puppies, kittens, and horses normal horse. The four components of S1 are indicated by numbers 1–4. The somewhat accentuated fourth component could be considered an ejection sound. S3 follows the onset of S2 by 0.14 s. S3 is followed by a soft low‐frequency sound. Vertical lines occur at 0.04‐s intervals. HEART SOUNDS: CARDIAC MURMURS  Diastolic murmurs-heard after S2 HEART SOUNDS: OTHER SYSTOLIC SOUNDS  Mitral or tricuspid stenosis  Pulmonic insufficiency  Two extra sounds occurs between S1 and S2.  Aortic insufficiency  Ejection sound or ejection click  Innocent diastolic murmurs  Systolic click  Continuous murmurs - Patent Ductus Arteriosus (PDA) HEART SOUNDS: CARDIAC MURMURS FURTHER READING: Duke’s Physiology of Domestic Animals. 2015. 13th edition.  Prolonged series of auditory vibrations emanating from the Reece et al. pages 417 to 427 Figure 39.1 Relationships between timing of heart sounds, cardiac events, and electrocardiogram. Electrical activity depicted on the ECG precedes cardiac heart or blood vessels mechanical activity shown by the phonocardiogram (Phono). The QRS complex  Cause by turbulence in flowing of blood or prolonged represents ventricular activation. The atrioventricular valves close (MC) as the vibrations ventricles eject blood through the semilunar valves and the first heart sound (S1) - alteration of the morphology of any one of the occurs at the R‐wave downstroke. The second heart sound (S2) occurs at the end four heart valves (insufficiency or stenosis) of ventricular contraction (i.e., ventricular systole) when the semilunar valves close (AC), approximately at the time of the T wave. The third heart sound (S3) - abnormal communication between the two sides occurs during the first half of diastole, during passive ventricular filling (e.g., of the heart or great vessels (interatrial septal between the T wave and the ensuing P wave). The fourth heart sound (S4) occurs defect, interventricular septal defect, patent late in diastole after atrial activation (P wave) and contraction. LA, left atrium; LV, ductus arteriosus) left ventricle; RA, right atrium; RV, right ventricle. - increased blood flow velocity through a normal valve orifice or vessel - changes to the blood viscosity  Systolic murmurs-occurs between S1 and S2  Results when blood regurgitates through incompetent (mitral and tricuspid valves) or as blood is ejected through the semilunar valves or through ventricular septal defect MODULE 5: VASCULAR PHYSIOLOGY TWO MAJOR FACTORS THAT INFLUENCE BLOOD FLOW  Pressure Gradient - difference in the pressure between the beginning and the end of a vessel (aorta – arterioles) - main driving force of flow through the vessel - Blood flows from an area with higher pressure (P1) coming from the heart, down to an area with lower pressure (P2) which are the individual vessels.  Resistance (Viscosity, Vessel length and radius) - is the one that reduces the flow of blood because of frictional looses, and the pressure will decrease the blood flow through the vessel - In general, the pressure would be higher from the start, and then will gradually diminish during the rest of the flow of blood.  Pressure Gradient (gravity) - important in establishing pressure gradient TWO MAJOR FACTORS THAT INFLUENCE BLOOD FLOW: GRAVITY FIGURE 9-41 Mammalian and avian circulation. Arteries progressively branch as they carry blood from the heart to the tissues. A separate small arterial branch delivers blood to each of the various organs. As a small artery enters the organ it is supplying, it branches into arterioles, which further branch into an extensive network of capillaries. The capillaries rejoin to form venules, which further unite to form small veins that leave the organ. The small veins progressively merge as they carry blood back to the heart.  BLOOD VESSELS ARTERIES - serves as a pipeline that delivers blood from the  Rapid transit passageways heart to the different parts of the body  Pressure reservoir  Connective tissue fibers - Important since organs depend on them, if one is malfunctioning, your organs could die - collagen (tensile strength)  Arteries - elastin (elasticity)  Aorta – the biggest one; attached to the heart  Arteries  Arterioles – fenestrate or have contact with capillaries  Veins - veins would return blood into the heart; and will