Back to AP I Lecture Notes, Power Points and Study Review Page
Notes - 4th Edition
The Structure of the Muscle Organ
Myology = the study of muscles – 40-50% of body mass is muscle.
Three main types of muscle tissue:
- striated muscle tissue due to it's striated appearance
- voluntary muscle because it can be consciously controlled
In general, moves bones
2. Cardiac = heart muscle tissue
- striated but involuntary - cannot normally be consciously controlled
- has a built in pacemaker system that gives the tissue autorhythmicity (pacemaker)
-lines hollow organs such as GI, blood vessels, skin
- non-striated, therefore called "smooth"
- sometimes exhibit autorhythmicity
Skeletal and smooth muscle cells are elongated and are called muscle fibers
Muscle contraction depends on two kinds of myofilaments – actin and myosin
Muscle terminology is similar
Sarcolemma – muscle plasma membrane
Sarcoplasm – cytoplasm of a muscle cell
Prefixes – myo, mys, and sarco all refer to muscle
Four main characteristics of muscle tissue
1. Excitability (irritability), responsiveness
- nerve tissue also has this property
- respond to stimuli by producing electrical impulses (action potentials)
- chemicals (either neurotransmitters or hormones) can trigger the impulse
- ability to shorten and thicken in order to generate force and do work
- contraction occurs in response to action potentials
- ability to be stretched (extended) without damage
- while one muscle is contracted, an opposing muscle is relaxed or being extended
- ability to return to its original shape after contraction or extension
Four main functions of muscle tissue-
1. Converts chemical energy to mechanical energy – this is the most distinguishing characteristic of muscle tissue
o The total number of muscle cells available for contraction determines the power of a muscle.
2. Movement or motion of the body & stabilization of posture and organs
- ex: sitting or standing possible due to steady contractions of muscles
- relies on coordinated functions of bones, joints and muscles
3. Movement of substances within the body
- ex: flow of blood, flow of substances through the GI tract
4. Generates heat – 85% of body heat generated by muscle contractions
- involuntary shivering can increase heat production (thermogenesis) immensely
Skeletal Muscle Tissue - general characteristics
Packaged in skeletal muscles that attach to and cover the bony skeleton
Has obvious stripes called striations
Is controlled voluntarily (i.e., by conscious control)
Contracts rapidly but tires easily
Is responsible for overall body motility
Is extremely adaptable and can exert forces ranging from a fraction of an ounce to over 70 pounds
Cardiac Muscle – general characteristics
Occurs only in the heart
Is striated like skeletal muscle but is not voluntary
Contracts at a fairly steady rate set by the heart’s pacemaker
Neural controls allow the heart to respond to changes in bodily needs
Smooth Muscle – general characteristics
Found in the walls of hollow visceral organs, such as the stomach, urinary bladder, and respiratory passages
Forces food and other substances through internal body channels
It is not striated and is involuntary
Skeletal Muscle Details
Each skeletal muscle is a discrete organ
Accessory components of skeletal muscle tissue
A. Connective tissue components: surrounds and protects the muscle tissue
• 3 main layers of connective tissue around the muscle tissue
1. Endomysium – is made from areolar connective tissue and separates and surrounds each individual muscle fiber within the fascicle
2. Perimysium - separates individual muscle fibers into bundles of 10-100 called fascicles and surrounds each fascicle.
3. Epimysium – covers and encircles the whole muscle. Made from dense irregular connective tissue.
• A sheet like extension of the epimysium is called an aponeurosis
B. Nerve Supply (from brain to spinal cord to motor neuron)
o Nerves that stimulate muscle contractions are called motor neurons.
(any nerve that causes a muscle contraction is a motor neuron)
o Each motor neuron has a certain number of skeletal muscle fibers that it stimulates .... one motor neuron and it's muscle fibers together is called a motor-unit
C. Attachments – most muscles cross joints and have at least 2 points of attachment:
1. Origin – on the bone that does not move.
2. Insertion – on the bone that does move.
Types of attachments
a. Fleshy (direct) – muscle’s epimysium is fused to the periosteum of a bone or the perichondrium of a cartilage.
b. Indirect via tendon or aponeuroses
1. Tendon - extension of organized dense connective tissue that connects muscle to periosteum of bone. Tendons may be further covered by connective tissue called tendon sheaths.
2. Aponeurosis (Ap-oh-new-ro-sis) - type of tendon that extends as a flat, broad sheet.
MICROSCOPIC ANATOMY OF A SKELETAL MUSCLE FIBER [USE PREFIX SARCO]
• Mesodermal - stem cells called “myoblasts” fuse to form each muscle fiber
• Satellite cells – some myoblasts remain unspecialized satellite cells between the muscle fibers and can fuse with damage fibers to repair.
• Each individual muscle cell is called a myofiber or muscle fiber.
Microscopic Anatomy of a Skeletal Muscle Fiber
• Sarcolemma is the cell membrane or plasma membrane.
• Sarcoplasm is the cytoplasm of a muscle fiber.
Contains lots of glycogen to provide stored energy
Myoglobin (oxygen binding molecule like hemoglobin of the blood) –
holds a reserve supply of oxygen in muscle cells
Lots of mitochondria in rows through out fiber
• Myofibrils - each muscle fiber is filled with multiple small structures called myofibrils which are the parallel contractile threads (elements) of the muscle fiber (sarcoplasm)
• Fibers produce striations [Dark (A) and Light (I) Bands]
• Filaments – subunits of myofibrils – 2 types: Thick and Thin
• Sarcomere = the filaments of a myofibril are arranged in compartments - (the basic functional unit of striated muscle fibers)
Parts of a sarcomere:
Composed of myofilaments made up of contractile proteins
Myofilaments are of two types – thick and thin
Thick is myosin filament
Thin is actin filament
• memory tool for which filament is the thin one and which is the thick one: If you stay active you stay thin
Ultrastructure of Myofilaments: Thick Filaments
Thick filaments are composed of the protein myosin
Each myosin molecule has a rod-like tail and two globular heads
Tails – two interwoven, heavy polypeptide chains
Heads – two smaller, light polypeptide chains called cross bridges
Cross bridges act as motors to generate the tension developed by contacting a muscle cell
During muscle contraction, myosin cross bridges attach to the active sites of actin filaments
Heads split ATP to generate energy for the muscle contraction
Ultrastructure of Myofilaments: Thin Filaments
Thin filaments are chiefly composed of the protein actin
Each actin molecule is a helical polymer of globular subunits called G actin
The subunits contain the active sites to which myosin heads attach during contraction
Tropomyosin and troponin are regulatory subunits bound to actin
In muscle contraction, calcium acts to remove the blocking action tropomyosin
Actin and myosin interact according to the sliding filament mechanism which involves actin and myosin sliding past each other but not shortening
• Sarcoplasmic reticulum Stores Ca++ during relaxation. A muscle contraction is triggered when the sarcoplasmic reticulum releases Ca++ through its Ca++ release channels, The Ca++ is released into the sarcoplasm surrounding the thick and thin filaments.
T- Tubules (Transverse)
• Transverse tubules are infoldings (invaginations) - of the sarcolemma that penetrate through the sarcoplasmic reticulum towards the center of the muscle fiber.
- As the transverse tubules pass through the sarcoplasmic reticulum...the sarcoplasmic reticulum forms dilated end sacs on each side of the transverse tubules called terminal cisterns....Each T-tubule and the terminal cistern on each side of it form what is called a Triad.
T- tubules conduct nerve-initiated electrical impulses to the deepest regions of the muscle cell and to every sacromere
The Sliding Model of Contraction
• Filament mechanism of contraction
o Myosin heads attach to thin filaments and pull them in toward the M
o Z discs come closer together
o Sarcomeres shorten
Summary of How a Muscle Contraction Occurs
1. Just prior to a muscle contraction.... ATP attaches to the ATP-binding sites on the myosin cross bridges (golf club heads). The ATP molecule is split and energy is transferred to the cross bridges. Therefore, it is "loaded" or "activated".
2. An action potential travels from a motor neuron, crosses the synapse and is received by the motor end plates of the muscle fiber. This causes Na channels to open in the sarcolemma. Na rushes in...this changes the resting potential of the sarcolemma....thus an action potential is traveling along the cell membrane (sarcolemma}.
