CH. 9-B

Wave (temporal) summation: 2 stimuli are received by a muscle in rapid succession. Muscle fibers don't have time to completely relax b/t stimuli, so twitches increase in force w/ each stimulus. Additional Ca2+ that is released with second stimulus stimulates more

shortening

If stimuli frequency increases, muscle tension reaches near maximum. Produces smooth, continuous contractions that add up (summation). Further increase in stimulus frequency causes muscle to progress to sustained, quivering contraction referred to as this.

If stimuli frequency further increase, muscle tension reaches maximum. Referred to as this because contractions “fuse” into one smooth sustained contraction plateau

-Prolonged muscle contractions lead to muscle fatigue

Types of stimulus: Subthreshold stimulus: stimulus not strong enough, so no contractions seen. Threshold stimulus: stimulus is strong enough to cause first observable contraction. Maximal stimulus: strongest stimulus that increases maximum contractile force (All motor units have been recruited)

Motor units with smallest muscle fibers are recruited first. Motor units with larger and

larger fibers are recruited as stimulus intensity increases. Largest motor units are

activated only for most powerful contractions

Concentric contractions: muscle shortens and does work (Example: biceps contract to pick up a book). Eccentric contractions: muscle lengthens and generates force (Example: laying a book down causes biceps to lengthen while generating a force)

Load is greater than the maximum tension muscle can generate, so muscle neither shortens nor lengthens

In isotonic contractions, actin filaments shorten and cause movement. In isometric contractions, cross bridges generate force, but actin filaments do not shorten (Myosin heads “spin their wheels” on same actin- binding site)

Move and detach cross bridges. Pump calcium back into SR. Pump Na+ out of and K+ back into cell after excitation-contraction coupling

-Available stores of ATP depleted in 4–6 seconds

-ATP is the only source of energy for contractile activities;

therefore, it must be regenerated quickly

Direct phosphorylation of ADP by creatine phosphate (CP). Anaerobic pathway: glycolysis and lactic acid formation. Aerobic pathway

CP is a unique molecule located in muscle fibers that donates a phosphate to ADP to instantly form ATP. Creatine kinase is enzyme that carries out transfer of phosphate. Muscle fibers have enough ATP and CP reserves to power cell for about 15 seconds

Creatine phosphate + ADP → creatine + ATP

Glycolysis: first step in glucose breakdown. Does not require oxygen. Glucose is broken into 2 pyruvic acid molecules. 2 ATPs are generated for each glucose broken down

-Low oxygen levels prevent pyruvic acid from entering aerobic respiration

phase

Normally, pyruvic acid enters mitochondria to start aerobic respiration phase; but, at high intensity activity, oxygen not available (Bulging muscles compress blood vessels, impairing oxygen delivery)

-If no oxygen, referred to as anaerobic glycolysis, pyruvic acid is converted to lactic acid

Lactic acid: Diffuses into bloodstream. Used as fuel by liver, kidneys, and heart. Converted back into pyruvic acid or glucose by liver

-Anaerobic respiration yields only 5% as much ATP as aerobic respiration, but produces ATP 2½ times faster

(Breaks glucose into CO2, H2O, and large amount ATP (32 can be produced))

Fuels used include glucose from glycogen stored in muscle fiber, then bloodborne glucose, and free fatty acids (Fatty acids are main fuel after 30 minutes of exercise)

Aerobic endurance: Length of time muscle contracts using aerobic pathways (Light-to-moderate activity, which can continue for hours)

Anaerobic threshold: Point at which muscle metabolism converts to anaerobic pathway

Possible causes include: Ionic imbalances can cause fatigue (Levels of K+, Na+ and Ca2+ can change disrupting membrane potential of muscle cell)

-Increased inorganic phosphage (Pi) from CP and ATP breakdown may interfere with calcium release from SR or hamper power

Decreased ATP and increased magnesium (As ATP levels drop, magnesium levels increase and this can interfere with voltage sensitive T tubule proteins)

0Decreased glycogen

-Lack of ATP is rarely a reason for fatigue, except in severely stressed muscles

For a muscle to return to its pre-exercise state: Oxygen reserves are replenished, Lactic acid is reconverted to pyruvic acid, Glycogen stores are replaced, ATP and creatine phosphate reserves are resynthesized

->Formerly referred to as “oxygen debt”

3. Frequency of stimulation: the higher the frequency, the greater the force (Stimuli are added together).

4. Degree of muscle stretch: muscle fibers with sarcomeres that are 80–120% their normal resting length generate more force

-sarcomere is less than 80% resting length, filaments overlap too much, and force decreases

-if sarcomere is greater than 120% of resting length, filaments do not

overlap enough so force decreases

-Muscle fiber type

-Load

-Recruitment

1. Speed of contraction – slow or fast fibers according to: Speed at which myosin ATPases split ATP. Pattern of electrical activity of motor neurons

2. Metabolic pathways used for ATP synthesis: Oxidative fibers: use aerobic pathways. Glycolytic fibers: use anaerobic glycolysis

Most muscles contain mixture of fiber types, resulting in a range of contractile speed and fatigue resistance

-All fibers in one motor unit are the same type

-Genetics dictate individual’s percentage of each

Slow oxidative fibers: low-intensity, endurance activities (Ex: maintaining posture)

Fast oxidative fibers: medium-intensity activities (Ex: sprinting or walking)

Fast glycolytic fibers: short-term intense or powerful movements (Ex: hitting a baseball)

