Mueller Flashcards

1
Q

How are bed rest and space flight similar?

A

Head Down Bed Rest (-6°): reversed (removed) influence of gravity on hydrostatic columns; inactivity leads to reduced muscle use and reduced loading of bone

Spaceflight: loss of influence of gravity on hydrostatic columns; relative inactivity due to reduced muscle effort and work, and reduced loading of bone

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2
Q

How does bedrest and space flight effect muscle mass/strenght? What effect does muscle loss have on the body?

A

Bedrest = reduced activity, lack of requirement to maintain upright posture
Spaceflight = reduced work against gravity, no “upright” in space
** the gravitational load is necessary to maintain postural muscle size and force; thus

Results in: muscle loss, mostly in lower limbs and back muscles (postural muscles)

Protein loss due to decreased protein synthesis rather than increased protein breakdown (not moving therefore don’t want to expend extra energy on synthesis of protein when you’re not going to use the muscles)

Can increase dietary protein to prevent decreases in protein synthesis

Effects of Muscle Loss:

oNegative protein balance (too much protein loss can be fatal)

oDecreased strength due to:
•Atrophy
•Altered motor control
•Changes in properties of contractile machinery
•Reduced efficiency of EC coupling
•Decreased tendon stiffness (makes contraction less efficient)

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3
Q

What effect does bedrest/space flight have on the skeletal system?

A
  1. Loss of bone mass and strength (due to increased excretion and decreased reabsorption of Ca++); can mimic osteoporotic changes similar to aging
    The magnitude of bone loss in bed rest is less than in spaceflight (because sometimes in bed rest you get up and while you lay you also do slight movement, in space you can’t escape the effect of no gravity)
  2. Action of muscles on bone required to promote bone building ; therefore less mechanical usage sensed by mechano-sensing osteocytes and results in bone unloading

Note: supplementing with vitamin D or Ca++ during bed rest does not prevent bone loss, so culprit is inactivity no a mineral

**Takes a long time after bed rest to recover from bone loss; resistance exercises can prevent bone loss during bed rest

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4
Q

What effect does bedrest/space flight have on metabolism?

A
  • Energy requirements reduced to basal metabolic rate (lower BMR in bed/space); small percentage of metabolism is due to energy expenditure from residual small movement and thermogenesis during digestion
  • Matching individual energy requirements is challenging (don’t want the patient to gain or lose too much weight)
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5
Q

What effect does bedrest/flight have on insulin?

A
  • Bed rest and spaceflight reduce insulin sensitivity (increase insulin resistance) due to decreased exercise
  • Exercising prior to bed rest can combat this effect
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6
Q

What are some of the other changes that occur during bedrest/space (not skeletalmuscular, not metabolism, not insulin)

A
  • Decrease in RBCs, erythropoietin (due to decreased exercise therefore there is a decreased energy requirement)
  • Vestibular system: balance issues, changes in gait
  • Emotional and Hormonal: associated with confinement and isolation
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7
Q

How does bedrest/spaceflight effect CV homeostasis?

A
  1. Immediate response (24 hours): = adaptations to hypovolemia and Na+ loss;
    reduced SNS activity and reduced vasocontriction , reduced vascular responsiveness to vasoconstrictors (decreased barorreceptor response); all effects lead to orthostatic hypotension/intolerance
    soo when you stand back up, blood flows back down to legs and the increase in blood there causes othorstatic intolerance
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8
Q

Explain the Astronaut Stand Test

A

asked astronauts to stand for 10 minutes after they returned from space;

Finishers: BP maintained by increasing HR (SV decreases) and increasing TPR greatly

Nonfinishers: could not maintain BP due to orthostatic intolerance; greater HR increase than finishers with similar decrease in SV, but TPR could not increase enough (BP fell)

Results suggest a problem due to reflex response or change in vasculature (in non-finishers, because you can’t increase TPR, means you can’t constrict the vasculature as well) more studies also prove this: that in response to an orthostatic challenge, there is less activation of the sympathetic nervous system to promote vasoconstriction following real or stimulated bed rest

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9
Q

What are some of the predisposing factors for othostatic intolerance?

