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Sports Training Physiology > Week 5 - Speed Endurance Training > Flashcards

Week 5 - Speed Endurance Training Flashcards

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Sports Trivia flashcards
1
Q

Define speed endurance

A

Ability to maintain a high speed for a prolonged period of time + to recover speed following short recovery periods.

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2
Q

Sports where speed endurance is a key fitness component

A

Track + field — 200-800m

Track Cycling — 500-1000m

Swimming — 50-200m

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3
Q

Value of speed endurance in team sports

A

25-40 sprints in a game, 2-4 secs

Work:Rest – 1:6

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4
Q

How long do bouts last for speed endurance production training

A

10-40s

Perf at max or near Max intensity

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5
Q

What is recovery/rest like for speed endurance production training

A

More than 5 times the exercise bout duration.

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6
Q

How long do bouts last for speed endurance maintenance training

A

5-90s

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7
Q

What is recovery/rest like for speed endurance maintenance training

A

Shorter rest period between bouts

1-3 times exercise duration.

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8
Q

Speed endurance production training vs speed endurance maintenance

Sessions per week

A

3 - 3

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9
Q

Speed endurance production training vs speed endurance maintenance

Weeks

A

3 - 3

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10
Q

Speed endurance production training vs speed endurance maintenance

Bouts per session

A

6-8 – 6-8

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11
Q

Speed endurance production training vs speed endurance maintenance

Recovery duration

A

120s - 40s

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12
Q

Describe a typical speed endurance training programme

A

Duration: 4-8 weeks

Sessions: 3-4

No. of bout reps per session: 4-12

Duration of exercise bout: 30s

Intensity of exercise bout: 90-100% of max speed

Recovery between bouts: 4-6mins

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13
Q

Energy Systems contributions to 30s Wingate test

A

PCR = approx 28% of total ATP req.

Oxidative phosphorylation contributes around 16%.

If you extended the sprint beyond 30s, then the contribution from aerobic metabolism would further ⬆️.

Remaining 56 % of ATP demand for 30s all out sprint, is provided by anaerobic glycolysis.

== Glycolysis = primary source of ATP during this prolonged sprint activity.

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14
Q

Why isn’t heavy reliance on anaerobic glycolysis sustainable for a long time?

A

Limited glycogen stores

Prod. of LA = ⬆️ H+ = Muscle acidosis

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15
Q

What does muscle acidosis inhibit?

A

Glycolysis + perhaps the contractile apparatus.

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16
Q

Diff in amount speed endurance training vs endurance training increases muscle glycogen stores

A

SET == 28%

End. training = 17%

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17
Q

By how much does SET ⬆️ muscle buffering capacity

A

8%

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18
Q

How does SET ⬆️ muscle buffering capacity

A

By ⬆️ no. of intramuscular buffers

+

⬆️ no. of H+ transporters (exporting H+ outside muscle + into bloodstream)

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19
Q

What are the intramuscular buffers?

A

Carnosine protein

Sodium phosphate

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20
Q

What type of transporters also transport H+ out of muscle fibre

A

Membrane embedded transporters

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21
Q

What buffer is there in the blood to neutralise H+

A

Bicarbonate buffer

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22
Q

What are 2 of the membrane transporters responsible for moving H+ out of muscle fibre?

A

Monocarboxylate transporter / MCT

Sodium-hydrogen exchanger / NHE

  • Evidence suggests these are ⬆️ as a result of SET.
23
Q

When is there a -ive membrane potential of -70milivolts?

A

Resting membrane pot.

When muscle fibre hasn’t been stimulated to contract.

24
Q

Charge wise, what does it mean when there’s a -ive membrane potential of -70 millivolts?

A

LOWER charge inside muscle

25
Q

Describe ion distribution in resting conditions

A

IN fibre = High conc of K+

OUTSIDE fibre = High conc. of Na+

26
Q

What is the resting membrane potential caused by?

A

Imbalance in no. of ions inside + outside fibre

27
Q

What happens when a signal arrives at the muscle fibre from a neurone

A

Electrical current causes membrane Na+ channels to OPEN.

28
Q

What happens once Na+ channels are open?

A

Na+ move into muscle fibre, causing membrane pot. to ⬆️ to a +ive 30 milivolt charge == AP.

+ive charge triggers neighbouring Na+ channels to open, leading to sodium influx further along membrane. — How AP is able to propagate along the sarcolemma + down T tubules.

