W11 - Adaptations (3.7) Flashcards Preview

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Flashcards in W11 - Adaptations (3.7) Deck (40):
1

Describe the 3 energy systems of skeletal muscle.

Graph.

  • power events (few seconds): 
    immediate E sources = ATP, CrP
  • several seconds - minute:
    non-oxidative breakdown of glycogen
  • 2 minutes and longer:
    oxidation of fat and glucose derived from circ.

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2

How does the oxygen consumption (= VO2) change w/ increasing intensity of exercise?

Explain.

Graph.

increases to ensure an increased rate of ATP generation

due to incr. tidal volume (1l) and incr. breathing frequency (60/min)

0, 50, 100, 150 W

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3

How does the VO2 of athletes differ from that of untrained people?

Graph.

increased VO2max
functional capacity of body's ability to generate aerobic power

→ O2 uptake by lungs sufficient even during higher intensities, plateaus later

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4

Which 3 steps limit the O2 transport from atmosphere to muscle?

How can they be influenced?

  1. O2 uptake by lungs depends on pulmonary ventilation  (↑ alveolar ventilation → ↑ O2 uptake)
  2. O2 delivery to muscle depends on cardiac output and O2 content (↑ CO → O2 delivery)
  3. extraction of O2 from blood by muscle depends on O2 delivery and PO2 gradient btw blood and mitochondria (↓ PO2 in mixed venous blood)

5

Values for

  • O2 content of ambient air
  • alveolar air

  • ambient air = 21%
  • alveolar air = 15%

NOTE: values don't change, even during exercise

6

Values for O2 consumption

  • at rest
  • of untrained person during exercise
  • of trained person during exercise

How does it affect alveolar ventilation?

  • at rest = 250ml/min
  • untrained person during exercise = 2500 - 3000ml/min
  • trained person during exercise = 4000 - 4500ml/min

​→ increases alveolar ventilation in order to meet its demands

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7

Why is the alveolar ventilation in trained people increased?

Values.

elevated vital capacity → higher reserves to elevate tidal volue
BUT: same breathing frequency as untrained persons during exercise (60/min)

  • resting tidal volume = 500ml
  • tidal volume in untrained = 1l
  • tidal volume in trained = 1.3l 

REMEMBER: VA = (TV - VD) * resp. rate

 

8

Values for

  • CO2 content of ambient air
  • alveolar air

  • ambient air = 0%
  • alveolar air = 5%

​NOTE: values don't change, even during exercise

9

How does the production of CO2 (= VCO2) change during exercise?

Values

  • at rest
  • of untrained person during exercise
  • of trained person during exercise

increases due to increased E demand in muscle

  • at rest = 200ml/min
  • untrained person during exercise = 2500ml/min
  • trained person during exercise = 3500ml/min

10

Values for O2 extraction

  • at rest
  • of a untrained person during exercise
  • of a trained person during exercise

O2 extraction = CO * ΔPO2,art-ven

  • at rest = 250ml/min
  • of a untrained person during exercise = 2700ml/min
  • of a trained person during exercise = 3750ml/min

→ during exercise ΔPO2,art-ven incr. to 150ml/l

11

How much O2 is normally stored in the body?

Where?

∽ 2l

  • 0.5l in the air of the lungs
  • 0.25l dissolved in the body uids
  • 1l combined with the Hb of the blood
  • 0.3l stored in the muscle fibers, combined mainly with myoglobin

12

Define oxygen debt.

 

in periods of incr. metabolic rate

  • O2 storages are rapidly depleted for aerobic metabolism (2l)
  • disturbances in ATP/CrP and lactic acid system (9l)

incr. O2 uptake to “repay” about 11.5l of O2
= O2 debt

13

Draw and explain the graph how O2 uptake increases during and after exercise.

incr. O2 uptake during + even after exercise

  • during exercise: reconstituting the ATP/CrP system and repaying the stored O2
    = alactic O2 debt ∽ 3.5l
  • after exercise: lowered level to remove lactic acid 
    = lactic acid O2 debt ∽ 8l

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14

Define anaerobic treshold.

Why is it physiologically important?