Load: muscles contract fastest when no load is added (The greater the load, the shorter the duration of contraction. The greater the load, the slower the contraction)

Recruitment: the more motor units contracting, the faster and more prolonged the contraction

Leads to increased: Muscle capillaries, Number of mitochondria, Myoglobin synthesis

-Results in greater endurance, strength, and resistance to fatigue

-May convert fast glycolytic fibers into fast oxidative fibers

(typically anaerobic), such as weight lifting or isometric exercises, leads to: Muscle hypertrophy (Due primarily to increase in fiber size)

-Increased mitochondria, myofilaments, glycogen stores, and connective tissue

-Increased muscle strength and size

Constant, slightly contracted state of all muscles

-Due to spinal reflexes (Groups of motor units are alternately activated in response to input from stretch receptors in muscles)

-Keeps muscles firm, healthy, and ready to respond

Disuse atrophy (degeneration and loss of mass) (Due to immobilization or loss of neural stimulation. Can begin almost immediately)

-Paralyzed muscles may atrophy to 1/4 of their initial size

-Fibrous connective tissue replaces lost muscle tissue

-Rehabilitation is impossible at this point

Found in walls of most hollow organs: Respiratory, digestive, urinary, reproductive, circulatory (except in smallest of blood vessels). Not found in heart – heart contains cardiac muscle, not smooth

-Most smooth muscle organized into sheets of tightly

packed fibers

Circular layer: fibers run around circumference of organ (Contraction causes lumen of organ to constrict)

-Alternating contractions and relaxations of layers mix and squeeze substances through lumen of hollow organs

Contain varicosities (bulbous swellings) of nerve fibers instead of neuromuscular junctions

(Varicosities store and release neurotransmitters into a widesynaptic cleft referred to as a diffuse junction. Innervated by the autonomic nervous system)

->Gap junctions are specialized cell connections that allow depolarization to spread from cell to cell

-There are no striations and no sarcomeres, but they do

contain overlapping thick and thin filaments

4. Intermediate filament–dense body network: Dense bodies: proteins that anchor filaments to sarcolemma at regular intervals. During contraction, areas of sarcolemma b/t dense bodies bulge outward (Make muscle cell look puffy. Looks like a lattice network)

Cells electrically coupled by gap junctions (AP transmitted from fiber to fiber)

• Some cells are self-excitatory (depolarize w/o external stimuli). Act as pacemakers for sheets of muscle. Rate and intensity of contraction may be modified by neural and

chemical stimuli

Contraction in smooth muscle is similar to skeletal muscle contraction in following ways:

• Actin & myosin interact by sliding filament mechanism

• Final trigger is increased intracellular Ca2+ level

• ATP energizes sliding process

• Contraction stops when Ca2+ is no longer available

Ca2+ binds to and activates calmodulin

• Activated calmodulin activates myosin (light chain)

kinase ->

Phosphorylates and activates myosin

Cross bridges interact with actin

• When intracellular Ca2+ levels drop ->myosin is

dephosphorylated ->relaxation

- Contraction in smooth muscle is thick filament (myosin) regulated

- Contraction in striated muscle is thin filament (actin) regulated

->Slower ATPases

->Myofilaments may latch together to save energy

Most smooth muscle maintain moderate degree of contraction constantly without fatiguing (Referred to as smooth muscle tone)

-Makes ATP via aerobic respiration pathways

Hormones and local chemicals

Some smooth muscle cells have no nerve supply. Depolarize spontaneously or in response to chemical stimuli. Chemical factors can include hormones, high CO2, pH, low oxygen

-Some smooth muscles respond to both neural and chemical stimuli

Length and tension changes: Can contract when b/t half and twice its resting length. Allows organ to have huge volume changes without becoming flabby when relaxed

Smooth muscle varies in different organs by:

1. Fiber arrangement and organization

2. Innervation

3. Responsiveness to various stimuli

-All smooth muscle is categorized as either: Unitary or Multiunit

Found in all hollow organs (not heart)

Has all common characteristics of smooth muscle:

• Arranged in opposing (longitudinal and circular) sheets

• Innervated by varicosities

• Often exhibit spontaneous action potentials

• Electrically coupled by gap junctions

• Respond to various chemical stimuli

Located in large airways in lungs, large arteries, arrector pili muscles, and iris of eye

-Very few gap junctions

-Different from skeletal muscle because, like unitary smooth muscle, it is

controlled by autonomic nervous system and hormones

Development:

Myoblasts: Immature muscle precursor cells that multiply. Myoblasts fuse together to create long, multinucleated cylindrical structures known as myotubes, which mature into skeletal muscle fibers. Cardiac and smooth muscle myoblasts do not fuse; instead, they link via gap junctions

-Group of inherited muscle- destroying diseases; generally appear in childhood

-Muscles enlarge due to fat and connective tissue deposits

-Muscle fibers atrophy and degenerate. Dystrophin (Links thin filaments to proteins of sarcolemma)

-Myoblast transfer therapy disappointing

-Coaxing dystrophic muscles to produce more utrophin

(protein similar to dystrophin) successful in mice. Dystrophin (Links thin filaments to proteins of sarcolemma)

-Viral gene therapy and infusion of stem cells with correct dystrophin genes show promise

Fragile sarcolemma tears-> Ca2+ entry ->damaged contractile fibers -> inflammatory cell

->muscle mass drops

Victims become clumsy and fall frequently; usually die of respiratory failure in 20s. (Dystrophin: Links thin filaments to proteins of sarcolemma)