In my recent post I summarised the evidence indicating that running, at least in amounts up to 50 minutes of vigorous activity per day, is likely to increase your life expectancy, but nonetheless some endurance runners suffer serious ill-health attributable at least in part to their running. There is unequivocal evidence indicating transient heart muscle damage after endurance event such as a marathon; and unequivocal evidence that endurance athletes are at increased long-term risk of heart rhythm disturbance, such as atrial fibrillation. There is quite strong evidence that many years of marathon training increases the risk of fibrosis of the heart muscle and calcification of the coronary arteries. While the beneficial effects appears to outweigh the adverse effects for the majority, at least some endurance athletes suffer serious adverse effects. On the other hand, the evidence that the benefits appear to outweigh the adverse effects in the majority suggests that is sensible to try to identify what causes the serious adverse effects and take steps to minimise them, thereby increasing the likelihood of being among those who derive more benefit than harm.
Although the mechanisms of cardiac damage are not well established, there is a great deal of evidence regarding plausible mechanisms. We are not detached observers who can afford the luxury of waiting until the mechanisms are established beyond doubt, like climate change deniers who prefer to wait until the outcome is certain before acting. Rather, we are each an experiment of one, and we must make our decision for action or inaction based on the current evidence.
Inflammation and myocardial fibrosis
Perhaps the most plausible mechanism for adverse cardiac effects is a mechanism based on inflammation. Prolonged mechanical stress on heart muscle produces damage, which in turn elicits an increase in cytokines, the chemical messengers that circulate in the blood and trigger the events of inflammation which lead to laying down of fibrous tissue. This is the body’s mechanism for repairing damage and increasing the strength of tissues. But the initial deposition of fibrous tissue is slap-dash and unless redundant fibres are removed, the future function of the relevant body tissue is likely to be impaired. In the long term calcium is deposited at the site of damage, making the tissues stiff and inflexible.
In the case of tissues such as the plantar fascia, the misaligned fibres cause the pain of plantar fasciitis and the deposited calcium gives rise to the heel spurs visible on x-ray. In the case of the heart muscle, misplaced fibrous tissue has the potential to interfere with the electrical conduction pathways producing disturbance of rhythm. In the case of the lining of blood vessels such as the coronary arteries, the process is a bit more complex. The accumulation of cholesterol at the sites of damage to the lining of the artery plays a key role in triggering the inflammatory response. The Wellcome Trust have produced an excellent video depicting the sequence of events.
Minimising the risks
From what we understand of the mechanism, there are three key things we can do to minimise the risk of damage:
1) Allow adequate recovery after heavy training and racing. Studies in animals and humans demonstrate that much of the fibrosis, though perhaps not all, resolves during an adequate recovery period.
2) Build up training gradually. The tissue trauma that initiates the inflammatory process is less if the tissues have been strengthened by gradual adaptation. This is illustrated by the fact that DOMS is more marked if you suddenly increase training volume.
3) Consume a diet that minimises chronic inflammation. Current evidence indicates that a Mediterranean diet, in which the pro-inflammatory omega 6 fats prevalent in the Western diet are balanced by omega 3 fats from fish and/or nuts and green leafy vegetables, is a heart-healthy diet.
It is noteworthy that these three strategies not only have the potential to reduce the risk of serious long term adverse effects on the heart, but are also likely to maximises the long term improvement in running performance.
In future posts I will discuss the more complex issue of cortisol and also the exacerbation of rhythm disturbances by excess potassium that is released from damaged muscle cells