Graph.

at VO2 = 1.5l/min. = anarobic threshold​​
VO2 above which aerobic E production is supplemented by anaerobic mechanisms, causing a sustained incr. in lactic acid

  • accumulates in blood → ↓pH (= metabolic acidosis)
  • combines w/ HCO3-, CO2 formed → ↑ exhaled CO2 (= VCO2)
  • ↑ respiratory quotient (= VCO2/VO2)
  • ↑ ventilation (unproportional incr. to HR)
  • cardiac output close to maximum

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15

How does the lactate level in the blood change during heavy exercise?

Explain.

  1. isovolumetric contr. of skeletal m. compresses vessels → no further blood flow, insufficient O2 delivery
  2. lactic acid generated during anaerobic E production accumulates in blood
  3. metabolized in liver (Cori cycle), but reaches maximum capacity at anaerobic threshold

NOTE: lactic acid elevates local blood flow

 

16

How does the heart rate change w/ increasing intensity of exercise?

Explain.

Graph.

incr. up to 3 times resting heart rate

contraction of sk. m. → ↑ metabolites → local vasodilation → ↓ MAP → arterial baroreceptors → ↑ HR

0, 50, 100, 150 W

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17

Values for HR

  • of untrained person at rest
  • of trained person at rest
  • during exercise

  • of untrained person at rest = 60 bpm
  • of trained person at rest = 50 bpm
    → physiological bradycardia
  • during exercise = 180 bpm

18

How does the stroke volume change w/ increasing intensity of exercise?

Explain.

Graph.

incr. up to 1.5 times resting stroke volume

contraction of sk. m → muscle pump → ↑ venous return → ↑ right atrial pressure → ↑ end-diastolic pressure → ↑ EDV → ↑ stroke volume

0, 50, 100, 150 W

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19

Values for stroke volume

  • at rest
  • of untrained person during exercise
  • of trained person during exercise

  • at rest = 70ml
  • of untrained person during exercise = 100ml
  • of trained person during exercise = 150ml

20

How does the cardiac output change w/ increasing intensity of exercise?

Explain.

Graph.

incr. up to 4-5 times resting CO

result of incr. HR and stroke volume

0, 50, 100, 150 W

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21

Values for stroke volume

  • at rest
  • of untrained person during exercise
  • of trained person during exercise

  • at rest = 5l/min
  • of untrained person during exercise = 18l/min
  • of trained person during exercise = 27l/min

22

How does the pulmonary pressure change during exercise?

Explain.

↑ CO → ↑ pulmonary art. pressure → dilation → ↓ pulmonary resistance

23

How does the arterial pressure change w/ increasing intensity of exercise?

Explain.

Graph.

  • strong incr. in systolic pressure due to vasoconstriction in inactive tissues triggered by symp. nervous system
  • slight incr. in diastolic pressure
  • incr. in MAP

BUT: TPR decreases as a result of vasodilation in skin vessels for thermoregulation offsetting incr. in MAP

0, 50, 100, 150 W

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24

How does the TPR change w/ increasing intensity of exercise?

Explain.

Graph.

decreases as a result of

  • vasodilation in skin vessels → thermoregulation
  • vasodilation of arterioles due to ↑ metabolites
  • capillary recruitment

NOTE: offsetting incr. in MAP

0, 50, 100, 150 W

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25

How does the AVDO change w/ increasing intensity of exercise?

Explain.

Graph.

increases bc mm. are avidly extracting O2 from blood stream

due to shift in Hb O2 dissociation curve

0, 50, 100, 150 W

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26

How is blood redistributed during exercise?

  • away from organs w/ no imm. nec. function
    • splanchnic 
    • kidney
    • skin
  • toward organs w/ imm. nec. function
    • brain
    • heart
    • working mm.
    • skin in case of core temp. elevation

27

List some further biochemical adaptations to exercise.

  • incr. control of citric acid cycle enzymes
  • conversion of glycogen phosphorylase b to a
  • vasoneogenesis
  • incr. maximal O2 uptake
  • hypertrophy of sk. muscle

28

Define circulatory shock.

Different types?

reduced CO and reduced arterial pressure due to pathology emerging in the vascular system

  • hypovolemic shock
  • cardiogenic shock
  • distributive shock
  • obstructive shock

29

What happens in case of a hypovolemic shock?

