8 - Oxygen 2 cardiovascular responses to exercise

In this lecture we're going to focus on the cardiovascular responses to exercise. And we'll look at both, incremental exercise, where exercise intensity progressively increases. But also, prolonged exercise at a given exercise intensity. Primary function of the cardiovascular system is to increase oxygen supply to the skeletal and the cardiac muscle. The VO2 during exercise is really determined by the cardiac output, and the oxygen extraction, or the aVO2 difference. And this is referred to as the thick equation. As you can see, cardiac output plays a key role in determining the VO2. An important function, other function of the cardiovascular system is to remove CO2 and heat from the contracting muscle. And finally, the main arterial blood pressure has to be maintained to insure that there's adequate profusion of the key organs, notably the brain. Its important to remember that mean arterial pressure is really the product of the cardiac output and the total peripheral resistance and we'll see during exercise the changes in regional blood flow and changes in cardiac output will interact to determine the mean arterial pressure response to exercise. If we begin by looking at incremental exercise we can, examine the changes in oxygen uptake, cardiac output and various tissue blood flows as we go from rest through light exercise, to heavy exercise and then to maximal exercise. You can see as we've shown before that oxygen uptake increases in proportion to the exercise intensity and as does cardiac output. And roughly for each liter of increase in oxygen there's about a five to six liter increase in cardiac output. It's a very large increase in muscle blood flow and the active skeletal muscles you can see at maximal exercise are getting close to 90% of the available cardiac output, the heart increases its activity during exercise and so there is a slight increase in the coronary blood flow and as we'll see in the next module when we talk about heat and fluid balance, an important way of removing heat during exercise is the evaporation of sweat which requires the transfer of heat to the surface of the body to the skin. You'll notice here that during light to heavy exercise there's an increase in skin blood flow, to facilitate this heat removal. But as you move to higher intensities, there's a reduction in skin blood flow as we approach the maximal cardiac output. And this really sets up, if you like, a competition between the muscle and the skin and the other important organs, the heart and the brain. that needs to be managed. We'll talk a little bit about that in the next module as well. Some of the vascular beds that are perhaps less important during exercise can be vasocontricted. So, the splanchnic region and the kidney will have less blood directed to them during exercise, and their vascular beds are vasoconstricted. Other inactive beds are those constricted and finally you can see the effectiveness of the system in as much as the cerebral blood flow is well maintained. And in fact some recent studies have suggested that cerebral blood flow may even go up slightly during exercise. What are the factors that mediate these cardiovascular responses to exercise? Well, the fundamental part of the cardiovascular response is the increase in skeletal muscle blood flow. And important factors that increase blood flow are metabolic vasodilators that are released from contracting muscle From the endothelial lining the blood vessels, and from the red blood cell itself. And these include factors such as endonicyne, ATP both from muscle and from the red blood cell, potassium, active oxygen species, and nitric oxide from the endothelial. Are being implicated in relaxing vascular smooth muscle and facilitating the increase in skeletal muscle blood flow during exercise. The so-called muscle pump, or the rhythmic contractions of blood vessels are thought to play a role. Some have suggested that early on in exercise the initial contractions can create a vacuum which facilitates blood flow into the muscle, but certainly with ongoing exercise, the action of the muscle pump is important in maintaining venous return to the heart. Given that there are valves in the vein, veins which facilitates the unidirectional flow back towards the heart. With the cessation of exercise, some people often experience dizziness and fainting. And post exercise hypotension. Is, usually thought to be due to cooling of the blood in the, in the lower extremities when the muscles are no longer contracting and that muscle pump is no longer facilitating venous return. There's some evidence of conduct, what's termed conductive vasodilation. Where there's a dilation in one part of the vasculature is transferred upstream, or distally, and this is thought to be mediated by this photo decolorization through gap junctons between the smooth muscle cells. And finally an important characteristic during exercise is what is being termed Functional sympatholysis. And what this means is that the basic constrictor effects of sympathetic nervous activation, or sympathetic nerves to blood vessels in the active skeletal muscle, is less effective during exercise than it is at rest. And it's thought that some of these metabolic vasodilators desensitize or make less effective sympathetic nerve activity during exercise. If we look at the whole body cardiovascular responses, then we see an increase in both cardiac output, and in the oxygen extraction. You can see this in this, in this graph and summarize for two groups a sedentary group and an athletic group. You'll see here that as VO2 increases there's an increase in cardiac output. And its largely similar between a sedentary and an athlete, athletic group. Except that an athlete is able to go to a much higher VO2. And as we'll see it's largely due to their ability to achieve a higher maximal cardiac output. The A-VO2 difference increases and the maximal A-VO2 difference is really not that different. There's a slight increase in the athletic group but most of the increase in VO2, maximal VO2, appears to be due to the increase in maximal cardiac output. Although cardiac output at any given VO2 is very similar between a sedentary person and an athletic person, their heart rate and stroke volume responses are quite different. One of the hallmark adaptations to exercise training is a reduction in heart rate at any given submaximal exercise intensity. And you can see here this reduction in heart rate. in the athletic group. Maximal heart rate, if anything, might be slightly lower in an athletic group, or unchanged. Stroke volume will increase in the early part of the exercise in both groups, and then it tends to level off. at moderate exercise intensities. There have been some studies suggesting, certainly in athletic populations, that stroke volume might continue to increase until leveling off at a higher exercise intensity. Part of the reason why stroke volume levels off is that with an increase in heart rate, the diastolic filling time becomes limiting, and it's perhaps not able, or the