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5. ADV PHYS > Exercise II > Flashcards

Exercise II Flashcards

1
Q

why does CO and ventilation rate rise during exercise in lung: list (5)

A

increase:

  • pulmonary blood flow/ ventilation rate for increased gas exchange
  • blood flow through exercising mm (incl heart)
  • maintain arterial pH, limit acidification and metabolite build up in ex mm
  • maintain/increase BP
  • blood flow to skin, prevent overheating
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2
Q

at VO2 max: ventilation at %

A

50%

~ 170L/min in healthy male

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3
Q

at VO2 max: arterial PO2, mixed venous PCO2 %

A

near normal

- respiration not limiting factor in exercise

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4
Q

at VO2 max: CO %

A

95%

- cardiovascular function is limiting factor at max exercise

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5
Q

cardiac function during exercise: untrained healthy person- stroke vol increases until % VO2? why does CO increase

A
  • 40% of VO2 max

- increase in CO due to HR increase

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6
Q

cardiac function during exercise: elite athlete- stroke vol increases due to

A
  • not only CO,
  • hypertrophy of L ventricular mm
  • increase vol of lumen too
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7
Q

list major responses during exercise (5)

A

increased:

  • HR and stroke vol
  • BP to increase flow (Darcy’s law)
  • reduced TPR (vasodilation in mm)
  • redirection of blood from visceral areas -> active mm
  • blood flow to skin (stop overheating)
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8
Q

response during exercise: activation of which para/sym and effect

A
  • activate sym
  • reduced para output
  • increase HR, circulating Ad and symp neurons increase contractility of ventricular myocytes
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9
Q

response during exercise: symp nn on vasoconstriction

A
  • constrict arterioles of organs not involved in exercise
  • renal, splanchnic beds (liver, spleen, GIT)
  • helps redistribute increased CO to exercising mm to help limit fall in TPR (when vasodilation in mm)
  • brain blood flow not affected (perfusion of brain under local vs central control)
  • 80% of increased CO channelled through mm
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10
Q

response during exercise: blood flow to exercising mm and features

A
  • from 1L/min -> 19 L/min
  • increased CO, locally induced vasodilation
  • low PO2, high PCO2, low pH, NO, K+, phosphate, adenosine, histamine, prostaglandins)
  • accumulated substances directly on vascular smooth mm cause relaxation = vasodilate
  • local control, matches blood flow to metabolic requirements of exercising mm
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11
Q

response during exercise: symp release onto å-adrenergic receptors

A
  • on walls of resistance vessels
  • limits blood flow to maintain BP, but effect of NAd modulated by local factors
  • increase exercise: ADH (vasopressin) and angiotensin II released (protect BP)
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12
Q

response during exercise: at rest % skeletal mm capillaries collapsed

A

50-80%

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13
Q

response during exercise: why decrease TPR

A
  • mm mass makes up most of body’s vascularised tissue

- BP only rise lil despite increase CO

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14
Q

response during exercise: increased flow and reduced compliance in v=

A
  • increase VR so increase CO (frank-starling relo)
  • skeletal mm pump
  • thoracic pump accelerate flow blood back to heart
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15
Q

response during exercise: thoracic pump

A
  • caused by more -ve pressure in thoracic cavity

- produced by inspiratory effort during exercise

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16
Q

mean arterial BP determined by:

A

CO x TPR

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17
Q

define systolic BP:

A
  • max BP in cardiac cycle

- when L ventricle ejects blood

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18
Q

systolic BP mostly effected by

A
  • changes in stroke vol

- arterial compliance

19
Q

define diastolic BP:

A
  • vol of blood remaining in aa at end of ventricular filling phase
20
Q

diastolic BP determined by:

A
  • resistance faced by blood when flows from aa to veins (TPR)
  • time allow for flow before ejection phase (HR)
  • recoil of elastic aa (esp aorta) during diastole increase diastolic P
21
Q

during whole body dynamic exercise: what effects on systolic BP

A
  • strong stimulation of sym NS
  • increased VR, increasing stroke vol
    = increase systolic BP
22
Q

during whole body dynamic exercise: what effects on diastolic BP

A
  • vasodilation of arterioles decreased TPR

- expected to decrease diastolic but not due to increase HR

23
Q

during whole body dynamic exercise: result of systolic and diastolic P for MAP

A
  • increase in mean arterial pressure
24
Q

control of CO sys: central command features

A
  • increased CO due to high centres f brain (learned reflex)
  • centres influence output from CV control centres in medulla
  • initial signals (somatic motor nn) cause skeletal mm to begin movement, paralleled by changed in output in autonomic NS
  • HR increases from 1st beat after initiation of exercise
  • central command feedforward control sys
25
Q

control of CO sys: mm metaboreflex features

A
  • depends on metabolic products accumulating in exercising mm, stimulate receptors feedback via sensory nn to medullary CV centre
  • aerobic ex: rise CO parallels O2 consumption
  • done by tight control of -ve feedback sys
  • mm metaboreflex: stimulate sym output in CV control centre in medulla
  • mechanoreceptors in mm, send sensory info on movement/ position of mm to medulla
26
Q

control of CO sys: local control features

A
  • changes in local env (low PO2, high PCO2, low pH, increased lvls of NO, K+, phosphate, adenosine, histamine, prostaglandins) due to increase metabolic rate in exercising mm
  • directly produce vasodilation of vascular smooth mm in walls of arterioles (ex mm)
  • reduces resistance in ex mm, for whole body= decrease TPR
  • lower TPR, skeletal mm pump/ thoracic pump increase VR = increase CO
27
Q

baroreceptor function: features

A
  • stretch receptors in walls of aortic/ carotid aa

- when stretched by high BP freq of AP from receptors INHIBIT sym output, activates para output

