Understand the distribution of cardiac output and how it is controlled in
different situations
At rest, only around 20% of cardiac output goes to the muscles. Around half goes to the liver and kidneys, around 14% to the brain, and the rest goes to the heart, skin, and other organs. Distribution depends on the opening and closing of pre-capillary sphincters, and local vasodilation/vasoconstriction, as discussed here.
Describe and understand what happens to cardiac output during exercise
Cardiac output, as I'm sure you know, increases dramatically during exercise. The distribution of cardiac output also changes: a larger proportion of cardiac output goes to the muscle, and less goes to other organs. Because cardiac output has increased so much, though, the absolute amount of blood that most organs get increases. There are two exceptions to this rule: the liver and kidneys both experience a decrease in cardiac output (both absolute and proportional).
Describe and understand the determinants of cardiac output during exercise
During exercise, sympathetic stimulation increases, causing vasoconstriction. This seems counterproductive given that vasoconstriction will reduce the flow of blood, but thankfully there's also something called "functional sympatholysis" (i.e. the "breaking off" of sympathetic stimulation). Areas of the body undergoing high levels of metabolism, such as working muscle, can produce local mediators that cause vasodilation, counteracting the vasoconstricting effects of sympathetic stimulation.
Describe the known determinants of local blood flow mediation
See previous post: Microcirculation and Blood Flow
Nitric oxide (NO) may also play a role. It has been discovered that haemoglobin releases NO when it becomes deoxygenated.
Describe and understand how the local control of blood flow conflicts with blood
pressure regulation
Vasodilation of capillaries causes a decrease in blood pressure, which would be bad if unchecked. (The opposite is true during vasoconstriction.) Thankfully, total peripheral resistance isn't the only determinant of blood pressure, the other being cardiac output. An increase in cardiac output can counteract a decrease in blood pressure due to local vasodilation (within limits, of course).
Understand the relationships between work rate and cardiovascular variables
As work rate increases, so too does heart rate and stroke volume (and hence cardiac output), arterial pressure (systolic increases to a much greater extent than diastolic), oxygen consumption, and arterio-venous oxygen difference. Peripheral resistance, however, decreases due to the vasodilation of capillaries in working muscle.
Describe and understand the origin of changes in the arterio-venous oxygen
difference during exercise
As you might recall from PHYL2001, the haemoglobin saturation curve shifts to the right when temperature is high and pH is low (which is what happens during exercise). A rightward shift indicates that more oxygen is released from haemoglobin at the same partial pressure of oxygen in solution. As more oxygen is being released from haemoglobin during exercise, the arterio-venous oxygen difference increases.
Describe and understand the changes in cardiovascular variables during exercise
During exercise, the baroreceptor's set point is reset to a higher blood pressure. Stimuli that reset the baroreceptors may include feedback from muscle chemosensors, muscle mechanoreceptors, or the motor cortex. Our normal blood pressure is then sensed as being too low, reducing the firing rate of baroreceptors. The nervous system then responds by increasing sympathetic stimulation and decreasing sympathetic stimulation. These changes in sympathetic and parasympathetic stimulation cause an increase in certain cardiovascular variables, such as heart rate.
Describe and understand adaptations in cardiovascular variables after repeated
exercise
Our bodies can adapt to repeated exercise. Fit people will tend to have a lower resting and exercise heart rate, but a greater oxygen uptake (a.k.a. VO2 max). I'm not entirely sure what the mechanisms are, though- maybe we'll find out in the next lecture?
Describe and understand the determinants of stroke volume
See previous post: Cardiac Loads
End-diastolic volume changes more in exercise than end-systolic volume. Interestingly enough, end-systolic volume changes even less when you are exercising in a supine (lying down) position, compared to exercising while standing up.
Describe and understand Starling’s capillary fluid balance and how it is affected by
exercise
See previous post: Microcirculation and Blood Flow
Remember, the switch from filtration to reabsorption depends on the pressure drop across the length of an arteriole. In exercise, this pressure drop is decreased, so the outward hydrostatic presssure is greater than the inward oncotic pressure over a longer distance. This leads to increased filtration during exercise, which in turn leads to oedema and a decrease in plasma volume during exercise.
Describe and understand cardiac drift
Cardiac drift refers to the phenomenon in which heart rate increases during exercise, even when work rate remains the same. Cardiac drift occurs because of the decrease in plasma volume during exercise (see above). A decrease in plasma volume lowers blood pressure, and heart rate increases in order to compensate (baroreceptor reflex).
Describe and understand blood pressure changes in exercise
Not really sure what to say here, other than that a higher heart rate leads to a higher diastolic pressure during exercise (my understanding was that it's because the next heart beat comes along before pressure can drop all the way down to resting diastolic pressure?). Mean arterial pressure also increases during exercise.
Describe and understand blood boosting
In blood doping (or blood boosting), athletes remove a litre of their blood around a month or so prior to a competition, and then reinfuse it. As such, their haematocrit (% of blood with red blood cells) increases. Blood doping increases VO2 max and exercise performance, but if you overdo it, the blood can become very viscous and difficult to pump around (as also mentioned here).
An alternative to blood doping is to add erythropoietin (EPO) to increase production of red blood cells. Recombinant EPO, made in the lab by microbes, can be detected as microbes glycosylate EPO differently to humans.
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