8 fiber types and muscle damage Flashcards
fiber types
TYPE IIB—Fast twitch—High Force—High Fatigue
TYPE IIA—Fast twitch—Moderate Force—Fatigue Resistant
TYPE I—Slow twitch—Low Tension—Fatigue Resistant
• More aerobic activities: use larger % of type I vs Endurance athletes: greater type I fiber proportionately
Size Principle of Muscle Fiber Recruitment
• Slow Oxidative (SO) fibers require less excitation to reach threshold and propagate an AP than Fast Oxidative Glycolysis (FOG) and Fast Glycolytic (FG).
o due to a smaller soma & axon & less inhibitory synapses
• Results in recruitment order…SO MU are recruited 1st during incremental ex, followed by a progressive ↑ in FOG and FG MU recruitment as ex intensity increases.
• Recruitment profile of MU is from TYPE I (low contraction tension, slow vel, and high fatigue resist) to TYPE II (high contraction strength, fast vel, and low fatigue resist)
Myofibrillar Disorganiztion
• myofibrillar disruption (primarily at the Z-disc) is relatively focal (often only a few sarcomeres per fiber) resulting in the breakage of the cytoskeletal proteins such as vimentin, laminin, and desmin.
• What happens to force transmission with mm damage?
o Depends on amount of mm damage. Decr 25-50% force production days to months following a single bout of ex
Exercise Induced Muscle Damage
• Delayed-onset of muscle soreness (DOMS)
1. Microscopic tears
2. Osmotic pressure changes causing fluid retention
3. Muscle spasms
4. Overstretching CT
5. Acute inflammation
6. Alteration in Ca2+ regulation
• DOMS: resuly of high-intensity or long-term eccentric or plyometric exercise
o Downhill running
o Hiking
o High-intensity RT
• Soreness usually peaks 36-48hrs after the exercise bout & can last as long as 3-4 days
• Extertional Rhabdomyolysis
DANGEROUS!!)
o Myoglobin spills over the blood into the urine & precipitates in the kidney causing renal failure & death
o Coca Cola urine + soreness→ get your Pt to the ER
o Large amount of muscle damage that the kidneys cant handle
GENERAL STEPS IN THE DEVELOPMENT OF DOMS
new ex using ecc mm action→ high forces = damage sarcolemma→ release of cytosolic enzymes & myoglobin→ damage to mm contractile myofibrils & non-contractible structures→ metabolites accumulate to abnormal levels in mm cell to produce more cell damage & reduced force capacity→ DOMS: considered to result from inflammation, tenderness, pain→ inflammation process begins…mm cell heals…the adaptive process makes the mm more resistant to damage from subsequent ex
MECHANISMS of DAMAGE #1—MECHANICAL
- Early in exercise (<10 min.) Type II fibers fatigue.
- Based on inability to regenerate ATP, they enter a rigor or high-stiffness state.
- Subsequent stretch of stiff fibers mechanically disrupts the fibers, resulting in cytoskeletal & myofibrillar damage.
• important bc explains protective effect of endurance training & transition of Type IIB→IIA
MECHANISMS of DAMAGE #2—CHEMICAL
- Early in exercise (<10 min.) Type II fibers fatigue.
- Based on inability to regenerate ATP, mitochondria lose their Ca2+ buffer capacity.
- Incr intracellular Ca2+ results in activation of the Ca2+ activated proteases, lysosomal proteases, etc.
• important bc it relates to the oxidative capacity of the muscle fiber.
Muscle Damage Changes in the SR—unregulated Ca2+ causes problems
• decr pH
• incr ADP, Pi
• Altered ionic balance
• Altered temperature
All factors may depress the rates of Ca2+ uptake & release→high [Ca2+] in cytosol…autolytic→reduced force capacity & soreness
Markers of mm damage: Creatine kinase (CK), Myoglobin (Mb), Troponin I (TI), Lactate Dehydrogenase (LDH), Alanin Aminotransferase (ALT)
IS THE PAIN OF ECCENTRIC EXERCISE DUE TO LACTIC ACID BUILDUP?
o NO!! pain from ecc ex is related to inflammatory response stimulating the very small sensory n endings in the mm & mm spindles rather than the buildup of any metabolic products
o Ecc contractions are more efficient—use less O2 than concentric contractions (aka lower metabolic cost) at same absolute workload
Lactic acid DOES NOT cause mm damage
Repeated Bout Effects of Exercise
• Existing mm damage/soreness doesn’t exacerbate subsequent mm damage or impair the repair process
• Single ex bout offers significant protection against muscle soreness in subsequent ex, with the effect lasting as long as 6 wks
Short Term Adaptation to Exercise= protective response
Strength Loss Following Eccentric Exercise
Strength loss of 25-50% after a single exercise bout & can last several weeks
• May not correlate with CK levels
Popping Sarcomere” Theory
• Muscle fiber damage may be the result of small differences along the length of a myofibril (due to sarcomere length diff).
• Resulting in diff sarcomere strength bc at longer sarcomere lengths on the descending limb of the length-tension curve, sarcomeres have less filament overlap and thus generate lower forces compared with their shorter counterparts in series.
o Longer & weaker sarcomere— FAILS FIRST bc less overlap, NOT OPTIMAL…disengagement “pop”→ titin breaks
Eccentric-exercise induced Myofibril Remodeling
• Adaptation occurs→build new sarcomere creating overlap by laying them down in series, which can incr excursion velocity (NOT FORCE)