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Chapter 21. Muscular System

Recommended Article: 【Biology】 Table of Contents for Biology

1. Muscle

2. Skeletal Muscle Contraction Model

3. Smooth Muscle Contraction Model

4. Cardiac Muscle Contraction Model

5. Exercise

6. Muscular System Disorders

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 across joints by tendons.

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 (e.g., tongue, sphincter, diaphragm)

○ Structure: Cylindrical multinucleated cells, cross-striations (transverse stripes, developed sarcomeres)

○ Multinucleated cells are a unique characteristic of skeletal muscles

○ Features: non-graded, abundant sarcoplasmic reticulum, 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 skeletal muscle is 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

○ Myostatin

○ Inhibits the development and growth of skeletal muscle

○ Involved in the formation and development of ligaments and tendons

② Cardiac Muscle (myocardium)

○ Structure: Branching shape, intercalated discs, cross-striations (developed sarcomeres), gap junctions and adherens junctions between muscle cells

○ Intercalated discs contain gap junctions that enable simultaneous signal transmission.

○ Intercalated discs also contain desmosomes.

○ Due to cell–cell adherens junctions, contraction occurs simultaneously → all cells act as a single functional unit.

○ Features: Graded, numerous mitochondria, calcium-troponin binding, high resting potential leading to action potential initiation with small stimuli

○ Tetanus not possible: During the plateau phase of cardiac muscle, a phenomenon similar to the absolute refractory period occurs, making overlapping muscle contractions impossible.

○ Regulation of Contraction: Involuntary regulation (involuntary control)

○ Among pacemakers, the sinoatrial (SA) node is regulated by the autonomic nervous system.

○ The sympathetic nervous system increases Ca²⁺ permeability, raising the pacemaking rate of the SA node, while the parasympathetic nervous system increases K⁺ permeability, lowering the pacemaking rate.

○ Cardiac muscle cells are regulated only by the sympathetic nervous system (regarding whether stroke volume increases).

③ Smooth Muscle (visceral muscle) (e.g., digestive tract, blood vessel walls, uterus)

○ Structure

○ Presence of gap junctions between muscle cells

○ Calcium does not bind directly to troponin; calmodulin is involved

○ Spindle-shaped, single-nucleus cells

○ No sarcomeres

○ Features: graded, 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 muscle, contraction of small arterioles, contraction of airways

○ Parasympathetic nervous system: contraction of visceral muscle, relaxation of small arterioles, relaxation of airways

○ Myosin phosphorylation (activates contraction) and dephosphorylation (inhibits contraction)

○ Aortic vascular smooth muscle self-regulates through its own stretch receptors

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 myofibrils” + “Aligned myofibrils” + …

④ Myofibrils have sarcomeres

○ Sarcomere: Basic unit of muscle contraction

○ Sarcomeres are distinguished by Z lines (Z disks), which are actin filament lines arranged perpendicular to the direction of the myofibrils.

⑤ Filaments within the sarcomere = Actin filaments (thin filaments) (bright) + Myosin filaments (thick filaments) (dark)

○ 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 is neither actin nor 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 chain

○ The tail of the heavy chain (150 nm) is coiled into a superhelix, forming oriented myosin filaments.

○ The head of the heavy chain (17 nm) contains an actin-binding site and an ATPase site, providing the driving force for sliding.

③ Light chain

○ Attached to the head of the heavy chain, it regulates 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 1^st. Muscle in a resting state (rigor): Myosin heads bind to actin filaments without ATP or ADP

② 2^nd. ATP binding: Myosin heads bind to ATP, detaching from actin filaments

③ 3^rd. Myosin heads possess ATPase activity, breaking down ATP into ADP and inorganic phosphate

④ 4^th. The myosin head has a high energy state and adopts various conformations.

⑤ 5^th. Cross-bridge formation: While adopting various conformations, the myosin head stands upright and binds to the actin filament.

○ [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 6^th. Sarcomere contraction: the myosin head, initially in a high-energy state, tilts downward as ADP and phosphate are released, shifting to a lower-energy state. During this process, the actin filament is pulled toward the center.

○ [Second Mechanical Action]

○ Although in a low-energy conformation, the myosin remains bound to the actin filament.

⑷ Calcium-Mediated Muscle Contraction Control: Human movement is controlled in the range of 5 to 10 Hz

① 1^st. Acetylcholine released at the synapse terminal of the neuromuscular junction triggers an action potential

○ 1^st - 1^st. Released acetylcholine diffuses into the synaptic cleft

○ 1^st - 2^nd. A graded potential is induced at the motor end plate.

○ 1^st - 3^rd. The graded potential depolarizes the muscle fiber, triggering an action potential in the muscle fiber.

