L4.2 Cardiovascular Responses Flashcards
What is the Fick principle?
What is MAP determined by?
VO2 = Q x (CaO2 (arterial O2 content) – CvO2 (venous O2 content))
MAP = Q x TPR
What are the cardiovascular responses to exercise?
- ↑Q → ↑O2 supply to skeletal & cardiac muscles
- Facilitate CO2 & heat removal
- Maintain mean arterial BP
What is the relationship between O2 consumption and Q during exercise?
- ↑exercise → ↑Q & O2 uptake
- Every ↑L of O2 uptake → need ~↑5L of Q
Where is Q directed/constricted/maintained during exercise?
- ↑Q → muscles (v.↑↑), skin (↓at max output), others – e.g. heat (↓at max output)
- ↓Q → splanchnic, renal
- ↔Q → Cerebral (blood diverted from skin and others at max output to ↔)
How is hyperaemia (increase blood flow) achieved during exercise?
- Metabolic vasodilators from contracting skeletal muscles, endothelium &/or RBC
- Muscle pumps (1st muscle contraction → ↑Blood flow) → maintains venous return
- Conducted vasodilation
- Dilates large arteries leads to dilation of distal capillaries
- Functional sympatholysis
- Blunts effect of sympathetic nerves (↑vasodilation)
- Desensitises sympathetic nerves
What are the vasodilator metabolites?
- K+, H+, adenosine, ATP (From muscles/RBC)
- Reactive Oxygen Species (ROS)
- NO, prostacyclin, PGE2
What are the cardiovascular responses from training?
- ↑VO2 max, due to ↑CO
- A-VO2 diff not that big
What is the BP response to exercise?
- Not markedly different btw trained & untrained
- Systole → influenced by Q
- Diastole → influenced by TPR
- ↑MAP → ↓HR (Baroreflex)
- Baroreflex is reset during exercise → allows a higher output
- Baroreflex reset by central command
What is the A-VO2 difference during exercise?
- ↑exercise → muscle use ↑O2
- At high intensity exercise → mixed CvO2 becomes closer to CaO2
- A-VO2 difference becomes smaller
What happens to CV during prolonged exercise?
- ↓SV (main determinant) → ↓CO
- ↓skin blood flow
- ↑TPR (counter drop in Q)
- ↑HR (counters ↓SV)
- ↓MAP & BV
What is the CV drift?
- ↑in HR → contributes to O2 drift
- Hyperthermia (↑temp → SA node depolarise more quickly)
- Dehydration (losing blood volume)
- ↑ plasma [A] (↑HR, related to dehydration & hypoglycaemia)
- Peripheral displacement of BV due to cutaneous vasodilation
How does autonomic innervations control CV parameters at different exercise intensities?
- Initial ↑HR due to ↓parasym activity
- Secondary ↑intensity → ↑HR from ↑sym activity
What is the effects of training on CV output?
And what are the microvascular adaptations?
- ↑Q by:
- ↑BV → ↑SV (major training adaptation) (from frank-starling mechanism → ↑SV from ↑BV)
- ↑heart size → ↑L. ventricular mass & size
- Heart more sensitive to adrenergic stimulation
- ↑capillary density & recruitment (major training adaptation) → ↑O2 delivery & exchange in muscles