Exam 3- Lecture 20 Flashcards
Spectrum of disease
reduced activity –> bedrest, microgravity –> casting –> SPI
What decreases initially when highly trained athletes are detrained?
- SV due to early blood volume loss
- dextran (antithrombotic) can reverse fall in SV
what is slower to reverse when highly trained athletes detrain?
- a-v O2 difference
- takes about 3 months for capillary density and mitochondrial activity to decrease
how quickly does VO2max reverse with detraining after short term training (10 weeks)
- complete in 8-12 weeks
- initial fall is due to decreased SV
what occurs after 3 months of detraining after a short term training (10 weeks)
- mitochondrial enzyme content completely returns to sedentary levels
- capillary density reverses partially to fully
do structural or functional adaptations persist longer?
structural adaptations
Long term MAY result in ….
structural adaptations that persists for “long” periods of time
How long does it take for VO2 max to decrease with bedrest?
20 days
explain the physiologic process that happens with bed rest:
supine position –> shift in blood volume to thoracic cavity –> stimulates atrial volume receptors can either:
increase ANP –> H2O excretion –> fall in plasma volume –> lower SV and VO2 max
OR
reflexively inhibit ADH and renal SNA –> increases sodium excretion –> fall in plasma volume –> lower SV and VO2 max
Cardiovascular consequence of bed rest
Reduced orthostatic tolerance:
- tendency to faint when standing
- reduced submaximal exercise tolerance
explain why people who have been on bed rest have a tendency to faint when standing
- lower plasma volume
- increase venous compliance due to excess CO stored in venous circulation
explain why people who have been on bedrest have reduced tolerance to submaximal exercise
- decreased exercise time
- due to decrease in enzymatic oxidative capacity
- higher HR at submax intensities
Muscular adaptations to disuse (casting)
- some neural and isometric tension can occur
- muscle atrophy
what is muscle atrophy
reduction in muscle size primarily through reduction in contractile proteins
does atrophy occur faster in disuse or detraining
disuse
degree of immobilization- induced atrophy is related to:
- degree of disuse or immobilization
- initial level of use –> most used get most atrophic
- duration of immobilization
what is muscle strength loss (due to disuse) correlated with?
- reduction in cross sectional area
- peaks at 6 months
What is the metabolic response to disuse?
- reduction in oxidative capacity and glycogen storage
- increased fatigability
- subtype reverts to pre-training fiber distribution
what does unloading a lower limb muscle to 5 weeks do?
- increases vulnerability to eccentric-exercise induced injury
- injury during reloading phase in rehab may be sufficient to prolong recovery
- emphasizes the use of low intensity exercise during the initial return to ambulation
irradiation
bilateral corticospinal activity occurs with intentional unilateral muscle activation via corpus callous and pyramidal decussation
what can maintain mitochondrial function and attenuate atrophy after immobilization?
heat
what occurs to calcium metabolism with disuse?
- balance between new bone formation and resorption is disrupted by prolonged bed rest, immobilization, weightlessness
Changes in BMD with detraining
occurs in adults > 50 years old
cessation of regular weight bearing exercise
may result in decreased spine BMD back to sedentary levels
Is disuse osteopenia reversible?
- yes –> takes days
- BMD changes take much longer –> 5-10x longer than immobilization period
- long term disuse osteopenia may result in a permeant reduction in BMD
