Heart health: Part I – Heart Disease and Cardiovascular Health
What you need to know about heart disease, rate variability, effect of exercise, nutrition and more
What is the most dreaded disease of the modern world? Most people would probably say: cancer. Yet, cancer is by far not the most prevalent cause of death. That place is actually firmly occupied by ischemic heart disease, according to statistics published by World Health Organization (WHO).
So it makes sense to try to do what you can to prevent being a part of this statistic. The article below explores a few potential causes of heart disease, discusses risk factors (including some of those that are not well known) and preventive measures (including some unconventional but very effective ones).
What makes your heart beat
On average, your heart pumps about 7,200 liters of blood per day. In an average lifetime, that equals about 2,628,000 liters (700,000 gallons) or about 2.5 billion contractions. That’s a massive amount of work!
As with any muscle, to maintain the strength and pace of these contractions, two variables must be present – the constant availability of fuel and proper functioning metabolism that utilizes this fuel to produce electric energy required to contract the muscle.
The heart is generally considered as a substrate omnivore with the capacity to oxidize fatty acids, carbohydrates, ketone bodies, lactate and even amino acids, the preferred substrate being fatty acids.
That said – energy deficit is a key contributor to heart failure. During high intensity exercise, for instance, the heart uses up to 90% of its oxidative capacity – so it has no excess capacity of energy generation over energy utilization.
Under these circumstances, it is very important that whatever oxidative capacity your heart does have for supplying energy to cover the immediate needs is utilized to the maximum – and that such capacity is increased to provide some buffer for more strenuous activities, should those take place. Ninety percent of the heart’s energy requirement is met by mitochondrial oxidative phosphorylation, which is finely tuned to energy need on a “pay as you go” basis. In fact, mitochondria (power plants of the cell) occupy more than 30% of the cardiac muscle cells’ volume.
What is heart disease?
With such dependency on constant uninterrupted generation of energy, it is not surprising that heart attacks are triggered by some sort of acute energy deficit. But heart attacks (ischemic heart failure) are not the only condition that may affect the heart.
Heart disease – often also referred to more broadly as “cardiovascular disease” is a general term used for a set of pathological conditions, including narrowed and blocked blood vessels, abnormal heart beat (arrhythmia), heart muscle tissue damage, various physical defects and malformations of the heart, cardiomyopathy and several others. Some of these abnormalities are present at birth (as what is called a “congenital heart disease”) – while some others are acquired later in life, as a result of various factors, primarily associated with lifestyle. And while mortality from congenital heart disease as a cause has been on a steady decline, given that the overall heart disease statistics show an increase in the number of associated deaths – it follows that most of those cases are related to factors are non-genetic and can and should be controlled.
In other words, many types of cardiovascular diseases are preventable, if you pay attention to a few key factors. As an added bonus consider this: if you look at the WHO mortality statistics above, stroke is consistently the number two killer worldwide – and many preventive measures we will be discussing today also significantly decrease the risk of stroke.
The role of cholesterol and fat in heart disease
Let’s start by addressing an elephant in the room. As you have probably heard – cholesterol levels and saturated fat intake have been implicated in cardiovascular disease for decades. It has been mistakenly thought – and actively promoted – that the amount of saturated fats you consume has a direct correlation with the risk of cardiovascular disease.
As we have previously discussed in the article on cholesterol [LINK] – this correlation is not quite as direct as you might think. The consumption of saturated fat cannot be looked at in isolation, without also considering the consumption of simple carbs, pro-inflammatory compounds and toxic chemicals. Saturated fat by itself is not your enemy – the same way as cholesterol by itself is not your enemy. Both have essential structural, regulatory and metabolic functions in your body.
The association of cholesterol with cardiovascular disease mainly comes from the fact that inflamed cholesterol plaques obstruct blood flow through arteries. However, merely because saturated fat may raise cholesterol, stating that saturated fat leads to heart disease is too much of a generalization. First – cholesterol (which is an essential molecule for many biological processes) can come in different forms. And the most dangerous form is very-low density (vLDL) particles that typically do not get synthesized with the increase in saturated fat (but it does get synthesized with the increase in carbohydrates). Furthermore, even low-density cholesterol by itself is not the culprit – it needs a set of certain conditions to potentially create arterial blockage – namely, endothelial inflammation and lesions – which your body “patches” with cholesterol that then gets calcified and hardened.
The real culprit behind arterial blockage, therefore is a set of conditions that lead to inflammation and calcification. You will get more information from a dedicated article on cholesterol, but, as a quick recap – here is what you need to do to avoid such inflammation in the first place:
- Reduce the consumption of inflammatory compounds – in the modern diets, vegetable oils are the biggest culprit – which is ironic, given how they are being promoted for heart health (totally not the case!);
- Reduce the consumption of carbohydrates. You don’t necessarily have to go into ketosis per se (although there is nothing wrong with that if you approach it correctly – but the discipline required makes it tough to maintain for a long time) – but the problem is that with modern-day diets the scale is significantly tipped towards simple carbohydrates – to a point where, maybe, up to a half of total energy consumption for a typical western diet comes from carbs. Many of these are simple carbs as well as grains and starches that are produced from pesticide-laden GMO crops. Inflammation from too much carbs and destruction that chemical pesticides bring with them is what creates endothelial dysfunction in the first place, raising the risk of cardiovascular disease;
- If you are a smoker – you need to quit. The list of damaging factors with cigarette smoke is too large to mention here (and it impacts much more than just your lungs, but rather – every organ in your body), but specifically within the context of arterial impact – smoking damages the lining of your arteries, leading to plaque build-up and arterial blockage. Given that it also increases blood clotting – the risk of heart attack or stroke is even higher. To top it off, carbon monoxide in smoke reduces the amount of blood oxygen (including the blood that the heart supplies to itself to work properly) and increases blood pressure. Quitting smoking is one of the absolute best things you can do to improve your health;
Does Exercise make your heart stronger?