3. As the action potential travels along....it travels dawn into each T-tubule... this triggers stored Ca++ in the SR to be released from the terminal cisterns (thus the triad function).
4. When the Ca++ is release from the terminal cisterns, it is released into the sarcoplasm around the thick and thin filaments of the myofibril. This increase in Ca++ levels causes tropomyosin to move away from the myosin binding site. Therefore, the myosin binding site is now exposed.
5. The myosin cross bridges (heads) snap into place spontaneously because they are already activated (step 1). When the cross bridges bind to the myosin binding sites on the actin....there is a change in shape. This stimulates the power stroke of contraction.
6. During the power stroke....the club head swivels or bends back towards the center of the sarcomere. It drags the actin with it towards the H Zone and pulls the thin filament back to overlap the thick filament. During the power stroke… ADP is released.
7. Once this is complete, ATP binds to the ATP binding site on the myosin...this causes the myosin cross bridge to release.
8. The ATP molecule is then split and reactivates the myosin cross bridge...this make the myosin head return to it's original shape...It is now ready to go through the process again and grab the next myosin binding site.
9. The action potentials occur one after another so the myosin cross bridges can bind, pull, release, bind, pull, release, bind, pull, release etc...this pulls the myosin binding sites (actin, thin filaments) back in a rowing fashion to overlap the thick filaments.-therefore, the muscle fiber and therefore, the muscle shortens (contracts).
10. The myosin cross bridges alternate which are binding and which are releasing... therefore, while one is released...the one next to it is binding so there is a hand over fist.. .assembly line. ...treadmill. ...belt like movement of the filaments.
Click here to hear the song, Myofibrils ---
Here are the words to this song:
Muscular Contraction Step by Step (taken from PowerPoint Slides)
• In order to contract, a skeletal muscle must:
• Be stimulated by a nerve ending
Propagate an electrical current, or action potential, along its sarcolemma
• Have a rise in intracellular Ca2+ levels, the final trigger for contraction
• Linking the electrical signal to the contraction is called excitation-contraction coupling
• Skeletal muscles are stimulated by motor neurons of the somatic nervous system
• Axons of these neurons travel in nerves to muscle cells
• Axons of motor neurons branch profusely as they enter muscles
• Each axonal branch forms a neuromuscular junction with a single muscle fiber
The neuromuscular junction is formed from:
Axonal endings, which have small membranous sacs (synaptic vesicles) that contain the neurotransmitter acetylcholine (ACh)
The motor end plate of a muscle, which is a specific part of the sarcolemma that contains ACh receptors and helps form the neuromuscular junction
Though exceedingly close, axonal ends and muscle fibers are always separated by a space called the synaptic cleft
• When a nerve impulse reaches the end of an axon at the neuromuscular junction:
• Voltage-regulated calcium channels open and allow Ca2+ to enter the axon
• Ca2+ inside the axon terminal causes axonal vesicles to fuse with the axonal membrane
This fusion releases ACh into the synaptic cleft via exocytosis
ACh diffuses across the synaptic cleft to ACh receptors on the sarcolemma
Binding of ACh to its receptors initiates an action potential in the muscle
Destruction of Acetylcholine
ACh bound to ACh receptors is quickly destroyed by the enzyme acetylcholinesterase
This destruction prevents continued muscle fiber contraction in the absence of additional stimuli
The destruction of ACh by acetylcholinesterase and its removal from the membrane receptors is the first thing that stops a contraction after the nerve stops sending ACh.
A transient depolarization event that includes polarity reversal of a sarcolemma (or nerve cell membrane) and the propagation of an action potential along the membrane
Role of Acetylcholine (ACh)
ACh binds its receptors at the motor end plate
Binding opens chemically (ligand) gated channels
Na+ and K+ diffuse out and the interior of the sarcolemma becomes less negative
This event is called depolarization
Initially, this is a local electrical event called end plate potential
Later, it ignites an action potential that spreads in all directions across the sarcolemma
Action Potential: Electrical Conditions of a Polarized Sarcolemma
The outside (extracellular) face is positive, while the inside face is negative
This difference in charge is the resting membrane potential
Action Potential: Electrical Conditions of a Polarized Sarcolemma
The predominant extracellular ion is Na+
The predominant intracellular ion is K+
The sarcolemma is relatively impermeable to both ions
Action Potential: Depolarization and Generation of the Action Potential
An axonal terminal of a motor neuron releases ACh and causes a patch of the sarcolemma to become permeable to Na+ (sodium channels open)
Action Potential: Depolarization and Generation of the Action Potential
Na+ enters the cell, and the resting potential is decreased (depolarization occurs)
If the stimulus is strong enough, an action potential is initiated
Action Potential: Propagation of the Action Potential
Polarity reversal of the initial patch of sarcolemma changes the permeability of the adjacent patch
Voltage-regulated Na+ channels now open in the adjacent patch causing it to depolarize
Action Potential: Propagation of the Action Potential
Thus, the action potential travels rapidly along the sarcolemma
Once initiated, the action potential is unstoppable, and ultimately results in the contraction of a muscle
Action Potential: Repolarization
Immediately after the depolarization wave passes, the sarcolemma permeability changes
Na+ channels close and K+ channels open
K+ diffuses from the cell, restoring the electrical polarity of the sarcolemma
Action Potential: Repolarization
Repolarization occurs in the same direction as depolarization, and must occur before the muscle can be stimulated again (refractory period)
The ionic concentration of the resting state is restored by the Na+-K+ pump
Myosin cross bridges alternately attach and detach
Thin filaments move toward the center of the sarcomere
Hydrolysis of ATP powers this cycling process
Ca2+ is removed into the SR and the muscle fiber relaxes
Sequential Events of Contraction
Cross bridge formation – myosin cross bridge attaches to actin filament
Working (power) stroke – myosin head pivots and pulls actin filament toward M line
Cross bridge detachment – ATP attaches to myosin head and the cross bridge detaches
“Cocking” of the myosin head – energy from hydrolysis of ATP cocks the myosin head into the high-energy state
Contraction of Skeletal Muscle Fibers
Contraction – refers to the activation of myosin’s cross bridges (force-generating sites)
Shortening occurs when the tension generated by the cross bridge exceeds forces opposing shortening
Contraction ends when cross bridges become inactive, the tension generated declines, and relaxation is induced
Contraction of Skeletal Muscle (Organ Level)
Contraction of muscle fibers (cells) and muscles (organs) is similar
The two types of muscle contractions are:
Isometric contraction – increasing muscle tension (muscle does not shorten during contraction)
Isotonic contraction – decreasing muscle length (muscle shortens during contraction)
Motor Unit: The Nerve-Muscle Functional Unit
A motor unit is a motor neuron and all the muscle fibers it supplies
The number of muscle fibers per motor unit can vary from four to several hundred
Muscles that control fine movements (fingers, eyes) have small motor units
Motor Unit: The Nerve-Muscle Functional Unit
Large weight-bearing muscles (thighs, hips) have large motor units
Muscle fibers from a motor unit are spread throughout the muscle; therefore, contraction of a single motor unit causes weak contraction of the entire muscle
A muscle twitch is the response of a muscle to a single, brief threshold stimulus - a single action potential of its motor neuron. The muscle fiber contracts quickly and then relaxes.
Every muscle twitch as seen on a myogram (a graphic recording of contractile activity) has three phases of a muscle twitch:
1. Latent period – first few milli-seconds after stimulation when excitation-contraction coupling is taking place
2. Period of contraction – cross bridges actively form and the muscle shortens
3. Period of relaxation – Ca2+ is reabsorbed into the SR, and muscle tension goes to zero
Graded Muscle Responses
Graded muscle responses are: (smooth contractions that vary in strength as different demands are placed on them)
Variations in the degree of muscle contraction
Required for proper control of skeletal movement
Responses are graded by:
Changing the frequency of stimulation
Changing the strength of the stimulus
Muscle Response to Varying Stimuli
A single stimulus results in a single contractile response – a muscle twitch
Frequently delivered stimuli (muscle does not have time to completely relax) increases contractile force – wave summation
Muscle Response to Varying Stimuli
More rapidly delivered stimuli result in incomplete tetanus
Tetanus is a smooth sustained muscle contraction resulting from high-frequency stimulation
If stimuli are given quickly enough, complete tetanus results
Muscle Response: Stimulation Strength
Threshold stimulus – the stimulus strength at which the first observable muscle contraction occurs
Beyond threshold, muscle contracts more vigorously as stimulus strength is increased
Force of contraction is precisely controlled by multiple motor unit summation
This phenomenon, called recruitment, brings more and more muscle fibers into play
Strong muscle contractions are controlled by increasing the voltage up to the maximum voltage.
