22-24) *** Adaptations to Aerobic Training *** Flashcards

1
Q

How do adaptations to training differ between Aerobic and Anaerobic Training?

A

Aerobic training:
- “Cardiorespiratory endurance training”
- Improves cardiac fxn and peripheral blood flow
- enhances metabolic capacity of mm fibers (mm generate more ATP)

Anaerobic training Improves:
- anaerobic metabolism
- Short-term, high intensity (explosive) exercise capacity
- Tolerance for acid-base imbalances
- Muscle Strength

Greatest athletic success comes from training both systems

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2
Q

Muscular Endurance vs Cardiorespiratory Endurance:
Define.
Which are improved with aerobic training?

A

Aerobic Training improves both!

Muscular Endurance: Ability of a single muscle or mm group to maintain high-intensity, repetitive or static contractions
- Highly related to Muscular strength and Anaerobic power development

Cardiorespiratory Endurance: Ability to sustain prolonged, dynamic whole-body exericise using large mm groups
- related to development of CV and Resp systems’ ability to use energy aerobically
- Ability to maintain O2 delivery to working mm during prolonged exercise and
- mm ability to use energy aerobically

Anaerobic power development: ATP produced anaerobically, trained aerobically

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3
Q

Cardiorespiratory Endurance Capacity

What is Maximal Endurance Capacity?
How does it change with Exercise?

A

Maximal Endurance Capacity: VO2max
- Highest rate of oxygen consumption attainable during maximal or exhaustive exercise
- Maximal Aerobic Power or Maximal Aerobic Capacity
- ↑Excerise intensity → o2 consumption will plateau or decrease slightly even w/ increases in workload

Endurance Training:
- Increases maximal endurance capacity: more O2 can be delivered to and used by active mm than in untrained state
- ↑VO2max
- ↑ capacity for intense exercise

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4
Q

Cardiorespiratory Endurance Capacity

How does Maximal Endurance Capacity change with endurance training?

A

Endurance Training:
- Increases maximal endurance capacity: more O2 can be delivered to and used by active mm than in untrained state
- ↑ VO2max
- ↑ capacity for intense exercise

Maximal Endurance Capacity: VO2max
- Highest rate of oxygen consumption attainable during maximal or exhaustive exercise
- Maximal Aerobic Power or Maximal Aerobic Capacity
- ↑Excerise intensity → o2 consumption will plateau or decrease slightly even w/ increases in workload

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5
Q

What is Submaximal Endurance Capacity? How does it change with Endurance training?

A

Submaximal Endurance Capacity:
- Ability to maintain peak speed or velocity during a set period of time
- Likely determined by both V̇O2max and Lactate threshold

Submaximal Endurance Capacity increases with training

ie the distance one can run in 30 minutes increases w/ training

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6
Q

Repeated challenges to cardiovascular/respiratory systems leads to ? to allow body to improve ?

A

Repeated challenges to cardiovascular/respiratory systems leads to adaptations to allow body to improve VO2max
- Goal: to improve VO2max and how long you can exercise near VO2max

Multiple CV adaptations occur in response to exercise training:
1. Heart rate
2. Stroke Volume
3. Blood Pressure
4. Cardiac output
5. Blood flow
6. The blood

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7
Q

What are 6 CV factors that adapt in response to training?

A

Multiple CV adaptations occur in response to exercise training:
1. Heart rate
2. Stroke Volume
3. Blood Pressure
4. Cardiac output
5. Blood flow
6. The blood

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8
Q

What is the (a-ṽ)O2difference
Does it respond to training?

A

Refers to oxygen transport system:
* (a-ṽ)O2difference: Arterial-venous O2 Difference
* Difference between arterial and venous O2
* Reflects amount of O2 extracted by the tissue
* As extraction of O2 ↑ (rate of O2 use ↑) → ↓ amount of O2 in venous blood → ↑ (a-v)O difference

  • Endurance training causes numerous changes in the oxygen transport system to allow it to function more effectively

Changing HR or SV changes CO which impacts V˙O2max

V˙O2max = highest rate of oxygen consumption obtainable during maximal or exhaustive exercise
~max
* V˙O2max = CO x (a-v)O2difference = rate of oxygen consumption
* CO = HR x SV

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9
Q

V˙O2max Equation?
- What is V˙O2max
- How does it relate to the oxygen transport system?