A

o Low vascular resistance below and after flight; low NE release during orthostatic stress after flight

oLow alpha-adrenergic (vasoconstriction) responsiveness before flight and changes in central nervous system control such as sympathetic response to baroreceptor input become impaired after flight

oAssociated with being taller, low resting BP, greater changes in resting lower limb distensibility, and absence of counter measures

oFemales have greater risk (decreased plasma volume, less baroreflex SNS excitation)

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10
Q

How does bedrest/spaceflight effect exercise capcity

A

results in a DECREASED exercise capacity due to:

  1. Cardiac mechanism (pump mechanisms): decreased plasma volume = decreased venous return = decreased stroke volume = decreased cardiac output
  2. Peripheral mechanism (not as important):
    decreased baseline and maximal muscle blood flow and decreased RBC volume = decreased capillarization in working muscles
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11
Q

What are some of the countermeasures that can be taken to offset effects of prolonged bed rest or spaceflight?

A

Primary types:
1. Nutritional (fluid and Na+ loading); attempts to restore PV (isotonic fluid infusion) but doesn’t really work because it increases PV initially, but then the body just loses it again

  1. Lower body negative pressure:
    induces a fluid shift from UPPER to LOWER part of the body (so that you don’t perceive an increase in fluid and cause hypovolemia); repeated daily sessions show benefit on orthostatic intolerance; prolonged use can cause fainting due to reduced BP at head level
  2. Exercise:
    single bouts of acute maximal exercise are beneficial in overcoming OI; used in combination with lower body negative pressure to prevent orthostatic intolerance and prevent the decrease exercise capacity ; resistive exercise (via high intensity loading) is the most effect to counteract loss of bone mass and strength and improves tendon stiffness
  3. Pharmacological:
    atropine = blocks muscarinic acetylcholine therefore it blocks PS (vagal reflex)
    Propranolol = beta blocker
    FLUDROCORTISONE = EFFECTIVE AGAINST OI
    MIDODRINE = ALPHA 1 AGONIST; stimulates arterial and venous vasocontriction
  4. Artificial gravity
    promising alternative approach (potitally mitigates bone loss, CV issues, muscle atrophy, and neurovestibular disturbances) ; acts on all physiological systems at once; rotates entire space vehicle or use on onboard centrifuge
  5. Thigh Cuffs
  6. Combination Measures:
    currently used in Spaceflight: exercise, fluid loading, anti G suit, LBNP
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12
Q

What are some of the spaceflight specific influences?

A
  • Launch activities (acceleration, excitement)
  • Confinement and isolation
  • Environment (light and pressure)
  • Conflict in visual and vestibular systems due to absence of usual directional cues (“space motion sickness”)
  • Re-entry acceleration profiles
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13
Q

What is maximal oxygen consumption? How is it related to sedentary individuals?

A
  • Level of physical conditioning influences the magnitude of maximal oxygen consumption
  • Sedentary individuals have the lowers maximal oxygen uptake

Both ends of the spectrum = extreme: in highly trained elite athletes, super high O2 consumtion and super positive cardiovascular health

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14
Q

How do you calculate oxygen consumption?

A
Fick Equation: VO2= CO x (CaO2-CvO2)
VO2= oxygen consumption
CO= cardiac output
CaO2= arterial blood oxygen content
CvO2= venous blood oxygen content
CaO2-CvO2= amount of O2 from each ml of blood transported to and consumed by the tissue
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15
Q

How does oxygen consumption (VO2) vary between rest and maximal exercise?

A

At Rest: VO2 is lower (mostly due to increase venous oxygen content)

Maximal Exercise:
VO2 is higher (~3 fold increase; mostly due to decrease in venous oxygen content)

Exercise can also increase arterial oxygen capacity slightly (due to splenic contraction and release of more RBCs)

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16
Q

What is the highest attributable fraction?

