The Motor (Efferent) System PDF

The Motor (Efferent) Division of the Nervous System: Autonomic and Somatic Motor Control Chapter 11  Efferent (Motor) Division Consists of TWO Subdivisions: 1) Somatic Motor subdivision: Innervates skeletal muscles of the body Responsible for voluntary movements...

The Motor (Efferent) Division of the Nervous System: Autonomic and Somatic Motor Control Chapter 11  Efferent (Motor) Division Consists of TWO Subdivisions: 1) Somatic Motor subdivision: Innervates skeletal muscles of the body Responsible for voluntary movements 2) Visceral Motor subdivision (a.k.a. Autonomic Nervous System, ANS): Regulates smooth muscle of digestive tract, blood vessels, ducts of glands, airways, urinary bladder, cardiac muscle, and secretion of salivary glands and some endocrine glands.  Features of the ANS Involuntary (you do not have conscious control of its output). Has two subdivisions: 1) Parasympathetic subdivision: “Rest and Digest” Prepares body for rest and digestion activities 2)Sympathetic subdivision: “Fight or flight” Prepares the body for energetic action However, these two subdivisions are always active, not just during times of rest or fighting. The dynamic balance in the output of these two subdivisions act to regulate homeostasis in the body. Most tissues, but not all, are under antagonistic regulation of the two ANS subdivision.  Autonomic Division: Homeostasis During “rest and digest” During “fight-or-flight” type type activities activities sympathetic parasympathetic output is output is higher than higher than sympathetic parasympathetic output. output.  Autonomic Control Centers Hypothalamus – Water balance, temperature, and hunger – Center for homeostasis integration Pons – Respiration, cardiac, and urinary bladder Medulla – Respiration, blood pressure Comparing the Sympathetic and Parasympathetic Subdivisions Autonomic pathways between CNS and Target cells consist of two neurons (i.e. they are di-synaptic). This is the case for both the sympathetic and parasympathetic subdivisions. axon axon Ganglion = cluster of cell bodies outside the CNS  Autonomic connections between the CNS and target tissue are di-synaptic. Preganglionic neuron: Postganglionic neuron: The preganglionic neuron synapses on the postganglionic neuron in the autonomic ganglion. The postganglionic neuron sends its axon out to synapse on the target tissue ( which may be an endocrine or exocrine gland cell, smooth muscle cell, or adipose cell). Comparing the Sympathetic and Parasympathetic Subdivisions Autonomic post-ganglionic axons form dispersed synapses on target cells. These dispersed synapses consist of varicosities (swellings along the axon) that release the neurotransmitter onto the surface of the target cell. The neurotransmitter receptors on the target cell are distributed across the surface of the target cell membrane, rather than at a specific synaptic location on the cell membrane, (as in a typical chemical synapse). Figure 11-8 The Sympathetic and Parasympathetic subdivisions differ in terms of: 1) Location of their pre- and post-ganglionic neurons. 2) The neurotransmitters used on target cells. 3) The receptors expressed by their target cells. Sympathetic versus Parasympathetic : Location of pre- and post-ganglionic cell bodies The cell bodies of the sympathetic preganglionic neurons are located in the thoracic and first two lumbar segments of the spinal cord. The cell bodies of the sympathetic post-ganglionic neurons are located in the sympathetic ganglion chain close to the spinal cord and three ganglia located along Aortic ganglia the aorta. The cell bodies of the parasympathetic preganglionic neurons are located in the pons, medulla and sacral segments of the spinal cord. The cell bodies of the parasympathetic post- ganglionic neurons are located close to or on the target tissue.  Sympathetic versus Parasympathetic: Neurotransmitters used Parasympathetic Pre- Sympathetic ganglionic neuron Pre-ganglionic neuron Sympathetic Post- Parasympathetic ganglionic neuron Produces fast Post-ganglionic synaptic response neuron Produces slow synaptic response Figure 11-7 Focus on the Sympathetic Subdivision: Examples of some actions Pupil dilation to allow more light to enter the eye increasing visual acuity. Promotes mucus secretion from the salivary glands to help increase cleaning of inhaled air. Increases rate and depth of breathing to increase gas exchange. Bronchiole dilation reducing resistance to airflow in the lungs. Speeds Heart Rate and increases the force of heart contraction increasing volume of blood pumped per beat. Blood vessel constriction of arteries supplying blood to the digestive tract. Promotes Lipolysis (Fat breakdown) to release stored energy. Sympathetic Target Tissues use Adrenergic Receptors Adrenergic receptors bind norepinephrine (and some also bind epinephrine released from the adrenal medulla). Adrenergic receptors are linked to G-proteins inside the target cell producing slow synaptic responses. Two general types of adrenergic receptors (a and b): 1) Alpha receptors (α): (two subtypes) - a1 receptors are found on most, but not all, target tissues of the sympathetic subdivision of ANS. Will cause smooth muscle contraction Respond most strongly to binding of norepinephrine. Will also bind epinephrine, but response is weak. - a2 receptors are found only on the smooth muscle of the digestive tract and secretory cells of the pancreas. Will cause digestive tract smooth muscle relaxation and decrease pancreatic secretions. Respond most strongly norepinephrine. Will also bind epinephrine, but response is weak. Sympathetic Target Tissues use Adrenergic Receptors 2) Beta Receptors (β): (three subtypes) – β 1 receptors are found on cardiac pacemaker cells, heart muscle cells, and smooth muscle of kidney arterioles. Will cause increase in heart rate, force of heart contraction, and increase secretion of renin (more later). Respond equally well to binding of norepinephrine and epinephrine. – β 2 receptors are found on smooth muscle of arterioles, bronchioles, digestive tract, and urinary bladder. Activated by epinephrine released from adrenal medulla. – Will causes relaxation of smooth muscles that they’re expressed on. – Will also respond to norepinephrine, but response is weak. However, are not innervated by sympathetic post-ganglionic neurons so don’t receive norepinephrine. Sympathetic Target Tissues use Adrenergic Receptors β 3 receptors are mostly found on adipose tissues (fat) cells. Activation will stimulate lipolysis (breakdown of stored fats). Respond most strongly to norepinephrine, but will also respond to epinephrine but response is weak. Medulla of the Adrenal Gland Focus on Parasympathetic Subdivision: Examples of some actions Constricts pupils decreasing visual acuity Stimulates salivation to preparing the oral cavity for food. Slows heart rate Constricts bronchioles increasing resistance to airflow in the lungs. Stimulates digestion by stimulating increased release of digestive acid and enzymes, and increased stomach and intestinal motility. Stimulates insulin secretion from the pancreas preparing the body to receive increased glucose and amino acids absorbed during a meal.  