8 fiber types and muscle damage Flashcards

1
Q

fiber types

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Size Principle of Muscle Fiber Recruitment

A

• 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Myofibrillar Disorganiztion

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Exercise Induced Muscle Damage

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

• Extertional Rhabdomyolysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MECHANISMS of DAMAGE #1—MECHANICAL

A
  1. Early in exercise (<10 min.) Type II fibers fatigue.
  2. Based on inability to regenerate ATP, they enter a rigor or high-stiffness state.
  3. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MECHANISMS of DAMAGE #2—CHEMICAL

A
  1. Early in exercise (<10 min.) Type II fibers fatigue.
  2. Based on inability to regenerate ATP, mitochondria lose their Ca2+ buffer capacity.
  3. 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IS THE PAIN OF ECCENTRIC EXERCISE DUE TO LACTIC ACID BUILDUP?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Repeated Bout Effects of Exercise

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Strength Loss Following Eccentric Exercise

A

Strength loss of 25-50% after a single exercise bout & can last several weeks
• May not correlate with CK levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Popping Sarcomere” Theory

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Eccentric-exercise induced Myofibril Remodeling

A

• Adaptation occurs→build new sarcomere creating overlap by laying them down in series, which can incr excursion velocity (NOT FORCE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly