Chapter 21. Muscular System
Recommended Article : 【Biology】 Table of Contents for Biology
1. Muscle
2. Model of Skeletal Muscle Contraction
3. Model of Smooth Muscle Contraction
4. Model of Cardiac Muscle Contraction
5. Exercise
1. Muscle
⑴ Components : Animal muscles are composed as follows:
① Water : 70%
② Proteins such as myosin, actin, myoglobin : 20%
⑵ Interaction Between Muscle and Skeleton
① The function of the muscular system is movement, and it interacts with the skeleton
② Muscles are connected to the skeleton by tendons, situated between joints
③ Muscles can only contract → Cooperative muscles (contracting in the same direction) and antagonistic muscles (contracting in opposite directions) act together
○ The statement “muscles can only contract” means there is no mechanism for generating tension in the relaxing direction
○ Contracted muscles naturally tend to relax into an equilibrium state
⑶ Classification
Figure. 1. Classification of muscles. From top to bottom: Skeletal muscle, cardiac muscle, smooth muscle [Footnote:1]
① Skeletal Muscle (skeletal muscle) (e.g., tongue, diaphragm, intercostal muscles)
○ Structure : Cylindrical multinucleated cells, cross-striations (transverse stripes, developed sarcomeres)
○ Multinucleated cells are a unique characteristic of skeletal muscles
○ Features : Non-uniform, abundant sarcoplasm, calcium-troponin binding
○ Frank-Starling Law : The law stating that muscle tension is influenced by muscle length
○ Maximum tension is achieved when actin and myosin filaments are maximally overlapped
○ When the sarcomere length is long : When the muscle contracts, the number of myosin cross-bridges increases, leading to an increase in total tension
○ When the sarcomere length is short : As the sarcomere length becomes shorter than the effective length of the muscle, the overlap between actin and myosin filaments decreases, resulting in decreased tension. If they no longer overlap, tension cannot be generated
Figure. 2. Frank-Starling Law
○ Tetanus Possible : The only muscle among the three muscles capable of tetanus
○ Twitch : A one-time muscle contraction pattern with constant size and shape, similar to an action potential
○ Tetanus : Continuous contraction without relaxation in skeletal muscles caused by repeating electrical stimulation at short intervals
○ Tetanus Possible : Short refractory period of skeletal muscle → High-frequency stimulation → Accumulation of intracellular Ca2+ → Overlapping contractions
○ Unfused Tetanus : Relatively low-frequency stimulation during contraction, resulting in uneven muscle contractions
○ Fused Tetanus : Relatively high-frequency stimulation during contraction, resulting in smooth and connected muscle contractions
Figure. 3. Muscle Fiber Tension Experiment and Twitch-Tetanus
○ Muscle Contraction Regulation : Voluntary regulation (voluntary control)
○ Regulated by the somatic motor nervous system, different from the autonomic nervous system, does not involve ganglia
○ Only contraction and excitation
○ Acetylcholine secretion at the neuromuscular junction leads to calcium binding to troponin, initiating muscle contraction
○ Model of Skeletal Muscle Contraction
② Cardiac Muscle (myocardium)
○ Structure : Branching shape, intercalated discs, cross-striations (developed sarcomeres), intercellular and intercalated junctions
○ Intercalated discs allow simultaneous signal transmission
○ Desmosomes are also present in intercalated discs
○ Intercellular attachment junctions lead to simultaneous contractions, causing all cells to act as a single functional unit
○ Features : Non-uniform, numerous mitochondria, calcium-troponin binding, high resting potential leading to action potential initiation with small stimuli
○ Inability to Tetanus : Similar to an absolute refractory period in cardiac muscle at resting potential, preventing overlapping contractions
○ Regulation of Contraction : Involuntary regulation (involuntary control)
○ Sinoatrial node regulates the heartbeat, controlled by the autonomic nervous system
○ Sympathetic nervous system increases calcium permeability, increasing heart rate, while the parasympathetic nervous system increases potassium permeability, decreasing heart rate