Focus on Parasympathetic Subdivision Neurotransmitter used by both the pre- and post- ganglionic neurons is Acetylcholine The parasympathetic receptors are called “cholinergic receptors” – Two types: Nicotinic receptors and muscarinic receptors. - Nicotinic receptors are expressed on post- ganglionic neurons of this subdivision (also expressed on sympathetic post-ganglionic neurons). - Activation produces fast synaptic response. - Muscarinic receptors are expressed on the target cells of the parasympathetic subdivision. – At least five subtypes of muscarinic receptors have been identified. – All are G protein-coupled producing slow synaptic responses in the target cell.  Summary of Sympathetic versus Parasympathetic Subdivisions In terms of Parasympathetic Sympathetic Location of pre-ganglionic Located in pons, medulla, Located in thoracic & neurons in the CNS & segments 2-4 of sacral lumbar segments of spinal spinal cord cord Location of autonomic Located on or very near Located in sympathetic ganglia target tissue chain of ganglia. Close to vertebral column, and along abdominal aorta. Receptor Types Post-ganglionic neurons Post-ganglionic neurons express nicotinic receptors express nicotinic receptors Target Cells express Target cell receptors muscarinic receptors express adrenergic receptors Neurotransmitter used Both pre & post-ganglionic Pre-ganglionic neurons neurons use Acetylcholine use ACh. Post-ganglionic as their neurotransmitter neurons use norepinephrine.  More On Cholinergic Receptors Acetylcholine (ACh) uses 2 types of receptors: 1) Nicotinic receptors: Called “nicotinic” because nicotine is an agonist for these receptors (i.e. They can also be activated by nicotine). – Found on dendrites and cell bodies of post-ganglionic neurons of both subdivisions of the ANS & on skeletal muscle fibers (more later). – Consists of four protein subunits that combine to form a chemically gated ion channel in the membrane of the target cell. – Has two receptor sites for ACh as part of the protein subunits that make up the ion channel, both sites must bind ACh for the channel to open. Channel allows both Na+ and K+ to move across the cell membrane producing a fast synaptic response. At the resting membrane potential more Na+ than moves in than K+ moves out => depolarization in the target cell!  More On ACh Receptors 2) Muscarinic Receptors: are called “muscarinic” because muscarine is an agonist for these receptors. – Found on cell membrane of target cells of parasympathetic post-ganglionic neurons, pacemaker cells of the heart, and other target cells of the parasympathetic subdivision. – Consists of a single protein subunit that spans the cell membrane. – All muscarinic receptors are linked to G-proteins. – Activated by binding one molecule of ACh, which activates a second messenger system, thus producing a slow synaptic response in the target cell.  Somatic Motor Division Function: Provides voluntary control of body movement. Neuron innervating a skeletal muscle fiber is called a somatic motor neuron. The cell body of a somatic motor neuron is located in CNS. – These neurons send their axons out to directly synapse on target cells, which are always skeletal muscle fibers. Ganglion: Cluster of neuronal cell bodies in PNS Nucleus: Cluster of neuronal cell bodies in the CNS  Somatic Motor Division In the somatic motor subdivision the connection between the CNS and the target (skeletal muscle fiber) is monosynatptic (as opposed to di- Cell body & synaptic as in the ANS). axon of a somatic So, the somatic motor neuron sends it motor axon out to synapse directly on the neuron target (skeletal muscle fiber). These axons may be many feet in length. The somatic motor axon may branch to synapse with multiple muscle fibers in a muscle. The axon terminals of a somatic motor axon forms a chemical synapse on a muscle fiber called a Neuromuscular junction  Structure of the Neuromuscular Junction Somatic motor axon Somatic muscle fiber Structure of the Neuromuscular Junction Somatic motor axon terminal Muscle fiber Figure 11-12 (3 of 3)  Events at the Neuromuscular Junction leading to muscle fiber contraction. (1) AP 1. Action potential comes down axon and depolarizes the axon terminal. 2. Depolarization of the axon terminal triggers opening of voltage gated Ca2+ channels in membrane of axon terminal. (3) 3. Ca2+ enters axon terminal and triggers binding of synaptic vesicles to docking proteins on the presynaptic membrane. (2) 4. ACh is released into the synaptic cleft, (4) diffuses across and binds to nicotinic receptors on motor end plate. 5. (see next slide).  Events at the Neuromuscular Junction leading to muscle fiber contraction 5. Binding of two molecules of ACh to the nicotinic receptor triggers the opening of the Na+/K+ channels in the motor end plate allowing Na+ influx/K+ efflux.. out Motor end plate in *At the resting membrane potential of the muscle fiber the driving force on Na+ into the cell is greater than the driving force on K+ out of the cell, so result is a depolarization that leads to muscle fiber contraction.  Summary of the Motor Division Motor Division consists of: Somatic Motor Division ANS ANS – Has central role in homeostasis – CNS control centers in the hypothalamus. – Divided into sympathetic and parasympathetic subdivisions – Consists of di-synaptic pathways between CNS and target tissues: – pre-ganglionic motor neuron with its cell body in the CNS, axon synapses on postganglionic motor neuron – Postganglionic motor neuron with its cell body in an autonomic ganglion, axon synapses on target tissue – Regulates gland secretion, smooth and cardiac muscle activity, and adipose cell fat storage. – Antagonistic regulation of most, but not all, target tissues.  Summary of the Motor Division Somatic Motor Division. – Somatic motor neurons control skeletal muscle contraction. – Somatic motor neuron cell body located in CNS. – Single long myelinated axon from somatic motor neuron to skeletal muscle fiber. (monosynaptic connection between CNS and muscle fiber) – Release of ACh at Neuromuscular junction leads to muscle fiber contraction. Chapter 12 Muscle  Lecture Topics: The functions of muscle tissue. The three types of muscle tissue found in the human body. Skeletal muscle terminology. Skeletal muscle structure. Skeletal muscle fiber structure and ultrastructure. The Sliding Filament Theory of Muscle Contraction. Molecular events of the sliding filament theory The roles of Troponin and Tropomyosin Excitation Contraction Coupling Events Skeletal Muscle Fiber Types The Motor Unit and Skeletal Muscle Contraction Isotonic vs Isometric Skeletal Muscle Contraction ATP and Muscle Contraction Factors that Contribute to Muscle Fatigue Characteristics of Skeletal vs. Cardiac vs. Smooth Muscle 3 Primary Functions of Muscle: 1) To produce movement. 2) To generate force for doing work Moving loads (objects) from one place to another. 3) To generate heat.  