② 2^nd. Action potential travels along the cell membrane and T-tubules.

○ Transverse tubule (T-tubule): A tubular structure formed by the invagination of the muscle cell membrane, transmitting membrane excitation into the cell interior.

○ The T-tubule membrane contains voltage-gated K⁺ channels necessary for generating action potentials.

③ 3^rd. Action potential induces Ca²⁺ release from the sarcoplasmic reticulum (a type of smooth endoplasmic reticulum)

○ 3^rd – 1^st. When the action potential reaches the T-tubule membrane (cell membrane), voltage-gated Ca²⁺ channels are activated.

○ 3^rd – 2^nd. Driven by the Ca²⁺ concentration gradient, Ca²⁺ moves from outside the cell into the cytoplasm.

○ 3^rd – 3^rd. The Ca²⁺ that has entered the cytoplasm opens the Ca²⁺-dependent Ca²⁺ release channels in the sarcoplasmic reticulum membrane.

○ 3^rd – 3^rd – 1^st. Action potential causes conformational change of the dihydropyridine (DHP) receptor on T-tubules

○ 3^rd – 3^rd – 2^nd. The calcium channels (ryanodine receptors) located in the sarcoplasmic reticulum membrane adjacent to the T-tubules are opened.

○ 3^rd – 4^th. Ca²⁺ moves from the sarcoplasmic reticulum membrane 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 4^th. When calcium ions bind to the thin filament and troponin, the myosin-binding sites are exposed.

○ Calcium ions do not bind to actin or myosin

○ Troponin complex binds to tropomyosin and actin filaments

○ 4^th – 1^st. Binding of Ca²⁺ to C subunit of troponin complex

○ 4^th – 2^nd. Shifting of tropomyosin position

○ 4^th – 3^rd. Exposure of myosin binding site on actin filament

Figure 6. Actin, tropomyosin, troponin complex, myosin head binding site

⑤ 5^th. [Sliding filament model] Myosin cross-bridges bind to actin.

○ As the number of myosin cross-bridges acting on the actin filament increases, the overall tension increases.

⑥ 6^th. [Sliding Filament Model] ATP hydrolysis causes rotational movement of myosin head → Actin-myosin interaction (repeated)

⑦ 7^th. Termination of action potential: Ca²⁺-ATPase in the sarcoplasmic reticulum membrane consumes ATP to transport Ca²⁺ from the cytoplasm into the lumen of the sarcoplasmic reticulum.

○ Active transport of Ca²⁺ occurs continuously, even beforehand.

○ However, the net flux of Ca²⁺ shifts toward the sarcoplasmic reticulum from the cytoplasm only after the action potential has ended.

○ Since the resting membrane potential of the muscle fiber membrane is –90 mV, which is equal to the equilibrium potential of K⁺, no hyperpolarization occurs.

⑧ 8^th. Removal of Ca²⁺ from troponin and re-covering of myosin binding sites by tropomyosin results in the termination of contractions.

⑨ 9^th. Muscle fiber relaxation

○ Requires new ATP supply and Ca²⁺ removal

○ When ATP detaches myosin from actin, the actin filament momentarily slips, causing the muscle fiber to relax.

Figure 7. Regulation of muscle contraction by calcium

⑸ Twitch Muscle Fibers

① Motor unit: a single motor neuron and all the muscle fibers it controls.

○ LMN (Lower Motor Neuron): spinal motor neurons that innervate skeletal muscle.

○ Twitch: the brief contraction that occurs as an action potential spreads through the T-tubule system (the smallest unit of contraction); follows the all-or-none law.

○ Tetanus: when action potentials arrive at a sufficiently high frequency so the fiber has no time to relax, twitches summate to produce a continuous, sustained contraction; occurs only in skeletal muscle.

○ If the firing frequency is low, periods of relaxation appear and the tension plot shows a saw-tooth oscillation (unfused/incomplete tetanus). If the interval between twitches is short, the muscle remains continuously contracted (fused/complete tetanus).

○ Tension is influenced by both the number of contracting fibers and the speed (rate) of contraction.

② (Antonym) Tonic muscle fibers: postural muscles; do not generate action potentials; does not follow all-or-none units.

③ Types of twitch fibers

○ Slow-twitch fibers (red fibers): oxidative/aerobic; ↑ mitochondria and myoglobin; well vascularized.

○ Oxidative fiber characteristics: rely primarily on aerobic metabolism—slower but endure longer (fatigue-resistant).

○ Compared with fast-twitch: less developed sarcoplasmic reticulum, slower Ca²⁺ pumping, longer cytosolic Ca²⁺ residence; twitch duration ≈ five times longer.

