Cardiovascular 3 Flashcards
Blood flow to the regions during exercise
- CO
- Cardiac output (total blood flow) increases as a function of exercise intensity.
- Most of this increase in cardiac output is distributed to contracting skeletal muscle and, to lesser extents, the heart and skin.
- By contrast, blood flows to some other regions decreases or remains constant.
Blood flows to the heart and skeletal muscle during exercise
- Cardiac output
- The femoral triangle
Cardiac output
- Cardiac output increases as a function of exercise
- As a response to an increase of work done by the heart the coronary blood flow increases
The femoral triangle
- Common femoral artery, femoral vein & femoral nerve
- The blood flow responses in contracting skeletal muscles and the contracting heart behaves in an almost identical fashion to an increase in work done by contracting muscle
How does muscle blood flow increase during exercise?
- The vascular resistance in contracting muscles decreases and then starts to plateau as work load increases
- MAP rises slightly at lower intensities but rises dramatically as higher intensities
- The first half of the rise in blood flow at lower intensities appears to be due to the fall in vascular resistance. The continued rise in blood flow up to maximum work load appears to be due to a rise in blood pressure
- A control in blood flow in this scenario appears to be due to a reduction vascular resistance at lower workloads and an increase in blood pressure at higher workloads
Connecting systemic and muscle responses
- CO & TPR
- Responses in previous slide (muscle) are very similar to systemic responses during ‘wholebody’ exercise (below).
- Most of the increase in cardiac output is due to an increase in skeletal muscle blood flow (plus blood flows to heart and skin).
- These increases in regional blood flows are achieved mainly via decreases in vascular resistances in these regions (muscle, heart, skin).
- Most of the decrease in TPR (systemic vascular resistance) is due to a decrease in vascular resistance in contracting muscles.
- The ‘flattening’ of the TPR response (below) is due to a similar response in skeletal muscle, but also due to increases in vascular resistances in the renal and splanchnic regions.
Haemodynamic aspect of how vascular resistance is adjusted
Vasodilation of blood vessels
- Increasing the radius of blood vessels decreases resistance
- Increasing radius of blood vessels also increases blood flow
Physiological aspect of how vascular resistance is adjusted
- Vasoconstriction - the reduction of the radius of a blood vessel and occurs due to the contraction of the vascular smooth muscle (VSM) layer
- Vasodilation - involves the relaxation of the vascular smooth muscle to allow the VSM to lengthen and allow the luminal radius to increase.
Muscle vasodilation is rapid and intensity-dependent
-leg blood flow
Muscle vasodilation is rapid and intensity-dependent
- Data from ten subjects who performed calf exercise at three intensities (% ‘peak force’).
- Intermittent, isometric contractions (1 s contraction, 2 s relaxation) for 300 s.
- The impulse is similar to the contraction force and represents the exercise intensity.
- Leg blood flow (“LBF”) measured during relaxation.
- Blood pressure measured continuously (responses not shown).
- Most of the increase in leg blood flow occurred within the first two contractions.
- This rapid response, as well as the total response, increases with intensity.
Vasodilation and reduction in vascular resistance accounts for most of the increase in leg blood flow.
Physiological control of vascular resistance and blood flows during exercise
- Neural (sympathetic vascular neurons)
- Mechanical (intramuscular pressure)
- Metabolic (muscle metabolites)
- Endothelial (e.g., nitic oxide)
- Humoral (erythrocytes, adrenaline)
- Thermal & other neural
As exercise intensity increases, the activity of sympathetic vascular neurons increases to reduce blood flow to these regions (liver, gastrointestinal tract, kidney and inactive muscles) through vasoconstriction
Training effects
- CO & TPR
- Responses after several months of aerobic training shown as dashed lines.
- The training-induced increase in cardiac output at the same relative intensity is accompanied by a similar increase in the decline in TPR.
- What would explain this effect on TPR?
Blood volume
- Volume of blood is proportional to the pressure of blood
- 70 ml/kg (female) to 75 ml/kg (male).
- 5 L in a 70 kg adult (where CO = 5 L/min).
- Most blood is in veins.
- Kidneys and hypothalamus are central to control of blood volume and long-term regulation of blood pressure.
- Endurance training increases blood volume.
Blood and O2
- Hematocrit (Hct) (amount of red blood cells as a proportion to the total amount of blood in a sample or vascular system = Males (45%), Females (42%)
- [Hb] = Males (16 g/100ml), Females (14 g/100ml)
- O2 /Hb = 1.39 ml/g
- %SaO2 (how much oxygen is bound to haemoglobin) = 97 -99 %
- CaO2 = 19-21 ml O2/100 ml blood
Gas and nutrient exchange
Gas and nutrient exchange occurs across the capillary wall within a tissue
O2 exchange from lungs to organs to cell
Oxygen enters the lung then diffuses into the pulmonary circulation then goes to the systemic arteries and then diffuses into the cells.
O2 exchange in a cell
- Most exchange of O2 occurs across walls of capillaries as blood transits from arteriolar (a) to venular (v) ends.
- O2 exchange occurs by diffusion and from areas of higher to lower concentration of O2 at a rate proportional to the concentration ‘gradient’.
- If the difference is higher the rate of exchange of oxygen will be higher
- The concentration of O2 - [O2 ] – in the blood decreases as blood transits the capillary and O2 leaves the blood.
- This creates an arterial-venous difference for O2 .
- The a-v [O2 ] is influenced by cell VO2 and blood flow (Q̇).
- The relationships between a-v [O2 ], Q̇ and V̇O2 can be represented by an equation.
- This equation can be rearranged and becomes the Fick equation for V̇O2 .
Fick equation and O2 exchange for a cell, organ and whole body
VO2 = Q x a-v (O2) VO2 = Q x (CaO2 - CvO2)
CvO2 - From systemic veins
CaO2 - To systemic arteries