Reason?

blood volume → impairs ventr. filling
→ ↓ CO and ↓ MAP

e.g. due to hemorrhage, exsiccocsis
most common type of circulatory shot

30

What happens in case of a cardiogenic shock?

Reason?

↓↓ CO → peripheral alterations

e.g. heart infarct affecting large ventricular masses

31

What happens in case of a distributive shock?

Reason?

loss of tone of peripheral vessels → ↓ MAP

e.g. due to bacterial infection, spinal shock

32

What happens in case of a obstructive shock?

 

obstruction of sufficient part of circulation

33

What are symptoms of a hemorrhagic shock?

List SOME.

  • signs of blood loss on scene and on the body of patient
  • pulse, heart beats frequent (sympathetic)
  • pulse feeble, can be easily suppressed (low MAP)
  • Psys < 70 mmHg (diastolic can not be measured)
  • skin pale, cool (vasoconstriction, sympathetic, loss of RBCs)
  • confusion, blurred conscience, communication difficulties (cerebral autoregulation fails at 60 mmHg MABP) 
  • breathing unfrequent, shallow (brain stem respiratory centers affected, weakness of respiratory muscles)
  • anuria (no filtration at 60 mmHg)
  • thirst (AT II, Vasopressin, low pressure baroreceptors)
  • metabolic acidosis, arterial pO2 can be normal

34

What are the stages of a hemorrhagic shock?

Graph.

  1. progressive stages:
    blood loss of 200 - 600ml → can be controlled by BP control mechanisms
  2. irreversible shock:
    blood loss of 1200+ ml → results in death in a few hours unless transfusions are applied

 

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35

Which negative feedback mechanism is the most important in order to restore blood pressure in case of a hemorrhagic shock?

Effects?

high pressure baroreceptor reflexes down to about 60-70 mmHg MAP

⇒ tachycardia, proper redistribution of cardiac output

36

Which negative feedback mechanisms are activated in order to restore blood pressure in case of a hemorrhagic shock?

 

  1. Low pressure baroreceptor reflexes (also contributing to volume control)
  2. peripheral and central chemoreflexes, Cushing reflex (at 20-40 mmHg MAP)
  3. restoration of plasma volume from extracellular space (Starling forces)
  4. anaeorobic metabolism in tissues with this ability (metabolic acidosis)
  5. AT II-aldosterone (vasoconstriction, volume saving, tubulo-glomerular feed-back, thirst)
  6. Vasopressin 
  7. decreased GFR as a result of reduced MAP, glomerulotubular feedback, anuria below 60 mmHg MAP restoration of urine flow when MAP is restored with limited delay
  8. restoration of RBC mass, several days after (EPO, reticulocytosis)

37

Which mechanisms prevail in uncompensated shock situations?

positive feedback mechanisms activated

  • ↓ coronary circulation due to reduced MAP, ↓ ventricular contractility, it further ↓ MAP
  • ↓ brain circulation reduces the activity of brainstem circulatory and breathing centers, loss of peripheral sympathetic tone, vasodilation, hypoxia, further ↓ MAP
  • endothelial damage due to hypoxia and low flow, closure of capillaries
  • anaerobic metabolism, lactic acid dilates vascular smooth muscle, low pH damages

38

What happens in case of acute mountain sickness?

At which heights can it usually appear?

3000+ m

↓ Pbar → ↓Palv → hypoxemia

  • stimulation of per. chemoreceptors
    hyperventilation + resp. alkalosis
  • stimulation of EPO production
    → ↑Hb → ↑O2 content
  • pulmonary vasoconstriction
    → ↑Ppul → right ventr. hypertrophy, pulm. edema
  • ↑ 2,3-BPG → unloading of O2 in tissue

39

What happens in case of adaptation to acute mountain sickness?

  • adaptation to resp. alkalosis
  • breathing driven by pO2 not by pCO2
  • biochemical adaptation to lower tissue pO2
  • incr. Ht (EPO)

​(Tibetian pop. has incr. expression of PHD2 gene which induces HIF2α for incr. RBC development)

40

What is the effect of microgravity on the cardiovascular system?

What happens after landing?

during space flights
missing gravitational effects

→ art. pressures equilibriate in the body (100 mmHg), venous orthostatic reflexes disappear

BUT: after landing rapid regain of venous orth. reflexes → fainting

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