The stonger the stimuli, the stronger the strength or force of skeletal muscle contactions.
Treppe: The Staircase Effect
When a muscle begins to contract its contractions may be only half as strong as those later in response to stimulus of the same strength
Staircase – increased contraction in response to multiple stimuli of the same strength
Contractions increase because:
There is increasing availability of Ca2+ in the sarcoplasm
Muscle enzyme systems become more efficient because heat is increased as muscle contracts
Is the constant, slightly contracted state of all muscles, which does not produce active movements
Keeps the muscles firm, healthy, and ready to respond to stimulus
Spinal reflexes account for muscle tone by:
Activating one motor unit and then another
Responding to activation of stretch receptors in muscles and tendons
In isotonic contractions, the muscle changes in length (decreasing the angle of the joint) and moves the load
The two types of isotonic contractions are concentric and eccentric
Concentric contractions – the muscle shortens and does work
Eccentric contractions – the muscle contracts as it lengthens
Tension increases to the muscle’s capacity, but the muscle neither shortens nor lengthens
Occurs if the load is greater than the tension the muscle is able to develop
Muscle Metabolism: Energy for Contraction
ATP is the only source used directly for contractile activity
As soon as available stores of ATP are hydrolyzed (4-6 seconds), they are regenerated by 3 pathways:
The interaction of ADP with creatine phosphate (CP)
Anaerobic glycolysis (sugar splitting)
Aerobic respiration in the mitochondria
Muscle Metabolism: Anaerobic Glycolysis
When muscle contractile activity reaches 70% of maximum:
Bulging muscles compress blood vessels
Oxygen delivery is impaired
Pyruvic acid is converted into lactic acid
Muscle Metabolism: Anaerobic Glycolysis
The lactic acid:
Diffuses into the bloodstream
Is picked up and used as fuel by the liver, kidneys, and heart
Is converted back into pyruvic acid by the liver
Muscle fatigue – the muscle is in a state of physiological inability to contract
Muscle fatigue occurs when:
ATP production fails to keep pace with ATP use
There is a relative deficit of ATP, causing contractures
Lactic acid accumulates in the muscle
Ionic imbalances are present
Intense exercise produces rapid muscle fatigue (with rapid recovery)
Na+-K+ pumps cannot restore ionic balances quickly enough
Low-intensity exercise produces slow-developing fatigue
SR is damaged and Ca2+ regulation is disrupted
Vigorous exercise causes dramatic changes in muscle chemistry
For a muscle to return to a resting state:
Oxygen reserves must be replenished
Lactic acid must be converted to pyruvic acid
Glycogen stores must be replaced
ATP and CP reserves must be resynthesized
Oxygen debt – the extra amount of O2 needed for the above restorative processes
Heat Production During Muscle Activity
Only 40% of the energy released in muscle activity is useful as work
The remaining 60% is given off as heat
Dangerous heat levels are prevented by radiation of heat from the skin and sweating
Force of Muscle Contraction
The force of contraction is affected by:
The number of muscle fibers contracting – the more motor fibers in a muscle, the stronger the contraction
The relative size of the muscle – the bulkier the muscle, the greater its strength
Degree of muscle stretch – muscles contract strongest when muscle fibers are 80-120% of their normal resting length
Muscle Fiber Type: 2 Functional Characteristics
Speed of contraction – determined by speed in which ATPases split ATP
(1) The two types of fibers are slow and fast
(2) ATP-forming pathways
Oxidative fibers – use aerobic pathways
Glycolytic fibers – use anaerobic glycolysis
These two criteria define three categories – slow oxidative fibers, fast oxidative fibers, and fast glycolytic fibers
Muscle Fiber Type: Speed of Contraction
Slow oxidative fibers contract slowly, have slow acting myosin ATPases, and are fatigue resistant
Fast oxidative fibers contract quickly, have fast myosin ATPases, and have moderate resistance to fatigue
Fast glycolytic fibers contract quickly, have fast myosin ATPases, and are easily fatigued
o Increase in efficiency of the respiratory system
o Increase in the efficiency of the circulatory system
o Increase in the number of myofibrils within the muscle cells
o Does not increase the number of muscle cells
o Increase in the number of mitochondria
Composed of spindle-shaped fibers with a diameter of 2-10 μm and lengths of several hundred μm
Lack the coarse connective tissue sheaths of skeletal muscle, but have fine endomysium
Organized into two layers (longitudinal and circular) of closely apposed fibers
Found in walls of hollow organs (except the heart)
Have essentially the same contractile mechanisms as skeletal muscle
When the longitudinal layer contracts, the organ dilates and contracts
When the circular layer contracts, the organ elongates
Peristalsis – alternating contractions and relaxations of smooth muscles that mix and squeeze substances through the lumen of hollow organs
Innervation of Smooth Muscle
Smooth muscle lacks neuromuscular junctions
Innervating nerves have bulbous swellings called varicosities
Varicosities release neurotransmitters into wide synaptic clefts called diffuse junctions
Microscopic Anatomy of Smooth Muscle
SR is less developed than in skeletal muscle and lacks a specific pattern
T tubules are absent
Plasma membranes have pouchlike infoldings called caveoli
Ca2+ is sequestered in the extracellular space near the caveoli, allowing rapid influx when channels are opened
There are no visible striations and no sarcomeres
Thin and thick filaments are present
Proportion and Organization of Myofilaments in Smooth Muscle
Ratio of thick to thin filaments is much lower than in skeletal muscle
Thick filaments have heads along their entire length
Thick and thin filaments are arranged diagonally, causing smooth muscle to contract in a corkscrew manner
Contraction of Smooth Muscle
Whole sheets of smooth muscle exhibit slow, synchronized contraction
They contract in unison
Action potentials are transmitted from cell to cell
Some smooth muscle cells:
Act as pacemakers and set the contractile pace for whole sheets of muscle
Are self-excitatory and depolarize without external stimuli
The final trigger for contractions is a rise in intracellular Ca2+
Ca2+ is released from the SR and from the extracellular space
Special Features of Smooth Muscle Contraction
Unique characteristics of smooth muscle include:
Smooth muscle tone
Slow, prolonged contractile activity
Low energy requirements
Response to stretch
Response to Stretch
Smooth muscle exhibits a phenomenon called stress-relaxation response in which:
Smooth muscle responds to stretch only briefly, and then adapts to its new
The new length, however, retains its ability to contract
This enables organs such as the stomach and bladder to temporarily store contents
Certain smooth muscles can divide and increase their numbers by undergoing hyperplasia
This is shown by estrogen’s effect on the uterus
At puberty, estrogen stimulates the synthesis of more smooth muscle, causing the uterus to grow to adult size
During pregnancy, estrogen stimulates uterine growth to accommodate the increasing size of the growing fetus
Types of Smooth Muscle: Single Unit
The cells of single-unit smooth muscle, commonly called visceral muscle:
Contract rhythmically as a unit
Are electrically coupled to one another via gap junctions
Often exhibit spontaneous action potentials
Are arranged in opposing sheets and exhibit stress-relaxation response
Types of Smooth Muscle: Multiunit
Multiunit smooth muscles are found:
In large airways to the lungs
In large arteries
In arrector pili muscles
Attached to hair follicles
In the internal eye muscles
Types of Smooth Muscle: Multiunit
Their characteristics include:
Rare gap junctions
Infrequent spontaneous depolarizations
Structurally independent muscle fibers
A rich nerve supply, which, with a number of muscle fibers, forms motor units
Graded contractions in response to neural stimuli
Muscular dystrophy – group of inherited muscle-destroying diseases where muscles enlarge due to fat and connective tissue deposits, but muscle fibers atrophy
Duchenne muscular dystrophy (DMD) – most common and serious form of muscular dystrophy
Inherited, sex-linked disease carried by females and expressed in males (1/3500)
Diagnosed between the ages of 2-10
Victims become clumsy and fall frequently as their muscles fail
Progresses from the extremities upward, and victims die of respiratory failure in their 20s
Caused by a lack of the cytoplasmic protein dystrophin that links the cytoskeleton to the extracellular matrix and stabilizes the sarcolemma
There is no cure, but myoblast transfer therapy shows promise
• mostly females (20-50yr)
• weakness of skeletal muscle from abnormal neuromuscular junction
• Autoimmune disease where antibodies attack ACh receptors
Muscle tissue develops from embryonic mesoderm cells called myoblasts
Multinucleated skeletal muscles form by fusion of myoblasts
The growth factor agrin stimulates the clustering of ACh receptors at newly forming motor end plates
As muscles are brought under the control of the somatic nervous system, the numbers of fast and slow fibers are also determined
Cardiac and smooth muscle myoblasts do not fuse but develop gap junctions at an early embryonic stage
Developmental Aspects: Regeneration
Cardiac and skeletal muscle become amitotic, but can lengthen and thicken
Myoblastlike satellite cells associated with skeletal muscle show very limited regenerative ability
Cardiac cells lack satellite cells
Smooth muscle has good regenerative ability – the greatest ability to regenerate of all the muscle types.
