W11 - Adaptations (3.7) Flashcards

(40 cards)

1
Q

Describe the 3 energy systems of skeletal muscle.

Graph.

A
  • 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
Q

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

Explain.

Graph.

A

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
Q

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

Graph.

A

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
Q

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

How can they be influenced?

A
  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)
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5
Q

Values for

  • O2 content of ambient air
  • alveolar air
A
  • ambient air = 21%
  • alveolar air = 15%

NOTE: values don’t change, even during exercise

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6
Q

Values for O2 consumption

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

How does it affect alveolar ventilation?

A
  • 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
Q

Why is the alveolar ventilation in trained people increased?

Values.

A

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

<u>REMEMBER</u>: VA = (TV - VD) * resp. rate

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8
Q

Values for

  • CO2 content of ambient air
  • alveolar air
A
  • ambient air = 0%
  • alveolar air = 5%

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

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9
Q

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

Values

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

increases due to increased E demand in muscle

  • at rest = 200ml/min
  • untrained person during exercise = 2500ml/min
  • trained person during exercise = 3500ml/min
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10
Q

Values for O2 extraction

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

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

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11
Q

How much O2 is normally stored in the body?

Where?

A

∽ 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
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12
Q

Define oxygen debt.

A

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

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13
Q

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

A

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
Q

Define anaerobic treshold.

Why is it physiologically important?

Graph.

A

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
Q

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

Explain.

A
  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

<u>NOTE:</u> lactic acid elevates local blood flow

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16
Q

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

Explain.

Graph.

A

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
Q

Values for HR

  • of untrained person at rest
  • of trained person at rest
  • during exercise
A
  • of untrained person at rest = 60 bpm
  • of trained person at rest = 50 bpm
    → physiological bradycardia
  • during exercise = 180 bpm
18
Q

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

Explain.

Graph.

A

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

19
Q

Values for stroke volume

  • at rest
  • of untrained person during exercise
  • of trained person during exercise
A
  • at rest = 70ml
  • of untrained person during exercise = 100ml
  • of trained person during exercise = 150ml
20
Q

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

Explain.

Graph.

A

incr. up to 4-5 times resting CO

result of incr. HR and stroke volume

0, 50, 100, 150 W

21
Q

Values for stroke volume

  • at rest
  • of untrained person during exercise
  • of trained person during exercise
A
  • at rest = 5l/min
  • of untrained person during exercise = 18l/min
  • of trained person during exercise = 27l/min
22
Q

How does the pulmonary pressure change during exercise?

Explain.

A

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

23
Q

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

Explain.

Graph.

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

<u><strong>BUT:</strong></u> TPR decreases as a result of vasodilation in skin vessels for thermoregulation offsetting incr. in MAP

0, 50, 100, 150 W

24
Q

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

Explain.

Graph.

A

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

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
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
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