Chapter 8 - Skeletal Muscle Function

Muscle flexors

Decrease joint angle

Muscle extensors

Increase joint angle

Functions of skeletal muscle

• Force production of locomotion and breathing

• Force production for postural support

• Heat production during cold stress

• Endocrine organ

Epimysium (most outside layer)

Surrounds entire muscle

Perimysium

Surrounds bundles of muscle fibers

• Fascicles

Endomysium

Surrounds individual muscle fibers

Sarcolemma

Muscle cell membrane

Contractile Proteins

Actin & myosin

Satellite Cells

• Increase number of nuclei in mature muscle fibers during exercise

• More nuclei allow for greater protein synthesis

Myonuclear Domain

• Volume of cytoplasm surrounding each nucleus

Myofibrils

Contain Actin and Myosin

Actin

• Thin filament

• Contains troponin and tropomyosin

Myosin

Thick filament

Sarcormere

Subdivision of myofibril

Z line

Divides each sarcomere

M line

Fine line in the middle of the H zone

H zone

Myosin filament with no overlap of actin is located in the center of a sarcomere

A band

Dark portions of the sarcomere where the myosin filaments are located

I band

Light regions of the sarcomere where actin is located primarily

Sarcoplasmic Reticulum

Membranous channels that surround each myofibril

• Storage site for calcium

• Terminal cisternae

Transverse tubules

Extend from sarcolemma to the sarcoplasmic reticulum

• Lies between terminal cisternae

Neuromuscular junction

Junction between motor neuron and muscle fiber

Motor end plate

Pocket formed around motor neuron by sarcolemma

Neuromuscular cleft

Short gap between neuron and muscle fiber

Hormone that depolarizes muscle fiber and causes end-plate potential

Acetylcholine

Endurance and resistance training stimulate enhanced adaptations of NMJ including:

1. Increased size of NMJ

2. Expanding number of synaptic vesicles which contain acetylcholine

3. Increased number of acetylcholine receptors on the postsynaptic membrane

Power stroke

Formation of cross-bridges between actin and myosin filaments

Sliding filament model of muscle contraction

Describes how muscular contraction works

• muscle shortening occurs due to the movement of actin filament over the myosin filament

Cross bridge formation

• Calcium binds to troponin which causes tropomyosin to be removed from active binding site

• Myosin head binds to the actin filament at the binding site

ATPase

Located on the head of the myosin cross-bridge which breaksdown ATP as fiber contracts

Excitation-contraction coupling

Depolarization of the motor end plate is coupled to muscular contraction

• action potentials travels down transverse tubules and cause release of Ca++ from SR

• Ca++ binds to troponin, exposes active site on actin

• Cross-bridge formation between actin and myosin

Excitation

1. Nerve signal arrives at the synaptic knob

2. Acetylcholine is released into the synaptic cleft and binds to receptors on the motor end plate, allowing sodium to enter the cell

3. Sodium influx causes depolarization that is conducted down tubules

Contraction

1. Depolarization of T-tubules causes release of ca++ from SR

2. CA++ binds to troponin, shifting typomyosin to uncover myosin binding sites

3. Myosin binds to actin to form cross bridge

4. Phosphate released from myosin cross-bridge movement (power stroke) and ADP is released

5. New ATP attaches to myosin, breaking cross-bridge, ATP breaks down to ADP+Pi and energizes myosin

Relaxation

1. Motor neurons stimulate ends, acetylcholine no longer released; the muscle fiber repolarizes

2. Ca++ is pumped back into SR and tropomyosin returns to its original position, covering myosin binding site on actin, muscle relaxation occurs

Muscle fatigue

• Decline in muscle power output

• D/t decrease in muscle force production at cross-bridge level

• Decrease in muscle shortening ability

• CNS and PNS fatigue

CNS fatigue

• Decrease in excitatory neurotransmitters in the motor cortex

• Reduces motor neuron activation to skeletal muscle

Mechansims responsible for muscular fatigue

• Decreased Ca++ release from SR

• Accumulation of metabolites the inhibit myofilament sensitivity to Ca++

• Pi, H+, lactate, free radicals

• Prevent cross bridge formation

Mechanisms responsible for muscle fatigue in prolonged duration

• Radical accumulation in muscle fibers that reduce number of cross-bridges bound to actin

