Physiology Lab - Skeletal Muscle

Smooth muscle

- no striation
- uninucleated
- nucleus centrally located

skeletal muscle

- striated
- multinucleated
- nucleus peripherally located

cardiac muscle

- striated
- uninucleated or binucleated
- nucleus centrally located

epimysium

surround the muscle group

perimysium

surrounds fasicle

endomysium

surrounds muscle fiber/cell

sarcomere

functional unit of muscle

striation

comes from arrangement of myofilaments within myofiber

myofilament

actin and myosin

myofiber

muscle cell

I-band

actin only; light region of sarcomere

A-band

myosin plus overlapping actin; dark region of sarcomere

H-band

myosin only; center of A-band

M-line

center of A band

thick filaments

myosin

thin filaments

actin

z-line

how sarcomeres are divided from each other, found in center of I band

sarcolemma

muscle plasma membrane

T tubules

extension of sarcolemma into muscle fiber; carry action potential to interior myofibrils

Sarcoplasmic reticulum

stores calcium ions

excitation-contraction coupling

pairs depolarization of neuron with depolarization of a muscle cell

steps of excitation-contraction coupling

- Ach is released into neuromuscular junction and binds to receptor site on sarcolemma
- action potential travels down T tubules causing Ca2+ channels to open
- intracellular Ca2+ concentration increases
- Ca2+ binds to troponin on thin filaments
- Tropomyosin moves away to allow myosin to attach to actin
- cross-bridge cycling begins and force is generated
- Ca2+ is reaccumulated by SR and muscle relaxes

Ca2+ is low

tropomyosin blocks myosin binding site on actin; no contraction

Ca2+ is present

Ca2+ binds to troponin complex which changes tropomyosin to allow myosin to bind to actin; contraction can occur

sliding filament theory

- ATP binds to myosin and causes myosin head to detach
- ATP hydrolyzed into ADP and P; myosin is in resting cocked position
- myosin binds to actin monomer forming crossbridge
- P is released; filaments slide past each other (powerstroke)
- ADP is released

motor unit

single motor neuron and the muscle fibers it innervates

small motor units

fine motor activities

large motor units

gross motor activities

recruitment

start using small motor units and add more as needed

isometric action

muscle contract and length remains; force generated is insufficient to overcome load

isotonic action

contraction tension remains constant and muscle changes length and moves the load

concentric action

muscle contracts and shortens

eccentric action

muscle contracts and lengthens

agonist

primary mover

synergist

muscle that assist agonist group

antagonist

muscles that oppose the agonist

Slow Twitch - Type I

- mostly aerobic respiration, not large amount of force, fatigue resistant, efficient, lots of mitochondria
- endurance athlete

Fast Twitch - Type IIX

- anaerobic glycolysis or direct phosphorylation of ADP
- less resistant to fatigue, high power output, rich in glycolytic enzymes, small number of mitochondria
- 100m sprint

Fast Twitch - Type IIA

- intermediate fibers, mix of Type I and Type IIX
- 800m sprint

hypertrophy

increase in muscle fiber diameter due to increase in myofibril size; muscle can exert more force due to proportionality of cross-sectional area and force

Muscle soreness

- from microscopic injury to muscle fibers
- 24-48 hrs after injury
- not from lactic acid accumulation

Rigor mortis

postmortem muscle stiffness due to rigor cross-bridges in absence of ATP

Sarcopenia

age related decline in muscle mass beginning around age 25 and occurs across lifespan

slow phase sarcopenia

10% muscle mass loss from age 25-50

rapid phase sarcopenia

additional 40% muscle mass loss from age 50-80

Muscular dystrophy

- group of hereditary muscle diseases that weaken skeletal muscle
- no cure and respiratory failure usually occurs early in life
- lack dystrophin protein

dystrophin protein

helps maintain structural integrity of sarcolemma