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 O 2 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 MRISwelling 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 zig- zagged 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