• Depletion of muscle glycogen reduces TCA intermediates

Muscle Proprioceptors

• Relative to muscle length

• Tension development by muscle

• Muscle spindle

• Golgi tendon organ

Muscle Spindles

Respond to change in muscle length that requires the finest degree of control

Intrafusal fibers

Run parallel to normal muscle fibers and insert into connective tissue within the muscle

Gamma motor neurons

Stimulate interfusal fibers to contract simultaneously with extrafusal fibers

Sensory nerve endings

Provides the central nervous system with continuous information concerning static muscle length

Stretch reflex or myotactic reflex

• Rapid stretch on muscle causes reflex contraction

• Knee-jerk reflex at the doctor when tapped on patellar tendon

Golgi Tendon Organ (GTO)

• Safety devices that prevent muscle damage during excessive force generation

• GTO stimulation results in reflex relaxation of muscle

• Send information to spinal cord and prevent motor neurons from firing causing muscle relaxation

• Relieves tension applied to muscle

Causes of muscle cramping

• Dehydration and electrolyte loss

• Electrolyte imbalance within interstitial space

• Discharge of acetylcholine at motor end plate

Altered neuromuscular control theory for muscular cramps

• Exercise-induced fatigue

• Increased muscle spindle activity

• Inhibition of golgi tendon organ function

• Increased stimulation of motor neuron innervating cramping muscle

• Decreased inhibitory drive to motor neurons innervating cramping muscle

Transient Receptor Potential Channels in the throat

The theory that activation of these ions can inhibit over-active motor neurons to prevent cramping

Type 1 Fibers

• Slow-twitch fibers

• Slow oxidative fibers

• light

• High amount of mitochondria

• Predominantly aerobic

• High efficiency

• High fatigue resistance

Type IIa fibers

Intermediate fibers

Fast oxidative glycolytic fibers

medium dark

High ATPase

Moderate efficiency

High/moderate mitochondria

Type IIx fibers

Fast-twitch fibers

Fast glycolyic fibers

dark

Low number of mitochondria

Anaerobic

High Vmax

Low efficiency

High ATPase

More crossbridges

Oxidative capacity

Number of capillaries, mitochondria, and amount of myoglobin

Fatigue resistant

Type of myosin ATPase

Speed of ATP degradation (high ATPase activity = high ATP breakdown capability)

Result in a high speed of muscle shortening

Abundance of contractile proteins within the fiber

Able to generate more force

Vmax

Speed of contraction is determined by rate of cross bridge cycling

Myosin ATPase activity

Maximal force production

Force per unit of cross sectional area

Maximal power output

Determined by force generation and shortening velocity

Muscle fiber efficiency

Measure of muscle fiber economy, lower amount of ATP used to generate force

Isometric (static exercise)

• Muscle exerts force without changing length

• Pulling against an immovable object

• Postural muscles during periods of sitting or standing

Dynamic muscle action

• Concentric, muscle shortens during force production

• Eccentric, muscle produces force but length increases

  • Associated with muscle fiber injury and delayed onset muscle soreness

Muscle twitch

After stimulation - short latent period exists- corresponding to depolarization of muscle fiber

• Tension develops due to cross bridge cycling

Diabetes and muscle

• Cachexia

• progressive loss of muscle mass

• aerobic and resistance training are protective

Myokines

Small signaling molecules released by skeletal muscle

Act as hormone or hormone messengers that affect a variety of other tissues

Production of myokines

• Stimulate glucose uptake and FFA oxidation

• Promote blood vessel growth

• Promote liver glucose production and TG breakdown

IL-6

• Pro-inflammatory and anti-inflammatory

• During exercise, produces anti-inflammatory effects

• Acute cytokines don’t increase with exercise

• inhibits pro-inflammatory cytokines

Proprioceptors

• Receptors that provide the CNS with information about body position

• Located in joints and muscles

Kinesthesia

• Relates to conscious recognition of the position of body parts with respect to one another

• Relates to limb movement rates

Free nerve ending joint proprioceptor

• Sensitive to touch and pressure

• Initially strongly stimulated at the beginning of the movement then adapt to become less sensitive to stimuli and movement ceases

Golgi type receptors - joint proprioceptor

• Found in ligaments around joints

• Similar to free nerve endings

Pacinian corpuscles joint proprioceptor

In tissue around joints

Detect rate of joint rotation