The Three Types of Muscle Tissue Skeletal muscle Aka: “Striated” muscle Cardiac muscle Smooth muscle This banding pattern is a result of the organization of the proteins that produce contraction in this type of muscle. Skeletal muscle = somatic muscle  The Three Types of Muscle Tissue Again this banding pattern is a result of the organization of the proteins that produce contraction in this type of muscle. Cardiac muscle = heart muscle  The Three Types of Muscle Tissue The same proteins are involved in contraction of smooth muscle as in the types of striated muscle tissue, but the proteins are not as organized as in striated muscle tissue hence the banding pattern is not seen. Smooth muscle = visceral muscle  Skeletal Muscle Usually attached to bones by tendons (but some attach to soft tissues, like the lips). Skeletal MuscleTerminology: Origin: attachment point to the skeletal element that doesn’t move when the muscle contracts. Usually close to the torso of the body. Triceps Insertion: attachment point to the skeletal muscle Biceps muscle element that moves when the muscle contracts. Usually more distal along the limb. Flexor: reduces the joint angle. Ex. Biceps muscle flexes the elbow joint. Extensor: increases the joint angle. Ex. Triceps muscle extends the elbow joint. Antagonistic muscle groups: flexor- extensor pairs move skeletal elements in opposite directions at a joint. (Ex. Biceps- Triceps muscles). Antagonistic Muscle Groups Contraction of the biceps muscle decreases the angle of the joint between the humerus and radius Humerus bone Joint angle Radius (~900) bone Antagonistic Muscle Groups Contraction of the triceps increases Joint the angle of the angle joint between the (~1800) humerus and radius  Anatomy Summary: Skeletal Muscle Contractile component of muscle. Attaches to the tendon at each end of the muscle. *Connective tissue of the muscle is the elastic component. Both the elastic and contractile components are important in normal muscle functioning.  The Muscle Fibers: Result of fusion of individual muscle cells during development of the muscle. Long and cylindrical in shape. Has multiple nuclei. Each muscle cell that fused to create the fiber contributes its nucleus. Ends of each muscle fiber are attached to the ends of the muscle. When muscle fibers contract, the muscle contracts. Ultrastructure of a Muscle Fiber Inside of a muscle fiber * *  T-tubules and the Sarcoplasmic Reticulum * T-tubules are small infoldings of the sarcolemma which have terminal cisternae of sarcoplasmic reticulum on both sides (all of which is referred to as a triad). The t-tubules conduct the muscle action potential deep into the muscle fiber, which triggers the release of calcium from the terminal cisternae leading to the contraction of the muscle.  Ultrastructure of Muscle Fibers: The Myofibril The myofibrils of a muscle fiber are composed of the proteins that interact to produce muscle contraction. The proteins compose thick and thin filaments that are organized into repeating units called sarcomeres that are linked to form a myofibril. So, a myofibril is a chain of sarcomeres. Thin filaments (pink) Thick filaments (purple) Each end of a myofibril is attached to the ends of the muscle fiber. The Proteins of the Sarcomere: Proteins of the Thick Filament Myosin is a “motor protein” consisting of a tail region, a hinge region, and a head region. 250 myosin molecules are bundled to form the thick filaments of a sarcomere. Flex points The Proteins of the Sarcomere: Proteins of the Thin Filament Thin filaments of the sarcomere are composed four proteins: Actin, Tropomyosin, Troponin, and Nebulin. 1) G-Actin: Globular Protein that polymerizes into F-actin chains that twist together to form the thin filaments. 2) Tropomyosin: covers myosin binding sites on the actin to prevent complete binding by the myosin head. 3) Troponin: involved in shifting the tropomyosin to expose the myosin binding sites during contraction. 4) Nebulin: aligns and supports the thin filament. It is not involved in contraction.  Actin and Myosin form crossbridges During contraction myosin heads of the thick filaments bind to the G-actin molecules of the thin filaments at myosin-head binding sites, forming what are called crossbridges between the thick and thin filaments. Crossbridges Thin filament Thick filament Ultrastructure of Muscle Fibers: The Sarcomere Sarcomere Terminology: A repeating unit of the myofibril. Includes a Z disk at each end, ½ of an I band, 1 A band, 1 H zone, and 1 M line. Z disk: Attachment site for thin filaments on the ends of the sarcomere and to the thin filaments of the adjacent sarcomere. I band: Region containing only thin filaments. A band: Encompasses the entire length of a thick filament. H zone: Clear zone in the A band that consists of thick filaments only. M line: Represents proteins that form the attachment site for thick filaments.  Sarcomeres (c) A band Sarcomere Z disk Z disk Myofibril M line I band H zone (d) Z disk Z disk M line During a muscle contraction, the interaction between the myosin heads and G-actin pulls the Z disks towards the M line….  Review: Ultrastructure of Muscle Fibers (c) A band Sarcomere Z disk Z disk Myofibril M line I band H zone (d) Titin Z disk Z disk M line M line Thick filaments  Review: Ultrastructure of Muscle Fibers (c) A band Sarcomere Z disk Z disk Myofibril M line I band H zone (d) Titin Z disk Z disk M line M line Thick filaments (e) Myosin heads Hinge Myosin tail region Myosin molecule  Review: Ultrastructure of Muscle Fibers (c) A band Sarcomere Z disk Z disk Myofibril M line I band H zone (d) Titin Z disk Z disk M line M line Thick filaments Thin filaments (e) Myosin heads Hinge Myosin tail region Myosin molecule  Review: Ultrastructure of Muscle Fibers (c) A band Sarcomere Z disk Z disk Myofibril M line I band H zone (d) Z disk Z disk M line M line Thick filaments Thin filaments (e) (f) Myosin heads Hinge Myosin tail region G-actin molecule Myosin molecule Actin chain  Accessory Proteins: Titin and Nebulin Titin acts like a spring that returns the sarcomere to its original length after contraction has occurred. Nebulin helps align and support the thin filament. * * Sliding Filament Theory of Muscle Contraction According to this theory of how muscle contraction occurs muscle contraction (following an action potential at the neuromuscular junction that spreads along the sarcolemma): 1. The thin filaments of the sarcomeres slide along the thick filaments 2. The Z disks on each end of the sarcomere are pulled towards the M line (starts midway along a muscle fiber and proceeds towards each end). 3. Because the sarcomeres of myofibrils are shortened in length. 4. Because the myofibrils are attached to each end of the muscle fiber the muscle fiber is shortened in length. 5. Because the ends of the muscle fibers are attached to the tendons at each end of the muscle overall muscle length is shortened. The molecular events that result in sliding of thin filament along thick filament: (Six Steps) Myosin filament Tight binding in the rigor Myosin ATP binds to its binding site 1 45° 2 state. The crossbridge is binding ATP on the myosin. Myosin then at a 45° angle relative to sites binding dissociates from actin. the filaments. site 1 2 3 4 G-actin molecule ADP ATP 1 2 3 4 1 2 3 4 5 At the end of the power stroke, 6 The ATPase activity of myosin the myosin head releases ADP 3 hydrolyzes the ATP. ADP and and resumes the tightly bound Pi remain bound to myosin. rigor state. ADP Contraction- Pi relaxation Pi Sliding 1 2 3 4 1 2 3 4 5 filament Actin filament moves toward M line. 90° Pi 1 2 3 4 5 Release of Pi initiates the power The myosin head swings over and stroke. The myosin head rotates 4 binds weakly to a new actin molecule. on its hinge, pushing the actin The crossbridge is now at 90º relative filament past it. to the filaments.  