28
Q

baroreceptor function: mechanism of inhibiting sym output

A

stimulate glutamate to nucleus of solitary tract (NTS) in brainstem - activate GABA neurons from caudal ventrolateral medulla (CVLM) to (RVLM)

  • baroreceptor induced inhibition of interneurons of RVLM
  • as they synapse w pregang sym neurons in SC, sym output = reduced
29
Q

baroreceptor function: resetting baroreceptors

A
  • increased BP needed for increased blood flow during ex.
  • ‘set point’ in baro reflex increased to higher BP, sensitivity (gain) reduced
  • initiated by input from higher centres of brain (via hypothalamus) and mm receptors (metaboreceptors, mm mechanoreceptors)
  • inhibit glutamate releasing neurons to RVLM - eventually = activate sym neurons
30
Q

baroreceptor function: most of increased HR at start of exercise due to

A

up to 100bpm

- due to reduced para inhibition on pacemaker cells of heart

31
Q

hormones/exercise: stimulation of sym NS

A
  • release Ad, some NAd = increase CO by direct effects on HR, strength contraction, decrease venous compliance for increased VR
  • hormones involved in vasoconstriction of arterioles in ab organs = redirect blood, maintaining BP
32
Q

hormones/exercise: role of Ad

A
  • mobilising energy substrates for use by ex mm
  • glycogenolysis, gluconeogenesis in liver, export of glucose into plasma
  • stimulates lipolysis and export of free fatty acids from adipose cells
  • plasma lvls of glucagon, growth hormone and cortisol rise during ex. release is activated by low plasma glucose lvls
  • these 3 hormones similar effect to Ad during ex.
  • synergistic w combined effect larger together vs solo
33
Q

hormones/exercise: insulin

A
  • released from Islets of langerhans in pancreas
  • due to nutrients entering plasma after meals, will move these nutrients into cells
  • convert them into storage compounds
  • during exercise insulin is decreased (compromise nutrients available)
  • Ad and NAd act on pancreatic cells to decrease synthesis/release of insulin
34
Q

what protein to take up glucose from plasma: skeletal mm

A
  • GLUT4 membrane transport protein
35
Q

GLUT4 mechanism: and during exercise issue of decreased insulin?

A
  • stored in membrane of cytoplasmic vesicles til binding of insulin to receptor on plasma membrane
  • vesicle fuses and GLUT4 active glucose transporter
  • during ex although insulin lvls decrease, specific pathways activated to insert GLUT4 into membrane
  • so ex mm don’t need insulin to take up plasma glucose
36
Q

long term endurance strength training: features

A
  • runners, weekend warriors
  • slight L ventricular hypertrophy from vol overload (sarcomeres added to increase L ventricular vol- end diastolic vol)
  • increased conc of myosin ATP increased contractility and increased ratio: para/sym stimulation of heart decreased HR at rest, exercise
37
Q

long term endurance strength training: increased O2 requirement

A
  • stimulates angiogenesis
  • increases density of microcirculation
  • elevation of enzymes for utilisation of both glucose, fatty acids as substrates for ATP generation
  • increased no./activity of mitochondria increase production of free radicals = response cells dev higher lvls antioxidant enzymes
38
Q

reductions in BP after long term endurance exercise: hypertension

A
  • advised to change lifestyle w respect to diet, increased exercise
  • ex shown to lower BP
  • lowering of BP due to vascular vs cardiac effects
39
Q

reductions in BP after long term endurance exercise: inhibition to sym input

A
  • inhibit sym input in vascular smooth mm = decrease vasoconstriction throughout body
  • decreased responsiveness to NAd and endothelin, increased release of NO (vasoconstrictors)
40
Q

reductions in BP after long term endurance exercise: angiogenesis activated-

A
  • increased density of capillaries in mm = decrease flow resistance
41
Q

reductions in BP after long term endurance exercise: cross-sectional area of vascular lumen effect

A
  • increases cross-sectional area

- reduced wall thickness in muscular aa

42
Q

reductions in BP after long term endurance exercise: result of all changes

A
  • reduced TPR

- reduced BP

43
Q

reduced SBP and DBP by? beneficial

A
  • SBP: 7.4 mmHg

- DBP: 5.8mmHg

44
Q

exercise also benefits:

A
  • artherosclerosis
  • obesity
  • diabetes
  • depression
  • Alzeheimer’s
  • insomnia

5. ADV PHYS (10 decks)

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