muscle 1.4 Flashcards
in one single motor unit muscle fibers are..
all the same
does a muscle have only 1 fiber type
no it has all 3 motor unit types
2 factors of total muscle tension development
1) amount of tension developed by each fiber
(frequency-tension relation, length-tension relation, fiber diameter, fiber type, fatigue)
2) number of fibers contracting at any time (number of fibers per motor unit, number of active motor units)
small motor units vs large motor units
small motor units : total tension the muscle produces increases in small steps by activating more motor units
large motor units : total tension the muscle produces increases in large steps by activating more motor units
size of a motor neuron
the diameter of the neuronal cell body (diamteter of its axon)
type 1 smallest diameter = smallest tension
type 2a slightly larger diameter= larger tension
type 2x biggest diameter =greatest tension
what makes the smaller diameters in muscle fibre types produce less tension?
there is the same number of sodium ions entering to cause excitatory synapse, but the difference is there greater depolarization
-motor units are spread out over a smaller surface in muscle fibre types with smaller diameters
what determines the velocity that a single muscle fiber shortens
1) the load on the fiber -> load on the whole muscle
2) the speed of the myosin type expressed in the fiber -> type of motor units in the muscle
when you increase motor unit recruitment, the load decreases on each motor unit which increases both force and velocity
what happens if there is denervation atrophy
neuron to the skeletal muscle was destroyed
-progressively smaller in diameter and amount of contractile proteins they contain will decrease
what happens if there is disuse atrophy
when the muscle is not used for a long period of time
-same thing, smaller diameter, amount of contractile proteins decrease
what happens when you exercise the muscle
increase amount of contractile activity, increase in size (hypertrophy), changes in capacity of ATP production and subtype of myosin they express
low intensity/long duration exercise leads to
- increase number of mithochondra in all muscle fibers
- myosin composition MAY shift in fast fibres from 2X to 2A
- increase in number of capillaries
all increase ability to sustain muscle contraction through OXIDATIVE metabolism
high intensity exercise
- increase in diameter (hypertrophy) due to satelite cell activation and increased synthesis of actin and myosin filaments -> more fibrils
- myosin in fast fibers could shift 2a to 2b
- increase synthesis of glycolytic enzymes
can you increase strength without hypertrophy?
yes increase synchronous of muscle units, enhance ability to recruit fast glycolytic motor neurons
can you change proportions of fibers in a muscle
can change fibres 2A to 2x but not from type 1 to 2
tone
resistance training can enhance tone
- more myofibrils are activated during RT, more energy being used = good for weight loss
- RT enhances background motor unit firing
- better at recruiting large motor units
transient hypertrophy
increase in muscle size that develops immediately following exercise (transitioning quickly)
chronic hypertrophy
increase in muscle size due to long term strength training, muscle fibres increase size and increased recruitment of muscle fibres and activation
neural adaptations happen first then hypertrophy
insulin like growth factor 1, anabolic steroids (androgens), myostatin
androgens influence on muscle strength and growth
myostatin is produced by skeletal muscle cells, it is a regulatory protein which inhibits muscle hypertrophy through negative feedback effect
-myostatin bad if you want to get big
-some people have myostatin deficiency
effects of aging
maximum force a muscle can generate decliness 30-40% between 30-80 years old
- average fibre diameter decreases, less PA
- intensity and duration of exercise in older individuals doesnt produce as much change
what causes exercise-induce muscle soreness
thought to be structural damage to the muscle cells and their membrane which activates the inflammation response
-releases histamines that activate endings of pain neurons in the muscle
eccentric produces most muscle soreness
acute muscle soreness
pain due to ischemia (not enough blood flow; oxygen to the muscle) or accumulation of hydrogen ions or lactate
doms
delayed onset muscle soreness
post - 12,24,48 hours after exercise
nothing to do with lactate, lactate gone after an hour
creatine kinase
structural member of the M LINE
- when the muscle is damaged it is torn apart and released
- CK is often used as a marker for muscle damage
what does strained muscle leads to
scar tissue
has collagen overtop which does not allow the muscle to stretch as nicely
antagonist
groups of muscles that produce oppositely directed movements at joint
fulcrum
point on which a lever rests or is supported and on which it pivots
first class lever
fulcrum is between load and effort
eg. semispinalis doing flexion and extension at head
second class lever
fulcrum at the end near the load
eg. soleus doing plantar flexion and dorsiflexion
third class
fulcrum at the start near the effort
eg. biceps doing flexion and extension
skeleton is a lever and fulcrum system
mechanical equilibrium of forearm
downward load x distance from the elbow = isometric tension exerted by the muscle X distance from the elbow
muscle cramps
involuntary tetanic contractions of skeletal muscles
AP’s firing higher rates than normal, sensory receptors and motor neurons in the area activated
caused by : electrolyte imbalances in extracellular fuid, over exercise, dehydration, chemical imbalances, hormonal imbalances, cholesterol lowering medications
-spicy foods reduce excess AP = less cramping
muscular dystrophy
genetic disease
- progressive degeneration of skeletal and cardiac muscle fibres
- absence of proteins that make up the costameres in striated muscle
costameres
clusters of structural and regulatory proteins that link the Z disks of the outermost myofibrils to the sarcolemma and extracellular matrix
-allow you to have lateral transmission from sarcomere to extracellular matrix
help stabilize the muscle
myasthenia gravis what is it? whats it caused by? treatment?
neuromuscular disorder charcterized by muscle fatigue and weakness that progressively worsened as the muscle is being used
caused from destruction of nicotinic Ach receptors proteins of the motor end plate, mediated by antibodies of a persons own immune system
treatment is adminestering acetylcholinesterase inhibitors, suprress immune function with glucocorticoids and removal of the thymus
