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Muscles &Muscle Tissue
Chapter 10
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Functions of Skeletal Muscles
Produce skeletal movement Maintain body position Support soft tissues Guard body openings Maintain body temperature
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Functional Characteristics of Muscle
Excitability (irritability) Can receive and respond to stimuli. Stimuli can include nerve impulses, stretch, hormones or changes in the chemical environment. Contractility – the ability to shorten with increasing tension. Extensibility – the ability to stretch. Elasticity – the ability to snap back (recoil) to their resting length after being stretched.
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Three types of muscle Skeletal Smooth Cardiac
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Characteristics of Skeletal Muscle
Striated Multinucleate (it is a syncytium) Voluntary Parallel fibers
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Organization of Connective Tissues
Figure 10–1
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Formation of Skeletal Muscle Fibers
Skeletal muscle cells are called fibers Formation of Skeletal Muscle Fibers
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Organization of Skeletal Muscle Fibers
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Anatomy of a myofibril
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A Triad Is formed by 1 T tubule and 2 terminal cisternae
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Sarcomeres Figure 10–4
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Muscle Striations A striped or striated pattern within myofibrils:
alternating dark, thick filaments (A bands) and light, thin filaments (I bands)
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M Lines and Z Lines M line: Z lines: the center of the A band
at midline of sarcomere Z lines: the centers of the I bands at 2 ends of sarcomere
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Zone of Overlap The densest, darkest area on a light micrograph
Where thick and thin filaments overlap
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The H Zone The area around the M line
Has thick filaments but no thin filaments
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Titin Are strands of protein
Reach from tips of thick filaments to the Z line Stabilize the filaments
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Sarcomere Structure
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Summary of skeletal muscle anatomy: muscles are made of fascicles
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Fascicles are made of fibers, fibers are made of myofibrils
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Level 1: Skeletal Muscle
Figure 10–6 (1 of 5)
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Level 2: Muscle Fascicle
Figure 10–6 (2 of 5)
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Level 3: Muscle Fiber Figure 10–6 (3 of 5)
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Level 4: Myofibril Figure 10–6 (4 of 5)
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Level 5: Sarcomere Figure 10–6 (5 of 5)
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Fibrils are divided into sarcomeres, sarcomeres are made of myofilaments
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Myofilaments are made of protein molecules
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A Thin Filament
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4 Thin Filament Proteins
F actin: is 2 twisted rows of globular G actin the active sites on G actin strands bind to myosin
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4 Thin Filament Proteins
Nebulin: holds F actin strands together
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4 Thin Filament Proteins
Tropomyosin: is a double strand prevents actin–myosin interaction
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4 Thin Filament Proteins
Troponin: a globular protein binds tropomyosin to G actin controlled by Ca2+
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Troponin and Tropomyosin
Figure 10–7b
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A Thick Filament Figure 10–7c
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Thick Filaments Contain twisted myosin subunits
Contain titin strands that recoil after stretching
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The Mysosin Molecule Figure 10–7d
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Muscle Contraction: the Sliding Filament Theory
Muscle contraction requires: Stimulus – the generation of an action potential. Crossbridge formation – interaction between the thick and thin myofilaments. This is triggered by Ca++ ions released from the sarcoplasmic reticulum. Energy – ATP to energize the myosin molecules.
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Sliding Filaments
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Skeletal Muscle Contraction
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T- tubules supply the stimulus, Sarcoplasmic Reticulum supplies the Ca++, Mitochondria supply the ATP.
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The Process of Contraction
Neural stimulation of sarcolemma: causes excitation–contraction coupling Cisternae of SR release Ca2+: which triggers interaction of thick and thin filaments consuming ATP and producing tension
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Skeletal Muscle Innervation
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Skeletal Muscle Innervation
Figure 10–10c
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The Neuromuscular Junction
Is the location of neural stimulation Action potential (electrical signal): travels along nerve axon ends at synaptic terminal
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A neuromuscular junction (NMJ).
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acetylcholine The actual synapse
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Synaptic Terminal Releases neurotransmitter (acetylcholine or ACh)
Into the synaptic cleft (gap between synaptic terminal and motor end plate)
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The Neurotransmitter Acetylcholine or ACh:
travels across the synaptic cleft binds to membrane receptors on sarcolemma (motor end plate) causes sodium–ion rush into sarcoplasm is quickly broken down by enzyme (acetylcholinesterase or AChE)
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Action Potential Generated by increase in sodium ions in sarcolemma
Travels along the T tubules Leads to excitation–contraction coupling
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Excitation–Contraction Coupling
Action potential reaches a triad: releasing Ca2+ triggering contraction Requires myosin heads to be in “cocked” position: loaded by ATP energy
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Exposing the Active Site
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The Contraction Cycle
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The Contraction Cycle
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The Contraction Cycle
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The Contraction Cycle
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5 Steps of the Contraction Cycle
Exposure of active sites Formation of cross-bridges Pivoting of myosin heads Detachment of cross-bridges Reactivation of myosin
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Show the animation
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A Review of Muscle Contraction
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Excitation-Contraction coupling
Stimulus or excitation is required for muscles to contract. In skeletal muscle, the stimulus is from a motor neuron. The stimulus is in the form of an action potential. This action potential starts at the neuromuscular junction (NMJ).