A

Inactivity (Cardiorespiratory fitness, CRF) has the highest attributable fraction (the percentage of deaths that could have been avoided if a particular risk factor was not present)

17
Q

What role does cardiac output have on determining oxygen consumption?

A

CO = HR x SV
Rest: HR = 60 bpm, SV = 70mL (CO = 4.2 L/min)
Exercise: HR = 180 bpm, SV = 110 mL (CO = 19.8 L); heart rate increases due to increase in SS activity and decreased PS activity
As heart rate increases with exercise the stroke volume cannot increase anymore because filling time decreases (therefore SV levels off as exercise continues)

18
Q

What determines SV?

A

Increased heart rate → decreased fill time
Increased contractility → decreased ESV (more blood ejected)
Increased preload → increased EDV
Increased afterload → increased ESV (less blood ejected)
Decreased ejection time → increased ESV (less blood ejected)

19
Q

How does bed rest effect maximal oxygen consumption in dynamic exercise?

A
  1. CO:
    at rest = no difference between exercise trained, control, and red rest;
    exercise = Bed rest &laquo_space;control &laquo_space;exercise trained
  2. O2 Extraction:
    at rest = no difference between exercise trained, control, and red rest;
    during exercise = bed rest = control control > exercise trained
    during exercise: bed rest = control = exercise trained
  3. SV
    at rest: bed rest < control = exercise trained
    during exercise: bed rest «< control &laquo_space;exercise trained
    *** this is what causes the major difference in CO and VO2 between bedrest/ exercised individuals!
20
Q

What is the relationship between CRF and O2 consumption?

A

Low cardiorespiratory fitness (CRF)= low maximal O2 consumption

21
Q

What is BMI and what does it tell you about heart disease/other problems?

A

Body Mass Index (BMI): weight (kg)/ height (m)2

The higher your BMI, the higher your risk for diseases like heart disease, HTN, type II diabetes etc.

However, cannot just rely on BMI, because studies show that obese men who were moderately fit had less than half the risk of dying than normal-weight men who were unfit

22
Q

What is a Hazard Ratio and what effect does CRF/exercise have on it?

A

Hazard Ratio (HR): indicatory of how much the risk is increased or decreased in one group relative to another for an all cause mortality (adjusts for confounders like smoking and high cholesterol)

Increasing CRF decreases hazard ratio

Largest benefit seen from making transition from most unfit group (Q1) to the next level of fitness (Q2) but with each increasing level of fitness there is still an increased benefit

23
Q

What is the effect on a person who is both physically active and highly sedentary

A
  1. Prolongers = spend more continuous periods engaging in sedentary behavior (ie. sitting down)
    - Have greater waist circumference than breakers (relationship stronger in those who were overweight or obese)
    - More sitting time = greater mortality, even among those who were physically active
  2. Breakers = break up sedentary time with more frequent periods of nonsedentary time
24
Q

What are some of the effects of inactivity on the body?

A
o	HTN
o	Congestive heart failure
o	Arrhythmias
o	Stroke
o	CAD
o	Diabetes
o	Obesity
25
Q

What are the three basic mechanism of daily caloric expenditure (not involving exercise)?

A
  1. BMR
  2. Non-exercise activity thermogenesis (NEAT)
  3. THermic effect of food
26
Q

Describe NEAT (non-exercise activity thermogenesis)

A
  • Based on posture- sitting, standing etc.
  • Obese individuals found to sit, on average, 2 hours per day longer than lean individuals
  • Results did not change when obese individuals lost weight or when lean individuals gained weight (this suggests that our NEAT behaviors are biologically determined.. not due to a physical effect of carrying more weight)
27
Q

What are some of the effects of exercise on regulation of arterial pressure?

A
decreased HR
decreases BP
increased SV
slightly increased CO
decreased TPR

all beneficial to decreasing BP and improving it for exercise

28
Q

What autonomic control changes are induced by physical activity?

A

exercise increases resting PS activity and decreases resting SS activity, making a person less susceptible to arrhythmias and decreasing resting BP