When I began this blog, the importance of exercise for reducing risks associated with cardiovascular disease (CVD) was the first idea that came to mind. Since then, however, I’ve been hesitant to write about it. The topic is so widely accepted and understood that it might come across as redundant or, worse, boring. I thought I might get caught up writing about something everyone already knows and isn’t particularly eager to read about.

But how well do we actually understand this connection? I bet we all know that exercise is good for your heart and can help prevent heart disease, but have you ever stopped to ask why or how?

Mortality rates from CVD have decreased over the past 50 years (British Heart Foundation, 2023), but it still remains one of the leading causes of death globally.

I finally decided to bite the bullet (no pun intended) and address the topic. Why not? If it’s such a universally-accepted fact, maybe more people will be interested in understanding the mechanisms behind how exercise reduces the risk of CVD.

Let’s go back to the basics for a second.

What do we already know?

1. CVD is a broad term encompassing numerous diseases that affect the heart and/or blood vessels. These include stroke and coronary heart disease (CHD), which may lead to a heart attack (known as myocardial infarction or MI in the medical field).
2. Atherosclerosis is thought to be the most important underlying cause of CVD. Although it’s a big word you may not have heard of, atherosclerosis is simply the narrowing of the blood vessels (mainly arteries). How does this happen? A build-up of plaque and fatty material within the blood vessel walls causes lesions to form and impedes blood flow.
3. Blood flow impedance due to atherosclerosis is bad enough, but over time, if the plaque becomes unstable, it may rupture and cause a blood clot. This can lead to a cardiovascular event, such as a stroke or heart attack.

Have a look at the figure below. It’s been simplified, but it’s a good visual representation of the progression of atherosclerosis.

Here’s the interesting thing: we all have plaque building up in our blood vessels. You currently have fatty deposits in your arteries, and I don’t need to know how healthy (or otherwise) you are in order to know that.

Now, before I give you a heart attack (pun intended), you should know this is normal. The truth is, plaque builds up in our blood vessels throughout our life, as early as in childhood, and there’s not much we can do to reverse it (McGill et al., 2000). Our best strategy is actually to limit plaque formation in the first place.

How do we do that?
It’s pretty simple: make good lifestyle choices.

• a healthy diet
• exercise
• maintaining a healthy weight
• cutting back on alcohol
• quitting smoking
• managing stress
• getting enough sleep

These can all be helpful strategies to reduce the risk of atherosclerosis, but I’m an exercise physiologist, so predictably, exercise is what I’d like to discuss further.

How can exercise help guard us against CVD?

There are multiple mechanisms and causal pathways that may be involved in mediating this association.

On the surface of it, one of the main ways it can do this is by reducing body fatness. Doing more exercise means that adipose tissue levels can be reduced, and this, in turn, increases health and reduces the risk of mortality. However, I’ve already written about adiposity here, so I won’t go into the details in this article. Please feel free to take a detour and read more about the importance of body fat and its distribution in my other article.

Now, in terms of the less visible mechanisms involved, there are a few.

Improving insulin sensitivity is one of them. Exercise helps increase insulin sensitivity in the liver and muscles. This means that blood glucose levels can be kept in check, reducing the risk of diabetes, damage to blood vessels (due to high sugar levels in the blood; Deighton, 2021), and hence atherosclerosis.

Another mechanism is by reducing chronic low-grade inflammation. I discuss this further in my article on adiposity, but briefly, exercise helps to reduce chronic inflammatory markers (some cytokines and C-reactive protein) and offers an anti-inflammatory response (mediated by interleukin-6; Mathur & Pedersen, 2008). This chronic inflammation has been linked to atherosclerosis, so reducing it is beneficial to cardiovascular health.

Exercise may also reduce the risk of thrombosis, meaning the formation of blood clots. It may be that exercise reduces platelet activation, lowers levels of clotting factors in the blood, and increases the breakdown of blood clots by enzymes. Whatever the mechanism, exercise appears to help reduce the risk of blood clot formation and therefore a cardiovascular event (Deighton, 2021).

Perhaps a well-understood mechanism is the alteration of the lipid profile: levels of fat and cholesterol in the blood. The most consistent findings indicate that exercise is associated with an increase in high-density lipoprotein, i.e. the good cholesterol that has a protective effect on our health. It helps to transfer excess cholesterol from the tissues to the liver for it to be excreted (Deighton, 2021). Exercise is also associated with a reduction in circulating triglycerides, or fats in the blood. Importantly, exercise can prevent the build-up of low-density lipoproteins, or bad cholesterol. This is crucial as LDL can easily enter the arterial wall once the endothelium has been damaged, and is therefore particularly atherogenic (Deighton, 2021).

