Basic Science Behind the Cardiovascular Benefits of Running
Running and improved cardiovascular health go hand in hand, but have you ever stopped to consider the exact science behind this well-known fact? Doctors have long touted the benefits of aerobic exercise, from lower mortality rates among athletes to decreased risk of disease, thanks to improved circulation. How, specifically, does exercise enhance the cardiovascular system? The answer to this question and the corresponding science is discussed below.
Cardiovascular Benefits of Exercise
The exact cardiovascular benefits of aerobic exercise are vast. For one, cardiorespiratory fitness has been conclusively linked with decreased cardiovascular disease1. A long-term study performed in France determined that men who partook in vigorous aerobic exercise had a 41% decreased mortality rate2 versus the general male population. Additionally, people who have been exercising for longer than six months predictably have lower heart rates3 both at rest and during exercise, and are able to pump approximately 20% more blood through their arteries. The volume of the heart increases, as well, which is also important for overall health.
Structural/Functional Adaptations in the Heart
Athletes experience increased cardiac stress and output during exercise, which initiates a number of structural adaptations. The four chambers of the heart increase in volume while the walls of the tissue surrounding this organ increase, allowing for improved activation and transport4 of endogenous cardiac stem and progenitor cells.
Evidence for the restructuring of the heart in response to exercise was shown by studying the aging process in veteran athletes5. Male athletes 56 + 6 years of age with 43 + 6 years of exercise experience were found to have smaller left and right ventricle volumes, yet similar wall thickness and cardiac mass when compared with younger athletes, aged 31 + 5 years.
On the other hand, in comparison to sedentary individuals their own age, the veteran athletes showed vast structural improvement, with larger left and right ventricle volumes, wall thicknesses, and blood-pumping abilities (measured by stroke volume). These studies helped to verify the effect of exercise on cardiac remodeling.
Cellular Adaptations in the Heart
There are two types of cardiac growth: pathological and physiological. With pathological, cardiomyocyte death is recorded, as well as fibrotic replacement and cardiac dysfunction. In physiological cardiac growth, cell hypertrophy (i.e. enlargement), activation of cardiac stem cells, improved cardiac function, and absence of cell death is observed. For athletes, physiological cardiac growth is experienced, and new research suggests this is due to activation of cardiac stem cells6, which have the ability to self-renew.
These stem cells improve cardiac function by increasing myocardial mass and promoting cardiomyocyte and capillary formation. These results can be distinguished from pathological cardiac growth, and are proven to be the result of exercise.
Molecular Adaptations in the Heart
There are a number of molecular mechanisms that produce physiological growth in an athlete’s cardiovascular system. The most common is insulin-like growth factor-1 (IGF-1). Endurance athletes have shown cardiomyocyte growth thanks to increased activity7 in the pathway for this particular growth factor in response to shear stress. As IGF-1 release increases, myocyte size is enhanced while fewer cell deaths are recorded.
To verify the correlation, when this activation pathway was removed in transgenic mice, the same cardiac gains were not observed8. Additionally, this IGF-1 pathway is not implicated in pathological cardiac growth, proving that this is an important molecular adaptation in the athlete’s heart.
Other growth factors that are important for cardiac adaptation are neuroregulin, bone morphogenetic protein-10 (BMP-10), and transforming growth factor beta. In conjunction with IGF-1, neuroregulin increases cardiac stem cell proliferation and corresponding benefits6. BMP-10 and transforming growth factor beta caused differentiation of the growth-inducing stem cells into three important categories: cardiomyocytes, endothelial cells, and vascular smooth muscle.
Vascular Structure/Function Adaptation
The cardiovascular system is lined with endothelial cells, which are integral in the vascular adaptations experienced by endurance athletes. The mechanism of adaptation is the release of vasoactive hormones that control the functionality of cardiovascular vessels.
One of the most important components produced in the endothelium is nitric oxide9, which causes smooth muscle cells to relax, blood vessels to dilate, prevents the build-up of fat in the arteries, and reduces the incidence of blood clots. For these reasons, nitric oxide is believed to be one of the largest mitigating factors for cardiovascular morbidity10.