○ Fast-twitch fibers (white fibers): sparse mitochondria and capillaries; produce rapid, powerful contractions but cannot be maintained; Type IIa and IIb are interconvertible.

○ Glycolytic fiber characteristics: rely mainly on glycolysis; larger diameter with low myoglobin, so they fatigue easily; fatigue is commonly attributed to lactate.

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 1^st Priority. ATP

○ ~ 5 mM (about 5 seconds)

○ Rigor mortis: State where muscles cannot relax due to ATP depletion

③ 2^nd Priority. Creatine Phosphate

○ Function: Regenerates ATP to counter ATP depletion

○ Creatine Phosphate + ADP → Creatine + ATP

○ Energy released when ATP is broken: 7.3 kcal

○ Energy released when the bond of creatine phosphoric acid is broken: 10.3 kcal

○ 20 ~ 40 mM, rapid energy source (about 20 seconds)

④ 3^rd Priority. Lactic Acid Fermentation: Human body doesn’t undergo alcohol fermentation or acetic acid fermentation

○ When energy sources are depleted: Glucose → Pyruvate → Lactate, with ATP obtained through glycolysis (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

○ Lactic fermentation occurs frequently in fast-twitch fibers, which are glycolysis-dependent.

○ Tomato as a recovery aid

○ More than 50% of tomatoes are glutamate

○ Glutamate converts pyruvate to alanine, reducing lactic acid production and fatigue

⑤ 4^th Priority. Glycogen

○ Stored in the liver and muscles for a day

○ Glycogen stored in a liver: Provides energy for the entire body

○ Glycogen stored in muscles: Provides energy only to muscles

○ Can participate in anaerobic and aerobic respiration through gluconeogenesis

⑥ 5^th 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)

Figure 8. The energy sources of muscle

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: regulated by epinephrine and norepinephrine released from sympathetic nerve endings through α and 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 9. Vasodilation Model

① 1^st. Acetylcholine secretion from parasympathetic nerve terminals

② 2^nd. Acetylcholine binds to muscarinic acetylcholine receptors on endothelial cells

○ Muscarinic acetylcholine receptors are G-protein-coupled receptors (GPCRs)

③ 3^rd. First signal transduction

○ 3^rd - 1^st. When GPCR is activated, the GDP of the G protein is replaced by GTP.

○ 3^rd - 2^nd. Activated G proteins convert PLC into IP3

○ 3^rd - 3^rd. IP3 acts on the sarcoplasmic reticulum, leading to Ca²⁺ release

○ 3^rd - 4^th. Ca²⁺ binds with calmodulin to form Ca2+-calmodulin complex

○ 3^rd - 5^th. Activated calmodulin activates NO synthase

○ 3^rd - 6^th. NO synthase promotes the reaction “Arginine + O2 → Citrulline + NO”

④ 4^th. NO produced in vascular endothelial cells diffuses directly into vascular smooth muscle cells.

⑤ 5^th. Second signal transduction

○ 5^th - 1^st. NO activates guanylyl cyclase, an enzyme present in the cytoplasm of smooth muscle cells

○ 5^th - 2^nd. 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

○ 5^th - 3^rd. cGMP activates Protein Kinase G (PKG)

○ 5^th - 4^th. PKG activates MLCP (Myosin Light Chain Phosphatase)

○ 5^th - 5^th. NO also activates K⁺ channels in the smooth muscle membrane, inducing hyperpolarization

⑥ 6^th. MLCP dephosphorylates myosin light chains

⑦ 7^th. Smooth muscle relaxation: Dephosphorylated myosin loses ATPase activity, causing actin-myosin cross-bridge detachment → Muscle relaxation

⑶ Vasoconstriction Model

① 1^st. Voltage-gated L-type Ca²⁺ channels allow calcium ions to enter the cell

② 2^nd. 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 3^rd. Ca2+-calmodulin activates MLCK (Myosin Light Chain Kinase)

④ 4^th. MLCK phosphorylates myosin light chains

⑤ 5^th. 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 potential of autorhythmic cells

① Autorhythmic cells: Sinoatrial (SA) node, Atrioventricular (AV) node, Purkinje fibers

Figure 10. Types of Pacemaker Cells

② Pacemaker potential: Focused on the SA node

Figure 11. Pacemaker Potential

○ 1^st. I_f acts as an open channel, allowing Na⁺ influx and K⁺ efflux in the initial stage, leading to a continuous net influx of cations.

○ 2^nd. Membrane potential rises.

○ 3^rd. Depolarization: When the membrane potential reaches threshold, Ca²⁺ rapidly flows in.

○ 4^th. Repolarization: K⁺ flows out with a delay, returning to the initial stage.

