exercise-induced cardiac fatigue

Is exercise-induced cardiac fatigue caused by damage to the heart muscle?

Regular Peak Performance readers will probably recall last year’s eye-opening article on the potential risks of sudden cardiac death and cardiac cell death during or immediately following prolonged endurance events (PP161, March 2002, p1). Although that article may have struck the fear of death (quite literally!) into many an aspiring marathoner, it highlighted the fact that the risks of strenuous endurance exercise should not be taken lightly, and both caution and common sense are needed when training for these types of events.

But before you take fright and swap your trainers for slippers, it is worth noting that the majority of sudden cardiac deaths during exercise occur in athletes with existing cardiovascular disease. In young athletes (under 35), sudden cardiac death is caused mainly by inherited structural and functional abnormalities, while in the over-35s it can be attributed primarily to coronary artery disease(1). Both of these conditions can be diagnosed through screening.

Rather than focusing on sudden cardiac death and unhealthy hearts, the purpose of this article is to inform readers about recent research findings on the effects of prolonged exercise on healthy hearts. We will take a look at current evidence on exercise-induced cardiac fatigue (EICF) and exercise-induced cardiac damage (EICD), along with their clinical implications, and finally home in on what it all means for you as an athlete.

EICF, defined as a reduction in cardiac function following prolonged strenuous exercise, is not a new concept. In a study carried out in the 1960s, athletes were found to exhibit a significant decrease in stroke volume (the amount of blood pumped out by the heart in a single beat) following a bout of prolonged exercise (2). This established a possible link between exhaustive exercise and the potential for a decrease in cardiac function. This is perfectly logical: after all, if skeletal muscle fatigues after a period of extended exercise, why not cardiac muscle too? However, the crucial difference is that the cardiac muscle has the essential job of supplying blood to vital organs and, unlike skeletal muscle, cannot simply ‘take a break’ during or following prolonged exercise.

Evidence for EICF has come from a number of studies examining cardiac function after prolonged exercise. Decreases in both systolic and diastolic function (blood pressure during and between heart beats) have been reported in ultra-endurance athletes immediately following half and full Ironman triathlons (3,4). More recently, EICF was demonstrated in athletes after the two-day Lowe Alpine Mountain marathon(5). In studies where follow-up assessments of cardiac function have been performed 1-2 days after a race, normal cardiac function has been restored, suggesting that EICF is likely to be a transient phenomenon (3,4).

The majority of endurance athletes, however, are highly unlikely to undertake such extreme competition. So what is the relevance of these studies to the general athletic population?

Well, the findings observed following ultra-endurance exercise have been replicated in experiments using less well-trained individuals covering shorter exercise distances. EICF has been demonstrated in healthy subjects following a 20km run (6) and a 60-minute cycle ride (7). It is therefore possible that EICF may affect mere mortals as well as the super-heroes taking part in ultra-endurance events.

It is important to note that the evidence is not beyond doubt since other studies have failed to demonstrate EICF either following (8) or during (9) similar bouts of prolonged exercise. Nevertheless, on balance there is compelling evidence to suggest that EICF does exist and that it occurs following a wide range of exercise durations and intensities in both trained and untrained subjects. It is worth noting, though, that there is no evidence to support the existence of EICF following periods of intense brief exercise. Indeed, if anything, short duration exercise actually enhances cardiac function in the short-term.

In studies of relatively short periods of endurance exercise (50-150 min), EICF has not always been observed. As a result, it has been suggested that exercise duration may be an important factor in determining the onset of EICF, although the existence of a critical ‘threshold’ has not been established. Other factors, such as temperature and humidity, altitude, hydration status, gender and age may also be significant, and differences in these variables may account for some of the conflicting findings in the current literature.

There is extensive evidence to support the existence of EICF, but what is actually causing the reduction in cardiac performance? By analogy with the response of skeletal muscle to prolonged strenuous exercise, which is known to generate significant but reparable tissue damage, researchers hypothesised that myocardial damage may be the underlying mechanism in EICF.