Developmental Aspects: After Birth
Muscular development reflects neuromuscular coordination
Development occurs head-to-toe, and proximal-to-distal
Peak natural neural control of muscles is achieved by mid-adolescence
Athletics and training can improve neuromuscular control
Developmental Aspects: Male and Female
There is a biological basis for greater strength in men than in women
Women’s skeletal muscle makes up 36% of their body mass
Men’s skeletal muscle makes up 42% of their body mass
Developmental Aspects: Male and Female
These differences are due primarily to the male sex hormone testosterone
With more muscle mass, men are generally stronger than women
Body strength per unit muscle mass, however, is the same in both sexes
Developmental Aspects: Age Related
With age, connective tissue increases and muscle fibers decrease
Muscles become stringier and more sinewy
By age 80, 50% of muscle mass is lost (sarcopenia)
Regular exercise reverses sarcopenia
Aging of the cardiovascular system affects every organ in the body
Atherosclerosis may block distal arteries, leading to intermittent claudication and causing severe pain in leg muscles
Related Clinical Terms
Hernia – protrusion of an organ through its body cavity wall
Myalgia – muscle pain
RICE – acronym for rest, ice, compression, elevation
Spasm – a sudden, involuntary smooth or skeletal muscle twitch; may be due to a chemical imbalance
Cramp is a prolonged spasm
Notes - 5th Edition
Dr. Steven Schwartz AP1 IRSC/PBCC
I. Types and Characteristics of Muscular Tissue (pp. 404–405)
A. In animals, muscle cells have evolved that are specialized for movement. (p. 404)
B. Skeletal muscle is the type of muscle that holds the body erect against the pull of gravity and produces its outwardly visible movement. (p. 404)
C. Muscle cells have five universal characteristics. (p. 404)
1. Responsiveness (excitability). Responsiveness is a property of all living cells, but muscle and nerve cells have developed this property to the highest degree.
2. Conductivity. Stimulation of a muscle fiber produces a wave of excitation that travels along the fiber and initiates muscle contraction.
3. Contractility. Muscle fibers are unique in their ability to shorten when stimulated, allowing them to pull on bones and other tissues.
4. Extensibility. In order to contract, a muscle cell must be able to stretch again between contractions; skeletal muscle fibers can stretch to as much as three times their contracted length.
5. Elasticity. When a muscle cell is stretched and then the tension released, it recoils to its original resting length.
C. Skeletal muscle may be defined as voluntary striated muscle that is usually attached to one or more bones. (pp. 404–405)
1. Skeletal muscle has light and dark transverse bands called striations. (Fig. 11.1)
2. Skeletal muscle is called voluntary because it is usually subject to conscious control; other types of muscle are involuntary, and they are never attached to bones.
3. A typical skeletal muscle cell is about 100 μm in diameter and 3 cm long; some are a thick as 500 μm and 30 cm long.
4. Because of their length, skeletal muscle cells are usually called muscle fibers of myofibers.
5. A skeletal muscle is composed of not only muscle cells but also fibrous connective tissue.
a. The endomysium surrounds each muscle fiber.
b. The perimysium bundles muscle fibers together into fascicles.
c. The epimysium encloses the entire muscle.
d. These connective tissues are continuous with collagen fibers of the matrix, which in turn are continuous with the collagen of the bone matrix.
6. The collagen of muscles is neither excitable nor contractile, but it is somewhat extensible and elastic.
a. The collagen resists excessive stretching when a muscle lengthens and protects the muscle from injury.
b. Some believe that the recoil of tendons contribute to power output and efficiency of a muscle; others feel that the elasticity in humans is negligible.
II. Microscopic Anatomy of Skeletal Muscle (pp. 405–410)
A. The muscle fiber has a complex, tightly organized internal structure that is closely tied to its contractile function (pp. 405–406)
1. The plasma membrane is called the sarcolemma, and its cytoplasm is the sarcoplasm.
a. The sarcoplasm is occupied mainly by long protein bundles called myofibrils about 1 μm in diameter. (Fig. 11.2)
b. It also contains glycogen, a starchlike carbohydrate, which stores energy, and the red pigment myoglobin, which stores oxygen.
2. Muscle fibers have multiple flattened or sausage-shaped nuclei pressed against the inside of the sarcolemma.
a. During embryonic development, several stem cells called myoblasts fuse to produce each muscle fiber, each contributing a nucleus.
b. Some myoblasts remain as unspecialized satellite cells between the muscle fiber and endomysium; these can multiply and produce new muscle fibers to some degree.
3. Most other organelles are packed into the spaces between the myofibrils.
a. The smooth endoplasmic reticulum, called the sarcoplasmic reticulum (SR), forms a network around each myofibril; it periodically has dilated end-sacs called terminal cisternae.
b. Osteocytes function to resorb or deposit bone matrix, contributing to the homeostatisis of bone density and blood concentrations of calcium and phosphate ions
c. The sarcolemma has tubular infolding called transverse (T) tubules that penetrate through the cell and open onto the other side.
i. Each tubule is closely associated with two terminal cisternae.
ii. A T tubule and its associated two terminal cisternae constitute a triad.
d. The sarcoplasmic reticulum is a reservoir of calcium ions; it has gated channels in its membranes that allow a flood of calcium ion into the cytosol where it activates muscle contraction.
e. The T tubule signals that SR when to release these calcium bursts.
B. Each myofibril is a bundle of parallel protein microfilaments called myofilaments; there are three kinds of myofilaments. (pp. 406–407)
1. The thick filaments are about 15 nm in diameter is each is made of several hundred myosin molecules. (Fig. 11.3a, b, d)
a. A myosin molecule is shaped like a golf club, with two chains intertwined to form a shaftlike tail and a double globular head projecting from the tail at an angle.
b. A thick filament may be likened to a bundle of 200 to 500 such “golf clubs,” with their heads directed outward around the bundle.
c. Half of the heads angle to the left and half to the right, with a bare zone in the middle.
2. The thin filaments, 7 nm in diameter, are composed of two intertwined strands of fibrous (F) actin. (Fig. 11.3c, d)
a. Each F actin strand is string of subunits called globular (G) actin.
b. Each G actin has an active site that can bind to the head of a myosin molecule.
c. A thin filament also has 40 to 60 molecules of the protein tropomyosin, which blocks active sites of some G actins when a muscle fiber is relaxed.
d. A calcium-binding protein, troponin, is bound to every tropomyosin molecule.
3. Elastic filaments, 1 nm in diameter, are made of a large protein called titin (connectin). (Fig. 11.5b)
a. Elastic filaments flank each thick filament and anchor it to a structure called the Z disc, helping to stabilize the thick filament.
4. Myosin and actin are called contractile proteins because they accomplish the shortening of the muscle fiber.
5. Tropomyosin and troponin are called regulatory proteins because they act like a switch to determine when the fiber can contract or not contract.
a. The action of these regulatory proteins depends on the availability of calcium ions, which bind to troponin.