A

V˙O2max: highest rate of oxygen consumption obtainable during maximal or exhaustive exercise
* V˙O2max = CO x (a-v)O2difference = rate of oxygen consumption
* CO = HR x SV

Endurance training → numerous changes in the oxygen transport system to allow it to function more effectively
* Changing HR or SV changes CO which impacts V˙O2max

  • (a-ṽ)O2difference: Arterial-venous O2 Difference
    • Difference between arterial and venous O2
    • Reflects amount of O2 extracted by the tissue
      • As extraction of O2 ↑ (rate of O2 use ↑) → ↓ amount of O2 in venous blood → ↑ (a-v)O difference
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10
Q

Heart size
* Cardiac hypertrophy or ?
* ?-induced; normal adaptation to training
* ? undergoes greatest adaptation
* Type of ? depends on type of exercise performed

A

Heart size
* Cardiac hypertrophy or athlete’s heart
* Training-induced; normal adaptation to training
* Left ventricle undergoes greatest adaptation
* Type of ventricular adaptation depends on type of exercise performed

Ventricular Adaptation to:
(1) Strength-based (static) training
* Concentric LV hypertrophy
* Due to pressure load
* LV wall thickening and minimal LV dilation

(2) Endurance-based training
* Eccentric LV hypertrophy
* Due to increases in volume load
* LV dilation and proportional LV wall thickening
* Increased plasma volume and diastolic filling time
* leads to LV dilation:
* Allows for increased left ventricular filling and increased SV
* Largely attributable to a training-induced increase in plasma volume that increases left ventricular EDV
* Decreased heart rate at rest due to increased parasympathetic tone, and during exercise at the same rate of work, increasing diastolic filling

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11
Q

Ventricular adaptation to Strength-Based (STATIC) training:
(vs Endurance)

A

Ventricular Adaptation to:
Strength-based (static) training
* Concentric LV hypertrophy (reduced ventricular volume)
* Due to pressure load
* LV wall thickening and minimal LV dilation

(2) Endurance-based training
* Eccentric LV hypertrophy
* Due to increases in volume load
* LV dilation and proportional LV wall thickening
* Increased plasma volume and diastolic filling time
* leads to LV dilation:
* Allows for increased left ventricular filling and increased SV
* Largely attributable to a training-induced increase in plasma volume that increases left ventricular EDV
* Decreased heart rate at rest due to increased parasympathetic tone, and during exercise at the same rate of work, increasing diastolic filling

Heart size
* Cardiac hypertrophy or athlete’s heart
* Training-induced; normal adaptation to training
* Left ventricle undergoes greatest adaptation
* Type of ventricular adaptation depends on type of exercise performed

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12
Q

Ventricular adaptation to Endurance Training
(vs Static/Strength)

A

Endurance-based training
* Eccentric LV hypertrophy
* Due to increases in volume load
* LV dilation and proportional LV wall thickening

Increased plasma volume and diastolic filling time
* leads to LV dilation (to account for extra Vol):
* Allows for increased left ventricular filling and increased SV
* Largely attributable to a training-induced increase in plasma volume that increases left ventricular EDV
* Frank starling: ↑EDV→ ↑SV
* Decreased heart rate at rest due to increased parasympathetic tone, and during exercise at the same rate of work, increasing diastolic filling

Ventricular Adaptation to:
Strength-based (static) training
* Concentric LV hypertrophy (reduced ventricular volume)
* Due to pressure load
* LV wall thickening and minimal LV dilation

Heart size
* Cardiac hypertrophy or athlete’s heart
* Training-induced; normal adaptation to training
* Left ventricle undergoes greatest adaptation
* Type of ventricular adaptation depends on type of exercise performed

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13
Q

Heart Size & VO2max:
* Highly trained endurance athletes have greater ? than non-endurance training athletes

LVID and LVM increase with endurance training

A

Heart size
* Highly trained endurance athletes have greater left ventricular masses than non-endurance training athletes
* Left ventricular mass highly correlated with VO2max (VO2max dependent on CO which depends on SV)

(cross-country skiers, endurance cyclists, long-distance runners)

Graph: literature review: LVID (left ventricular internal diameter; index of chamber size), MVT (mean wall thickness), LVM (left ventricular mass)
* LVID and LVM increase with endurance training
* Longitudinal studies show increases with heart size with training and decreases with detraining

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14
Q

CV adaptations to training: Stroke Volume

Stroke Volume increases following Endurance Training, why?