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Excitation-contraction coupling
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Show NMJ animation
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Micrograph of an NMJ
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A Synapse Synaptic vesicles
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Tension and Sarcomere Length
Figure 10–14
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Length–Tension Relationship
Number of pivoting cross-bridges depends on: amount of overlap between thick and thin fibers Optimum overlap produces greatest amount of tension: too much or too little reduces efficiency
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Length–Tension Relationship
Normal resting sarcomere length: is 75% to 130% of optimal length
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Frequency of Stimulation
A single neural stimulation produces: a single contraction or twitch which lasts about 7–100 msec Sustained muscular contractions: require many repeated stimuli
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Tension in a Twitch Length of twitch depends on type of muscle
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Myogram A graph of twitch tension development
Figure 10–15b (Navigator)
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3 Phases of Twitch Latent period before contraction:
the action potential moves through sarcolemma causing Ca2+ release
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3 Phases of Twitch Contraction phase: calcium ions bind
tension builds to peak
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3 Phases of Twitch Relaxation phase: Ca2+ levels fall
active sites are covered tension falls to resting levels
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Treppe A stair-step increase in twitch tension Figure 10–16a
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Treppe Repeated stimulations immediately after relaxation phase:
stimulus frequency < 50/second Causes a series of contractions with increasing tension
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Wave Summation Increasing tension or summation of twitches
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Wave Summation Repeated stimulations before the end of relaxation phase: stimulus frequency > 50/second Causes increasing tension or summation of twitches
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Incomplete Tetanus Twitches reach maximum tension Figure 10–16c
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Incomplete Tetanus If rapid stimulation continues and muscle is not allowed to relax, twitches reach maximum level of tension
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Complete Tetanus Figure 10–16d
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Complete Tetanus If stimulation frequency is high enough, muscle never begins to relax, and is in continuous contraction
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Comparative speed of different muscles
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Tension Produced by Whole Skeletal Muscles
Depends on: internal tension produced by muscle fibers external tension exerted by muscle fibers on elastic extracellular fibers total number of muscle fibers stimulated
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Motor Units in a Skeletal Muscle
Figure 10–17
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Motor Units in a Skeletal Muscle
Contain hundreds of muscle fibers That contract at the same time Controlled by a single motor neuron
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Recruitment (Multiple Motor Unit Summation)
In a whole muscle or group of muscles, smooth motion and increasing tension is produced by slowly increasing size or number of motor units stimulated
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Maximum Tension Achieved when all motor units reach tetanus
Can be sustained only a very short time
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Sustained Tension Less than maximum tension
Allows motor units to rest in rotation
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2 Types of Skeletal Muscle Tension
Isotonic contraction Isometric contraction
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Isotonic Contraction Figure 10–18a, b
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Isotonic Contraction Skeletal muscle changes length:
resulting in motion If muscle tension > resistance: muscle shortens (concentric contraction) If muscle tension < resistance: muscle lengthens (eccentric contraction)
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Isometric Contraction
Figure 10–18c, d
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Isometric Contraction
Skeletal muscle develops tension, but is prevented from changing length Note: Iso = same, metric = measure
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Resistance and Speed of Contraction
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Resistance and Speed of Contraction
Are inversely related The heavier the resistance on a muscle: the longer it takes for shortening to begin and the less the muscle will shorten
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ATP and Muscle Contraction
Sustained muscle contraction uses a lot of ATP energy Muscles store enough energy to start contraction Muscle fibers must manufacture more ATP as needed
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ATP and CP Reserves Adenosine triphosphate (ATP):
the active energy molecule Creatine phosphate (CP): the storage molecule for excess ATP energy in resting muscle
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Recharging ATP Energy recharges ADP to ATP:
using the enzyme creatine phosphokinase (CPK) When CP is used up, other mechanisms generate ATP
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Energy Storage in Muscle Fiber
Table 10–2
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ATP Generation Cells produce ATP in 2 ways:
aerobic metabolism of fatty acids in the mitochondria anaerobic glycolysis in the cytoplasm
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Aerobic Metabolism Is the primary energy source of resting muscles
Breaks down fatty acids Produces 34 ATP molecules per glucose molecule
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Anaerobic Glycolysis Is the primary energy source for peak muscular activity Produces 2 ATP molecules per molecule of glucose Breaks down glucose from glycogen stored in skeletal muscles
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Anaerobic Metabolism: a losing proposition
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Energy Use and Muscle Activity
At peak exertion: muscles lack oxygen to support mitochondria muscles rely on glycolysis for ATP pyruvic acid builds up, is converted to lactic acid