○ Cardiac muscle cells only receive regulation of the sympathetic nervous system (determines stroke volume)
③ Smooth Muscle (visceral muscle) (e.g., digestive tract, blood vessel walls, uterus)
○ Structure
○ Intercellular junctions between muscle cells
○ Calmodulin is involved in calcium-troponin binding instead of direct binding of calcium to troponin
○ Spindle-shaped mononucleated cells
○ No sarcomeres
○ Features : Non-uniform, underdeveloped T-tubules
○ Slow contraction and relaxation due to the absence of well-developed T-tubules
○ Single-unit smooth muscle and multi-unit smooth muscle exist : Single-unit smooth muscle is more common
○ Regulation of Contraction : Involuntary regulation (involuntary control)
○ Sympathetic nervous system : Relaxation of visceral muscles, constriction of small arteries, contraction of airways
○ Parasympathetic nervous system : Contraction of visceral muscles, dilation of small arteries, relaxation of airways
○ Myosin phosphorylation (activation of contraction) and dephosphorylation (inhibition of contraction)
○ Smooth muscle in arterial walls has intrinsic pacemaker cells for self-regulation
④ Comparison of Skeletal Muscle, Cardiac Muscle, and Smooth Muscle
Table. 1. Comparison of Skeletal Muscle, Cardiac Muscle, and Smooth Muscle
⑷ Structure of Skeletal Muscle : Arrangement of fibers in parallel creating a striated pattern
① Muscle = “Bundles of muscle fibers surrounded by muscle fascia” + “Bundles of muscle fibers surrounded by muscle fascia” + …
② One bundle of muscle fibers = “Muscle fibers (muscle cells)” + “Muscle fibers (muscle cells)” + …
③ One muscle fiber = “Aligned muscle origin fibers” + “Aligned muscle origin fibers” + …
④ Muscle origin fibers have sarcomeres
○ Sarcomere : Basic unit of muscle contraction
○ Sarcomeres are defined by actin filaments perpendicular to myosin filaments in the direction of the muscle fiber
⑤ Filaments within the sarcomere = Actin filaments (thin filaments) + Myosin filaments (thick filaments)
○ M Line : Central line of the sarcomere that anchors myosin filaments
○ Named after “middle line” or “M line”
○ H Zone (Helle Zone) : Part of the sarcomere around the M Line where there are no actin filaments
○ I Band (Light Band) : Area near the Z Line where only actin filaments are present, appears brightest under a microscope
○ A Band (Dark Band) : Part corresponding to myosin filaments (dark), includes the H Zone
Figure. 4. Structure of Filaments within Sarcomere
⑥ Calculation of Changes in Muscle Contraction and Relaxation
○ Formula 1: Total length = A Band + I Band
○ Formula 2: A Band = H Zone + α (overlapping region)
○ Formula 3: A Band = Constant
○ During contraction : Total length decreases, I Band decreases, α increases, causing H Zone to decrease (because A Band = Constant)
○ During relaxation : Total length increases, I Band increases, α decreases, causing H Zone to increase (because A Band = Constant)
2. Model of Skeletal Muscle Contraction
⑴ Regulation of Muscle Contraction
① Skeletal muscles are regulated by the somatic motor nervous system rather than the autonomic nervous system
② When the somatic motor nervous system secretes acetylcholine, calcium binds to troponin, initiating muscle contraction
○ Note that troponin does not include actin or myosin
③ Lag time : The time difference between the initiation of a brain response and the initiation of a muscle response
⑵ Enzymatic Action of Myosin
① Myosin is composed of two heavy chains and two light chains
② Heavy Chains
○ The tail of the heavy chain (150 nm) forms a helical structure and constitutes direction-oriented myosin filaments
○ The head of the heavy chain (17 nm) contains actin-binding sites and ATPase sites, providing energy for movement
③ Light Chains : Attached to the head of the heavy chain, regulate ATPase activity
⑶ Sliding Filament Model of Muscle Contraction : ATP breakdown results in two mechanical actions
Figure. 5. Sliding Filament Model of Muscle Contraction
① 1st. Muscle in a resting state (rigor) : Myosin heads bind to actin filaments without ATP or ADP
