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
2
Q
at VO2 max: ventilation at %
A
50%
~ 170L/min in healthy male
3
Q
at VO2 max: arterial PO2, mixed venous PCO2 %
A
near normal
- respiration not limiting factor in exercise
4
Q
at VO2 max: CO %
A
95%
- cardiovascular function is limiting factor at max exercise
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
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
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)
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
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
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
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)
12
Q
response during exercise: at rest % skeletal mm capillaries collapsed
A
50-80%
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
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
15
Q
response during exercise: thoracic pump
A
- caused by more -ve pressure in thoracic cavity
- produced by inspiratory effort during exercise
16
Q
mean arterial BP determined by:
A
CO x TPR
17
Q
define systolic BP:
A
- max BP in cardiac cycle
- when L ventricle ejects blood
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
control of CO sys: mm metaboreflex features
- 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
control of CO sys: local control features
- 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
baroreceptor function: features
- 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
baroreceptor function: mechanism of inhibiting sym output
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
baroreceptor function: resetting baroreceptors
- 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
baroreceptor function: most of increased HR at start of exercise due to
up to 100bpm
| - due to reduced para inhibition on pacemaker cells of heart
31
hormones/exercise: stimulation of sym NS
- 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
hormones/exercise: role of Ad
- 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
hormones/exercise: insulin
- 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
what protein to take up glucose from plasma: skeletal mm
- GLUT4 membrane transport protein
35
GLUT4 mechanism: and during exercise issue of decreased insulin?
- 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
long term endurance strength training: features
- 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
long term endurance strength training: increased O2 requirement
- 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
reductions in BP after long term endurance exercise: hypertension
- 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
reductions in BP after long term endurance exercise: inhibition to sym input
- inhibit sym input in vascular smooth mm = decrease vasoconstriction throughout body
- decreased responsiveness to NAd and endothelin, increased release of NO (vasoconstrictors)
40
reductions in BP after long term endurance exercise: angiogenesis activated-
- increased density of capillaries in mm = decrease flow resistance
41
reductions in BP after long term endurance exercise: cross-sectional area of vascular lumen effect
- increases cross-sectional area
| - reduced wall thickness in muscular aa
42
reductions in BP after long term endurance exercise: result of all changes
- reduced TPR
| - reduced BP
43
reduced SBP and DBP by? beneficial
- SBP: 7.4 mmHg
| - DBP: 5.8mmHg
44
exercise also benefits:
- artherosclerosis
- obesity
- diabetes
- depression
- Alzeheimer's
- insomnia