Tight binding in the rigor 1 state. The crossbridge is at a 45° angle relative to the filaments. Myosin 45 ° filament Myosin ATP binding binding sites site 1 2 3 4 G-actin molecule  Tight binding in the rigor ATP binds to its binding site 1 state. The crossbridge is 2 on the myosin. Myosin then at a 45° angle relative to dissociates from actin. the filaments. Myosin 45 ° filament Myosin ATP ATP binding binding sites site 2 3 4 1 2 3 4 1 G-actin molecule  The ATPase activity of myosin 3 hydrolyzes the ATP. ADP and Pi remain bound to myosin. ADP Pi 1 2 3 4  The ATPase activity of myosin The myosin head swings over 3 hydrolyzes the ATP. ADP and 4 and binds weakly to a new Pi remain bound to myosin. actin molecule. The cross- bridge is now at 90º relative to the filaments. ADP 90° Pi Pi 1 2 3 4 1 2 3 4  Release of Pi initiates the power 5 stroke. The myosin head rotates on its hinge, pushing the actin filament past it. Pi 1 2 3 4 5 Actin filament moves toward M line.  Release of Pi initiates the power At the end of the power stroke, 5 stroke. The myosin head rotates 6 the myosin head releases ADP on its hinge, pushing the actin and resumes the tightly bound filament past it. rigor state. ADP Pi 1 2 3 4 1 2 3 4 5 5 Actin filament moves toward M line. The Regulatory Role of Tropomyosin and Troponin in Muscle Contraction IN RELAXED STATE FUNCTION OF MUSCLE FIBER: Tropomyosin partially covers the myosin binding sites Prevents myosin from binding fully and releasing Pi So myosin head can’t undergo power stroke  Regulatory Role of Tropomyosin and Troponin in Muscle Contraction (b) Initiation of contraction 1 Ca2+ levels increase in cytosol. Ca2+ binds to 4 Power stroke 2 troponin. 3 Tropomyosin shifts, Pi Troponin-Ca2+ exposing binding ADP 3 complex pulls site on G-actin tropomyosin away from G-actin binding site. TN Myosin binds 4 to actin and completes power stroke. 2 5 Actin filament G-actin moves 5 moves. 1 Cytosolic Ca2+ Excitation-Contraction Coupling: The link between the muscle action potential and muscle contraction. Somatic motor neuron 1 releases ACh at neuro- muscular junction. (a) 1 Axon terminal of Muscle fiber ACh somatic motor neuron Motor end plate T-tubule Sarcoplasmic reticulum Ca2+ DHP receptor Tropomyosin Troponin Z disk Actin M line Myosin head Myosin thick filament Excitation-Contraction Coupling Somatic motor neuron Net entry of Na+ through ACh 1 releases ACh at neuro- 2 receptor-channel initiates muscular junction. a muscle action potential. (a) 1 Axon terminal of Muscle fiber ACh somatic motor neuron potential K+ 2 Action potential Na+ Motor end plate T-tubule Sarcoplasmic reticulum Ca2+ DHP receptor Tropomyosin Troponin Z disk Actin M line Myosin head Myosin thick filament Excitation-Contraction Coupling Action potential in 3 t-tubule alters conformation of DHP receptor. (b) 3 Ca2+ Excitation-Contraction Coupling Action potential in DHP receptor opens Ca2+ 3 t-tubule alters 4 release channels in conformation of sarcoplasmic reticulum DHP receptor. and Ca2+ enters cytoplasm. (b) 4 3 Ca2+ Ca2+ released Excitation-Contraction Coupling Action potential in DHP receptor opens Ca2+ 3 t-tubule alters 4 5 Ca2+ binds to troponin, release channels in conformation of allowing strong actin- sarcoplasmic reticulum DHP receptor. myosin binding. and Ca2+ enters cytoplasm. (b) 4 3 Ca2+ Ca2+ released 5 Excitation-Contraction Coupling Action potential in DHP receptor opens Ca2+ 3 t-tubule alters 4 5 Ca2+ binds to troponin, release channels in conformation of allowing strong actin- sarcoplasmic reticulum DHP receptor. myosin binding. and Ca2+ enters cytoplasm. (b) 4 3 Ca2+ Ca2+ released 5 6 Myosin thick filament M line 6 Myosin heads execute power stroke.  Excitation-Contraction Coupling Action potential in DHP receptor opens Ca2+ 3 t-tubule alters 4 5 Ca2+ binds to troponin, release channels in conformation of allowing strong actin- sarcoplasmic reticulum DHP receptor. myosin binding. and Ca2+ enters cytoplasm. (b) 4 3 Ca2+ Ca2+ released 5 7 6 Myosin thick filament M line Distance actin moves Actin filament slides 6 Myosin heads execute 7 toward center of power stroke. sarcomere. A muscle fiber contracts completely and then repolarizes. That is it is an all-or-none event.  When a muscle fiber repolarizes… The Ca2+ channels on SR close Ca2+ pumps on SR pump Ca2+ back into the SR This pulls Ca2+ off troponin Tropomyosin shifts back to partially cover myosin binding sites on G-actin molecules. Sarcomere is returned to its original length with help of titin (like a spring!). As the sarcomeres are returned to their original length, the muscle fiber returns to original length (it “relaxes”). As the muscle fibers relax the muscle relaxes.  Skeletal Muscle Fiber Types There are three skeletal muscle fiber types: 1) Slow-twitch oxidative fibers 2) Fast twitch oxidative fibers 3) Fast-twitch glycolytic fibers  Characteristics of the Three skeletal muscle fiber types Fiber type Slow Twitch Fast Twitch Fast twitch Oxidative oxidative glycolytic Characteristic Fibers (Type I) fibers fibers (Type IIa) (Type IIb) Myosin type Slow (0.1ms) Fast Fast (0.1ms) (0.01ms) Twitch Long (75ms) Short Short (7.5ms) duration (7.5ms) Fatigue High moderate low resistance resistance Color Deep red Pinkish White (lots of myoglobin) (less myoglobin) (little myoglobin) Used for Endurance Walking Fast postural (moderate) movements  Muscle Fibers and Motor Units Most skeletal muscles are a mixture of muscle fiber types. Muscle fibers in a skeletal muscle are organized into motor units: A motor unit is composed of the motor neuron and all the muscle fibers it innervates. It is the basic functional unit of a skeletal muscle. The nervous system works in terms of motor units. The smallest possible contraction you can make with a skeletal muscle involves activation of a motor unit. Motor Units Recall that the cell body of a somatic motor neuron is located in the ventral horn of the spinal cord. The motor neurons send their axons out through the ventral root to innervate a group of muscle fibers in a skeletal muscle (color coded here). In this illustration this muscle has three motor units (MU 1, MU 2, and MU 3). Most muscles consist of 100s or even 1000s of motor units.  Motor Units and Muscle Movements When a motor unit is activated, all the muscle fibers in that unit contract completely and then relax (i.e. it is an all-or-none event). The number of muscle fibers in a motor unit determines the amount of force generated when that motor unit is activated. The more muscle fibers in a motor unit, the more force it generates when it is activated. Muscles used for fine movements (eg. finger muscles) have few muscle fibers per motor unit (small motor units). These small motor units allow you to make fine movements with your fingers. Muscles used for gross movements (hip or shoulder muscles) have large numbers of muscle fibers per motor unit (large motor units). This allows these muscles to generate enough force to move your whole arm or leg.  