I read an account by a housebound ME patient about being able to handle very short car trips as a passenger, while longer ones flare their symptoms even though they remain as idle as possible. Such a flare could only plausibly be induced by sensory stimuli during the trip, among which vehicle motion, ambient noise from the vehicle, surrounding vehicles and the road, bumps in the road and sunlight / UVs (when looking through the windows or the windshield). While it is acknowledged that active cognitive exertion and sensory / passive cognitive exertion are standalone PEM triggers, and that they can provoke PEM of the same intensity as that induced by physical activity, neither has yielded much insight into PEM until now. Few research studies have investigated their involvement in this regard. First, there does not seem to be a recognition that studying sensory exertion would lead to designing less strenuous repeated exertion tests than the 2-day CPET. They would be less dangerous and more accessible to moderate and severe patients, and they may be as effective -- at least for the needs of research --. In particular, a simple test with a virtual reality headset could be devised. To minimize physical activity and external sensory stimuli, a patient would lie flat in a calm, dark, temperature-regulated room. With the VR headset, they could then be subjected to scenarii involving varying amounts of sensory exertion, ranging from a dark bedroom to a car trip, a busy urban setting, a concert and so forth. Importantly, such a setup enables choosing the type of sensory stimuli as well as the duration of each scenario. Second, does the fact that sensory and cognitive exertion are standalone PEM triggers suggest that PEM from physical activity may not originate from a problem with muscles themselves, but rather that the latter results from the involvement of organs and biological pathways that are common to both types of exertion? Although evidence is suggestive or lacking, the hypotheses of cerebrovascular issues (e.g. cerebral perfusion), cerebral inflammation and neuronal signalling in general come to mind. Under this light, central sensitization may be evoked too, but it does not seem plausible as the onset of PEM is delayed at least by a few hours after terminating exposure to a sensory trigger.