Muscle Physiology Flashcards
Transverse (T-) Tubules
Invaginations of the sarcolemma
Transmit action potential into interior muscle cell
Closely apposed to sarcoplasmic reticulum (SR)
Sarcoplasmic Reticulum (SR)
Membranous sac underlying the sarcolemma
Responsible for calcium storage, release and reuptake
Integral to muscle contraction
Terminal Cisternae
Bulbous enlargements of the SR
Store and release calcium
“Triade”
SR, T Tubules, Terminal Cisternae
Sarcolemma
Muscle cell membrane
Contains sarcoplasm, cellular proteins, organelles and myofibrils
Myofibrils
Divided into individual contractile units – sarcomeres Thick filaments (myosin) Thin filaments (actin) Troponin and tropomyosin are located on actin protein
Titin / Connectin
Serves as a spring to link Z-disk and M-line
Maintains actin/myosin position
Molecular blueprint
Nebulin
Molecular ruler
Incorporated into and co-extensive with actin
Extends from Z-disk to end of actin myofilament
Precisely regulates actin length (caps actin, determines length)
Obscurin
Intimately surrounds sarcomere, primarily at Z-disk and M-band regions
Coordinates assembly and organization of SR with myofilaments
Myosin
2 heavy chain polypeptides (MHC) Light meromyosin (LMM): intertwine in double helix formation to form molecular backbone Heavy meromyosin (HMM): project outward to form neck (S2) and globular head (S1) MHC isoforms (I, IIa, IIx, and IIb) are determined by ATPase activity and contribute to contraction velocity
Neck region - Myosin
4 light chain polypeptides (MLC)
Each S1/S2 complex contains 1 essential (ELC) and 1 regulatory (RLC) light chain
MLC isoforms fine tune contraction velocity
Actin
Comprises majority of thin myofilament
Arranged in double helix formation
Contains myosin binding sites
Tropomyosin
Resides in groove along length of actin protein
Blocks myosin binding site under resting conditions
Troponin
Spaced at regular intervals along length of actin protein
3 distinct subunits (TI, TC, and TT)
Regulates position of tropomyosin relative to myosin binding site (Steric Block Model)
Sequence of Events:
1 Action potential is propagated along the sarcolemma and into the T-tubules
2 This stimulates the release of calcium (Ca+) from the SR
3 Ca+ binds to Troponin C, resulting in a conformation change that pulls tropomyosin away from myosin binding site on actin filament
4 Hydrolysis of ATP “cocks” myosin head
5 “Cocked” myosin head binds to actin and contraction occurs
6 Hydrolysis of ATP detaches myosin head from actin
7 This sequence continues as long as Ca+ is available
Ca+ is released as long as action potentials are present
Ca+ is resorbed and recycled by the SR
8 In the absence of action potentials, the SR resorbs Ca+ from the sarcoplasm
9 In the absence of Ca+ troponin and tropomyosin return to their resting states, blocking the myosin/actin binding site
Histochemical analysis of metabolic characteristics:
Type I: Slow oxidative
Type IIa: Fast oxidative-glycolytic
Type IIb/x: Fast glycolytic
Muscle Fiber Type - Changes?
Myosin isoforms are genetically determined
In general, exercise training does not override a myocyte’s intrinsic, genetically determined qualities (e.g. type I ↔ II)
However, exercise may alter histochemical characteristics, resulting in intermediate changes (e.g. type IIa ↔ IIb)
Myoplasticity
Changes in use and environment can generate alterations in structural and enzymatic protein content
Predominantly due to changes in gene expression
Some post-translational alterations contribute
Gene expression can be influenced by:
Contractile activity (e.g. endurance exercise, e-stim, denervation)
Loading conditions (e.g. resistance training, microgravity)
Substrate availability (e.g. nutrition)
Hormones (e.g. insulin, IGF, thyroid, etc)
Environment (e.g. hypoxia, trauma)
Myoplastic adaptation can occur at the level of:
Structure (e.g. cross-sectional area)
Type (e.g. MHC isomer)
Metabolism (e.g. mitochondrial density, oxidative capacity)
Energy storage (e.g. intracellular lipid content)
Capillary density, capillary : fiber ratio
Function (force production, contraction velocity, fatigue resistance
Adaptations to Endurance Training
Increased oxidative capacity
Increased mitochondrial density
Increased expression of type I fibers
Reduced expression of type IIb fibers (in days)
Reduced expression of type IIa fibers (in years)
Little change in CSA or glycolytic capacity
These adaptations result in:
Delayed onset of metabolic acidosis
Increased fatigue resistance
Increased oxygen consumption
Adaptations to Resistance Training:
Increased CSA (in all fiber types)
Increased number of nuclei / cell
Reduced mitochondrial density (due to hypertrophy)
Reduced expression of type I fibers
Reduced expression of type IIb fibers
Increased expression of type IIa fibers
Little change in capillarity or enzymatic capacity (oxidative or glycolytic)
These adaptations result in:
Increased contractility
Improved elasticity
Improved neuromotor recruitment
Duchenne’s and Physical Therapy
Have pt perform resistance exercises that strengthen and tone Mm
Stronger muscles can help to delay the impending weakness
Range of motion exercises and stretching
Flexibility can help ease the severity of joint contractures
Evaluate for braces
Keep tendons and muscles stretched and avoiding painful contractures
Aquatic therapy
Water exercises and swimming help to tone and strengthen muscles and joints
Decreases stress where the body is already weak
Place emphasis on mobility
Goal of physical therapy
PTs treat people with muscular dystrophy to provide them with independence for as long as possible by focusing on movement.
Develop large muscle groups improve strength and increase endurance