If each motor unit contracts in an “all-or-none” fashion, how can muscles create graded contractions of varying force? The nervous system can vary the force of contraction of a muscle in two ways: 1. By varying the type of motor units being activated in the muscle Small motor units have fewer muscle fibers and thus produce less force. So, if the task requires only a little force the nervous system will activate small motor units. Large motor units have many muscle fibers and thus produce greater force. So, if the task requires a greater force the nervous system will activate larger motor units. …The Nervous System Can Vary The Force of Contraction in Two Ways… 2. The nervous system can change the force of muscle contraction by changing the number of motor units that are being activated at any one time during the contraction. The force of contraction can be increased by recruiting additional motor units into the contraction. This is called “motor unit recruitment”. Motor Unit Recruitment occurs in a stereotyped way during a muscle contraction: During a contraction: Nervous system first activates a few small motor units in a muscle to produce a small amount of force. These small motor units are composed of slow twitch oxidative fibers. To increase the force of contraction the nervous system increases the number and size of the motor units being activated. As max force of contraction for the muscle is approached, the largest motor units in the muscle are activated, which are composed of fast twitch glycolytic fibers. Motor Unit Recruitment The fast twitch glycolytic fibers can’t sustain contraction for long period, so force of contraction drops as these motor units fatigue and drop out of the contraction. However, for most skeletal muscles it is possible to sustain submaximal contractions for relatively long periods. This is accomplished by “asynchronous recruitment”. In asynchronous recruitment: The nervous system alternates activation of motor units so that different motor units are maintaining the contraction at different times. This allows a sustained submaximal contraction of the muscle for relatively long periods. Two types of muscle contraction generate force: 1. Isotonic contractions: Muscle contracts, generates force, shortens in length, and moves a load. Two subtypes: Concentric action the muscle generates force during shortening. Eccentric action the muscle generates force during lengthening. 2. Isometric contractions: Muscle contracts, and generates force, but doesn’t shorten in length, and doesn’t move a load. Isotonic vs Isometric Contractions Series Elastic Elements in Muscle Connective tissue Muscle fibers ATP is required in steady supply during muscle contraction: ATP is needed: During contraction for release of myosin heads from the actin, To provide the energy to move of the myosin head from 45o to 90o angle. During relaxation of muscle fiber to provide energy for the Ca2+ pump to move Ca2+ ions back into the sarcoplasmic reticulum After excitation-contraction coupling to provide energy to the Na+/K+ ATPase pumps in the sarcolemma that restore the Na+ and K+ concentration gradients between the inside and outside of the muscle fiber.  Muscle Fatigue: Fatigue is defined as a condition in which an active muscle is no longer able to generate its expected power output. Cause of fatigue are uncertain and are actively being researched. It is probably the result of a combination of factors. Classically fatigue has been divided into: - Central Fatigue (i.e. fatigue of the CNS and Motor Neurons). - Peripheral Fatigue (i.e. fatigue due to factors in the muscle fiber)  Factors in Central Fatigue Maybe due to psychological factors (i.e. bored with repeated activity). It has also been proposed that lowered blood pH due to lactic acid production by muscles may contribute. Diminished supply of ACh at the neuromuscular junction.  Factors in Peripheral Fatigue Extended submaximal exercise. – Thought to cause depletion of glycogen stores in the muscle which may affect Ca2+ from the SR. Short-duration maximal exertion. – Believed to cause increased levels of inorganic phosphate (Pi) in the muscle fibers which: – May slow Pi release from myosin head during contraction resulting in altering the powerstroke. – Another possibility is that the Pi combines with Ca2+ preventing the Ca2+ from being taken back up into the SR and so decreases calcium release from the SR during subsequent contractions. Ion imbalances resulting from prolonged muscle activity. – With each muscle action potential K+ leaves the muscle fiber hyperpolarizing the muscle fiber membrane potential and so moving it away from the threshold for triggering subsequent muscle fiber action potential. Characteristics of Skeletal vs. Cardiac vs. Smooth Muscle Skeletal Muscle Characteristics: Appearance under microscope: Striated Where found in body: Attached to skeletal elements Control: Voluntary (somatic motor subdivision) Morphology of cellular components: Muscle fiber is long, cylindrical with multiple nuclei Contraction is all-or-none. Contraction Speed: Faster than smooth and cardiac Internal cellular structure: Sarcoplasmic reticulum & T-tubules Characteristics of Skeletal vs. Cardiac vs. Smooth Muscle Cardiac Muscle Characteristics: Appearance under microscope: Striated Where found in body: heart Control: Involuntary (ANS innervation) Morphology of cellular components: Individual muscle cells, branched with single nucleus Contraction is graded (is NOT all-or-none) Contraction Speed: Intermediate Internal cellular structure: Sarcoplasmic reticulum & T-tubules Characteristics of Skeletal vs. Cardiac vs. Smooth Muscle Smooth Muscle Characteristics: Appearance under microscope: No striations Where found in body: walls of digestive tract, blood vessels, bronchioles, ducts of glands, ureter, and urinary bladder. Control: Involuntary (ANS innervation) Morphology of cellular components: Individual muscle cells, fusiform in shape with single nucleus Contraction is graded (is NOT all-or-none) Contraction Speed: Slowest of the three types of muscle Internal cellular structure: Little Sarcoplasmic reticulum & NO T-tubules (Caveloae bring Ca2+ in from extracellular fluid to supplement SR)  Chapters 14,15,16 Cardiovascular System 1 The Cardiovascular System is composed of three elements: Heart Blood Blood vessels  3 Kinds of Blood Vessels 1. Arteries: Carry blood away from the heart Arterioles: The smallest arteries 2. Veins: Carry blood returning to the heart Venules: The smallest veins 3. Capillaries: Connect arterial side of system to venous side. Networks of capillaries called “capillary beds” are found in the tissues of the body. Walls of the capillaries are one cell layer thick. All exchange of gases, wastes, and nutrients between the blood & cells of the body tissues occurs across the walls of the capillaries.  