Another major risk factor for CVD that can be managed with exercise is hypertension, or high blood pressure. It appears that exercise can acutely and chronically reduce blood pressure values. In fact, an acute bout of exercise can result in a transient reduction in blood pressure (Miyashita et al., 2008). The way it does this is through vasodilation, or the widening of blood vessels, which reduces the resistance in the vessels to blood flow. This happens as exercise helps the body release vasodilatory substances (Hamer, 2006). Over the long term, chronic aerobic exercise results in a reduction in hypertension (Kokkinos et al., 1995). The mechanisms for this include increased insulin sensitivity, vascular structural changes (which I will discuss in the next paragraph), as well an increase in blood vessel formation, or what we call angiogenesis (Kokkinos et al., 1995; Gambardella et al., 2020; White et al., 1998).

The final mechanism I will discuss is the alteration in endothelial function brought about by exercise. This is closely linked to hypertension. Endothelial cells are able to release substances which diffuse into and interact with the smooth muscle layer beneath them (see diagram), resulting in vasodilation and influencing blood flow. This is called flow-mediated dilation, and it mostly occurs in response to a short duration of exercise (Tinken et al., 2008).

In the first couple of weeks of training, the shear stress in the endothelium due to increased blood flow and friction in the blood vessels results in an increase in nitric oxide synthase activity. This is an enzyme that catalyses nitric oxide production (Schuler et al., 2013). And what does nitric oxide do? It’s a potent vasodilator, which widens blood vessels.

However, this flow-mediated dilation decreases after a couple of weeks of training, if exercise is maintained (Tinken et al., 2008). Why does this happen, you might be wondering?

If you continue to exercise for multiple weeks, structural changes begin to occur, reducing the importance of flow-mediated dilation. In fact, after 8 weeks of training, we can see an increase in dilator capacity, which is a surrogate marker for structural remodelling. This basically means that with a few weeks of training, the blood vessels change shape. The walls become thinner, and the lumen becomes wider, making it easier for blood to flow through and improving vascular function (Tinken et al., 2008).

These are all mechanisms we believe are at play, but has it been shown that exercise actually decreases CVD incidence?

Yes, it absolutely has. And we’ve known this for a while.

I want to take us back a little to the mid-1900s, when the association between physical activity and lower rates of heart attacks began to gain attention.

In 1953, Professor Jerry Morris and his colleagues published a paper on the link between coronary heart disease (CHD) and physical activity. They were interested in those who worked on London buses. In particular, they looked at the difference in rates of CHD between the bus drivers and the conductors.

The nature of their occupations meant the bus drivers were sedentary for most of the day, whereas the conductors were on their feet, and therefore, more active. It turned out that the bus conductors experienced roughly half the number of heart attacks compared to bus drivers.

This was a landmark study in the ‘exercise for health’ field.

22 years later, in 1975, Professor Ralph Paffenbarger, along with his colleagues, published a study conducted on dockworkers. They found that those workers who had jobs involving light to moderate physical activity were twice as likely to die from CHD as those who did high-intensity physical activity. This indicated there was some sort of protective effect imparted by heavy physical activity – some threshold of activity intensity above which one is less likely to die from CHD.

There’s a lot more evidence available to support the link between physical activity and CVD – a lot of it done much more recently. But what two claims can we extrapolate from these two studies?

1. Those who do physical activity are less likely to develop CVD than those who are sedentary (Morris et al., 1953).
2. Those who do repeated bursts of high-intensity physical activity are at lower risk of developing CVD compared to those who do light or moderate physical activity (Paffenbarger & Hale, 1975).

This is all super interesting, at least to me. But does this mean that the only way to reduce the risk of CVD is to do a lot of high-intensity exercise?

Not necessarily.

How much exercise should you do to lower your risk of CVD?

The thing about exercise is that doing any amount is better than doing none at all. This applies in the case of CVD too. Arem et al. (2015) found that doing the minimum recommended physical activity (i.e. 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity exercise per week) reduces the risk of mortality due to CVD (as well as cancer) by about 31% compared to those who do no leisure-time physical activity.

Doing 3-5 times the recommended minimum leisure-time physical activity only decreases risk by another 8%, bringing one’s decreased risk to 39%. This is where it plateaus. Doing any more exercise will not reduce your risk of CVD mortality any further.

But here’s the really interesting part. Even if you don’t meet the minimum recommended physical activity guidelines, you could still reduce your risk of mortality due to CVD by 20%! That’s truly amazing. It shows that even doing a little exercise can be helpful, even if you’re not prepared to commit to daily gym time just yet.

Some even recommend doing moderate-intensity activity! It’s easier to maintain over the long term and can still help reduce hypertension. Additionally, it can help prevent musculoskeletal injuries and exercise-induced cardiac events, which generally occur when very inactive individuals do an acute bout of high-intensity exercise (Kokkinos et al., 1995).