A

Stroke volume:
Increases at rest and with submaximal/maximal exercise intensity following endurance training

(1)Left ventricle fills more completely during diastole after aerobic training (increased EDV)
* ↑Plasma volume w training → ↑EDV → ↑Dilation → ↑SV

(2)Heart rate of trained heart is lower at rest and during the same exercise intensity than untrained heart, ↓HR →↑diastolic filling
* Increased stretch of ventricles and force of contraction increases SV (Frank-Starling mechanism)

SV plateaus at about 40-60% VO2max

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15
Q

What is the Ejection Fraction (EF)? Why does EF increase after aerobic training?

A

Ejection fraction: proportion of the end-diastolic volume (EDV) that is pumped out with each beat
EF = (EDV - ESV)/EDV

Aerobic Training:
- LV fills more completely during diastole → ↑EDV
- ↑LV wall MASS →↑contractile force and ↓ESV (push out more blood)

facilitated by decreased peripheral resistance with training
* More blood enters the left ventricle and a greater % of what enters is forced out with each contraction, resulting in increased SV

Stroke volume is the amount of blood the heart pumps with each beat. SV = EDV-ESV.

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16
Q

CV Adaptations to training HR

HR: How does aerobic training lead to HR changes at rest? During submaximal exercise? During Recovery?

A

Heart Rate adaptions to Aerobic Training
- Major impact at rest, during submax exercise & recovery period
- Resting HR ↓ w/ Endurance Training

Training-Induced Bradycardia (very slow HR)

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17
Q

Resting Bradycardia in athletes:
Three possible explanations

A

Training-induced Bradycardia: Low resting HR in elite athletes
(1) Due to ↑ Parasympathetic (Vagal) Tone → ↓HR
(2) ↓ Sympathetic Tone
(3) ↓Intrinsic HR (set by SA node in absence of neural/hormonal input)
- Remodelling of SAN
- Changes properties of ion channels and Ca++ handling
- Causes bradycardias associated with SAN disease

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18
Q

How does aerobic training alter submaximal HR?

A

During Submaximal training, aerobic training →↓HR at any given intensity
- Larger decreases seen at higher intensities

Trained Heart performs less work (lower HR and Higher SV) to maintain CO at a specific intensity

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19
Q

Aerobic training and HRmax:
Does aerobic training alter maximum heart rate?

A

Maximum heart rate (HRmax):
* Stable and remains relatively unchanged
after endurance training

* Determined by age
* Exception: highly trained endurance athletes may have lower HRmax values than untrained people at same age

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20
Q

At maximal or near-maximal exercise intensities, ? and ? provide optimal CO

A

At maximal or near-maximal exercise intensities, HR and SV provide optimal CO
CO=HR x SV
- If HR is too fast → ↓diastolic filling time → ↓SV
- Highly trained athletes may have lower HRmax as hearts have adapted to training by Increasing SV so lower HRmax can provide optimal CO

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21
Q

What is Heart Rate Recovery?
How does it change with Endurance Training?

A

Heart Rate Recovery (HRR): Measure of Cardiorespiratory Fitness
- HR remains elevated after exercise, slowly returning to resting level
- HR Recovery period = period of time it takes to return to resting HR

After Endurance training:
- HR returns to resting more quickly after exercise in both maximal and submaximal exercise (Faster recovery)

Cannot compare HRR between individuals but can use it to track personal progress
B/c other factors affects HRR (Core body temp)

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22
Q

How does Cardiac Output change with Aerobic Training?
- At rest?
- Submaximal Exercise
- Maximal Exercise

A

CO = HR x SV

Rest and during submaximal exercise:
- Little change in CO; matches VO2

Max CO may increase in response to aerobic training:
- Largely responsible for increased VO2max
- Increased due to increase in SVmax as HRmax changes very little

CO = HR x SV
- SV increases with Training
- HR decreases with training at rest and during exercise

Fick eq’n CO affects O2 delivery

23
Q

Bloodflow: What are 4 factors that increase BF in response to exercise?