New tests for EICD

Testing this hypothesis by obtaining samples of cardiac muscle tissue from athletes would be difficult, impractical and downright unethical. Fortunately, though, highly-sensitive and specific tests to detect blood-borne markers of myocardial cell damage have been developed, and these offer a quick and reliable method of assessing the extent of EICD. Cardiac troponins I and T are regulatory proteins which form part of the cardiac contractile apparatus. Following damage to the cardiac muscle tissue, these troponins are released into the circulation, with the amount released corresponding to the severity of the damage (10).

Evidence of troponin release following prolonged endurance exercise has been reported by a number of investigators (11, 12), although some have failed to find it (13). These inconsistencies may be attributed to some of the confounding variables (climate, gender, age etc) referred to above.

Most of the studies examining EICD have used highly fit individuals who are accustomed to performing extraordinary volumes of endurance exercise in extreme environments. So how likely is it that a person of good physical fitness will exhibit cardiac damage over shorter distances, such as a marathon? The latest data suggests that elevated cardiac troponins (reflecting minimal cardiac damage) are evident even at this level. On completion of the London Marathon, the majority of a sample of recreational runners demonstrated cardiac troponin T values above the upper reference limit for a normal population, although these values were below the level expected after an acute myocardial infarction (heart attack) (14).

The clinical cut-off for diagnosis of myocardial infarction using cardiac troponin T has been established at 0.1 micrograms per litre, with any values above this level indicating the presence of major cardiac injury(15). Since the increases in cardiac troponin T which have been reported following strenuous endurance exercise are substantially lower than those observed after myocardial infarction, and often do not exceed the clinical cut-off, cardiac damage, while present, is likely to be minimal.

So should athletes be worried about EICD? The current evidence requires careful interpretation, and there are a couple of factors to consider. First, troponin release may be lower in highly trained athletes than in untrained individuals, suggesting that EICD may be part of the normal cardiac adaptation to endurance exercise; secondly, in studies where follow-up samples have been obtained 24-48 hours after exercise, it has been demonstrated that elevated cardiac troponin T levels return rapidly to baseline. This suggests that EICD is temporary, by contrast with myocardial infarction, which results in irreversible damage and, ultimately, cell death (necrosis).

Cardiac necrosis is characterised by a continuous release of cardiac troponins, which originate from the breakdown of the contractile apparatus in the muscle tissue. Cardiac troponin T levels remain elevated for at least seven days after a heart attack, which is much longer than after prolonged exercise. It is probable that these post-exercise elevations are caused by membrane damage of the cardiac cells, resulting in a release of troponin from the cell interior, not by breakdown or necrosis of the entire cell.

Now let’s return to the question whether EICD underpins EICF. Studies have shown simultaneous exercise-induced cardiac damage and fatigue following prolonged exercise(9,10), but only limited correlation between these two phenomena has been established. It is not, therefore, possible to confirm a link between cardiac fatigue and cardiac damage at present, although research work is continuing in this area.

In summary, the investigation of EICF and EICD is an important area in which more research is needed to provide a better understanding of the response of the heart to prolonged exercise. Although it is clear that EICF exists, alterations in cardiac function have been shown to be transient in nature, and any cardiac damage that may occur is likely to be minimal and reversible. Thus, there need be no panic about undertaking regular endurance training, which will, in fact, ultimately benefit the heart and reduce the risk of major heart disease in the long-term. However, it is pertinent to remind people embarking on intensive training programmes (especially sedentary older people) that it is advisable to undergo a full cardiovascular screening and to take a sensible approach towards an exercise programme. Progressively building up the number of exercise sessions per week and gradually increasing duration and intensity with time is the best way to improve fitness and cardiovascular health while preventing undue strain on the heart.

Natalie Middleton, Rob Shave

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Tagged in Exercise & Physiology
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