Difference between revisions of "Muscles - Anatomy & Physiology"

Revision as of 10:03, 24 July 2008

BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY

Introduction

Muscle mass accounts for a large majority of the carcass weight of domestic animals. Muscular contraction is necessary for voluntary and involuntary movement of limbs, stabilization of joints, maintaining luminal diameter (in the case of arteries, bowel, etc), and to produce heat. The number of muscle fibers an individual possesses is determined by genetics and is set at birth, although muscle size and type (i.e. glycolytic to oxidative and vice versa) can be altered. Further muscle development therefore occurs by hypertrophy, rather than hyperplasia of muscle fibers. Three types of muscle can be described:

Skeletal (aka Striated, Somatic, Voluntary)
Smooth (aka Visceral)
Cardiac

Skeletal Muscle

Striated muscle - Copyright RVC 2008

Each muscle is composed of multiple fascicles, each of which consists of a bundle of muscle fibers
Muscle "fiber" means a single cell, which are multi-nucleate, and known as syncitia
Within each fiber are groups of parallel, longitudinal myofibrils
- Myofibrils are arranged as sarcomeres, bound by Z-discs, which are the functional unit of muscle contraction
- Each sarcomere contains 2 separate groups of myofilaments:
  - Thin filament, containing Actin, located centrally
  - Thick filament, containing Myosin, originating from either side of each Z-disc
Two basic types of skeletal myofibre:
- Primary: Oxidative
  - Grossly red
  - High myoglobin level
  - Slow rate of contraction
  - High oxidative activity
  - Function - postural, sustained activity
- Secondary: Glycolytic
  - Grossly white
  - Low myoglobin level
  - Fast rate of contraction
  - High glycolytic activity
  - Function - exercise, bursts of activity
Neurogenic Contraction: Muscle activation is initiated by a nervous impulse crossing the Neuromuscular Junction to individual muscle fibers
- The neurotransmitter, Acetylcholine (Ach), binds receptors in the muscle fiber to open Na+ channels
- This causes a wave of depolarization along the sarcoplasmic membrane, further opening voltage-gated Na+ channels, which propagates the signal along the sarcolemma
- Depolarization of the sarcoplasmic reticulum causes Calcium to be released, which activates muscle contraction
  - Muscle contraction occurs when (thin) Actin filaments slide past (thick) Myosin filaments
  - Myosin heads bind Actin subunits, forming cross-bridges, hydrolyzing ATP and providing energy for contraction
  - Myosin heads undergo power stroke, displacing Actin and releasing ADP and Pi
Control of skeletal muscle activity is regulated by the thin filament
- In the off state, tropomyosin coiled-coils block the helical grooves of the actin filament
- Tropomyosin movement relieves the steric block, allowing access to myosin binding sites
  - Calcium regulates muscle contraction by binding troponin-C, which is attached to the thin filament
  - This causes inhibition of the steric block keeping Actin and Myosin from interacting
Increased Calcium causes a negative feedback inhibition of Ca release, and it is pumped back into the sarcoplasmic reticulum by the Ca/ATPase pump

Cardiac Muscle

Structural: striated but uninucleate, highly vascularized
Gap junctions concentrated at intercalated discs
- Myogenic Contraction spreads cell to cell and does not depend on nervous imput to individual cells
- Areas of low electrical resistance allow rapid spread of action potentials
- Contraction is regulated by autonomic neurons and circulating hormones
Contractile mechanism similar to skeletal muscle: increase cytosolic Ca
- Ca influx across plasma membrane AND sarcoplasmic reticulum
Action potential has a prolonged plateau phase

Smooth Muscle

Smooth muscle - Copyright RVC 2008

Smooth muscle lacks troponin
Control of smooth muscle contraction involves thin and thick filament regulation
Thin filament regulation is carried out by the actin binding protein, Caldesmon, which binds the thin filament and blocks myosin access
- Calmodulin (activated by binding Ca) binds caldesmon and causes its dissociation from actin, enabling contraction
Thick filament regulation occurs by the phosphorylation of the regulatory light chain (RLC)
- Calmodulin-Ca binds and activates myosin light chain kinase (MLCK)
- MLCK then phosphorylates RLC, turning myosin on
- Myosin light chain phosphatase (MLCP) switches myosin off

Tendon

Histology of tendon (Courtesy of RVC Histology images)

Consists of dense collagen type 1 fibres and fibroblasts (tenocytes)

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