Document 16053220

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Concentric Contraction
Shortening of muscle
Force is generated
Train: increase strength
Isometric Contraction
No change in length
Force is generated
Train: specific to joint angle
Eccentric Contraction
Lengthening of muscle
Force is generated
Ability to generate most force
Utilizes less O2 than concentric
More hypertrophy and strength gains
More muscle damage
Acute Muscle Soreness
Blood flow plays an important part
Build up of LA stimulates pain
receptors
Soreness disappears when you stop
activity
Delayed Onset of Muscle Soreness
(DOMS)
Eccentric work (pain peaks after 48
hours)
Isometric work (pain peaks after 12
hours)
LA disappears in one hour
Eccentric contractions cause most
damage
Could be due to:
Strains in the MU
Popping of sarcomeres
Stretching produces over-extended
sarcomeres
May be that myosin heads are
“loosely” bound during eccentric
contractions and heads are “popped
off” the chain, causing damage
Lactic Acid Theory
Not likely
Why not?
Spasm Theory
Spasm due to ischemia
Release of p substance that causes
pain stimulus
Pain reflex: muscle continues to
contract
Break spasm by: massage, ice, and
stretching
p substance is unknown
Connective Tissue Theory
4 substances: LDH, 3mH (increases
in urine), hydroxyproline (HP), and
CPK
CPK and LDH leak into blood when
muscle breaks down
HP increases in blood and urine when
break down connective tissue
All four are markers of muscle
damage
DOMS: 5 components
Structural components of skeletal muscle
and CT are disrupted
Structural damage causes a change in
permeability in muscle cell, allowing high
levels of calcium into cells (kills cells)
High calcium causes a release of
proteolytic enzymes
Fragments of broken protein leak into
serum/blood and lead to an immune
response; WBC flood the area
Histamine response: fluid flows to area,
swelling and heat production, stimulates
pain receptors
Can analyze damage via
MRI
Swelling
Muscle protein in blood
Impaired substrate utilization
Decrease in strength and ROM
Decrease in motor control
If entire muscle is not damaged,
small areas can recover
In resting state, z lines are zigzagged
Connection between titin and
myomesin is broken, distorting the
myofibril arrangement
Desmin (connects z lines of different
myofibrils) is gone 3 days post
exercise
Fibronectin (connects membrane to
matrix inside fiber) is also disrupted
Most damage is repaired after
10 days
Soreness decreases with repeated
bouts
Adaptation
Use of NSAIDS and DOMS
Short term pain/repair
– Actual
– Placebo
Long term pain/repair
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