② 2nd. ATP binding : Myosin heads bind to ATP, detaching from actin filaments
③ 3rd. Myosin heads possess ATPase activity, breaking down ATP into ADP and inorganic phosphate
④ 4th. Myosin heads at high energy levels assume various structures
⑤ 5th. Cross-bridge formation : Myosin heads, with high energy, stand upright and bind to actin filaments
○ [First Mechanical Action]
○ Still in a high-energy state
○ If myosin heads do not bind to actin, the process cannot proceed to the next step
⑥ 6th. Muscle contraction : Myosin heads with high energy release ADP and phosphate, transitioning to a low-energy state by tilting the head downward, causing actin filaments to slide toward the center
○ [Second Mechanical Action]
○ A low-energy structure, still with myosin heads bound to actin filaments
⑷ Calcium-Mediated Muscle Contraction Control : Human movement is controlled in the range of 5 to 10 Hz
① 1st. Acetylcholine released at the synapse terminal of the neuromuscular junction triggers an action potential
○ 1st - 1st. Released acetylcholine diffuses into the synaptic cleft
○ 1st - 2nd. Generates an end-plate potential at the motor endplate
○ 1st - 3rd. End-plate potential opens the muscle fiber, inducing an action potential
② 2nd. Action potential travels along the sarcolemma and T-tubules
○ T-Tubules : Tubular structures formed by invagination of the sarcolemma, transmit excitation inward
○ Voltage-gated K+ channels in the T-tubule membrane generate action potentials
③ 3rd. Action potential induces Ca2+ release from the sarcoplasmic reticulum (a type of sarcoplasmic reticulum)
○ 3rd – 1st. Voltage-gated Ca2+ channels in the sarcolemma (cell membrane) are activated when the action potential reaches
○ 3rd – 2nd. Ca2+ moves from outside the cell to the sarcoplasm due to Ca2+ concentration gradient
○ 3rd – 3rd. Ca2+ inside the cell triggers the opening of the Ca2+-release channel on the sarcoplasmic reticulum membrane
○ 3rd – 3rd – 1st. Action potential causes conformational change in the dihydropyridine (DHP) receptor on T-tubules
○ 3rd – 3rd – 2nd. Ca2+-release channels (ryanodine receptors) on the sarcoplasmic reticulum membrane adjacent to T-tubules open
○ 3rd – 4th. Ca2+ moves from the sarcoplasmic reticulum to the cytoplasm due to Ca2+ concentration gradient
○ As calcium is supplied from the sarcoplasmic reticulum, external calcium supply is unnecessary for skeletal muscle contraction
④ 4th. Calcium ions bind to troponin and expose the myosin-binding sites on actin filaments
○ Calcium ions do not bind to actin or myosin
○ Troponin complex binds to tropomyosin and actin filaments
○ 4th – 1st. Binding of Ca2+ to C subunit of troponin complex
○ 4th – 2nd. Shifting of tropomyosin position
○ 4th – 3rd. Exposure of myosin binding site on actin filament
Figure 6. Actin, tropomyosin, troponin complex, myosin head binding site
⑤ 5th. [Thin Filament Model] Binding of myosin cross-bridge to actin
○ Increase in the number of myosin cross-bridges acting on actin filaments leads to increased overall tension
⑥ 6th. [Sliding Filament Model] ATP hydrolysis causes rotational movement of myosin head → Actin-myosin interaction (repeated)
⑦ 7th. Termination of action potential : Sarcoplasmic reticulum Ca2+ ATPase consumes ATP, leading to the movement of Ca2+ from the cytoplasm to the sarcoplasmic reticulum
○ Active transport of Ca2+ continuously occurs as discussed before
○ However, the net flow of Ca2+ from the cytoplasm to the sarcoplasmic reticulum occurs after the action potential ends
○ The resting membrane potential of muscle fiber is -90 mV, so it doesn’t experience hyperpolarization like K+ equilibrium potential
⑧ 8th. Removal of Ca2+ from troponin and re-covering of myosin binding sites by tropomyosin results in relaxation
⑨ 9th. Muscle fiber relaxation
○ Requires new ATP supply and Ca2+ removal
○ When ATP detaches myosin from actin, actin filaments slide, leading to muscle fiber relaxation
Figure 7. Regulation of muscle contraction by calcium
⑸ Excitation-Contraction Coupling in Skeletal Muscle
① Motor Unit : A motor neuron and the muscle fibers it controls