6. At least seven other accessory proteins occur in the thick and thin filaments or are associated with them; the most clinically important is dystrophin.
a. Dystrophin is an enormous protein located between the sarcolemma and the outermost myofilaments; it links actin filaments to a peripheral protein on the inner face of the sarcolemma. (Fig. 11.4)
b. The peripheral protein in turn is linked to transmembrane proteins that connect with proteins external to the fiber that ultimately link with the basal lamina and to the endomysium.
c. Dystrophin is therefore a key element in transferring the forces of myofilament movement to the connective tissue of the muscle as a whole.
d. Genetic defects in dystrophin are responsible for muscular dystrophe.
C. Striations are a precise array of the abundant myosin and actin found in skeletal and cardiac muscle. (pp. 407–410) (Fig. 11.5)
1. Striated muscle has dark A (anisotropic) bands and lighter I (isotropic) bands, referring to their effect on polarized light.
a. Each A band consists of thick filaments lying side by side.
i. Part of the A band is especially dark, hwere each thick filament is surrounded by thin filaments.
ii. In the middle of the A band is a light region called the H band, into which thin filaments do not reach.
iii. The thick filaments originate at a dark M line in the middle of the H band.
b. Each light I band is bisected by a dark narrow Z disc (Z line), which provides anchorage for the thin filaments and elastic filaments.
c. Each segment of a myofibril from one Z disc to the next is called a sarcomere; it is the functional contractile unit of the muscle fiber.
i. A muscle shortens because its individual sarcomeres shorten and pull the Z discs closer together.
ii. Dystrophin and the linking proteins pull on the extracellular proteins of the muscle.
iii. The Z discs pull on the sarcolemma to achieve overall shortening of the cell.
d. The terminology of muscle fiber structure is shown in Table 11.1.
III. The Nerve–Muscle Relationship (pp. 410–413)
A. The relationship between nerve and muscle cells is important to understanding muscle contraction because skeletal muscle never contracts unless it is stimulated by a nerve (or artificially with electrodes). (p. 410)
B. Nerve cells called somatic motor neurons, with cell bodies in the brainstem and spinal cord, stimulate muscle fibers via their axons, called somatic motor fibers; a single motor fiber and all the muscle fibers it innervates are collectively called a motor unit. (pp. 410–411) (Fig. 11.6)
1. The muscle fibers of a single motor unit are not clustered together but are dispersed throughout a muscle, so that their stimulation causes a weak contraction over a wide area.
2. On average, about 200 muscle fibers are innervated by each motor neuron, but wide variation exists for different purposes.
a. Small motor units are present where fine control is needed, such as in the muscles of eye movement (3 to 6 muscle fibers per neuron).
b. Large motor units are present where strength is more important than fine control, such as in the gastrocnemius (1,000 muscle fibers per neuron).
3. Multiple motor units also have the advantage of allowing “shifts” in muscle contraction, so that when some units become fatigued, others can take over.
C. The point where a nerve fiber meets its target cell is a synapse, and when the target cell is a muscle fiber, the synapse is called a neuromuscular junction (NMJ) or motor end plate. (pp. 411–413) (Fig. 11.7) (Table 11.2)
1. One nerve fiber stimulates the muscle fiber at several points within the NMJ; each terminal branch of the nerve fiber has its own synapse point to the muscle fiber.
2. At each synapse, the nerve fiber ends in a bulbous swelling called a synaptic knob, which is separated from the muscle fiber by a narrow space 60–100 nm wide called the synaptic cleft.
a. A third cell, a Schwann cell, envelopes the entire junction.
b. A synaptic knob contains spheroidal organelles called synaptic vesicles, which are filled with acetylcholine (ACh).
c. ACh is released into the synaptic cleft when the nerve impulse reaches the nerve endings.
d. The muscle fiber has about 50 million ACh receptors incorporated into its sarcolemma, which contains numerous infoldings at the junction called junctional folds that increase surface area for receptors.
e. A deficiency of ACh receptors leads to the muscle paralysis of myasthenia gravis.
3. The muscle fiber and the Schwann cell of the NMJ are surrounded by a basal lamina that separates them from the surrounding connective tissue.
a. The basal lamina bases through the synaptic cleft and fills it.
b. Both the sarcolemma and the basal lamina within the cleft contain the enzyme acetylcholinesterase (AChE), which breaks down ACh.
Insight 11.1 Neuromuscular Toxins and Paralysis
D. Muscle fibers and neurons are considered electrically excitable cells because their plasma membranes exhibit voltage changes in response to stimulation. (p. 412–413)
1. The study of the electrical activity of cells is called electrophysiology.
2. In an unstimulated (resting) cell, more anions (negative ions) are found on the inside of the plasma membrane than on the outside; the membrane is therefore polarized, or charged.
a. In a resting muscle cell, Na+ is in excess in the extracellular fluid (ECF) and K+ is in excess in the intracellular fluid (ICF).
b. Anions such a proteins, nucleic acids, and phosphates are also inside the ICF and cannot cross the membrane.
3. A difference in electrical charge between two points is called an electrical potential, or voltage.
a. The voltage across the sarcolemma of a muscle cell is only about –90 mV and is called the resting membrane potential (RMP).
b. The negative sign indicates that the negative charge is greater on the inside of the membrane.
c. The resting membrane potential is maintained by the sodium–potassium pump.
4. When a nerve or muscle cell is stimulated, ion gates open in the plasma membrane and Na+ diffuses down its concentration gradient into the cell.
a. These cations override the negative charges in the ICF, and the inside of the membrane briefly becomes positive, a change termed depolarization.
5. The Na+ gates then close and the K+ gates open; K+ rushes out of the cell turning the inside of the membrane negative again.
a. This change is termed repolarization.
6. The voltage shift of depolarization followed by repolarization is called an action potential.
7. Action potentials perpetuate themselves along a membrane; a wave of action potentials moving along a nerve fiber is called a nerve impulse or nerve signal.
IV. Behavior of Skeletal Muscle Fibers (pp. 414–420)
A. The process of muscle contraction and relaxation has four major phases: excitation; excitation–contraction coupling; contraction; and relaxation. (p. 414) (Figs. 11.8, 11.9, 11.10, 11.11)
B. Excitation is the process in which action potentials in the nerve fiber lead to action potentials in the muscle fiber; it can be divided into five steps. (p. 414) (Fig. 11.8)
1. A nerve signal arrives at a synaptic knob and stimulates voltage-regulated Ca2+ gates to open; calcium ions enter the synaptic knob.
2. Ca2+ stimulates exocytosis of synaptic vesicles, which release ACh into the synaptic cleft.
3. ACh diffuses across the synaptic cleft and binds to receptor proteins on the sarcolemma.
4. The receptors are ligand-regulated ion gates that bind two ACh molecules to open.
a. When the gates are opened, Na+ diffuses into the cell and K+ diffuses out; the sarcolemma reverses polarity from –90 mV to +75 mV, then falls back again as K+ diffuses out.
b. This rapid fluctuation in membrane voltage at the motor end plate is called end-plate potential (EPP).
5. Areas adjacent to the NMJ have ion-specific voltage-regulated gates that open in response to the EPP, allowing flow of Na+ in and K+ out, generating an action potential; the muscle fiber is now excited.
C. Excitation–contraction coupling refers to the events that link the action potentials on the sarcolemma to activation of the myofilaments; this process has four steps that follow from excitation. (p. 414) (Fig. 11.9)
1. (6) A wave of action potentials spreads from the end plate in all directions, and enters the T tubules, continuing down them into the sarcoplasm.
2. (7) Action potentials open voltage-regulated ion gates in the T tubules.
a. These gates are linked to calcium channels in the terminal cisternae of the sarcoplasmic reticulum (SR).
a. When the channels in the SR open, Ca2+ diffuses out of the SR and into the cytosol down its concentration gradient.
3. (8) Calcium binds to the troponin of the thin filaments.
4. (9) The troponin–tropomyosin complex changes shape, exposing active sites on the actin filaments that can bind to myosin heads.
C. Contraction is the step in which the muscle fiber develops tension and may shorten; the mechanism of contraction was proposed in 1954 by Hanson and Huxley as the sliding filament theory. The process can be divided into four steps that follow excitation–contraction coupling. (pp. 414–418) (Fig. 11.10)
1. (10) Myosin ATPase hydrolyzes ATP that is bound to the myosin head; the energy released activates the head by changing its shape into a “cocked” position.