The Heart The heart is located in the thoracic cavity just under the sternum. The apex of the heart is to the lower left. The major arteries and veins that carry away from the heart and back to the heart, respectively, attach to the base of the heart. Base of heart  Structure of the Heart The mammalian heart has four chambers: two on the left and two on the right. The heart has four valves that keep the blood flowing in the right direction. The aortic semilunar valve is obscured in this figure.  Structure of the Heart: Heart Valves The A-V valves (atrioventricular) close when the ventricles of the heart contract, keeping blood from being pushed back into the atria from the ventricles. The closing of these valves causes the “lub” sound (S1 sound) of a heartbeat. The semi-lunar valves close when the ventricles relax, preventing blood from flowing back into the ventricles from the aorta and pulmonary trunk as pressure drops in the ventricles during relaxation. The closing of these valves causes the “dub” sound (S2 sound) of a heartbeat.  Functional Model of the Cardiovascular System The right side of the heart receives blood from the systemic circulation (body) and pumps it through the pulmonary circulation (lungs). The left side receives blood from the and pumps it to the systemic circulation.  Blood flow: Pressure Gradient in Blood Vessels For blood to flow there has be a pressure gradient across the system. This pressure gradient is created primarily by the contraction of the heart. With regard to the blood vessels, the pressure is highest in the aorta and lowest in the venae cavae.  Blood Flow: The Heart and Arteries Contraction of the heart creates pressure that pushes blood into the arteries. The walls of the larger arteries have elasticity, which allows them to stretch as blood is pushed out of the heart when it contracts. The stretching of the walls of the arteries stores energy. (a) Ventricular contraction Arterioles 1 2 3 1 Ventricle contracts. 2 Aortic valve is pushed opened. 3 Aorta and arteries stretch and store pressure in elastic walls.  Blood Flow: Elastic Recoil in Arteries When the heart relaxes, the arterial walls recoil, releasing the stored energy and pushing the blood through the arterioles, capillaries, and veins. (b) Ventricular relaxation 1 2 3 1 Ventricle relaxes and expands 2 Aortic valve shuts, in volume. preventing flow back into heart. 3 Elastic recoil of arteries sends blood forward into rest of circulatory system.  Blood Flow: Pressure in veins is low Because the pressure pushing the blood through the vessels is low in veins, the veins have valves that keep the blood from backing up. Contraction of skeletal muscle squeezes on the veins pushing the blood toward the heart.  The Heart Muscle: Myocardium To generate the pressure required to push the blood through the circulatory system the heart wall is composed mostly of cardiac muscle called the myocardium. The myocardium consists of cardiac contractile cells and autorhythmic (pacemaker) cells.  Cardiac Muscle versus Skeletal Muscle Cardiac muscle cells are single cells that are branched and have a single nucleus. Skeletal muscle fibers are long, cylindrical, and have multiple nuclei. Cardiac muscle cells have intercalated disks consisting of: – Desmosomes: intracellular attachments that hold the cardiac muscle cells together and allow force to be transferred across the heart as it contracts. – Gap Junctions that provide electrical connection between cardiac muscle cells – Skeletal muscle fibers don’t have intercalated disks. T-tubules of cardiac muscle cells are larger in diameter than those in skeletal muscle fibers, and they branch. Sarcoplasmic reticulum is smaller in volume in cardiac muscle cells than in skeletal muscle fibers. Some of the Ca2+ for contraction in cardiac muscle cells comes from the ECF. Mitochondria in cardiac muscle cells are larger than those in skeletal muscle to provide energy for constant activity. Remember your heart beats constantly your entire life.  The Heart Muscle: Cardiac Muscle The ventricles contract from the apex up to the base of the heart. So the spiral arrangement of the myocardium of the ventricles pushes the blood up towards the base of the heart (red arrow) and out through the semilunar valves during ventricular contraction. aorta Pulmonary trunk  Cardiac Muscle: Excitation-contraction coupling and relaxation in cardiac muscle cells. Excitation Relaxation 9 10 1 Action potential enters Ca2+ induced Ca2+ release Ca2+ Ca2+ 3 Na+ 2 K+ from adjacent cell. 1 ECF ATP 2 Voltage-gated Ca2+ ICF channels open. Ca2+ Ryanodine Ca2+ 3 Na+ enters cell. receptor-channel 3 Ca2+ induces Ca2+ release 2 through ryanodine 3 receptor-channels (RyR). SR Sarcoplasmic reticulum Ca2+ 4 Local release causes Ca2+ (SR) stores Ca2+ spark. T-tubule 5 Summed Ca2+ Sparks 4 ATP create a Ca2+ signal. Ca2+ Ca2+ spark 8 2+ 6 Ca ions bind to troponin 5 to initiate contraction. 7 Relaxation occurs when Ca2+ signal Ca2+ unbinds from troponin. Ca2+ 6 7 Actin 8 Ca2+ is pumped back into the sarcoplasmic reticulum for storage. 9 Ca2+ is exchanged with Na+. Contraction Relaxation Myosin 10 Na+ gradient is maintained by the Na+-K+-ATPase.  “Calcium-induced Calcium release” Accounts for two important properties of cardiac muscle cell contraction: 1. The amount of Ca++ released from the SR depends on the amount of Ca++ that enters the cell from the extracellular fluid. – The more Ca++ that enters, the more Ca++ released from SR 2. The amount of Ca++ released from the SR determines the force of contraction of the cardiac muscle cell. – The more Ca++ released, the greater the force of contraction. Calcium induced Calcium release in the context of the function of the heart as a blood pump: The more Ca++ that enters the cardiac muscle cells of the heart The more Ca++ released from the SR in those cells So the greater the force of contraction, thus The greater the volume of blood pumped into the circulation per contraction. Sympathetic Input to cardiac contractile muscle cells modulates the force of contraction, and so ejection volume. Cardiac contractile muscle cells receive only sympathetic autonomic innervation. Release of norepinephrine onto β1 receptors expressed on cardiac muscle cells initiates a second messenger system that increases the number of voltage-gated Ca++ channels that open in response to an action potential. This increases the amount of Ca++ that enters the cell from the ECF This increases the amount of Ca++ released from the sarcoplasmic reticulum This increases the force of contraction, and thus increases the volume of blood ejected from the heart per contraction. Sympathetic input to the cardiac contractile muscle cells also increases the rate of relaxation of these cells. Activation of β1 receptors on a cardiac muscle cell also enhances re-uptake of Ca++ by the SR, allowing the cell to relax more quickly so can be ready to contract again sooner.  Sympathetic input to autorythmic cells (pacemaker cells): The heart also has pacemaker cells that initiate an action potential that spreads through the myocardium leading to contraction of the cardiac muscle cells. These pacemaker cells receive both sympathetic and parasympathetic innervation that regulates heart rate (more on parasympathetic input later). Sympathetic input to β1 receptors on pacemaker cells increases rate at which pacemaker cells initiate action potentials, thus increasing heart rate.  