heart is not able to be optimally filled at very high heart rates, in terms of blood pressure, the systolic blood pressure tends to increase during incremental exercise, in parallel with the increase in cardiac output, the diastolic blood pressure, or the the pressure in the circulation when the heart is relaxing, is largely determined by the overall peripheral resistance and it tends to stay relatively constant during an incremental exercise and it may even fall slightly at higher exercise intensities due to the increase in muscle blood flow, mean arterial blood pressure, which is the weighted average of the systolic and the diastolic blood pressures, tends to increase slightly during incremental exercise. This is one of the few situations where both mean arterial blood pressure and heart rate increase simutaneously. And the baroreflex is still operative, but it's reset to a slightly higher set point to allow for those simultaneous increases. If we look at more prolonged exercise at a given exercise intensity, this slide summarizes the changes that you see in various cardiovascular parameters. Of two hours of exercise in recently well trained subjects in the absence of supplemented fluid ingestion so they become progressively dehydrated and you can see a slight reduction in the blood volume over time. We'll come back to this a little bit later in the, in the course in a module on heat and fluids and discuss that in more detail. Over time, what we tend to see is a slow increase in heart rate, we refer to as the cardiovascular drift. There is a reduction in stroke volume over time because of the changes in central blood volume, and the increase in heart rate The card, as a result the cardio output drops slightly. There's a slight increase in peripheral resistance over time as the phaser construction and inactive vascular beds, including the skin ultimately and a slight reduction in the arterial blood pressure, and during prolonged exercise particularly in the heat. This may have limiting effects. In relation to the cardiovascular drift, as I said, there's an increase in heart rate and a slight decrease in stroke volume. Some of the factors that have been implicated in that include hyperthermia and dehydration. And we'll touch on those in the next module. An increase in plasma adrenalin over time will contribute to an increase in heart rate and the peripheral displacement of blood, particularly to the more compliant cutaneous circulation has been implicated in these cardiovascular adapta changes during prolonged exercise. Some people have suggested that compression garments which are often used in sporting contexts act to minimize this peripheral displacement, and one of the reasons for their use that's been advocated relates to these hydrostatic effects on the peripheral circulation. In terms of the neural control of the circulation we see two important regulatory factors - the so-called central command or the descending activation of the heart, and some of the vascular responses linked to motor cortical activation. And this has really been described since the early 1900's when even the anticipation of exercise can result in a slight increase in heart rate. In central command if you'd like, sets the basic level of cardiovascular activity during exercise. It's also a central command that resets the baroreflex. The other important mechanism is feedback. Feedback from the contracting muscles themselves, and small nerve endings, the so-called type-3 and type-4 ephrins. In skeletal muscle can feed back and modify the cardiovascular system. And there are recent results suggesting that they are quite important for the cardiovascular responses to exercise. The baroreceptor, albeit reset to a slightly higher set point, also operates during exercise. And has an important role in modulating the cardiovascular responses to exercise. If we look at the autonomic control during incremental exercise, we can see the interaction between the parasympathetic nervous system and the sympathetic nervous system. During the early increase in heart rate most of that is due to turning off the vagus nerve, the parasympathetic nerve to the heart which is inhibitory at rest so turning it off will result in an increase in heart rate. With increasing exercise intensity, you see increased sympathetic nerve activity as reflected by the increasing plasma noradrenaline levels, and also the muscle sympathetic nerve activity, measured directly in muscle sympathetic nerves increasing. This increased sympathetic activity results in reductions in splanchnic blood flow, and renal blood flow, as I showed you in that early table. And with progressive increase as you can see, the slight increase in lactate as the sympathetic nerves activate glycogen breakdown in muscle. So at least during incremental exercise, withdrawal of the parasympathetic nerves and activation of the sympathetic nerves contribute to the increased heart rate. In patients who've had cardiac transplants, and are therefore denovated, their resting heart rate tends to be slightly higher, because of the removal of the influence of the vagus. And during exercise, the increase in heart rate is slightly sluggish. Because of the lack of sympathetic innovation. And these patients rely more on circulating adrenaline released from the adrenal medulla. Over time, there's evidence of some reinnovation of the transplanted heart as reflected by a slightly improved heart rate response to exercise. In the earlier slides, when I showed you the difference between the cardiovascular responses, between a sedentary group and an athletic group. And there are, clearly, cardiovascular adaptations to exercise training. There's a reduction in heart rate during submaximal, and possibly also maximal exercise and this is associated with an increase stroke volume during sub maximal exercise but importantly also during maximal exercise, so important adaptations which enable this increase in stroke volume to occur include an expansion of blood volume which facilitates the filling of the ventricles, increases in diastolic volume and therefore increases subsequent stroke volume. There's also an increase in the heart size, and left ventricular hypotrophy, both in the mass of the ventricle but also the chamber size is an important adaptation which facilitates an increase in maximum stroke volume and maximum cardiac output. It's been shown that to train hard is slightly more sensitive to adrenergic stimulation, and other vascular changes include an increase in arterial diameter and compliance, which might have been official effects in terms of vascular control, and may contribute to the health benefits of exercise in terms of cardiovascular risk. And finally, there's an increase in capillary density, and recruitment, during exercise, which acts to facilitate oxygen delivery to the contracting muscle. And you can see, in the micrograph here, the diffences in capillary density between an untrained muscle, and a trained muscle. this increased angiogenesis being an important peripheral vascular adaption to endurance exercise training.