A

(1) ↑ Capillarization
- ↑ # of capillaries per mm fiber

(2) Greater recruitment of existing capillaries
- Not all capillaries in a tissue are open at one time
- ↑BF to working mm

(3) More effective BF redistribution from inactive regions
- Redistribution of CO; ↑BF to active tissues

(4) ↑ Total Blood Flow

24
Q

Why is increased MM Capillarization a benefit?

A

Capillarization central for O2 and nutrient delivery to mm
High capillary density:
- Large mm to blood exchange SA
- Short O2 diffusion distance (closer to fibres)
- High blood cell mean transit time (move faster through bed)

25
Q

Capillarization in sk mm is caused by?

A

Exercise - most potent stimulator for angiogenesis in skeletal muscle
- During exercise VEGF is secreted from mm fibres to interstitium
VEGF:
- Vascular endothelial growth factor
- Determines degree of capillary growth

Exercise →↑VEGF →↑Capillary growth →↑ capillary:fibre ratio

26
Q

Recruitment of Capillaries and increased capillarization combine to cause:

A

Greater recruitment of existing capillaries
* Not all capillaries in a given tissue are open at one time
* Existing capillaries in trained muscles can be recruited and opened to flow

Increased capillarization and increased capillary recruitment combine to increase cross- sectional area for exchange between the vascular system and metabolically active muscle fibers (↑BF)

27
Q

Redistribution of BF why is it controversial?

A

Redistribution of CO to increase blood flow to active muscles
* Controversial: Blood flow can increase to more active fibers even within a specific muscle group
* Study: Endurance-trained rats can redistribute blood flow to their most active tissues during exercise better than untrained rats
* Trained rats distribute blood to most oxidative fibers and away from glycolytic fibers
* Difficult to replicate findings in humans; human skeletal muscle has mixed fiber types

Rats have a single fiber type in a particular mm (ie mm types are segregated) whereas humans have mixed fibre types within a single mm

28
Q

BP: How does Blood pressure change with Aerobic training?
* Resting
* Submaximal intensity
* Maximal intensity

A
  • Resting blood pressure does not change significantly in healthy subjects in response to endurance training
  • Submaximal exercise intensity: blood pressure is reduced
  • Maximal exercise intensity: systolic blood pressure is increased and diastolic pressure is decreased
    • Hypertrophy →↑ strength of contraction → systolic BP
  • ↑vasodilation → ↓ diastolic BP

  • Modest reduction in resting blood pressure after training in borderline or moderately hypertensive individuals
  • FYI: Reductions in both systolic and diastolic blood pressure of ~ 6 – 7 mmHg
29
Q

BV: How does endurance training impact total Blood Volume?

A

Endurance training increases total blood volume
* Effect larger at higher training intensities
* Increased blood volume due to increase in plasma volume and volume of red blood cells

Plasma volume is responsible for the increase in blood volume during first 2 weeks:
Two Phases leading to increased Plasma Volume:

Phase 1: Increases in plasma proteins
* Intense exercise → proteins (albumin) leave vascular space and move into interstitial fluid → proteins are returned in greater numbers through lymph system → results in rapid plasma volume increase within the first hour of recovery form the first training bout

Phase 2: Increased protein synthesis
* Upregulation of protein synthesis with repeated exercise (ADH, aldosterone)
* Increased reabsorption of water and sodium in kidneys increases plasma volume

30
Q

BV increases due to ? and ?