○ Lower Motor Neuron (LMN) : Motor neuron controlling skeletal muscles
○ Excitation : Brief contraction generated as the action potential propagates through the T-tubule system (minimal contractile unit)
○ Tetanus : When the frequency of action potentials is high enough, individual twitches merge into a continuous and sustained contraction; found only in skeletal muscles
○ If action potential frequency is low, there is a relaxation phase in muscles, resulting in a “twitching gear” appearance (incomplete tetanus), while short intervals between twitches lead to continuous muscle contraction (complete tetanus)
○ Tension depends on the number of contracting muscle fibers and the speed of contraction
② ( Antonym ) Tonic Muscle Fiber : Postural muscles, no action potential, nonfunctional unit
③ Types of Skeletal Muscle Fibers
○ Slow-twitch Fiber (Red Muscle Fiber) : Aerobic, abundant mitochondria and myoglobin, well-distributed blood vessels
○ Oxidative Fiber Characteristic: Primarily relies on aerobic respiration, slow but long-lasting
○ Compared to fast-twitch fiber: Fewer sarcoplasmic reticula, slower Ca2+ pumping, longer Ca2+ residence time, five times longer contraction duration
○ Fast-twitch Fiber (White Muscle Fiber) : Few mitochondria and blood vessels, quick and strong contraction but not sustained, fast-twitch muscles (Type IIa, Type IIb) can convert between each other
○ Glycolytic Fiber Characteristic: Primarily relies on glycolysis, easily fatigued due to thicker diameter and lower myoglobin content; fatigue associated with lactic acid
Table 2. Comparison of Slow-Twitch and Fast-Twitch Muscle Fibers
⑹ Energy Supply in Muscle Contraction : Various supply methods based on muscle fiber types
① Generally, ATP, creatine phosphate, lactic acid fermentation, glycogen, fat, protein in order
② 1st Priority. ATP
○ ~ 5 mM (about 5 seconds)
○ Rigor : State where muscles cannot relax due to ATP depletion
③ 2nd Priority. Creatine Phosphate
○ Function : Regenerates ATP to counter ATP depletion
○ Creatine Phosphate + ADP → Creatine + ATP
○ 20 ~ 40 mM, rapid energy source (about 20 seconds)
④ 3rd Priority. Lactic Acid Fermentation : Human body doesn’t undergo alcohol fermentation or acetic acid fermentation
○ Energy depletion : Glucose → Pyruvate → Lactic Acid, ATP generated through this process (Glucose → Pyruvate)
○ Accumulated lactic acid returns to the blood within an hour and is broken down in the liver (Cori cycle), so it’s less relevant to muscle soreness
○ In muscles: Pyruvate formation is much faster than lactic acid, leading to more NADH than NAD+
○ In liver: Since pyruvate has been resynthesized into glucose, more NAD+ than NADH is present
○ When lactic acid arrives, it reacts with abundant NAD+ to form pyruvate
○ Frequent in glycolytic fibers, which are fast-twitch fibers
○ Tomato as a recovery aid
○ More than 50% of tomatoes are glutamate
○ Glutamate converts pyruvate to alanine, reducing lactic acid production and fatigue
⑤ 4th Priority. Glycogen
○ Stored in the liver and muscles for a day
○ Liver-stored glycogen : Provides energy for the entire body
○ Muscle-stored glycogen : Provides energy only to muscles
○ Can participate in anaerobic and aerobic respiration through gluconeogenesis
⑥ 5th Priority. Fat
○ Carbohydrates (50 ~ 60%) → Fat (20 ~ 35%) → Protein (5 ~ 15%) in order of energy source usage
○ Energy source for aerobic respiration ( ∴ Ineffective in oxygen-deprived conditions)
3. Smooth Muscle Contraction Model
⑴ Regulation of Smooth Muscle Contraction
① Sympathetic Nervous System : Relaxation of visceral muscles, constriction of
arterioles
② Parasympathetic Nervous System : Contraction of visceral muscles, relaxation of arterioles
③ Aorta Smooth Muscle : Self-regulation through intrinsic stretch receptors
④ Other Blood Vessels : Controlled by epinephrine and norepinephrine from sympathetic nerve endings and α, β receptors
○ α receptors : Vasoconstriction → Reduced blood flow to visceral muscles → Relaxation of visceral muscles
○ β receptors : Vasodilation → Increased blood flow to cardiac and other smooth muscles → Contraction of cardiac and other smooth muscles
