Chapter 13 - Physiology of Training Flashcards

1
Q

What are the principles of training?

A

Overload, Specificity, Reversibility

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2
Q

What is overload?

A

Training effect with exercising beyond normal. The body adapts to the changes in some way, shape or form.

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3
Q

What is Specificity?

A

The type of training specific to muscle fibers, energy systems, velocity of contraction and type of contraction.

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4
Q

What is Reversibility?

A

Gains are lost when overload is removed. “Use it, or lose it”.

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5
Q

What is VO2 max?

A

The maximal ability to transport and utilize O2.

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6
Q

What is the VO2 equation?

A

VO2 max = Q max x a-VO2 diff.

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7
Q

What type of exercise increases VO2 max?

A

Exercise that is dynamic and uses large muscle groups.

20-60mins 3-5 times per week. 50-80% VO2 max.

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8
Q

What are the expected increases in VO2 max?

A

Average = 15-20%
2-3% in those with high initial VO2 max (requires intensity of over 70% of VO2 max)
Up to 50% in those with low initial VO2 max (training intensity of 40-50% of VO2 max)

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9
Q

What role does genetics play in VO2 max?

A

Accounts for about 50% of VO2 max.

Prerequisite for very high VO2 max.

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10
Q

What factor is influenced by genetics?

A

Muscle fiber type - mitochondria

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11
Q

What accounts for differences in VO2 max between males and females?

A

Males have a larger heart and more hemoglobin to pump oxygen around the body.

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12
Q

Improving VO2 Max: What is the calculation of VO2 max?

A

VO2 max = HRmax x SVmax x (a-VO2)max

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13
Q

What are the two main factors that influence an increase in VO2 max?

A

Stroke volume and Arterial-venous difference

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14
Q

What happens when doing shorter duration training (4 months)?

A

There is a greater increase in Stroke Volume than there is in a-VO2 difference

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15
Q

What happens when doing longer duration training (8 months)?

A

There is a greater increase in a-VO2 difference than there is in stroke volume.

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16
Q

Differences in Vo2 max in different populations are primarily due to….

A

differences in Stroke Volume max!

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17
Q

What are the 3 main factors that can elicit a change in Stroke Volume?

A

INCREASING End-Diastolic Volume (EDV): Preload
DECREASING Total Peripheral Resistance (TPR): Afterload
INCREASING Contractility

18
Q

What is EDV and how can we increase Preload?

A

The ability of the heart to fill up with blood.
INCREASE plasma volume
INCREASE filling time and venous return
INCREASE ventricular volume

19
Q

Why is there increased contractility?

A

Because of the frank-starling mechanism

20
Q

Why is there a decreased Total Peripheral Resistance? (afterload)

A

Because there is a DECREASE in arterial (aorta) constriction and there is an INCREASE in maximal muscle blood flow with no change in MAP

21
Q

When do the changes in stroke volume occur?

A

They occur rapidly. There is an 11% increase in plasma volume, 7% increase in VO2, and a 10% increase in stroke volume within 6 days of training!

22
Q

Increased a-VO2 difference: What is a-VO2 difference?

A

It is O2 extraction. There is an increase in muscle blood flow and a decrease in SNS vasoconstriction

23
Q

How does a-VO2 difference change with training?

A

It increases

24
Q

An increased a-VO2 difference results in an improved ability of the muscle to extract O2 from the blood… What changes allow this to happen?

A

There is an INCREASE in capillary density (slows blood flow through the muscle)
There is also an INCREASE in the mitochondrial number

25
Endurance training affect the maintenance of homeostasis: What happens to the body's ability to maintain homeostasis (steady state) during exercise after endurance training?
There is a more rapid shift from rest to steady-state. There is a reduced reliance on glycogen stores. There are CV and thermoregulatory adaptations. And it is due to neural and hormonal adaptations (also structural and biochemical changes in muscle)
26
What are the endurance training-induced changes in fiber type and capillarity?
There is a fast-to-slow twitch shift in muscle fiber type. | There is an increased number of capillaries.
27
Why is there a fast-to-slow shift in muscle fiber type?
1. Reduction in fast myosin - increase in slow myosin 2. INCREASED number of capillaries 3. Mitochondria in the muscle and the extent of change is influenced by duration of training and genetics
28
Why is there a change in mitochondria in the muscle from endurance training?
- Mitochondrial content increases quickly - Depends on intensity and duration of training - Can increase 50-100% within first 6 weeks.
29
Why is there an increased number of capillaries from endurance training?
- enhanced diffusion of oxygen | - increased removal of wastes
30
All of the changes in increased endurance performance are due to...
Changes in muscle metabolism
31
Mitochondrial Number & Performance: What are the 3 steps that ADP stimulates ATP production?
1. ATP-PC 2. Glycolysis 3. Oxidative phosphorylation
32
What metabolic systems becomes the primary source during steady state?
Oxidative phosphorylation
33
An increased number of mitochondria is observed after training: How does this affect the ADP needed to increase ATP production and VO2?
Lower ADP is needed to increase ATP production and VO2. (1 mitochondria splits into 2!) PCr responds immediately to ADP and the need for ATP
34
How is oxygen deficit affected after training?
It is lower after training due to: - same VO2 at lower ADP - energy requirement met by oxidative ATP production at the onset of exercise - faster rise in VO2 curve and steady state is reached earlier
35
What are the results from having the oxygen deficit affected after training?
- less lactate and H+ formation - less reliance on Anaerobic glycolysis - decrease in glycolytic enzymes (PFK) - less PC depletion
36
Why are ADP levels at the same VO2 after training?
They are lower. It is accomplished by more mitochondria
37
What are the end results of lower oxygen deficit after training?
Reach steady state quicker.
38
ESSAY QUESTION!!! | Biochemical Adaptations and Plasma Gluecose Concentration
After endurance training there is an increased utilization of FAT and sparing of PLASMA GLUECOSE and MUSCLE GLYCOGEN.
39
How is the increased utilization of FAT and sparing of PLASMA GLUECOSE and MUSCLE GLYCOGEN accomplished?
1. Transportation of FFA into the muscle by: INCREASED capillary density and INCREASED fatty acid binding protein and fatty acid translocase 2. Transportation of FFA from the cytoplasm to the mitochondria by: INCREASED mitochondrial number. (there are higher levels of CPT 1 and fatty acid translocase = faster transport to mitochondria) 3. Mitochondrial oxidation of FFA by: INCREASED enzymes of beta oxidation. INCREASED rate of acetyl-CoA formation. HIGH CITRATE level inhibits PFK and glycolysis
40
Biochemical Adaptations and Lactate: How is lactate produced?
Pyruvate + NADH = (LDH) = lactate + NAD
41
How do we get lactate accumulation?
Production - removal (lactate shuttle and cori cycle)
42
Endurance training causes adaptations that produce less blood lactate levels at the same workloads...
Blood lactate is affected by changes in production and removal.