A

BV increases due to increased plasma volume and increased volume of RBC

Plasma volume is responsible for the increase in blood volume during first 2 weeks:
Two Phases leading to increased Plasma Volume:

Phase 1: Increases in plasma proteins
* Intense exercise → proteins (albumin) leave vascular space and move into interstitial fluid → proteins are returned in greater numbers through lymph system → results in rapid plasma volume increase within the first hour of recovery form the first training bout

Phase 2: Increased protein synthesis
* Upregulation of protein synthesis with repeated exercise (ADH, aldosterone)
* Increased reabsorption of water and sodium in kidneys increases plasma volume

31
Q

BV increases due to increased plasma volume and volume of RBCs
What are the two phases that lead to Increased Plasma Volume

A

Plasma volume is responsible for the increase in blood volume during first 2 weeks:
Two Phases leading to increased Plasma Volume:

Phase 1: Increases in plasma proteins
* Intense exercise → proteins (albumin) leave vascular space (into interstitial fluid) → ↑ number of proteins returned through lymph system → results in rapid plasma volume increase within the first hour of recovery form the first training bout

Phase 2: Increased protein synthesis
* Upregulation of protein synthesis with repeated exercise (↑ADH, ↑aldosterone)
* Increased reabsorption of water and sodium in kidneys increases plasma volume

Recall: ↑Plasma volume → ↑EDV → ↑SV

↑ADH → ↑ H2O reabsorption
↑Aldosterone → ↑ Na+ reabsorption (water follows)

32
Q

BV increases due to increased plasma volume and volume of RBCs
Why is increasing RBC volume a benefit?

A

Volume of red blood cells
* Increases with endurance training
* Increased oxygen-carrying capacity

Hematocrit may decrease (%RBC)
* Hematocrit = red blood cell volume/ total
blood volume
* Trained athlete’s hematocrit can decrease so athlete appears anemic

Increased plasma volume increases more than RBC volume
* Decreases viscosity (prevents thickening of blood)

Plasma volume is responsible for the increase in blood volume during first 2 weeks:
Two Phases leading to increased Plasma Volume:

Phase 1: Increases in plasma proteins
* Intense exercise → proteins (albumin) leave vascular space (into interstitial fluid) → ↑ number of proteins returned through lymph system → results in rapid plasma volume increase within the first hour of recovery form the first training bout

Phase 2: Increased protein synthesis
* Upregulation of protein synthesis with repeated exercise (↑ADH, ↑aldosterone)
* Increased reabsorption of water and sodium in kidneys increases plasma volume
↑ADH → ↑ H2O reabsorption
↑Aldosterone → ↑ Na+ reabsorption (water follows)

Recall: ↑Plasma volume → ↑EDV → ↑SV

33
Q

Adaptations in Muscle

How do MM fibre types change with endurance training?
Type I vs Type II

A

Adaptations with endurance training:
Muscle fiber type:
Type I oxidative muscle
* Increased cross-sectional area with training (change depends on intensity/duration/length of program)

Type II fast twitch
* Do not change in cross-sectional area with endurance training

34
Q

How does Capillary supply to mm change with aerobic training?

A

Capillary supply:
* Increased muscle fiber capillarization
* Important change with training that causes an increase in VO2max
* Diffusion of O2 from the capillary to the mitochondria is a major factor limiting the maximal rate of O2 consumption by the muscle

mm fibre closer to capillary will increase rate of O2 entering Mitochondria

35
Q

How does myoglobin Content change with endurance training?

A

Adaptations with endurance training:
Myoglobin content:
* Shuttle O2 from cell membrane to the mitochondria
* Acts as reserve to release O2 to mitochondria in transition from rest to exercise
* Muscle myoglobin increases 75 – 80% with endurance training

36
Q

How does Mitochondrial Function change with endurance training?

A

Mitochondrial function
* Increase in number and size of MIT
* Increases ability to use O2 and produce ATP aerobically
* Increase activity of MIT oxidative enzymes

Mito are bigger, with increased activity of oxidative enzymes leading to increased aerobic metabolism

Mitochondrial changes induced by aerobic training may result in glycogen sparing
* A slower rate of utilization of muscle glycogen and enhanced reliance on fat as a fuel source at a given exercise intensity

  • Study: FYI: MIT number increased 15% and size increased 35% during 27 weeks of exercise

Training induced increases in VO2max may be limited by the circulatory system’s ability to transport O2 than by the muscle’s oxidative potential

37
Q

Mitochondrial Quality improved by exercise training: (role of PGC-1α)?