⑤ Key feature : Regulation of smooth muscle contraction by phosphorylation and dephosphorylation of myosin
⑵ Vasodilation Model : Nitric oxide ( NO ) plays a crucial role
Figure 8. Vasodilation Model
① 1st. Acetylcholine secretion from parasympathetic nerve terminals
② 2nd. Acetylcholine binds to muscarinic acetylcholine receptors on endothelial cells
○ Muscarinic acetylcholine receptors are G-protein-coupled receptors (GPCRs)
③ 3rd. First signal transduction
○ 3rd - 1st. G-protein-coupled receptors (GPCRs) activate by replacing GDP with GTP in G proteins
○ 3rd - 2nd. Activated G proteins convert PLC into IP3
○ 3rd - 3rd. IP3 acts on the sarcoplasmic reticulum, leading to Ca2+ release
○ 3rd - 4th. Ca2+ binds with calmodulin to form Ca2+-calmodulin complex
○ 3rd - 5th. Activated calmodulin activates NO synthase
○ 3rd - 6th. NO synthase promotes the reaction “Arginine + O2 → Citrulline + NO”
④ 4th. Generated NO from endothelial cells diffuses into the smooth muscle cell
⑤ 5th. Second signal transduction
○ 5th - 1st. NO activates guanylyl cyclase, an enzyme present in the cytoplasm of smooth muscle cells
○ 5th - 2nd. Guanylyl cyclase produces cGMP + ppi from GTP
○ cGMP is converted to GMP by PDE (phosphodiesterase)
○ PDE inhibitors lead to increased cGMP, causing hyperpolarization in smooth muscle cells
○ Sildenafil (Viagra™), vardenafil (Levitra™), tadalafil (Cialis™) inhibit cGMP degradation, promoting vasodilation
○ 5th - 3rd. cGMP activates Protein Kinase G (PKG)
○ 5th - 4th. PKG activates MLCP (Myosin Light Chain Phosphatase)
○ 5th - 5th. NO also activates K+ channels in the smooth muscle membrane, inducing hyperpolarization
⑥ 6th. MLCP dephosphorylates myosin light chains
⑦ 7th. Smooth muscle relaxation : Dephosphorylated myosin loses ATPase activity, causing actin-myosin cross-bridge detachment → Muscle relaxation
⑶ Vasoconstriction Model
① 1st. Voltage-gated L-type Ca2+ channels allow calcium ions to enter the cell
② 2nd. Increased calcium ions lead to the formation of Ca2+-calmodulin complex within the smooth muscle cell
○ Note: In the vasodilation model, Ca2+-calmodulin is generated within endothelial cells
③ 3rd. Ca2+-calmodulin activates MLCK (Myosin Light Chain Kinase)
④ 4th. MLCK phosphorylates myosin light chains
⑤ 5th. Smooth muscle contraction : Phosphorylated myosin loses ATPase activity, leading to actin-myosin cross-bridge formation and muscle contraction
4. Cardiac Muscle Contraction Model
⑴ Pacemaker Cell Action Potentials
① Pacemaker cells : Sinoatrial (SA) node, Atrioventricular (AV) node, Purkinje fibers
Figure. 9. Types of Pacemaker Cells
② Pacemaker potential : Focused on the SA node
Figure. 10. Pacemaker Potential
○ 1st. If Channel: Na+ influx, K+ efflux, continuous net cation influx during the initial phase through an open channel
○ 2nd. Membrane depolarization
○ 3rd. Depolarization : Rapid Ca2+ influx when membrane potential reaches the threshold
○ 4th. Repolarization : Delayed K+ efflux during the initial phase
○ Note the requirement of Ca2+ influx for generating action potentials in the SA node
③ The SA node is influenced by the sympathetic and parasympathetic nervous systems
○ Sympathetic : Shortening of diastole, increased heart rate
○ Parasympathetic : Prolonging diastole, decreased heart rate
⑵ Ventricular Action Potential Plateaus
Figure. 11. Ventricular Action Potential and ECG
① Channels
○ Voltage characteristics of K+ rectifier channels
Figure. 12. Voltage Characteristics of K+ Rectifier Channels
② 1st. Phase 4 (Resting phase)
○ Resting membrane potential of ventricular cells maintained around -90 mV by K+ rectifier channels remaining open on the inner membrane
○ Na+ and Ca2+ channels are closed
③ 2nd. Phase 0 (Depolarization) : Fast action potential
○ 2nd - 1st. Na+ influx into ventricular cells via action potential, causing membrane depolarization
○ 2nd - 2nd. Rapid voltage-gated Na+ channels open when membrane potential surpasses -70 mV, depolarizing the membrane
○ 2nd - 3rd. Rapid K+ channels close as membrane potential surpasses -70 mV
○ 2nd - 4th. Overshoot: Membrane potential rapidly rises until Na+ channels close around 20 mV