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Muscle Metabolism
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Muscle Metabolism Figure 10–20b
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Muscle Metabolism Figure 10–20c
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Results of Muscle Fatigue
Depletion of metabolic reserves Damage to sarcolemma and sarcoplasmic reticulum Low pH (lactic acid) Muscle exhaustion and pain
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The Recovery Period The time required after exertion for muscles to return to normal Oxygen becomes available Mitochondrial activity resumes
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The Cori Cycle The removal and recycling of lactic acid by the liver
Liver converts lactic acid to pyruvic acid Glucose is released to recharge muscle glycogen reserves
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Oxygen Debt After exercise:
the body needs more oxygen than usual to normalize metabolic activities resulting in heavy breathing
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Muscle Performance Power: Endurance: Power and endurance depend on:
the maximum amount of tension produced Endurance: the amount of time an activity can be sustained Power and endurance depend on: the types of muscle fibers physical conditioning
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3 Types of Skeletal Muscle Fibers
Fast fibers Slow fibers Intermediate fibers
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Fast Fibers Contract very quickly
Have large diameter, large glycogen reserves, few mitochondria Have strong contractions, fatigue quickly
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Slow Fibers Are slow to contract, slow to fatigue
Have small diameter, more mitochondria Have high oxygen supply Contain myoglobin (red pigment, binds oxygen)
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Intermediate Fibers Are mid-sized Have low myoglobin
Have more capillaries than fast fiber, slower to fatigue
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Fast versus Slow Fibers
Figure 10–21
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Comparing Skeletal Muscle Fibers
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Muscles and Fiber Types
White muscle: mostly fast fibers pale (e.g., chicken breast) Red muscle: mostly slow fibers dark (e.g., chicken legs) Most human muscles: mixed fibers pink
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Muscle Hypertrophy Muscle growth from heavy training:
increases diameter of muscle fibers increases number of myofibrils increases mitochondria, glycogen reserves
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Muscle Atrophy Lack of muscle activity:
reduces muscle size, tone, and power
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Structure of Cardiac Tissue
Cardiac muscle is striated, found only in the heart Figure 10–22
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7 Characteristics of Cardiocytes
Unlike skeletal muscle, cardiac muscle cells (cardiocytes): are small have a single nucleus have short, wide T tubules
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7 Characteristics of Cardiocytes
have no triads have SR with no terminal cisternae are aerobic (high in myoglobin, mitochondria) have intercalated discs
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Intercalated Discs Are specialized contact points between cardiocytes
Join cell membranes of adjacent cardiocytes (gap junctions, desmosomes)
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Functions of Intercalated Discs
Maintain structure Enhance molecular and electrical connections Conduct action potentials
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Coordination of Cardiocytes
Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells
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4 Functions of Cardiac Tissue
Automaticity: contraction without neural stimulation controlled by pacemaker cells Variable contraction tension: controlled by nervous system
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4 Functions of Cardiac Tissue
Extended contraction time Prevention of wave summation and tetanic contractions by cell membranes
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Structure of Smooth Muscle
Nonstriated tissue Figure 10–23
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Comparing Smooth and Striated Muscle
Different internal organization of actin and myosin Different functional characteristics
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8 Characteristics of Smooth Muscle Cells
Long, slender, and spindle shaped Have a single, central nucleus Have no T tubules, myofibrils, or sarcomeres Have no tendons or aponeuroses
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8 Characteristics of Smooth Muscle Cells
Have scattered myosin fibers Myosin fibers have more heads per thick filament Have thin filaments attached to dense bodies Dense bodies transmit contractions from cell to cell
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Functional Characteristics of Smooth Muscle
Excitation–contraction coupling Length–tension relationships Control of contractions Smooth muscle tone
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Excitation–Contraction Coupling
Free Ca2+ in cytoplasm triggers contraction Ca2+ binds with calmodulin: in the sarcoplasm activates myosin light chain kinase Enzyme breaks down ATP, initiates contraction
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Length–Tension Relationships
Thick and thin filaments are scattered Resting length not related to tension development Functions over a wide range of lengths (plasticity)
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Control of Contractions
Subdivisions: multiunit smooth muscle cells: connected to motor neurons visceral smooth muscle cells: not connected to motor neurons rhythmic cycles of activity controlled by pacesetter cells
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Smooth Muscle Tone Maintains normal levels of activity
Modified by neural, hormonal, or chemical factors
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Smooth Muscle
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Varicosities
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Skeletal Smooth Diameter 10 - 100 m 3 - 8 m Connective tissue
Epi-, Peri- & Endomysium Endomysium only SR Yes, complex Barely, simple T - tubules yes no Sarcomeres Gap Junctions voluntary Neurotransmitters Acetylcholine (Ach) Ach, epinephrine, norepinephrine, et al Regeneration Very little Lots, for muscle
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Future governors of Califorina?
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