A

Training → ↑biogenesis of new Mito; ↓ degradation of Mito; clears damaged Mito (mitophagy)

PGC-1α expression enhanced by both endurance and resistance training
* Regulatory protein involved in
(1) MIT biogenesis and
(2) replacement of old weakened MIT

Improves capacity to generate ATP by oxidative phosphorylation

38
Q

Glycogen sparing may be a result of mitochondrial changes, how?
What two factors are upregulated?

A

Mitochondrial changes induced by aerobic training may result in glycogen sparing
* A slower rate of utilization of muscle glycogen and enhanced reliance on fat as a fuel source at a given exercise intensity
* PGC-1α upregulated in skeletal muscle
* PDK4 upregulated in skeletal muscle

PGC-1α upregulated in skeletal muscle
* Improves capacity to generate ATP by oxidative phosphorylation

PDK4 upregulated in skeletal muscle
* Inhibits of carbohydrate oxidation
* Inhibits PDH activity which increases the influx of acetyl-coA from beta- oxidation into the Kreb’s cycle → enhances FA oxidation
* Reestablishment and/or sparing of the muscle glycogen stores and intracellular homeostasis after exercise

39
Q

Role of PGC-1α and PDK4 in skeletal muscle?

A

PGC-1α upregulated in skeletal muscle w/ endurance exercise
* Improves capacity to generate ATP by oxidative phosphorylation

PDK4 upregulated in skeletal muscle
* Inhibits of carbohydrate oxidation
* Inhibits PDH activity which increases the influx of acetyl-coA from beta- oxidation into the Kreb’s cycle → enhances FA oxidation (pyruvate won’t be converted to AcetylCoA (instead AcetylCoA from FA oxidation)
* Reestablishment and/or sparing of the muscle glycogen stores and intracellular homeostasis after exercise

40
Q

Pulmonary Ventilation adaptions in response to training:

A

Pulmonary ventilation:
Following endurance training:
At rest: pulmonary ventilation unchanged*
At maximal exercise intensity: ventilation is **substantially increased
*
* Support increase in VO2max

Increase in maximal pulmonary ventilation due to:
1) increased tidal volume
2) increased rate of breathing at maximal exercise

FYI: Untrained: 100 – 120 L/min prior to endurance training; 130 – 150 L/min
after endurance training
: Training results in elite athletes having rates of 180 – 200 L/min

41
Q

Exercise induced arterial hypoxemia:

A

Exercise-induced arterial hypoxemia → arterial O2 saturation decreases below 96% due to large right heart CO directed to the lung during exercise and consequently a decrease in the time the blood spends in the lung

In highly trained elite athletes/endurance training:
* Capacity for O2 transport may not be able to meet the demands of the limbs and cardiovascular system

42
Q

Pulmonary Diffusion adaptations to Training:

= Gas exchange in alveoli

A

Pulmonary Diffusion after training:
At Rest/Submax exercise: pulmonary diffusion (gas echange in alveoli) is unchanged

At Max intensity: Pulmonary Diffusion increases
- ↑ Pulmonary BF (esp to upper regions of lungs)
- ↑ Ventilation = more air in lungs
- ↑ # Alveoli involved in diffusion

43
Q

Arterial Venous O2 difference adaptations in response to exercise training?

A

Arterial-venous (a-v) oxygen difference:
At maximal exercise intensity:
*(a-v)O2difference increases
* Lower mixed venous O2 content → blood returning to the heart (mixture of venous blood from all body parts, not just active tissue) contains less O2 than it would in an untrained person
* Greater O2 extraction by active tissues due to greater oxidative capacity of active muscle fibers and a more effective distribution of blood flow to active tissues

44
Q

Metabolic Adaptations to Training

Lactate threshold adaptations to endurance training:

A

Training: can exercise at a higher percentage of VO2max before lactate begins to accumulate in the blood

-↑ MIT oxidative enxymes, MIT size and number → increased MIT capacity to generate ATP aerobically → ↑ Lactate Threshold
* Allows trained person to sustain a high percentage of aerobic capacity during prolonged
exercise without accumulating blood lactate

Lactate threshold (LT)→ the exercise intensity or relative intensity at which blood lactate begins to increase above baseline concentration
* The point at which during incremental exercise lactate production exceeds the rate of lactate clearance or removal

Aerobic/endurance training induces intracellular changes that enhance a muscle fiber’s capacity to aerobically generate ATP

45
Q

Respiratory Exchange Ratio: adaptations ot training?