All this means is that there is a clear dose-response relationship between leisure-time physical activity and CVD mortality risk. Up to a certain point, doing more activity incrementally reduces your risk, but the greatest benefit is gleaned from starting to do some exercise, not from doubling or tripling your exercise time.

How do you know that the physical activity you’re doing is enough to help reduce your risk of developing CVD?

Let’s be honest, it can be challenging to keep up the exercise when you don’t see any immediate benefits. Disease endpoints of CVD only become apparent later in life, so it’s difficult to see how exercise is helping when we won’t know whether we’ll see clinical manifestations of the disease until later.

Regardless, you should keep up the exercise. You’ll likely thank yourself later.

References

Arem, H., Moore, S. C., Patel, A., Hartge, P., Berrington de Gonzalez, A., Visvanathan, K., Campbell, P. T., Freedman, M., Weiderpass, E., Adami, H. O., Linet, M. S., Lee, I.-M., & Matthews, C. E. (2015). Leisure Time Physical Activity and Mortality. JAMA Internal Medicine, 175(6), 959. https://doi.org/10.1001/jamainternmed.2015.0533

British Heart Foundation. (2023). Heart and Circulatory Disease Statistics 2023 Published by British Heart Foundation (BHF). https://www.bhf.org.uk/-/media/files/for-professionals/research/heart-statistics/bhf-statistics-compendium-2023.pdf

Deighton, K. (2021). Cardio-metabolic risk factors. In D. J. Stensel, A. E. Hardman, & J. M. R. Gill (Eds.), Physical Activity and Health. Routledge. https://doi.org/10.4324/9780203095270

Gambardella, J., Morelli, M. B., Wang, X., & Santulli, G. (2020). Pathophysiological mechanisms underlying the beneficial effects of physical activity in hypertension. The Journal of Clinical Hypertension, 22(2), 291–295. https://doi.org/10.1111/jch.13804

Hamer, M. (2006). The Anti-Hypertensive Effects of Exercise. Sports Medicine, 36(2), 109–116. https://doi.org/10.2165/00007256-200636020-00002

Kokkinos, P. F., Narayan, P., Colleran, J. A., Pittaras, A., Notargiacomo, A., Reda, D., & Papademetriou, V. (1995). Effects of Regular Exercise on Blood Pressure and Left Ventricular Hypertrophy in African-American Men with Severe Hypertension. New England Journal of Medicine, 333(22), 1462–1467. https://doi.org/10.1056/nejm199511303332204

Mathur, N., & Pedersen, B. K. (2008). Exercise as a Mean to Control Low-Grade Systemic Inflammation. Mediators of Inflammation, 2008, 1–6. https://doi.org/10.1155/2008/109502

McGill, H. C., McMahan, C. A., Zieske, A. W., Tracy, R. E., Malcom, G. T., Herderick, E. E., & Strong, J. P. (2000). Association of Coronary Heart Disease Risk Factors With Microscopic Qualities of Coronary Atherosclerosis in Youth. Circulation, 102(4), 374–379. https://doi.org/10.1161/01.cir.102.4.374

Miyashita, M., Burns, S. F., & Stensel, D. J. (2008). Accumulating short bouts of brisk walking reduces postprandial plasma triacylglycerol concentrations and resting blood pressure in healthy young men. The American Journal of Clinical Nutrition, 88(5), 1225–1231. https://doi.org/10.3945/ajcn.2008.26493

Morris, J. N., Heady, J. A., Raffle, P. A. B., Roberts, C. G., & Parks, J. W. (1953). CORONARY HEART-DISEASE AND PHYSICAL ACTIVITY OF WORK. The Lancet, 262(6796), 1111–1120. https://doi.org/10.1016/s0140-6736(53)91495-0

Paffenbarger, R. S., & Hale, W. E. (1975). Work Activity and Coronary Heart Mortality. New England Journal of Medicine, 292(11), 545–550. https://doi.org/10.1056/nejm197503132921101

Schuler, G., Adams, V., & Goto, Y. (2013). Role of exercise in the prevention of cardiovascular disease: results, mechanisms, and new perspectives. European Heart Journal, 34(24), 1790–1799. https://doi.org/10.1093/eurheartj/eht111

Tinken, T. M., Thijssen, D. H. J., Black, M. A., Cable, N. T., & Green, D. J. (2008). Time Course of Change in Vasodilator Function and Capacity in Response to Exercise Training in Humans. The Journal of Physiology, 586(20), 5003–5012. https://doi.org/10.1113/jphysiol.2008.158014

White, F. C., Bloor, C. M., McKirnan, M. D., & Carroll, S. M. (1998). Exercise training in swine promotes growth of arteriolar bed and capillary angiogenesis in heart. Journal of Applied Physiology, 85(3), 1160–1168. https://doi.org/10.1152/jappl.1998.85.3.1160