I’ve talked here at the blog on many occasions about the health benefits of exercise. Once again, I’ll point out that those many benefits are undeniable.
Over the years, many studies have been devoted to questions like:
How little exercise is needed to produce those benefits?
What intensity is needed to enjoy those benefits?
Answers to those questions have guided the development of the various consensus guidelines about exercise as a part of healthy living. Check out the guidelines from the American Heart Association, World Health Organization, or the U.S. Centers for Disease Control.
Recently, though, there’s been increased attention paid to the potential issue of harm that might come to the heart because of too much exercise. The surprising–and rather serendipitous–finding of unusual scarring, or fibrosis, in the hearts of long-time marathoners has raised many important questions. In clinical practice, we usually associate such findings with serious heart problems. Yet the affected athletes may have gone a lifetime without any indication of a heart problem.
At least a couple working hypotheses have emerged:
1, Repeated episodes of seemingly routine, but intense exercise produces the harm, or
2. Increased inflammation from each episode, or a prolonged inflammatory state, produces the harm.
For now, let’s focus on the first hypothesis. And let’s consider the possibility that with even just a short period of intense exercise, a small amount of harm, or damage might come to the heart….and that little by little this damage accumulates over the years.
In today’s blog post, we’ll lay the necessary foundation for our discussion by developing some of the vocabulary we’ll need. In my next two posts, I’ll talk about what’s known regarding acute heart injury after running and after triathlon, specifically.
Skeletal Muscle and CPK
It’s long been known that periods of exercise can lead to skeletal muscle injury. In the early 1970s it was recognized that this injury was associated with release of proteins from the muscle cells into the bloodstream where they could be detected and quantified. The primary example is creatine phosphokinase (CPK), an enzyme that catalyzes the reversible reaction between creatine and phosphocreatine and is central to the muscle’s energy metabolism. When CPK is measured in the bloodstream as an indicator of muscle injury, we call the CPK a biomarker for muscle injury.
By the late 1970s enough investigation had been completed to know that elevation of the CPK could be mild in the case of recreational exercise or quite severe after efforts such as marathon running.
Heart Muscle and CPK-MB
It turns out that there are actually 3 different forms, or isoenzymes, of CPK. One of those forms, the CPK-MB is found almost exclusively in heart muscle. More than 98% of the body’s CPK-MB is found in the heart, while the remaining 2% is found in skeletal muscle. As a result, the CPK-MB can be used as a specific biomarker for heart muscle injury.
In clinical practice, a blood test showing elevation of the CPK-MB was used for many years as our way of confirming the diagnosis of acute myocardial infarction (MI), the condition that results from sudden, complete blockage of one of the coronary arteries. In the case of acute MI, there is a very characteristic pattern to the CPK-MB elevation found in the blood, with a rise in level very soon after the coronary artery becomes blocked, a peak level about 24 hours later, then a slow return to normal over several days’ time.
Exercise and the Cardiac Biomarkers
Around the time of the 1979 Boston Marathon, Dr. Arthur Siegel from Boston was interested in the newly available CPK-MB biomarker and enlisted 15 male marathoners to serve as subjects for a study. In their training leading up to the race, these runners were found to have borderline or slightly elevated blood levels of CPK-MB despite being completely healthy from a heart standpoint.
When their CPK-MB levels were checked 24 hours after the Marathon, there were elevations of up to 21 times normal, again without any other overt sign of a heart problem.
This was the first of many, many studies on cardiac biomarkers and exercise. We’ll talk about the results of these studies in more complete detail in my next two blog posts.
Today, the CPK-MB is seldom used clinically for the purpose of identifying cardiac injury. Instead, we measure cardiac troponin (cTn) which is even more specific for cardiac injury than the CPK-MB. But this newer biomarker works much the same way: with acute MI, there is a steady rise in the cTn to a peak level about 24 hours later, then a slow, gradual return to normal over several days’ time.
Exercise and Cardiac Structure and Function
In modern cardiology practice, we have many different diagnostic tests that help us define the heart’s structure and to asses its function. For the purpose of our discussion here, the important options are the echocardiogram (using ultrasound), the CT scan (using x-rays), and the MRI (using a powerful magnet).
In recent years, investigators have used these imaging tests to study the structure and function of the heart immediately after periods of intense exercise like marathon running or long-distance triathlon. The findings are intriguing.
Stay tuned for my next blog post devoted to acute heart injury–biomarkers and imaging tests–specifically after running events.