Sympathetic input to the heart: In summary, the sympathetic input to the heart is important in: Regulating the force of heart muscle contraction. Regulating the volume of blood pumped per contraction. Regulating the rate of heart contraction. The volume of blood pumped by heart per contraction is important in determining blood pressure (pressure exerted by the blood in blood vessels). Hypertension = high blood pressure on the arterial side of the circulation.  Sympathetic input to the heart: Treatment strategies for high blood pressure include: Calcium channel blocker: blocking Ca++ channels reduces the amount of Ca++ allowed to enter the cell, reducing the force of contraction and ejection volume, thus reducing arterial blood pressure. β blockers: Blocking β1 receptors reduces force and rate of contraction, reducing blood volume ejected during contraction, reducing arterial blood pressure. Action Potentials in Cardiac Autorhythmic Cells The membrane potential of the pacemaker cells is unstable. If channels on the pacemaker cells are permeable to both K+ and Na+ and open when the membrane potential reaches -60mV, allowing a slow influx of Na+ resulting in a slow depolarization called a pacemaker potential. When threshold is reached an action potential is initiated. Rapid depolarization repolarization Slow Depolarization (pacemaker potential) Allow slow influx of Na+ Action potentials in cardiac contractile muscle cells: The action potential initiated by the pacemaker cells spreads through the heart muscle. The action potential in a cardiac contractile cell is triggered by entry of positive ions from adjacent cells through gap junctions. The action potential in a cardiac muscle cell can be divided into 5 phases numbered 0-4.  Action potentials in cardiac muscle cells: The resting membrane PNa PX = Permeability to ion X potential of a cardiac muscle +20 1 2 PK and PCa cell is about -90 mV, and is 0 Membrane potential (mV) stable (phase 4). As well as -20 having K+ leak channels, -40 0 3 PK and PCa these cells have special -60 PNa gated K+ channels, called -80 4 4 fast potassium channels, -100 that are open at the resting 0 100 200 Time (msec) 300 membrane potential, Phase Membrane channels resulting in increased 0 1 Na+ channels open Na+ channels close membrane permeability to 2 Ca2+ channels open; fast K+ channels close K+ and causing the resting 3 4 Ca2+ channels close; slow K+ channels open Resting potential membrane potential to be close to the EK+ (-90mV).  Action potentials in cardiac muscle cells: PX = Permeability to ion X When a wave of +20 depolarization enters 0 Membrane potential (mV) the cardiac muscle cell -20 through the gap -40 0 junctions, voltage -60 PNa gated Na+ channels -80 are triggered to open -100 allowing Na+ to enter 0 100 200 Time (msec) 300 and causing rapid Phase Membrane channels depolarization of the 0 Na+ channels open Na+ flows in depolarization membrane potential (phase 0)  Action potentials in cardiac muscle cells: PX = Permeability to ion X During phase 0 membrane 1 PNa +20 potential depolarizes to about 0 +20mV before the voltage gated Membrane potential (mV) Na+ channels close. These -20 channels are similar to the -40 0 voltage gated Na+ channels in -60 PNa neurons, and have an -80 inactivation gate that remains closed for about 200msec. -100 0 100 200 300 During this time these channels Time (msec) are refractory so another action Phase Membrane channels potential cannot be initiated in 0 Na+ channels open the cardiac muscle cell. 1 Na+ channels close  Action potentials in cardiac muscle cells: During phase 1, PNa PX = Permeability to ion X 1 membrane potential +20 2 PK and PCa briefly repolarizes as K+ 0 ions move out across the Membrane potential (mV) -20 membrane through the K+ -40 0 leak channels and the PNa fast K+ channels. -60 -80 However, towards the end -100 of phase 1 the fast 0 100 200 300 potassium channels Time (msec) Phase Membrane channels close and voltage gated 0 Na+ channels open Ca2+ channels open, 1 Na+ channels close decreasing K+ outflow 2 Ca2+ channels open; fast K+ channels close and allowing Ca2+ to flow in. This results in a plateau in the membrane potential (phase 2)  Action potentials in cardiac muscle cells: The voltage gated Ca2+ channels remain open for about 100msec. PX = Permeability to ion X PNa As they close, slow, voltage +20 1 gated K+ channels open. These 2 PK and PCa 0 channels are similar to the voltage Membrane potential (mV) gated K+ channels in neurons. -20 3 PK and PCa -40 0 As the slow, voltage gated K+ PNa channels open, the membrane’s -60 permeability to K+ increases and -80 membrane potential rapidly -100 repolarizes (Phase 3). As 0 100 200 300 membrane potential approaches Time (msec) the resting membrane potential, Phase Membrane channels the fast K+ channels open helping 0 Na+ channels open to bring the membrane potential 1 Na+ channels close to -90mV (back to Phase 4). 2 Ca2+ channels open; fast K+ channels close 3 Ca2+ channels close; slow K+ channels open Action potentials in cardiac muscle cells: PNa PX = Permeability to ion X 1 +20 2 PK and PCa 0 Membrane potential (mV) -20 3 PK and PCa -40 0 -60 PNa -80 4 4 -100 0 100 200 300 Time (msec) Phase Membrane channels 0 Na+ channels open 1 Na+ channels close 2 Ca2+ channels open; fast K+ channels close 3 Ca2+ channels close; slow K+ channels open 4 Resting potential Coodinated Contraction of the Heart Muscle Contraction of the heart occurs in an orderly fashion: 1.First the atria contract pushing blood into the ventricles. 2.Then the ventricles contract pushing blood into the circulation. The basis of this orderly contraction is a conduction system within the heart called the intrinsic conduction system. Intrinsic conduction system of the heart consists of: SA node, is located in the upper wall of the right atrium and is composed of the pacemaker cells of the heart. AV node, located at top of the septum between the ventricles. – Receives pacemaker action potential and relays it to the conduction system of the ventricles. – Delays transmission of action potential to the ventricles for 0.1msec to allow the atria time to finish contracting. Purkinje fibers comprise the conduction system of the ventricles and make up the bundle of His, the left and right bundle branches. The cells of the AV node (50 bpm) and Purkinje fibers (25-40 bpm) are also autorhythmic and can act as the pacemaker for the heart under abnormal conditions. However, they cannot maintain a normal cardiac rhythm. All of these cells are modified cardiac muscle cells that have lost their contractile capabilities. Intrinsic conduction system of the heart 1 1 SA node AV node THE CONDUCTING SYSTEM 1 SA node depolarizes. OF THE HEART SA node Internodal pathways AV node A-V bundle Bundle branches Purkinje fibers Purple shading in steps 2–5 represents depolarization.  