Structural Components of a Sarcomere
Sarcomere - The contractile units of muscle Structural units of myofibrils Form a visible, striped or
striated pattern within myofibrils Alternating dark, thick filaments (A bands) and light, thin filaments (I
bands)
Structural Components of a Sarcomeres (continued)
The A Band M line - The center of the A band at midline of sarcomere The H Band - The area around the M line,
has thick filaments but no thin filaments Zone of overlap- The densest, darkest area on a light micrograph whe
thick and thin filaments overlap
The I Band Z lines The centers of the I bands at two ends of sarcomere Titin - Are strands of protein Reach fro
tips of thick filaments to the Z line Stabilize the filaments
Thin Filaments - Actin Thick Filaments - Myosin Sliding Filaments and Muscle Contraction
F-actin (filamentous actin) - Is two twisted rows of globular G- Contain about 300 twisted myosin subunits Sliding filament theory: Thin filaments of
actin, with active sites to bind myosin Contain titin strands that recoil after stretching sarcomere slide toward M line, alongside thick
Nebulin - Holds F-actin strands together The mysosin molecule filaments
Tropomyosin - Is a double strand which prevents actin–myosin Tail - Binds to other myosin molecules The width of A zone stays the same
interaction Head - Made of two globular protein subunits Z lines move closer together
Troponin - A globular protein, Binds tropomyosin to G-actin, Reaches the nearest thin filament Skeletal Muscle Contraction
controlled by Ca2+ Myosin Action - During contraction, myosin heads: The process of contraction
Initiating Contraction Interact with actin filaments, forming cross-bridges, Neural stimulation of sarcolemma
Ca2+ binds to receptor on troponin molecule pivot, producing motion excitation–contraction coupling
Troponin–tropomyosin complex changes Muscle fiber contraction
Exposes active site of F-actin Interaction of thick and thin filaments
Tension production
Components of The Neuromuscular Junction Skeletal Muscle Contraction
The Control of Skeletal Muscle Activity The Contraction Cycle
The neuromuscular junction (NMJ) Contraction Cycle Begins •Relaxation
Special intercellular connection between the nervous system and Active-Site Exposure •Contraction duration depends on:
skeletal muscle fiber Cross-Bridge Formation Duration of neural stimulus
Controls calcium ion release into the sarcoplasm Myosin Head Pivoting Number of free calcium ions in sarcoplasm
Excitation–Contraction Coupling Cross-Bridge Detachment Availability of ATP
Action potential reaches a triad Myosin Reactivation •Relaxation
Releasing Ca2+ Fiber Shortening •Ca2+ concentrations fall
Triggering contraction As sarcomeres shorten, muscle pulls together, producing•Ca2+ detaches from troponin
Requires myosin heads to be in “cocked” position tension •Active sites are re-covered by tropomyosin
Loaded by ATP energy Muscle shortening can occur at both ends of the muscle,•Rigor Mortis
or at only one end of the muscle •A fixed muscular contraction after death
This depends on the way the muscle is attached at the •Caused when:
ends •Ion pumps cease to function; ran out of ATP
Summary •Calcium builds up in the sarcoplasm
Skeletal muscle fibers shorten as thin filaments slide between thick
filaments
Free Ca2+ in the sarcoplasm triggers contraction
SR releases Ca2+ when a motor neuron stimulates the muscle fiber
ATP Generation
Contraction is an active process Cells produce ATP in two ways
Relaxation and return to resting length are passive Aerobic metabolism of fatty acids in the
mitochondria Anaerobic glycolysis in the
cytoplasm
Aerobic Metabolism At peak activity, energy is provided by
Is the primary energy source of resting muscles anaerobic reactions that generate lactic acid
Energy to Power Contractions Breaks down fatty acids
ATP Provides Energy for Muscle Contraction as a by-product
Produces 34 ATP molecules per glucose molecule Muscle Fatigue
Sustained muscle contraction uses a lot of ATP energy
Muscles store enough energy to start contraction Glycolysis When muscles can no longer perform a
Is the primary energy source for peak muscular required activity, they are fatigued
Muscle fibers must manufacture more ATP as needed
activity Results of Muscle Fatigue
ATP and CP Reserves Produces two ATP molecules per molecule of
Adenosine triphosphate (ATP) Depletion of metabolic reserves
The active energy molecule glucose Damage to sarcolemma and sarcoplasmic
Creatine phosphate (CP) Breaks down glucose from glycogen stored in reticulum
skeletal muscles Low pH (lactic acid)
The storage molecule for excess ATP energy in resting muscle Energy Use and the Level of Muscular Activity
Energy recharges ADP to ATP Muscle exhaustion and pain
Skeletal muscles at rest metabolize fatty acids and
Using the enzyme creatine kinase (CK)
When CP is used up, other mechanisms generate ATP store glycogen
During light activity, muscles generate ATP through
anaerobic breakdown of carbohydrates, lipids, or
