Cardiac Muscle Structure and Function PDF

RAK College of Medical sciences General structure and functions of cardiac muscle Dr. Rasha Abuelgasim MBBS, MSc, PhD Physiology Office 216 Department of Physiology  Learning Objectives 1. Describe the structure and function of cardiac muscle. 2. Explain how cardiac muscle myofi...

RAK College of Medical sciences General structure and functions of cardiac muscle Dr. Rasha Abuelgasim MBBS, MSc, PhD Physiology Office 216 Department of Physiology  Learning Objectives 1. Describe the structure and function of cardiac muscle. 2. Explain how cardiac muscle myofilaments and contraction are regulated 3. Explain the contractile cardiac myocyte action potential. 4. Explain the absence of tetanus in the contractile cardiac myocyte.  CARDIAC MUSCLE Cardiac muscle is a striated fiber containing the same arrangements of contractile filaments as skeletal muscle. intercalated discs :These intercalated discs join the muscle fibers end-to-end. They are highly specialized attachment sites which prevent the cells from pulling apart. On the lateral component of the intercalated discs are gap junctions which permit the cells to act as an electrical syncytium.  There are two types of cardiac muscle cells: conducting and contractile. Conducting cardiac muscle cells are 1% of the cardiac muscle cells. These are large diameter cells that do not produce tension, instead they are specialized for excitation. They constitute a network in the heart known as a conduction system. They are connected to the contractile cells by gap junctions. The conducting fibers are filled mostly with glycogen and have few myofilaments. These cells are the intrinsic pacemakers.  Contractile cardiac muscle cells are slow oxidative muscle fibers. These fibers form the walls of the heart, shorten and produce tension. They use glucose and fatty acids as substrates.  Characteristics of cardiac muscle: Histology Functional syncytium Source of energy Blood flow Oxygen consumption Metabolism Automaticity Rhythmicity Conductivity Action potential Recruitment Histology Connections between the fibers (intercalated discs and gap junctions) Functional syncytium  Source of energy Fat 60 %(main source) CHO 35% Ketones and amino acid 5%  Blood flow Cardiac muscle receive blood supply during diastole Left ventricle (diastole) Right ventricle (systole and diastole)  Oxygen consumption and Metabolism Consume high amount of oxygen Aerobic metabolism Anaerobic metabolism provide less than 1%  Automaticity and Rhythmicity Conductive system discharge the action potential Rhythmic contraction without external stimuli unlike the skeletal muscles  Types of cardiac muscle There are two types of cardiac muscle cells: conducting and contractile. Conducting cardiac muscle cells are 1% of the cardiac muscle cells. These are large diameter cells that do not produce tension, instead they are specialized for excitation. They constitute a network in the heart known as a conduction system. They are connected to the contractile cells by gap junctions. The conducting fibers are filled mostly with glycogen and have few myofilaments. These cells are the intrinsic pacemakers. Conductivity  Contractile cardiac muscle cells are slow oxidative muscle fibers. These fibers form the walls of the heart, shorten and produce tension. They use fatty acids and glucose as substrates.  Electrical –Contraction (E-C) Coupling As in skeletal muscle, contraction in cardiac muscle is dependent on the entry of Ca++ from the T tubule. Depolarization of the T tubule membrane opens the voltage gated Ca++ channels (dihydropyridine receptor), permitting the entry of a small amount of Ca++. This Ca++ opens the Ca++ gated Ca++ channel (ryanodine receptor) on the sarcoplasmic reticulum (SR) thereby releasing a lot of Ca++ into the cytoplasm. In turn, Ca++ binds to troponin which unmasks the actin (thin filament), cross bridges form, and shortening occurs. With repolarization of the T tubule membrane, no further Ca++ enters the cells and the SR CaATPase removes Ca++ from the cytoplasm. This removal of Ca++ ends the contractile cycle and the muscle relaxes. There are two other proteins located at the plasma membrane which help to return Ca++ to its basal level inside the cardiac muscle cell. The plasma membrane CaATPase uses ATP to actively pump Ca++ out. The Na+ - Ca++ exchanger transports Na+ into the cell for each Ca++ moved out of the cell (i.e., exchanges Na+ for Ca++).  Membrane activation in contractile cardiac cells The action potential of the contractile cardiac muscle fiber is longer in duration (200-220 msec) than that seen in skeletal muscle (2 msec). In cardiac cells there are four phases to the action potential.  Action potential of the contracting cardiomyocyte Phase 0, voltage gated Na+ channels open. Phase 1, voltage gated Na channels inactivate and voltage gated K+ channels open. Phase 2 (plateau), voltage gated Ca++ channels (L type) open and voltage gated K channels remain open. Phase 3, only voltage gated K+ channels are open and cells repolarize. Phase 4, all of the voltage gated channels are closed and the resting membrane potential is restored by the Na/K ATPase.  Note that the entry of Ca++ in phase 2 is essential for initiating contraction and triggering the opening of the Ca++ gated Ca++ release channel (ryanodine receptor). One other point, each action potential results in one contraction. One contraction (twitch) is ~250 msec, almost the same duration as the action potential (200 msec). This is due to the prolonged plateau phase 2.  Refractory period and absence of tetanus Recall that these voltage gated Na+ channels must undergo a conformational change from an “inactivated” state to a “closed” state before they can reopen and initiate another action potential. As a consequence of phase 2, the voltage gated Na+ channels remain “inactivated” for an extended period of time and do not “close” until repolarization in phase 3 (180 msec). This time period during which the voltage gated Na+ channels are inactivated is called the absolute refractory period. No amount of stimulus can cause an action potential during the absolute refractory period.  Note that the absolute refractory period (180 msec) is almost equal in duration to the action potential (200-220 msec). From ~180 msec to 200 msec is called the relative refractory period. During this time period, a second action potential can be fired but the stimulus required is greater than normal. This is because there are fewer voltage gated Na channels in the “closed” state and therefore it is harder to reach threshold  An important point regarding the refractory period is that contractions cannot sum and therefore there is no fused tetanus (summed contractions). Fused tetanus in the heart would lead to death as it would prevent the rhythmic pumping of blood.  The absolute refractory period of the cardiac muscle action potential refers to the time interval when the voltage gated sodium channels are inactivated. The absolute refractory period lasts 180 msec. The action potential lasts 200-220 msec. A single contraction is 250 msec.  Absence of muscle fiber recruitment The contractile cells of the heart act as an electrical syncytium with all of the cells contracting during a single beat. Therefore it is not possible to increase the force of contraction by fiber recruitment. Instead the heart has developed other strategies to increase the force of contraction.  KEY CONCEPTS Cardiac muscle have two sets of overlapping protein myofilaments, actin and myosin, the relative sliding of which produces shortening and generates force. This process involves cross bridge formation between actin and myosin which is driven by ATP. In cardiac muscle, coupling between the membrane action potentials and contraction is mediated by calcium ions. In cardiac muscle Ca++ regulates the thin filament (actin) to enable cross bridge formation.  Cardiac muscle is regulated by the autonomic nervous system and hormones. Relaxation of cardiac muscle, like skeletal muscle, is by removal of Ca++. The force of contraction in cardiac muscle is increased by stretch (Frank-Starling law). This is in contrast to skeletal muscle which increases force either by recruiting more muscle fibers or by summing twitches (fused tetanus). Thank you