○ Note that for the sinoatrial (SA) node to generate an action potential, Ca²⁺ influx is required.

③ The SA node is influenced by the sympathetic and parasympathetic nervous systems:

○ Sympathetic nerves: shorten diastolic length, increasing heart rate.

○ Parasympathetic nerves: prolong diastolic length, decreasing heart rate.

⑵ Plateau potential of ventricular muscle

Figure 12. Ventricular Action Potential and ECG

① Channels

○ Voltage characteristics of K⁺ rectifier channels

Figure 13. Voltage Characteristics of K⁺ Rectifier Channels

② 1^st. Phase 4 (Resting phase)

○ The resting membrane potential of ventricular muscle cells is steadily maintained at –90 mV, which corresponds to the equilibrium potential of K⁺, due to the continuously open K⁺ rectifier channels on the inner side of the cell membrane.

○ Na+ and Ca²⁺ channels are closed

③ 2^nd. Phase 0 (Depolarization): Fast action potential

○ 2^nd - 1^st. During the action potential, Na⁺ flows into the ventricular muscle cell, causing the membrane potential to rise.

○ 2^nd - 2^nd. When the membrane potential rises above the threshold potential of –70 mV, the voltage-gated Na⁺ channels open rapidly.

○ 2^nd - 3^rd. When the membrane potential rises above the threshold potential of –70 mV, the K⁺ channels close rapidly.

○ 2^nd - 4^th. Overshoot: the membrane potential rapidly increases up to +20 mV, at which point the Na⁺ channels close.

○ 2^nd - 5^th. The L-type (long-opening) Ca²⁺ channels open when the membrane potential exceeds –40 mV, allowing sustained influx of Ca²⁺.

④ 3^rd. Phase 1 (Early Repolarization)

○ 3^rd - 1^st. Membrane potential exceeds 0 mV

○ 3^rd - 2^nd. A few K⁺ channels briefly open and close, reducing membrane potential near 0 mV

⑤ 4^th. Phase 2 (Plateau phase)

○ 4^th - 1^st. L-type Ca²⁺ channels remain open, allowing continued Ca²⁺ influx

○ 4^th - 2^nd. K⁺ efflux through delayed rectifier K⁺ channels

○ 4^th - 3^rd. 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 5^th. Phase 3 (Repolarization): Diastole

○ 5^th - 1^st. Gradual inactivation of Ca²⁺ channels

○ 5^th - 2^nd. K⁺ efflux surpasses Ca²⁺ influx, reducing membrane potential toward -90 mV

○ 5^th - 3^rd. Ion pumps like sarcolemmal Na⁺-Ca²⁺ exchanger, Ca²⁺-ATPase, Na⁺-K⁺-ATPase operate to maintain ionic concentration homeostasis.

⑶ Ventricular muscle contraction

① Ventricular contraction occurs during the plateau phase of the ventricular action potential.

② Muscle Contraction: Troponin binds with Ca²⁺ upon Ca²⁺ influx, leading to muscle contraction

○ 1^st. Voltage-gated Ca²⁺ channels on the cell membrane open

○ 2^nd. Extracellular Ca²⁺ enters the cell

○ 3^rd. Ca²⁺-dependent channels in the sarcoplasmic reticulum (RyR) open

○ 4^th. Massive release of Ca²⁺ from the sarcoplasmic reticulum

○ 5^th. Muscle contraction

③ Muscle Relaxation: Removal of Ca²⁺ prevents troponin from binding with Ca²⁺, leading to muscle relaxation

○ 1^st. Ca²⁺ pump in the sarcoplasmic reticulum: Ca²⁺ removal

○ 2^nd. Ca²⁺ transported out of the cell by Na⁺-Ca²⁺ exchanger, Ca²⁺-ATPase, Na⁺-K⁺-ATPase

○ Cardiotonic drugs inhibit the Na⁺/K⁺ pump, causing the heart to remain in a sustained state of contraction.

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 Muscle contraction with constant force when not at maximum load

② 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 14. 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

○ 1^st. Eccentric contraction uses ATP, but muscles often lengthen as they work

○ 2^nd. Muscles contract even when they’re pulled by external forces, causing some actin fibers to bounce out

○ 3^rd. A few actin fibers break as a few can withstand the load

○ 4^th. Biological reactions like inflammation occur to protect wounds

○ 5^th. Heat or temporary muscle swelling (bulk-up) occurs, muscles appear larger

○ 6^th. Muscle soreness occurs

○ 7^th. Subsequent exercise of the same kind lessens the severity of muscle soreness

○ The milder intensity of muscle pain is similar to an immune response.

○ Immunity generally lasts for about one year.

Input: 2015.07.25 22:41

Edited: 2022.04.26 02:15