When blood flow and shear rate increase (as occurs during strenuous exercise) within the endothelium, nitric oxide is released. This phenomenon promotes vascular adaptation and arterial remodeling. Exercise – even in short bouts – causes vascular dilation, meaning that blood flow is improved throughout the cardiac system, and this change is nitric oxide dependent11.
After five to thirty minutes of exercise, blood flow is decreased (dependent on exercise intensity and duration), while dilatation is increased 1 – 24 hours post exercise. Blood vessels return to normal baseline function 24 – 48 hours post exercise. The initial reduction in flow-mediated dilatation is linked to oxidative stress and reduced endothelial arginine, both of which stimulate adaptations over time for improved cardiac efficiency12.
Another vascular adaptation caused by exercise is the increased diameter of conduit arteries13. When arteries are enlarged, blood flow is improved and the risk of blood clots significantly decreases. Exercise improves vascular health by first improving endothelial function, which in turn promotes structural adaptation. Interestingly, a study14 was performed which looked at the artery diameter of squash players in their dominant vs. non-dominant arm.
This effect from exercise is entirely dependent on intensity and duration of exercise, as the dominant arm exhibited larger arterial diameters than the non-dominant arm; however, both were still increased over the sedentary population. The arterial walls of athletes are also thinner, which further helps to improve blood flow.
Negative Effects of Exercise on Cardiac Health
In recent years, scientists have uncovered the other side of the coin: can exercise harm cardiovascular health? Of course, news outlets often sensationalize deaths during marathons or ultra-distance events, failing to recognize that thousands of participants finished the race with no (serious) adverse reactions.
However, a small percentage of athletes develop morphological changes in their hearts that are consistent with pathological modifications indicative of cell death and increased risk of cardiac arrest. A study performed in 199115 examined almost 1,000 elite athletes. Approximately 0.5% showed maximal wall thickness in the left ventricle had been reached, which can be indicative of higher risk of cardiac disease. In some instances, a family history of heart disease or an underlying heart condition can make extreme cardiac exercise dangerous, especially when exercise-induced cardiac growth impedes natural function due to a preexisting condition.
Optimizing Cardiac Benefits
The next obvious question is how to utilize the knowledge presented here in order to optimize the benefits of the vast research that has been performed in the cardiovascular field.
How much exercise?
From the studies described here, as well as additional studies put forth, reduction in cardiovascular disease risk is most clearly linked to exercise volume as the most consistent indicator of disease. In general, greater aerobic exercise volume leads to a lower risk16 of heart attack or stroke. Significant differences were observed between casual exercisers (those who worked out 2 – 3 times per week) versus committed exercisers (those who worked out 4 – 5 times per week), especially among the aging population.
Main disparities included stiffer ventricles in casual exercisers than committed exercises and insignificant differences in left ventricle flexibility. The stiffness of the left ventricle is an important indicator17 for cardiovascular disease risk, meaning that the amount of exercise one performs per week is indeed significant.
The next question is whether the intensity of exercise plays a role in cardiovascular health. A study18 was recently performed that looked at patients of cardiometabolic disease, which includes heart failure, high blood pressure, obesity, coronary artery disease, and metabolic syndrome. After completing a course of high-intensity interval training (HIIT; i.e. bouts of exercise greater than 85% of VO2 peak or greater than 90% peak heart rate, followed by 2 – 3 minutes of active recovery), a significant increase in VO2 max was observed. In addition, results were far greater after high-intensity interval training than when moderate-intensity continuous training (MICT) was performed instead.
In fact, HIIT improved cardiac fitness by almost twice as much as MICT. This phenomenon was also observed in healthy participants. However, in order to maintain all-around health, a mixture of low intensity and high-intensity exercise should be performed. Overall, even limited exercise leads to cardiovascular benefits, especially among individuals with the highest risk of cardiovascular disease.
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