To our knowledge this is the first study on the prevalence of ETM and the correlation with detailed characteristics of normal life migraine attacks. The two main findings in this study were; i) ETM attacks were reported by 38% of migraineurs and more than half of those quit the offending sport as a result. ii) During normal life attacks, neck pain as the initial migraine symptom was reported more frequently in migraineurs with ETM attacks compared to migraineurs without ETM attacks.
Several migraine triggers have been reported by migraine patients. Exercise, although not as commonly reported as stress or sleeping disturbance for instance, is one of them [1, 6, 7]. There is much debate on the existence of these triggers as presumed triggers can co-occur with the migraine just by chance and recall bias is likely to affect retrospective studies. Only few studies reported on patients who were prospectively followed and who were consistently able to trigger attacks by exercising [2, 8].
To minimize the possibility that presumed sport provoked attacks in our patients were actually normal life attacks occurring coincidentally during or after exercise, we asked these patients if they had quit the offending exercise because of migraine complaints. This was the case in more than half of patients reporting ETM. Furthermore these patients were able to practice lower intensity exercise in which they experienced no attacks. Both findings make chance as a possible explanation for the relation between exercise and ETM less likely.
If we consider the relation between exercise and migraine to be causal, then what is the underlying pathophysiological mechanism? One possible mechanism is dysfunction of neuropeptides like hypocretin which play a role in regulating sleep and arousal and which are located in brainstem structures which are selectively activated during migraine attacks. Patients often report that sleep is able to end a migraine attack [9], and sleep quality is negatively affected by intense severe exercise [10]. So possibly exercise can influence this hypocretin pathway and thereby trigger attacks.
A second possible mechanism is of cardiovascular origin. Aerobic exercise increases cardiac output and systolic blood pressure. Possibly this rise in cardiac output and systolic blood pressure triggers ETM attacks. This hypothesis is supported by the observation that the use of beta-blockers (which lower the cardiac output and systolic blood pressure) can prevent the occurrence of ETM attacks. It also has been shown that migraineurs have an impaired autonomic control of cerebral vasoreactivity [11], making them more vulnerable for major cardiovascular changes. The fact that in our study the majority of patients with ETM attacks stopped practicing high-intensity exercise, but were able to continue other low-intensity exercise, favors the hypothesis that rises in cardiac output and blood pressure are factors possibly associated with ETM attacks.
A third explanation is based upon an unfavorable energy metabolism. Athletes exercising at an intensity above their aerobic threshold will switch to anaerobic metabolism. The byproduct of this anaerobic exercise is lactate. Magnetic resonance spectroscopy (MRS) showed that higher brain lactate levels were associated with a higher migraine frequency [12]. A different MRS study concluded that energy metabolism in migraineurs is defective, with a slow rate of phosphocreatine recovery after exercise of the muscle in migraineurs [13]. So, while high-intensity exercise leads to a rise in blood lactate, and migraineurs have a defective energy metabolism and a higher brain lactate is associated with a higher migraine frequency, this could explain the triggering of migraine attacks by high-intensity exercise.
We found that neck pain as the initial migraine symptom was more prevalent in migraineurs with ETM. No previous studies reported that specific migraine symptoms were more prevalent in patients experiencing ETM attacks. During the pain phase in migraine the trigeminal complex is activated and neuropeptides are released at the peripheral nerve endings [14]. Neck pain in migraine attacks can be explained by the activation of upper cervical nerve fibers which have their endings in the trigeminal caudalis. Possibly the increased occurrence of neck pain in the ETM group is comparable with allodynia, as patients with allodynia reported more triggers than patients without allodynia [15].
Limitations
One limitation is the retrospective design of the study, thus recall bias could have influenced results. Furthermore, when patients are questioned if specific events could trigger attacks, their answers are subject to belief and conceptions. However unlike well-known triggers like stress and certain foods, exercise is generally not regarded as a trigger, so this bias might be limited. As this was a clinic based study in a headache center, migraine patients in this study could have been more severely affected than those in the general population. Possibly this may have influenced the lifetime prevalence of ETM attacks reported in this study. In the future prospective diary studies should be conducted, in which every exercise activity (and also other possible confounding triggers) and migraine attack needs to be recorded.