Electrical Conduction in Heart 1 1 SA node AV node 2 THE CONDUCTING SYSTEM 1 SA node depolarizes. OF THE HEART 2 Electrical activity goes rapidly to AV node via SA node internodal pathways. Internodal pathways AV node A-V bundle Bundle branches Purkinje fibers Purple shading in steps 2–5 represents depolarization.  Electrical Conduction in Heart 1 1 SA node AV node 2 THE CONDUCTING SYSTEM 1 SA node depolarizes. OF THE HEART 2 Electrical activity goes rapidly to AV node via SA node internodal pathways. 3 Internodal pathways 3 Depolarization spreads more slowly across atria. Conduction slows through AV node. AV node A-V bundle Bundle branches Purkinje fibers Purple shading in steps 2–5 represents depolarization.  Electrical Conduction in Heart 1 1 SA node AV node 2 THE CONDUCTING SYSTEM 1 SA node depolarizes. OF THE HEART 2 Electrical activity goes rapidly to AV node via SA node internodal pathways. 3 Internodal pathways 3 Depolarization spreads more slowly across atria. Conduction slows through AV node. AV node 4 Depolarization moves A-V bundle rapidly through ventricular 4 Bundle branches conducting system to the Purkinje apex of the heart. fibers Purple shading in steps 2–5 represents depolarization.  Electrical Conduction in Heart 1 1 SA node AV node 2 THE CONDUCTING SYSTEM 1 SA node depolarizes. OF THE HEART 2 Electrical activity goes rapidly to AV node via SA node internodal pathways. 3 Internodal pathways 3 Depolarization spreads more slowly across atria. Conduction slows through AV node. AV node 4 Depolarization moves A-V bundle rapidly through ventricular 4 Bundle branches conducting system to the Purkinje apex of the heart. fibers 5 Depolarization wave 5 spreads upward from the apex. Purple shading in steps 2–5 represents depolarization. Figure 14-18, steps 1–5  The Electrocardiogram (ECG) It is possible to record the pacemaker action potential as it is conducted through the myocardium using electrodes placed on the body surface. Such a recording of electrical activity is called and electrocardiogram or ECG. As each part of the heart depolarizes it causes a deflection in the ECG recording. Example of an ECG The five major deflection waves in the ECG recording are: P wave, Q wave, R wave, S wave, and T wave. Each cooresponds to the depolarization or repolarization of part of the heart. ECG deflection waves: P- wave: depolarization of the atria Q- wave: depolarization of the septum (wall between the ventricles) R- wave: depolarization of lower part of ventricles S- wave: depolarization of upper part of ventricle T- wave: repolarization of ventricles  ECG deflection waves: P wave: atrial START depolarization P Correspondance The end R between an ECG P T and electrical QS P Atria contract. events in the Repolarization ELECTRICAL R cardiac cycle. P T EVENTS OF THE CARDIAC CYCLE QS P Q wave Q These electrical ST segment R events lead to the P QS R wave R mechanical Ventricles contract. R P Q events of the P QS S wave cardiac cycle.  Electrical events of the cardiac cycle lead to mechanical events of the cardiac cycle: The mechanical events of the cardiac cycle include: Contraction of the myocardium of the atria and ventricles. The movement of blood from atria into ventricles and from the ventricles into the circulation. The opening and closing of the heart valves that keep the blood moving in the right direction through the heart. Cardiac Mechanical Function Terminology: Diastole: Time during which cardiac muscle is relaxed Systole: Time during which cardiac muscle is contracting Atrial systole: time during which atria are contracting Atrial diastole: time during which atria are relaxing Ventricular diastole: time during which ventricles are relaxing Ventricular systole: time during which ventricles are contracting  Mechanical Events of the cardiac Cycle Late diastole: both sets of Blood flows from the circulation 1 chambers are relaxed and directly through the atria and into START ventricles fill passively. the ventricles Isovolumic ventricular 5 relaxation: as ventricles relax, pressure in ventricles Atrial systole: atrial contraction 2 forces a small amount of falls, blood flows back into cups of semilunar valves additional blood into ventricles. and snaps them closed. Most of the filling of the Closing of semilunar ventricles occurs as a result of valves causes the pressure from the previous S2 sound (“dub) contraction. Contraction of the atria only pushes the last bit of blood into the ventricles. The The volume of volume of the blood in the left blood ejected ventricle at the end of diastole from the left is called the end-diastolic Ventriclei nto the volume (EDV) and is normally circulation is normally 135ml. 70ml and is called the stroke volume. The volume of blood left in the left ventricle Is called the end systolic volume and is normally 65ml. Isovolumic ventricular Ventricular ejection: 3 contraction: first phase of 4 as ventricular pressure ventricular contraction pushes rises and exceeds AV valves closed but does not pressure in the arteries, create enough pressure to open the semilunar valves semilunar valves. open and blood is ejected. Closing of the AV valves causes S1 Vales are pushed open by pressure sound (“lub”) of blood.  Mechanical Events of the cardiac Cycle In cardiac physiology the focus is on the function of the left ventricle. Left ventricular pressure-volume changes during one cardiac cycle A = ventricular contraction just completed. Begin KEY ventricle relaxation. 65ml of blood remain in the left EDV = End-diastolic volume ventricle following the previous contraction (ESV). ESV = End-systolic volume A-B = blood flows into left ventricle from atrium. Stroke volume 120 D Left ventricular pressure (mm Hg) B = Max ventricular filling. EDV=135ml ESV B-C = Isovolumetric Contraction. Left ventricle is 80 C contracting but pressure not yet great enough to push One open aortic semilunar valve. Volume of left ventricle cardiac cycle remains 135ml. 40 EDV C = Aortic Valve Opens B C-D = Blood pushed out into aorta. Stroke volume = A 70ml. ESV = 65ml 0 65 100 135 Left ventricular volume (mL) D-A = Isovolumetric relaxation Mechanical Events of the cardiac Cycle KEY EDV = End-diastolic volume ESV = End-systolic volume 120 Left ventricular pressure (mm Hg) 80 AV valve pushed opened by blood flowing in through the atria. 65ml of blood remain in the left ventricle after 40 previous contraction A 0 65 100 135 Left ventricular volume (mL) Mechanical Events of the cardiac Cycle KEY EDV = End-diastolic volume ESV = End-systolic volume 120 Left ventricular pressure (mm Hg) 80 Blood flows into ventricle while relaxed. Volume of blood rise to 135ml (EDV) 40 EDV B A 0 65 100 135 Left ventricular volume (mL) Mechanical Events of the cardiac Cycle KEY EDV = End-diastolic volume ESV = End-systolic volume 120 Left ventricular pressure (mm Hg) 80 C AV valves closed as blood is pushed up towards the base Isovolumetric of the heart. Aortic valve still contraction 40 closed. Volume of left Ventricle remains 135ml EDV B A 0 65 100 135 Left ventricular volume (mL) Mechanical Events of the cardiac Cycle KEY EDV = End-diastolic volume ESV = End-systolic volume Stroke volume 120 D Left ventricular pressure (mm Hg) ESV Ventricular ejection. Blood pushed from left ventricle Isovolumetric into aorta. 70ml ejected.