Lecture 29 Flashcards

(44 cards)

1
Q
A
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2
Q

Three main ATP sources in muscle?

A

Creatine phosphate, anaerobic glycolysis, aerobic respiration.

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3
Q

Creatine phosphate system role?

A

Transfers phosphate to ADP via creatine kinase for rapid ATP; lasts ~15 s.

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4
Q

When is anaerobic glycolysis used?

A

When CP stores fall (~10–15 s); provides ATP for 30–40 s, up to 2 minutes.

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5
Q

Does anaerobic glycolysis require oxygen?

A

No, it is anaerobic.

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6
Q

What does anaerobic glycolysis produce?

A

2 ATP per glucose and lactate.

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7
Q

Aerobic respiration role?

A

Uses oxygen for ATP production; dominant for long-duration activities.

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8
Q

Fuel sources for aerobic metabolism?

A

Pyruvate, fatty acids, amino acids.

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9
Q

How long can aerobic metabolism sustain activity?

A

Several minutes to hours.

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10
Q

Is lactate responsible for DOMS?

A

No, lactate is removed within ~30 minutes.

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11
Q

Is lactate responsible for cramps?

A

No; cramps relate to injury, low blood flow, overactive neurons, or Ca2+ buildup.

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12
Q

Cause of exercise acidosis?

A

ATP hydrolysis and CO2 production, not lactate.

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13
Q

What happens to lactate in the liver?

A

Converted back to glucose via gluconeogenesis.

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14
Q

Is lactate used by the brain?

A

Yes, it is a metabolic fuel source.

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15
Q

What is lactate threshold?

A

<4 mmol/L; good indicator of performance.

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16
Q

Peripheral fatigue definition?

A

Reduced ability to generate force due to muscle-level mechanisms.

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17
Q

Causes of peripheral fatigue?

A

Low SR Ca2+ release, depleted CP/oxygen/nutrients, low ACh release, low pH.

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18
Q

Central fatigue definition?

A

Reduced voluntary activation from spinal or supraspinal origins.

19
Q

Causes of central fatigue?

A

Protective reflexes, reduced motor drive, inhibitory feedback from fatigued muscle.

20
Q

Oxygen consumption after exercise increases because?

A

Higher body temperature, elevated heart/lung activity, tissue repair.

21
Q

Do muscles increase fibre number with training?

A

No; hypertrophy occurs, not hyperplasia.

22
Q

Endurance training adaptations?

A

Type IIx → IIa shift, ↑capillaries, ↑mitochondria, improved respiratory muscle efficiency.

23
Q

Strength training adaptations?

A

Type IIx → IIb shift, ↑capillaries/mitochondria, ↑bone density.

24
Q

Exercise-induced muscle damage signs?

A

Torn sarcolemma, disrupted Z-discs, elevated myoglobin and creatine kinase.

25
Difference between spasm and cramp?
Spasm = painless single contraction; cramp = painful sustained contraction.
26
Cause of cramps?
Low blood flow, overuse, injury, electrolyte imbalance.
27
DOMS timeline?
12–48 hours post-exercise.
28
Mechanism behind DOMS?
Microscopic muscle damage.
29
Muscle regeneration mechanism?
Hypertrophy; satellite cells assist repair.
30
Effect of aging on muscle?
Loss of muscle mass, replaced by connective/adipose tissue; slower reflexes.
31
Neural adaptation sites?
Supraspinal (corticospinal/cortical circuits) and spinal (motor neurons, interneurons).
32
Motor unit synchronization patterns?
Highest in weightlifters, intermediate untrained, lowest musicians.
33
Does size principle change with training?
No, recruitment order is preserved.
34
Role of muscle spindles?
Detect stretch, trigger stretch reflex to prevent injury.
35
What do spindles increase during stretch?
Motor unit recruitment or rate coding.
36
Role of Golgi tendon organs?
Inhibit excessive force; prevent injury from over-contraction.
37
Flexion reflex function?
Withdraw limb from painful stimulus.
38
Crossed extensor reflex function?
Support body weight during withdrawal.
39
Cardiac muscle key features?
Intercalated discs, desmosomes, gap junctions, uni-nucleated.
40
Why can't cardiac muscle tetanize?
Long refractory period prevents tetanus.
41
How does cardiac muscle resist fatigue?
High mitochondrial content; aerobic metabolism.
42
Smooth muscle features?
Non-striated, involuntary, spindle-shaped cells.
43
Smooth muscle contraction speed?
Slow onset, long-lasting.
44
Smooth muscle stretch ability?
Can stretch and still contract effectively.