2. (11) With ADP and phosphate still bound, the activated myosin head binds to an exposed active site on the thin filament, forming a cross bridge.
3. (12) Myosin releases the ADP and phosphate and flexes into a bent, low energy shape, tugging the thin filament along with it; this is called the power stroke.
4. (13) Upon binding to another ATP, myosin releases the actin; it is now prepared to repeat the process by hydrolyzing the ATP and recocking (the recovery stroke). It will then attach to a new active site farther down.
a. When one myosin releases an actin, many other heads on the same thick filament are still bound to actin on the thin filament so it does not slide back.
b. Even though the muscle fiber contracts, the myofilaments do not become shorter; instead, the thin filaments slide over the thick ones.
c. The cycle of power and recovery is repeated many times by each myosin head, at a rate of about five strokes per second.
D. When stimulation ceases, a muscle fiber relaxes and returns to it resting length; the process can be divided into five steps that follow the contraction phase. (p. 419) (Fig. 11.11)
1. (14) Nerve signals stop arriving at the NMJ, so the synaptic knob stops releasing ACh.
2. (15) As ACh dissociates from the receptor, AChE breaks it down; the synaptic knob reabsorbs the fragments as usual, but now no new ACh replaces that which is broken down.
3. (16) Active transport pumps in the SR pump Ca2+ from the cytosol back into the cisternae.
a. The Ca2+ in the cisternae binds to a protein called calsequestrin and is stored until stimulation occurs again.
b. Active transport requires ATP; therefore ATP is needed for both muscle contraction and muscle relaxation.
4. (17) As Ca2+ dissociates from troponin, it is pumped into the SR and not replaced.
5. (18) Tropomyosin moves back into position, blocking the active sites of the actin filament and preventing myosin binding.
6. A muscle returns to its resting length with the aid of two forces.
a. Its intracellular and perhaps extracellular elastic components stretch it, like a recoiling rubber band.
b. The contraction of an antagonist muscle lengthens it; for example, contraction of the triceps brachii stretches the biceps brachii.
Insight 11.2 Rigor Mortis
E. The amount of tension a muscle generates depends on how stretched or contracted it was before it was stimulated; this principle is termed the length–tension relationship. (p. 420) (Figure 11.12)
1. If a muscle fiber is overly contracted at rest, then upon stimulation the thick filaments can contract no farther than the Z discs and the contraction is weak.
2. If a muscle fiber is too stretched, then upon stimulation there is little overlap between thick and thin filaments, and the myosin heads cannot get a good grip on the actin and the contraction is weak.
3. Muscle has an optimum resting length at which it can respond with greatest force; the central nervous system continually adjusts the length of resting muscles in a state of partial contraction called muscle tone.
V. Behavior of Whole Muscles (pp. 420–425)
A. A nerve–muscle preparation, such as the gastrocnemius and sciatic nerve from a frog attached to stimulating electrodes, can be used to record a chart of stimulation and muscle contraction called a myogram. (p. 421)
1. A weak (subthreshold) electrical stimulus causes no contraction; as voltage is increased the threshold is reached—the minimum voltage necessary to generate an action potential and cause contraction.
a. The action potential triggers the release of Ca2+ into the cytosol and activates the sliding filament mechanism.
b. At threshold or higher, a stimulus causes a quick cycle of contraction and relaxation called a twitch. (Fig. 11.13)
2. A delay, or latent period, of about 2 milliseconds occurs between the onset of the stimulus and the onset of the twitch.
a. During this time excitation, excitation–contraction coupling, and tensing of elastic components occurs.
b. The force generated is called internal tension, and it does not show up on the myogram because the muscle does not yet shorten.
3. Once elastic components are taut, the muscle begins to produce external tension; this is called the contraction phase of the twitch.
a. The resisting load in a preparation is the sensor of the recording apparatus, so the movement is recorded on the myogram.
b. In the body, the resisting load is usually a bone.
4. The contraction phase is short-lived because the SR reabsorbs Ca2+ before the muscle develops maximum force; as the Ca2+ level falls, muscle tension declines during the relaxation phase.
a. The muscle is quicker to contract than it is to relax.
b. The entire twitch lasts from 7 to 100 msec.
Insight 11.3 Galvani, Volta, and Animal Electricity
B. Although electrical excitation of a muscle fiber obeys an all-or-none law, muscle fibers do not exhibit all-or-none twitches in response to excitation. (pp. 421–423)
1. Twitches vary in strength for a number of reasons:
a. Twitch strength varies with stimulation frequency: stimuli arriving close together produce stronger twitches than those arriving far apart.
b. Twitches vary with the concentration of Ca2+ in the sarcoplasm, which can vary with stimulation frequency.
c. Twitch strength depends on how stretched the muscle was just before stimulation (length–tension relationship).
d. Twitches vary with the temperature of the muscle; warmer muscle contracts more strongly.
e. Twitches are weaker when the pH of the sarcoplasm falls below normal, producing fatigue.
f. Twitches vary with the state of hydration of the muscle, which affect overlap between filaments and ability of myosin to form cross-bridges with actin.
2. Muscles must be able to contract with variable strength for different tasks, so it is not surprising that twitches vary in strength.
3. Stimulus intensity and stimulus frequency have contrasting effects. (Fig. 11.14)
a. At threshold, a weak twitch occurs, and if voltage is increased, twitches are stronger.
i. Higher voltages excite more and more nerve fibers in the motor nerve and thus stimulate more motor units.
ii. This effect is called recruitment or multiple motor unit (MMU) summation.
b. Even at constant voltage, a higher frequency of stimulation produces stronger twitches than does a lower frequency.
c. Up to 10 stimuli per second, a muscle produces an identical twitch for each stimulus and recovers fully between twitches. (Fig. 11.15a)
d. Between 10 and 20 stimuli per second, the muscle recovers fully between twitches, but each twitch develops more tension than the one before it; this pattern is called treppe or the staircase phenomenon. (Fig. 11.15b)
i. One cause of treppe is that the SR does not have time to completely reabsorb all the Ca+2 released.
ii. Another factor is that the heat of each twitch causes muscle enzymes to work more efficiently
e. At higher stimulus frequency (20–40 stimuli per second) each new stimulus arrives before the previous twitch is over; each new twitch “piggybacks” on the previous one and generates higher tension. (Fig. 11.15c)
i. This phenomenon is called temporal summation or wave summation.
ii. It produces a state of sustained fluttering contraction called incomplete tetanus.
f. At still higher frequency (40–50 stimuli per second) the muscle has no time to relax at all and the twitches fuse into a smooth, prolonged contraction called complete tetanus. (Fig. 11.15d)
i. This state should not be confused with the disease tetanus caused by the tetanus toxin.
ii. Complete tetanus rarely if ever occurs in the body.
C. Contraction does not always mean the shortening of a muscle; it may mean only that the muscle is producing internal tension. (pp. 423–425)
1. Physiologists speak of isotonic versus isometric contraction, and concentric versus eccentric contraction.
2. Isometric contraction is contraction without a change in length. (Fig. 11.16a)
a. Isometric contraction of antagonistic muscles at a joint maintains joint stability.
b. Isometric contraction of postural muscles keeps the body erect.
3. Isotonic contraction is contraction with a change in length but no change in tension. (Fig. 11.16b)
a. Isotonic contraction moves a load as the muscle shortens.
4. Isometric and Isotonic contraction are both phases of normal muscular action. (Fig. 11.17)
5. Isotonic contraction has two forms: concentric and eccentric.
a. In concentric contraction, a muscle shortens as it maintains tension, such as when the biceps brachii contracts and flexes the elbow to lift a weight.
b. In eccentric contraction, a muscle lengthens as it maintains tension, such as when the biceps brachii lengthens as a weight is lowered.
VI. Muscle Metabolism (pp. 425–430)
A. All muscle contraction depends on ATP, and the supply of ATP depends on the availability of oxygen and organic energy sources such as glucose and fatty acids. (pp. 425–426)
1. The two main sources of ATP synthesis are anaerobic fermentation and aerobic respiration; during the course of exercise, different mechanisms produce ATP depending on duration. (Fig. 11.18)
a. Anaerobic fermentation allows the cell to produce ATP in the absence of oxygen, but yield is limited and lactic acid, a toxic end product, is a major factor in muscle fatigue.
b. Aerobic respiration produces more ATP and less toxic end products, but requires a continual supply of oxygen.
c. In a resting muscle, most ATP is generated by the aerobic respiration of fatty acids.
2. Immediate energy such as that needed for a 100 m dash relies on oxygen stored in myoglobin.
a. The muscle borrows phosphate groups from other molecules and transfers them to ADP to form ATP; two enzymes systems control these transfers. (Fig. 11.19)
i. Myokinase transfers phosphate from one ADP to another to form ATP.
ii. Creatine kinase obtains phosphate from creatine phosphate (CP) and donates it to ADP to make ATP.
b. ATP and CP, collectively called the phosphagen system, provide nearly all the energy used for short bursts of intense activity, such as sprinting for 6 seconds.
3. As the phosphagen system is exhausted, the muscles shift into anaerobic fermentation for short-term energy until cardiopulmonary function can catch up with the oxygen demand
a. During this period, muscles obtain glucose from the blood and from their own stored glycogen.
b. The pathway from glycogen to lactic acid, called the glycogen–lactic acid system, produces enough ATP for 30 to 40 seconds of maximum activity.
4. After 40 seconds or so, the respiratory and cardiovascular system deliver oxygen to the muscles fast enough for aerobic respiration to meet most of the ATP demand.
a. Aerobic respiration produces much more ATP and is a very efficient means of meeting the ATP demands of prolonged exercise.
b. Oxygen consumption rises for 3 to 4 minutes and then levels off at a steady state in which ATP production keeps pace with demand.
c. Little lactic acid accumulates under steady state, but the depletion of glycogen and blood glucose, together with loss of fluid and electrolytes, set limits to endurance and performance even when lactic acid does not.
B. Muscle fatigue is the progressive weakness and loss of contractility that results from prolonged use of the muscles. (pp. 426–427)
1. Fatigue has multiple causes.
a. ATP synthesis declines as glycogen is consumed.
b. An ATP shortage slows down the sodium–potassium pumps, which affects the resting membrane potential and muscle excitability.
c. Lactic acid lowers the pH of the sarcoplasm, inhibiting enzymes.
d. The accumulation of K+ in the ECF lowers the membrane potential.
e. Motor nerve fibers use up their ACh (junctional fatigue).
f. The CNS fatigues by processes not yet understood, so that less signal output to the muscles occurs.
2. The maximum oxygen uptake (Vo2max) is the point at which the rate of oxygen consumption reaches a plateau and does not increase further; it determines a person’s ability to maintain high-intensity exercise for more than 4 to 5 minutes.
a. Vo2max is proportional to body size, peaks at around age 20, and is usually greater in males than in females.
b. It can be twice as great in a trained endurance athlete as in an untrained person.
i. A typical sedentary adult weighing 160 pounds has a Vo2max of about 35 mL/min/kg.
ii. An elite endurance athlete of the same weight can have a Vo2max of about 70 mL/min/kg.
iii. Lance Armstrong’s Vo2max was measured at 83.8 mL/min/kg.
Insight 11.4 Beating Fatigue—Some Athletic Strategies and Their Hazards
C. Oxygen debt is the difference between the resting rate of oxygen consumption and the elevated rater after exercise; it is also known as excess postexercise oxygen consumption (EPOC). (pp. 427–428)
1. Typically about 11 L of extra oxygen is consumed after strenuous exercise and is used for the following purposes:
a. Replacing the body’s depleted oxygen reserves, such as oxygen in myoglobin and hemoglobin, dissolved in the blood plasma, and in the air in lungs.
b. Replenishing the phosphagen system by synthesizing ATP and transferring phosphates to creatine to restore ATP and CP levels.
c. Oxidizing lactic acid to pyruvic acid in the kidneys, cardiac muscle, and especially the liver, where pyruvic acid is then converted into glucose.
d. Serving the elevated metabolic rate resulting from body heating.
D. Muscle fibers can be classed according to their physiological characteristics. (pp. 428–429) (Table 11.3)
1. Slow oxidative (SO), slow-twitch, red, or type I fibers have relatively abundant mitochondria, myoglobin, and blood capillaries and a deep red color.
a. SO fibers do not fatigue easily and exhibit a relatively long twitch (~100 msec) in response to a single stimulus
b. Examples are the soleus muscle of the calf and the postural muscles.
2. Fast glycolytic (FG), fast-twitch, white, or type II fibers are adapted for quick responses but not for fatigue resistance.
a. They are rich in enzymes of the phosphagen and glycogen–lactic acid systems.
b. Their SR releases and reabsorbs Ca2+ quickly.
c. FG fibers are poorer in mitochondria, myoglobin, and blood capillaries than SO fibers, so they are relatively pale.
e. They produce twitches as short as 7.5 msec.
f. Examples are the gastrocnemius of the calf, brachii of the arm, and muscles of eye movement.
3. Some authorities recognize two subtypes of FG fibers called types IIA and IIB.
a. Type IIB is the common type just described, whereas IIA, or intermediate fibers, combine fast twitch with fatigue resistance.
i. Type IIA is rare except in some endurance-trained athletes.
b. The fiber types can be distinguished histologically with stains for mitochondrial enzymes. (Fig. 11.20)
4. All muscle fibers of a single motor unit are of the same physiological type.
5. Nearly all muscles are composed of both SO and FG fibers, but the proportions differ.
a. Muscles composed mainly of SO fibers are called red muscles and those composed mainly of FG fibers are called white muscles.
b. The proportions differ even in a single muscle in people with different types and levels of physical activity. (Table 11.4)
c. Heredity may play a role in whether a person is a “born sprinter” or “born marathoner.”
d. Sometimes when two or more muscles appear to have the same function, they may have different proportions of SO to FG fibers and so actually allow a wider range of function.
E. Humans have far more muscular strength than is normally used, and muscles can generate more tension than the bones and tendons can withstand. (pp. 429–430)
1. Muscular strength depends on anatomical and physiological factors:
a. Muscle strength is primarily determined by muscle size.
b. Fascicle arrangement contributes to strength; pinnate muscles such as the quadriceps femoris are stronger than parallel muscles such as the sartorius, which in turn are stronger than circular muscles such as the orbicularis oculi.
c. Large motor units produce stronger contractions than small ones.
d. Recruitment, or multiple motor unit (MMU) summation produces a stronger muscle contraction.
e. Temporal summation of action potentials causes stronger contraction.
f. The length–tension relationship contributes in that a muscle resting at optimum length can contract more forcefully.
g. Fatigue contributes in that fatigued muscles contract more weakly.
2. Resistance exercise, such as weight lifting, can stimulate muscle growth even if only done a few minutes at a time a few times a week.
a. Growth results primarily form cellular enlargement, not cell division.
b. Myofibrils grow thicker and split longitudinally when they reach a certain size.
c. Muscle fibers are incapable of mitosis, but some evidence indicates that they may also split longitudinally as they enlarge.
3. Endurance (aerobic) exercise, such as jogging and swimming, improves the fatigue resistance of the muscles.
a. Slow-twitch fibers produce more mitochondria and glycogen and acquire a greater density of blood capillaries with endurance exercise.
b. This form of exercise also improves skeletal strength, increases red blood cell count and oxygen transport capacity, and enhances cardiovascular, respiratory, and nervous system function.
4. Cross-training incorporates elements of both resistance training and endurance training for optimal performance.
VII. Cardiac and Smooth Muscle (pp. 430–434)
A. Any of the three types of muscle cells can be called myocytes, a term preferable to muscle fibers for smooth and cardiac muscle cells because they are relatively short and have only one nucleus. (p. 430)
B. Cardiac and smooth muscle are termed involuntary muscles because they are usually not subject to conscious control. (p. 430)
C. Cardiac muscle cells are also called cardiocytes; cardiac muscle is limited to the heart, where its function is to pump blood. (p. 430)
1. To fulfill its function, cardiac muscle must have five properties: (Table 11.5)
a. It must contract with a regular rhythm.
b. The cells of a given heart chamber must contract in unison.
c. Each contraction must last long enough to expel blood from the chamber.
d. The muscle must function in sleep and wakefulness.
e. It must be highly resistant to fatigue.