29
Q

What happens if membrane is stimulated when not at a -ive 70 millivolt charge

A

AP won’t occur as readily or won’t be as strong, potentially inhibiting the propagation + strength of AP.

— Inhibiting contraction force — a loss of muscle excitability.

30
Q

What is the 1st step to returning membrane pot to resting levels

A

Opening of K+ channels so that K+ can flow from inside to outside fibre.

31
Q

What happens when K+ flows from inside to outside muscle fibre?

A

Brings pot. down to -ive 100 millivolts, overshooting the -ive 70 millivolt target.

For this reason, a Na+/K+ ATPase pump is present in memb. — To move K+ back into fibre + Na+ out of fibre — restoring -ive 70 millivolt memb. pot.

32
Q

What happens when APs repeatedly arrive at muscle at a maximal rate?

A

Accumulation of K+ outside muscle fibre causes reduced muscle excitability

33
Q

What does SET do to for the Na+/K+ ATPase pumps?

A

⬆️ the no. of them

34
Q

What does SET do in relation to adapt of mitochondria?

A

⬆️ mit. mass

35
Q

What does SET do in relation to adapt of enzymes?

A

⬆️ no. + activity of important enzymes in Krebs cycle + ETC. These incl:

  • Citrate synthase, 1st enzyme of Krebs cycle.
  • Cytochrome C oxidase, important enzyme in ETC.
36
Q

What is perf. during repeated sprint bouts partly dependent on?

A

Ind. ability to replenish their PCr stores before next sprint.

37
Q

What does replenishing PCr require?

A

ATP (mostly provided by aerobic system)

38
Q

How much lactate is shuttled to type 1 muscle fibres?

What happens there?

Where does the rest of the lactate go?

A

Around 75-80%

Oxidised by mit. to form glucose.

Other portion of lactate is shuttled out of muscle via bloodstream to heart + liver where its converted to glucose.

– Then released back into bloodstream + taken up by muscle.

39
Q

Lactate shuttle hypothesis

A

Means by which lactate can act as a substrate for ATP prod. by refuelling muscle w/ glucose that can enter glycolysis.

40
Q

What are the ways in which SET improves the lactate recycling process

A

⬆️ abundance of mit. = ⬆️ the oxidation of lactate w/in muscle itself.

⬆️ movement of lactate out of muscle due to larger no. of cap. available.

41
Q

Give a summary of physiological adapt. to SET

A

⬆️ in muscle glycogen

⬆️ glycolytic enzymes

⬆️ buffering capacity + H+ transporters

⬆️ Na+ K+ ATPase

⬆️ in muscle capillerization + oxidative capacity

⬆️ type 2a muscle fibres

42
Q

What does SET improve in already trained endurance athletes

A

Economy

VO2 max

Endurance perf (3-10km)

43
Q

How does SET improve endurance performance

A

⬆️ VO2 max

⬆️ exercise economy

⬆️ speed of VO2 kinetics

⬆️ lipid metabolism

44
Q

How does SET improve endurance performance

Explain ⬆️ lipid metabolism

A

⬇️ utilisation of limited glycogen stores + red. prod. of LA

45
Q

Describe a training session being an example of Speed endurance PRODUCTION

A

12 reps

30 s running at 100% max speed

6 min recovery between reps

46
Q

Fibre type changes following SET

A

⬆️ type 2

⬇️ type 1

47
Q

During a 30-s all-out cycle sprint, 56% of ATP is provided by the…

A

Glycolysis system

48
Q

Following SET there is an increase in muscle carnosine concentration. This is important because it…

A

Buffers H+

49
Q

Why is there a negative muscle fibre membrane potential at rest?

A

More +ively charged ions OUTSIDE muscle fibre

50
Q

What does an accumulation of K+ outside the muscle fibre result in?

A

⬇️ muscle excitability

51
Q

An increase in Na+-K+ ATPase pumps after SET will help maintain muscle excitability by…

A

Preventing accumulation of K+ outside muscle fibre

52
Q

What does SET result in in relation to capillary density

A

⬆️ capillary density + capillary-fibre ratio

53
Q

What has SET been shown to improve?

A

Repeated sprint performance

Individual sprint performance

Endurance performance

54
Q

Which of the following does not contribute to the improved endurance performance after SET?

a. Increased mitochondrial number
b. Increased cardiac output
c. Improved economy
d. Speeding of VO2 kinetics

A

b. Increased cardiac output

Sports Training Physiology (13 decks)

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