amino acids
Sarcomere - The contractile units of muscle Structural units of myofibrils Form a visible, striped or
striated pattern within myofibrils Alternating dark, thick filaments (A bands) and light, thin filaments (I
bands)
Structural Components of a Sarcomeres (continued)
The A Band M line - The center of the A band at midline of sarcomere The H Band - The area around the M line,
has thick filaments but no thin filaments Zone of overlap- The densest, darkest area on a light micrograph whe
thick and thin filaments overlap
The I Band Z lines The centers of the I bands at two ends of sarcomere Titin - Are strands of protein Reach fro
tips of thick filaments to the Z line Stabilize the filaments
Thin Filaments - Actin Thick Filaments - Myosin Sliding Filaments and Muscle Contraction
F-actin (filamentous actin) - Is two twisted rows of globular G- Contain about 300 twisted myosin subunits Sliding filament theory: Thin filaments of
actin, with active sites to bind myosin Contain titin strands that recoil after stretching sarcomere slide toward M line, alongside thick
Nebulin - Holds F-actin strands together The mysosin molecule filaments
Tropomyosin - Is a double strand which prevents actin–myosin Tail - Binds to other myosin molecules The width of A zone stays the same
interaction Head - Made of two globular protein subunits Z lines move closer together
Troponin - A globular protein, Binds tropomyosin to G-actin, Reaches the nearest thin filament Skeletal Muscle Contraction
controlled by Ca2+ Myosin Action - During contraction, myosin heads: The process of contraction
Initiating Contraction Interact with actin filaments, forming cross-bridges, Neural stimulation of sarcolemma
Ca2+ binds to receptor on troponin molecule pivot, producing motion excitation–contraction coupling
Troponin–tropomyosin complex changes Muscle fiber contraction
Exposes active site of F-actin Interaction of thick and thin filaments
Tension production
Components of The Neuromuscular Junction Skeletal Muscle Contraction
The Control of Skeletal Muscle Activity The Contraction Cycle
The neuromuscular junction (NMJ) Contraction Cycle Begins •Relaxation
Special intercellular connection between the nervous system and Active-Site Exposure •Contraction duration depends on:
skeletal muscle fiber Cross-Bridge Formation Duration of neural stimulus
Controls calcium ion release into the sarcoplasm Myosin Head Pivoting Number of free calcium ions in sarcoplasm
Excitation–Contraction Coupling Cross-Bridge Detachment Availability of ATP
Action potential reaches a triad Myosin Reactivation •Relaxation
Releasing Ca2+ Fiber Shortening •Ca2+ concentrations fall
Triggering contraction As sarcomeres shorten, muscle pulls together, producing•Ca2+ detaches from troponin
Requires myosin heads to be in “cocked” position tension •Active sites are re-covered by tropomyosin
Loaded by ATP energy Muscle shortening can occur at both ends of the muscle,•Rigor Mortis
or at only one end of the muscle •A fixed muscular contraction after death
This depends on the way the muscle is attached at the •Caused when:
ends •Ion pumps cease to function; ran out of ATP
Summary •Calcium builds up in the sarcoplasm
Skeletal muscle fibers shorten as thin filaments slide between thick
filaments
Free Ca2+ in the sarcoplasm triggers contraction
SR releases Ca2+ when a motor neuron stimulates the muscle fiber
ATP Generation
Contraction is an active process Cells produce ATP in two ways
Relaxation and return to resting length are passive Aerobic metabolism of fatty acids in the
mitochondria Anaerobic glycolysis in the
cytoplasm
Aerobic Metabolism At peak activity, energy is provided by
Is the primary energy source of resting muscles anaerobic reactions that generate lactic acid
Energy to Power Contractions Breaks down fatty acids
ATP Provides Energy for Muscle Contraction as a by-product
Produces 34 ATP molecules per glucose molecule Muscle Fatigue
Sustained muscle contraction uses a lot of ATP energy
Muscles store enough energy to start contraction Glycolysis When muscles can no longer perform a
Is the primary energy source for peak muscular required activity, they are fatigued
Muscle fibers must manufacture more ATP as needed
activity Results of Muscle Fatigue
ATP and CP Reserves Produces two ATP molecules per molecule of
Adenosine triphosphate (ATP) Depletion of metabolic reserves
The active energy molecule glucose Damage to sarcolemma and sarcoplasmic
Creatine phosphate (CP) Breaks down glucose from glycogen stored in reticulum
skeletal muscles Low pH (lactic acid)
The storage molecule for excess ATP energy in resting muscle Energy Use and the Level of Muscular Activity
Energy recharges ADP to ATP Muscle exhaustion and pain
Skeletal muscles at rest metabolize fatty acids and
Using the enzyme creatine kinase (CK)
When CP is used up, other mechanisms generate ATP store glycogen
During light activity, muscles generate ATP through
anaerobic breakdown of carbohydrates, lipids, or
amino acids