2. Cardiac muscle is striated like skeletal muscle but has shorter and thicker cells with uneven, notched ends. (Fig. 19.11)
3. Each myocyte is joined to several others at its ends through linkages called intercalated discs.
a. These discs appear as thick dark lines in stained tissue sections.
b. An intercalated disc has electrical gap junctions that allow each myocyte to stimulate neighbors and mechanical junctions to hold the myocytes together.
4. The sarcoplasmic reticulum of cardiocytes is less developed than in skeletal muscle but has larger T tubules.
5. Damaged cardiac muscle is repaired by fibrosis; although mitosis has been detected in cardiac myocytes following heart attacks, it does not produce significant regenerated muscle.
6. Cardiac muscle contains a built-in pacemaker that rhythmically sets off a wave of electrical excitation.
a. Cardiac muscle is said to be autorhythmic because of this ability.
b. The heart does receive fibers from the autonomic nervous system that can increase or decrease heart rate and contraction strength.
c. Cardiac muscle does not exhibit quick twitches but maintains tension for 200–250 msec.
7. Cardiac muscle uses aerobic respiration almost exclusively.
a. It is rich in myoglobin and glycogen and has large mitochondria that fill 25% of the cell.
b. It is adaptable with respect to fuel, but vulnerable to lack of oxygen.
c. Because little anaerobic fermentation takes place, cardiac muscle is highly resistant to fatigue.
D. Smooth muscle is composed of myocytes with a fusiform shape, about 30–200 μm long, 5–10 μm wide at the middle, and tapering to a point at each end; there is only one nucleus. (pp. 431–434)
1. Thick and thin filaments are both present, but they are not aligned and produce no visible striations.
2. Z discs are absent and in their place are protein plaques on the inner plasma membrane and protein masses called dense bodies in arrays in the cytoplasm.
3. Their cytoplasm contains an extensive cytoskeleton of intermediate fibers, which are also attached to the plasma membrane. (Fig. 11.24)
4. The sarcoplasmic reticulum is scanty, and there are no T tubules.
a. Ca2+ for contraction comes mainly from the ECF by way of channels in the sarcolemma.
b. During relaxation, Ca2+ is pumped back out of the cell.
5. Some smooth muscle has not nerve supply, but when nerve fibers are present, they are autonomic, not somatic.
6. Smooth muscle is capable of mitosis and hyperplasia.
7. There are two functional types of smooth muscle: multiunit and single-unit. (Fig. 11.21)
a. Multiunit smooth muscle occurs in some large arteries and pulmonary air passages, in piloerector muscles, and in the iris.
i. Its autonomic nerve innervation is similar to the motor nerve innervation of skeletal muscle, with motor units that contract independently.
b. Single-unit smooth muscle is more widespread, occurring in most blood vessels and in the digestive, respiratory, urinary, and reproductive tracts.
i. It is also called visceral muscle.
ii. In hollow organs, it forms two or more layers, and inner circular layer and an outer longitudinal layer. (Fig. 11.22)
iii. Its name refers to the fact that myocytes are electrically coupled to each other by gap junctions, so that cells directly stimulate each other and can contract as a unit.
8. Smooth muscle contraction is involuntary and does not require nerve stimulation.
a. Some smooth muscle contracts in response to chemical stimuli and in response to stretch.
b. Some single-unit smooth muscle, especially in the stomach and intestines, has pacemaker cells that set off waves of contraction; thus it is autorhythmic.
c. Most smooth muscle is innervated by autonomic nerve fibers that can trigger or modify its contraction.
i. These nerve fibers stimulate smooth muscle with either acetylcholine or norepinephrine.
ii. The nerves have contrasting effects in different locations, such as relaxing smooth muscle in the arteries while contracting smooth muscle in the bronchioles.
d. In single-unit smooth muscle, each autonomic nerve fiber has up to 20,000 beadlike swellings called varicosities along its length consisting of synaptic vesicles and a few mitochondria. (Figs. 11.21, 11.23)
e. Instead of approaching any one myocyte, the nerve fiber passes among several myocytes and stimulates all of them when it releases neurotransmitter.
i. The muscle cells do not have motor end plates, but instead have receptor sites on their surface.
f. These nerve–muscle relationships are called diffuse junctions because there is no one-to-one relationship between nerve fiber and myocyte.
9. Contraction in smooth muscle is triggered by Ca2+, energized by ATP, and involves sliding of thin filaments over thick filaments, but the mechanism of excitation–contraction coupling is very different.
a. Most Ca2+ comes from the extracellular fluid, not from the sarcoplasmic reticulum.
b. Calcium channels in the sarcolemma admit the Ca2+, but they are of different types, including voltage regulated, ligand-regulated, and mechanically regulated (respond to stretch).
c. Smooth muscle has no troponin; instead, calcium binds to a protein called calmodulin, associated with thick filaments.
i. Calmodulin activates the enzyme myosin light-chain kinase, which adds a phosphate to a protein on the myosin head.
ii. This phosphate addition activates myosin ATPase, so that myosin can bind to actin and hydrolyze ATP.
d. Thick filaments pull on thin filaments, which in turn pull on the dense bodies and membrane plaques, transferring force to the plasma membrane and shortening the entire cell.
e. When a smooth muscle cell contracts, it puckers and twists somewhat like wringing out a wet towel. (Fig. 11.24)
f. Compared to skeletal muscle, smooth muscle is very slow to contract and relax.
i. The latent period between stimulation and contraction in smooth muscle is 50–100 msec, compared with 2 msec in skeletal muscle.
ii. Tension in smooth muscle peaks about 0.5 sec after stimulus and then declines over a period of 1 to 2 sec.
iii. Smooth muscle’s myosin ATPase is a slow enzyme, and the pumps that remove Ca2+ from the cell are also slow.
g. As Ca2+ falls, myosin’s ability to hydrolyze ATP drops, but it does not detach from actin immediately; its latch bridge mechanism enables it to remain attached to actin for a prolonged time without consuming ATP.
h. Smooth muscle often exhibits tetanus and is highly resistant to fatigue.
i. It makes ATP aerobically, but its ATP requirement is small.
ii. It requires 10 to 300 times less ATP as does skeletal muscle to maintain the same amount of tension.
i. Smooth muscle’s fatigue resistance and latch-bridge mechanism allow maintenance of smooth muscle tone (tonic contraction) that keeps arteries in a state of partial constriction called vasomotor tone.
i. A loss of vasomotor tone can cause a dangerous drop in blood pressure.
j. Smooth muscle tone also keep the intestines partially contracted.
10. Stretch alone sometimes causes smooth muscle to contract.
a. Distension of the esophagus with food or the colon with feces causes a wave of contraction called peristalsis.
b. Smooth muscle exhibits a reaction called the stress-relaxation response or receptive relaxation response. When stretched, it briefly contracts and resists, but then relaxes.
i. This response allows hollow organs such as the urinary bladder to fill, without the smooth muscle in the walls expelling the contents immediately.
ii. Smooth muscle is also not subject to the limitations of the length–tension relationships as is skeletal muscle, so that even when stretched, smooth muscle can contract forcefully, such as when emptying a full urinary bladder.
c. Three features contribute to smooth muscle’s ability to stretch extensively and then contract powerfully:
i. It has no Z discs, so thick filaments do not butt up against them and stop contracting.
ii. The thick and thin filaments are not arranged in orderly sarcomeres, so having too little overlap for cross-bridging does not occur.
iii. The thick filaments have myosin heads along their entire length, with no bare zone, so cross bridges can form anywhere.
d. Smooth muscle also exhibits plasticity—the ability to adjust its tension to the degree of stretch; an organ such as the bladder can be greatly stretched yet not become flabby when empty.
E. The muscular system suffers few diseases but does have some common dysfunctions. (Table 11.6)
Insight 11.5 Muscular Dystrophy and Myasthenia Gravis(Fig. 11.25)
Additional information on topics mentioned in Chapter 11 can be found in the chapters listed below.
Chapter 2: Anaerobic and aerobic ATP synthesis
Chapter 3: The sodium–potassium pump
Chapter 5: The three types of muscular tissue
Chapter 10: Composition of a skeletal muscle
Chapter 12: Neurotransmitters
Chapter 12: Electrophysiology
Chapter 12: Action potentials
Chapter 12: All-or-none law
Chapter 19: Cardiac muscle
Chapter 29: Effects of aging on the muscular system
Back to AP I Lecture Notes, Power Points and Study Review Page