Skeletal Muscle: Fatigue and Soreness

KIN 3515

Fatigue

the decrease in muscle power output with exercise, causing a decrease in force generation and shortening velocity, and impaired generation at the crossbridge level.

Muscle fatigue factors

CNS (reduced motor neuron output and depletion of excitatory NT in neuronal vesicles) and skeletal muscle factors (fiber type composition, intensity/duration of exercise, state of fitness/nutrition, accumulation of lactate, H+, ADP, and Pi, and disruption of electrolyte balance due to depletion of glycogen→ depletion of TCA intermediates.)

Immediate muscle soreness

related to acidosis due to lactic acid formation, resolves within minutes/hours, and occurs immediately after or during exercise

Delayed onset mucle soreness (DOMS)

not caused by lactic acid formation, can last 3-4 days, and occurs 24-38 hours post exercise. Not observed following concentric exercise, only observed following eccentric exercise.

Connective tissue hypothesis

overstretching and perhaps tears in portions of the connective tissue harness, theory to explain DOMS

Muscle tissue hypothesis

minute tears in muscle tissue and/or damage to the sarcomere with accompanying release of creatine kinase, myoglobin, and troponin 1 into the blood'; theory to explain DOMS

Inflammatory hypothesis

acute inflammation and increased WBC in blood with soreness, theory to explain DOMS

Spasm hypothesis

Osmotic pressure changes causing fluid retention in surrounding tissues, alteration in cells mechanisms for calcium regulation causes spasms; theory to explain DOMS

Plasma creatine kinase (CK) activity

increased CK concentration indicate leakiness in the sarcolemma, plasma concentration of CK increasing following exercise with predominantly eccentric contractions

SR structure and function can be altered by

changes in pH, intramuscular high-energy phosphates, ionic imbalance, and temperature shifts.

Changes in SR effects

depresses rate of calcium uptake and release and increases free calcium in the cytosol of damaged fibers.

Increased cytosolic free calcium effects

May contribute to autolytic processes in damaged muscle fibers causing degradation to both contractile and non-contractile structures. Degradation leads to reduced force capacity and muscle soreness.