A

Respiratory exchange ratio → RER = VCO2 / VO2 = CO2 produced/ O2 consumed
* Reflects the composition of the mixture of substrates being used as an energy source

Following endurance training:
* RER decreases at both absolute and relative submaximal exercise intensities
* Due to greater utilization of free fatty acids instead of carbohydrates at those work rates

RER ~ 0.7 to 1.0
* Low RER (0.7) indicates increased reliance on fats for energy production;
- high RER (1.0) reflects higher contribution of carbohydrates for energy production

46
Q

Fat Catabolism: changes with endurance training

A

Fat catabolism:
* Increased ability to oxidize FA (triacylglycerols stored within active muscle during steady-rate exercise)
* Facilitated release of FA from adipose tissue, higher quantity of fat-mobilizing enzymes
- Can exercise at higher absolute level of submax before fatigue occurs from glycogen depletion

Biochemical changes (increased MIT enzyme activity) drive FA oxidation (Decrease RER)

47
Q

Carbohydrate catabolism: changes with endurance exercise?

A

Carbohydrate catabolism:
* Increased ability to oxidize carbohydrate (pyruvate)

Important:
1) provides faster aerobic capacity than from fat breakdown
2) liberates 6% more energy than fat

(Review: Fat provides more energy than CHO but more O2 needed to oxidize fat than CHO)

48
Q

Integrated Adaptations to Chronic Endurance Exercise

During maximal exercise CO increases considerably and is largely responsible for the increase in ?

Increased maximal CO is the result of the increase in maximal ? that occurs with training induced changes in cardiac structure and function

A

VO2max = CO x (a-v)O2difference = rate of oxygen consumption

During maximal exercise CO increases considerably and is largely responsible for the increase in VO2max

Increased maximal CO is the result of the increase in maximal SV that occurs with training induced changes in cardiac structure and function

49
Q

Two Theories as to what limits Aerobic power and endurance performance

A

Limits of VO2max

Theory 1: Utilization theory:
* VO2max limited due to lack of sufficient MIT enzymes
* But: Endurance training increases oxidative enzymes, MIT number and size

Theory 2: Central and peripheral cardiovascular factors:
* VO2max limited due to central and peripheral cardiovascular factors the affect delivery of O2 to the active tissues
* Improvement in VO2max is seen following endurance training due to increased blood volume, increased CO (via SV), improved perfusion of active muscles with blood

50
Q

? is major limiter of endurance performance

A

Available O2 supply is major limiter of endurance performance
* O2 transport to working muscles not MIT/oxidative enzymes limits VO2max

Summary: not only cardiovascular factors but skeletal muscle adaptations (↑ MIT content and respiratory capacity of the muscle fibers) contribute to ability to perform prolonged high intensity submaximal exercise

51
Q

Long-Term improvement in Aerobic Power and endurance?

A

VO2max obtained within 12 – 18 months of intense endurance exercise

Endurance performance can continue to improve
* Ability to perform at increasingly higher
percentages of VO2max for extended periods

52
Q

Most important component in physical fitness is:

A

Cardiorespiratory fitness → most important component of physical fitness
* Low endurance capacity leads to fatigue, even in activities that are not aerobic
* Fatigue is a major deterrent to optimal performance
* Fatigue can hinder the athlete’s total performance

All athletes regardless of sport can benefit from maximizing cardiorespiratory endurance

Fatigue can hinder the athlete’s total performance * FYI:
1. Muscular strength is decreased
2. Reaction and movement times are prolonged
3. Agility and neuromuscular coordination are reduced
4. Whole-body movement speed is slowed
5. Concentration and alertness are reduced

53
Q

2 Goals of Aerobic Training

A

Goals of aerobic training:
1. Enhance central circulatory capacity to deliver O2
2. Increase active muscle’s capacity to consume O2

Improve capacity to generate ATP by oxidative phosphorylation

54
Q

4 Factors influencing outcomes of aerobic training?

A

Factors influencing outcomes of aerobic training:
1. Initial level of cardiovascular fitness
2. Training frequency
3. Training duration
4. Training intensity