You have probably heard countless times that exercising trains your cardiovascular system and is, therefore, good for you. Millions of heart-health conscious individuals typically resort to aerobic exercise because it seems to get their heart rates up the most. The truth of the matter is, however, that they are all doing it wrong.
But first – let’s look at what is currently known about the impact of exercise on heart health.
There is no doubt that exercise is beneficial for the heart (as well as many other organs and systems in your body). Exercise leads to major adaptations in skeletal muscle, including an increase in capillary supply correlated with increased mitochondrial volume (the more mitochondria you have – the higher the theoretical capacity of the heart to produce energy). In contrast, heart failure is associated with an overall disarray in mitochondrial structure and decrease in mitochondrial cristae surface (those folds inside mitochondria, the surface area of which is directly correlated with their capacity to use more oxygen and generate more energy), suggesting a drop in oxidative capacity of the working heart muscle.
Adaptive responses of the heart to endurance training include reduction to resting and submaximal exercise heart rate and increase in end-diastolic dimension (an increase in the diameter of the relaxed ventricle when the heart is filling up with blood following the contraction). This leads to nonpathological cardiac hypertrophy, improved ventricular function and increase in the resistance of the heart to ischemic insult.
Exercise training improves endothelial function (endothelial dysfunction is another common reason for heart failure – as you recall, endothelial dysfunction can often be a direct result of consuming too much inflammatory cooking oils [LINK]. This doesn’t mean you can ever exercise your way out of a bad diet, but this fact is still something to consider.
Exercise also improves coronary perfusion, decreases peripheral resistance, and induces cardiac and skeletal muscle cell remodeling, leading to increased oxygen uptake, substrate oxidation, and resistance to fatigue.
But it is usually HOW and HOW MUCH you exercise that matters the most. Although aerobic (cardio) exercise is considered a staple for heart health, when you start doing meaningless aerobics for too long at too high of an intensity – you are actually doing yourself more harm than good (which is, by the way, confirmed by a reduction in HRV following intense aerobic exercise). We are not going to go into the details of what makes aerobic exercise good or bad (we have previously discussed this specifically [LINK]), but just keep in mind that the goal here is not to crank up your heart rate as much as possible for as long as possible. – excessive endurance exercise actually has adverse cardiovascular effects. Elite athletes – who often push their limits too much in going “longer and faster” – are at a higher risk of heart arrhythmias and coronary artery calcification than those who only exercise moderately.
Most types of exercise represents a stress for the body – and blood samples following exercise might even contain biomarkers typically associated with heart damage. When such stress is repetitive and prolonged – this leads to remodeling of the heart tissue (scarring of the walls, thicker, less elastic tissue, changes in heart rhythm, etc.). Don’t get this wrong – exercise is still very beneficial overall – but too much of it is not. Studies on rats, designed to imitate cardio endurance training, showed that animals with previously healthy hearts developed multiple dysfunctions at the end of such experiments (cardiac fibrosis, arrhythmias and changes in ventricular function). If you don’t think studies on mice can be indicative of what is happening to people – a study published in the journal of applied physiology in 1985 indicated that 50% of the examined veteran endurance athletes exhibited some degree of myocardial fibrosis (scarring of the heart muscle), directly correlated with the number of years spent training for and running marathons.
Let’s address the fundamental misunderstanding about exercise and the heart. Most people think that the heart only gets stronger and “better” when it is being pushed too hard – that’s why intense aerobic exercise is usually their choice. In reality, any exercise is good for the heart – because any exercise will raise the demand for oxygen and, thus – for the blood delivering this oxygen. By regularly placing higher demands on your heart to deliver this oxygenated blood, you are making it stronger (your heart is a muscle) and more efficient (as any muscle, your heart adapts with time by increasing the number of mitochondria necessary to produce energy for itself – so that as it gets more efficient, it requires less effort to keep up with energy needs to work). You don’t have to stress it too much for that purpose – it’s a natural adaptation process that will happen even if you don’t raise and maintain your elevated heartbeat for long periods of time (which happens with intense aerobic exercise). If you recall the discussions in previous articles, even if you are moving heavy weight for a limited number of repetitions (which, by itself, may not require as much oxygen during the exercise, while your muscles use anaerobic metabolism to quickly produce energy for movement), your system will catch up shortly after to repay the “energy debt”, clean up the by-products of anaerobic metabolism and regenerate some glycogen. Your heart will start pumping more blood more often – and will adapt and strengthen as a result.
One of the benefits of exercise is that it improves electrical stability of the heart and general heart rate variability (HRV) (although typically not during the exercise – but rather after it). What is heart rate variability and why is it important? Let’s take a closer look.
(Continued in Part II…)