Biology 105 Lecture 10: Muscles

T. Irving 1997
Revised A.Howard 02/14/00

Goals of this section

1. Describe the anatomy of a whole muscle. What is an antagonistic pair?
2. Describe twitches and tetani
3. Describe anatomy of muscle fibers
4. Describe the sliding filament theory
5. Describe a neuromuscular junction and how muscle action potentials are initiated and conducted

Muscle

• Typically attached to bones via tendons
• Origin of a muscle is on a stationary bone
• Insertion is on the end that moves
• Muscles can only actively shorten
• Muscles must work in antagonistic pairs

Muscle Physiology

• Twitches are single contractions
• Muscle twitches show a latent period, contraction period, relaxation period
• Many twitches can fuse to form a sustained contraction or tetanus
• Muscles eventually fatigue
  
• For muscles to contract, nervous stimulation must exceed a threshold value
• Twitch fibers show an all or none response
• Whole muscles vary in strength of contraction due to the number of fibers stimulated
• Maximum stimulus is one in which no crease in force is observed

Effects of Exercise

• Endurance increases because of build up of ATP in muscles and increased tolerance to lactate
• Strength increases not by increasing the number of fibers but by enlarging the fibers that are already there.
• Exercise increases size of heart muscle
• Resting heart rate decreases
• Lung capacity increase
• Body fat decreases
• Bone density increases
• Blood cholesterol and fat levels decrease
• Blood pressure decrease
• There can be too much of a good thing
• Sports injuries can build up and actually decrease long term well being

Muscle Fibers

• Skeletal muscle fibers are long, multinucleated cells (50 - 200 microns diameter)
• Muscle fibers come in many types:
• Twitch fibers show an all or none response to nervous stimuli
• Tonic fibers display a graded response - multiply innervated
• Red fibers contain lots of myoglobin, sustained contractions
• White fibers optimized for fast contractions - glycolysis, oxygen debt
• Fibers packed with structures called myofibrils (2-3 microns diameter)
• Many mitochondria

Myofibrils and sarcomeres

• A myofibril consists of many 2-3 micron long sarcomeres laid end to end
• In the light microscope, sarcomeres show a banding pattern (striations)
• A-band, I band, Z-line, and M-line, H-zone
• Underlying structure can be seen only at electron microscope level
   
• Sarcomere consists of actin containing thin filaments
• Myosin containing thick filaments
• I band contains only thin filaments
• H-zone only thick
• A-band both thick and thin

Molecular mechanism of muscle contraction

• Sarcomeres shorten by sliding of thin filaments past thick filaments:
  i.e. I-band changes length
• Thin filaments slide because of the action of crossbridges on thin filaments
• Crossbridges hydrolyze ATP and somehow pull thin filaments towards the middle of the A-band by a repetitive cycling action
• How exactly this is done is not known
• Popular theory is the so-called "swinging crossbridge" theory
• Crossbridges are imagined to "row" along thin filaments

Regeneration of ATP

• ATP supplies would be quickly exhausted if it weren't for a "backup system" which keeps ATP at an adequate level to support contraction for short periods
• creatine ~P + ADP ----> ATP + creatine
• As phosphocreatine is used up, ATP is regenerated by glycolysis
• If O₂ not present process called fermentation
  • Lactic acid builds up
  • "oxygen debt"
  • "Paid back" in the liver when O₂ available

Nervous control of muscle contraction

• Muscle is an electrically excitable tissue
• Cell membranes much like nerve cell membranes
• Maintained at resting potential of -60 -90 mV
• Motor neurons synapse with muscle fibers at neuromuscular junction
• Synapse use ACh (acetylcholine)
• Binding of ACh to post -synaptic binding sites causes depolarization of the sarcolemma
• Muscle action potentials travel along the sarcolemma and then down the T-tubular system
• Calcium is stored in a special type of endoplasmic reticulum called the sarcoplasmic reticulum (SR)
• Parts of this come very close to the T-tubules

Calcium released from SR causes muscle contraction

• . . . When an action potential arrives in the T tubules
• Ca²⁺ ions are released from sarcoplasmic reticulum and diffuse into the myofibrils
• Ca²⁺ binds to Troponin, a protein on the thin filament which causes another protein tropomyosin to shift position on the thin filament uncovering myosin binding sites
• Myosin can now bind to thin filaments causing contraction
• When stimulation ceases, Ca²⁺ is reabsorbed into SR and contraction ceases