○ 2nd - 5th. L-type Ca2+ channels open when membrane potential is above -40 mV, allowing sustained Ca2+ influx
④ 3rd. Phase 1 (Early Repolarization)
○ 3rd - 1st. Membrane potential exceeds 0 mV
○ 3rd - 2nd. A few K+ channels briefly open and close, reducing membrane potential near 0 mV
⑤ 4th. Phase 2 (Plateau phase)
○ 4th - 1st. L-type Ca2+ channels remain open, allowing continued Ca2+ influx
○ 4th - 2nd. K+ efflux through delayed rectifier K+ channels
○ 4th - 3rd. Ca2+ influx and K+ efflux balance, maintaining membrane potential around 0 mV
○ Plateau phase resembles the absolute refractory period in nerve cell axons, resulting in no tetanus
⑥ 5th. Phase 3 (Repolarization) : Diastole
○ 5th - 1st. Gradual inactivation of Ca2+ channels
○ 5th - 2nd. K+ efflux surpasses Ca2+ influx, reducing membrane potential toward -90 mV
○ 5th - 3rd. Ion pumps like sarcolemmal Na+-Ca2+ exchanger, Ca2+-ATPase, Na+-K+-ATPase adjust ion concentrations
⑶ Ventricular Contraction
① Ventricular contraction during the plateau phase of ventricular action potential
② Muscle Contraction : Troponin binds with Ca2+ upon Ca2+ influx, leading to muscle contraction
○ 1st. Voltage-gated Ca2+ channels on the cell membrane open
○ 2nd. Extracellular Ca2+ enters the cell
○ 3rd. Ca2+-dependent channels in the sarcoplasmic reticulum (RyR) open
○ 4th. Massive release of Ca2+ from the sarcoplasmic reticulum
○ 5th. Muscle contraction
③ Muscle Relaxation : Removal of Ca2+ prevents troponin from binding with Ca2+, leading to muscle relaxation
○ 1st. Ca2+ pump in the sarcoplasmic reticulum : Ca2+ removal
○ 2nd. Ca2+ transported out of the cell by Na+-Ca2+ exchanger, Ca2+-ATPase, Na+-K+-ATPase
○ Inotropic agents inhibit the Na+ / K+ pump, maintaining continuous contraction of the heart.
5. Exercise
⑴ Classification of Exercise based on Regulation
① Reflexive exercise : Involuntary, stereotypic
② Rhythmic exercise : Stereotypic
③ Voluntary exercise : Goal-directed
⑵ Classification of Exercise based on Load
① Isometric contraction : Muscle contraction with constant force when not at maximum load
② Isotonic contraction : Muscle contraction with constant length at maximum load
⑶ Examples of Exercise
① Situation : Left foot steps on a tack
② Reaction : Left
leg bends, right leg extends
○ Flexor muscles: Inner muscles
○ Extensor muscles: Outer muscles
○ Flexor contracts, extensor relaxes when leg bends
○ Flexor relaxes, extensor contracts when leg extends
③ Diagram
Figure. 13. Reflex Action to Noxious Stimulus
6. Muscular System Disorders
⑴ Multiple Sclerosis
⑵ Myasthenia Gravis
① Duchenne Muscular Dystrophy (DMD)
⑶ Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s Disease
① Onset : Degeneration of motor neurons in the spinal cord and brainstem, leading to atrophy of associated muscles
⑷ Spinal Muscular Atrophy (SMA)
① Rare condition causing progressive muscle atrophy due to SMN1 gene deficiency
② Occurs in approximately 1 in 10,000 individuals
⑸ Delayed Onset Muscle Soreness (DOMS)
① Definition : Muscle soreness occurring long after intense exercise
② Muscle Contraction Types
○ Geometric contraction : Muscle neither contracts nor elongates during ATP consumption
○ Concentric contraction : Muscle contracts during ATP consumption, similar to what was previously learned
○ Example: Climbing uphill, bending knees to exert force on the ground
○ Eccentric contraction : Muscle elongates during ATP consumption
○ Example: Descending, muscles that extend the knees receive force from the ground’s impact, causing them to elongate
③ Mechanism
○ 1st. Eccentric contraction uses ATP, but muscles often lengthen as they work
○ 2nd. Muscles contract even when they’re pulled by external forces, causing some actin fibers to bounce out
○ 3rd. A few actin fibers break as a few can withstand the load
○ 4th. Biological reactions like inflammation occur to protect wounds
○ 5th. Heat or temporary muscle swelling (bulk-up) occurs, muscles appear larger
○ 6th. Muscle soreness occurs
○ 7th. Subsequent exercise of the same kind lessens the severity of muscle soreness
○ Similar to immune responses, this lessening of soreness lasts for about a year
Input : 2015.07.25 22:41
Edited : 2022.04.26 02:15