The effects of exercise on dynamic sleep morphology in healthy controls and patients with chronic fatigue syndrome, 2013, Kishi et al

The effects of exercise on dynamic sleep morphology in healthy controls and patients with chronic fatigue syndrome

Akifumi Kishi, Fumiharu Togo, Dane B Cook, Marc Klapholz, Yoshiharu Yamamoto, David M Rapoport, Benjamin H Natelson

Published: 2013

(Line breaks added)

Abstract
Effects of exercise on dynamic aspects of sleep have not been studied. We hypothesized exercise altered dynamic sleep morphology differently for healthy controls relative to chronic fatigue syndrome (CFS) patients.

Sixteen controls (38 ± 9 years) and 17 CFS patients (41 ± 8 years) underwent polysomnography on baseline nights and nights after maximal exercise testing. We calculated transition probabilities and rates (as a measure of relative and temporal transition frequency, respectively) between sleep stages and cumulative duration distributions (as a measure of continuity) of each sleep stage and sleep as a whole.

After exercise, controls showed a significantly greater probability of transition from N1 to N2 and a lower rate of transition from N1 to wake than at baseline; CFS showed a significantly greater probability of transition from N2 to N3 and a lower rate of transition from N2 to N1. These findings suggest improved quality of sleep after exercise.

After exercise, controls had improved sleep continuity, whereas CFS had less continuous N1 and more continuous rapid eye movement (REM) sleep. However, CFS had a significantly greater probability and rate of transition from REM to wake than controls. Probability of transition from REM to wake correlated significantly with increases in subjective fatigue, pain, and sleepiness overnight in CFS – suggesting these transitions may relate to patient complaints of unrefreshing sleep.

Thus, exercise promoted transitions to deeper sleep stages and inhibited transitions to lighter sleep stages for controls and CFS, but CFS also reported increased fatigue and continued to have REM sleep disruption. This dissociation suggests possible mechanistic pathways for the underlying pathology of CFS.

Link | PDF (Physiological Reports) [Open Access]

 

I could only find two studies that monitored sleep quality after an exercise test. The other one is:

Sleep is not disrupted by exercise in patients with chronic fatigue syndrome, 2010, Togo et al (thread)

Most of the authors are the same, including Benjamin Natelson.

Still haven't read these. But I feel like there should be more studies on this.

Insomnia after exercise or heavy cognitive activity is maybe my most objective symptom. If I do a lot of activity, I can be almost certain that that night I'll feel far more "wired" at my usual bedtime, like I just drank caffeine, and it'll take at least an hour or two longer than normal to fall asleep.

I've seen this mentioned by others a lot as well. Maybe we should do a poll thread about how many people experience this?

 

Both studies used Fukuda. So basically this has never really been tested in ME/CFS.

 

Interesting, but waking from sleep or disrupted sleep cycles once sleep has been initiated is only one aspect of ME/CFS sleep issues, others include trouble initiating sleep (as mentioned by others here), shifting in the internal clock, excessive sleeping and unrefreshing sleep can be more than implied in the abstract, for example following a ‘good night’s’ sleep I can wake feeling significantly iller than when I went to sleep requiring several hours rest before I can begin any activity.

It is good to have a putative mechanism that would not necessarily be amenable to treatment by sleep hygiene measures, certainly I think it is also interest that at least some of us find trying to impose a presumed normal sleep pattern can make the situation much worse.

Then of course there is those of us who experience night sweats, currently apposite for me as I lie debating which will be more disruptive to my sleep remaining in damp clothing or getting up to change into dry clothing.

 

I've noticed this kind of pattern from my wearable sleep data. REM sleep very often initiated every 1.5h and after that waking up. Few days ago it happened 5 times in a row. Sure, the data might be somewhat unreliable but I do remember seeing lots of different dreams and waking up often.

I've had same kind of problems and at least on winters I've got a life hack for it. My problem has been that normal blanket gets too hot for me and thin blanket too cold for me. I then realized that I could lower my room temperature! Got it down to 18℃ from 22℃ and now I can sleep and sweat less with the normal blanket.

 

A poll sounds like a good idea. Cognitive efforts reduce my sleep quality and duration.

 

This is brutal for me during the cold winter months when I don't heat my room for sleeping. I feel chilled and frozen. So now I keep dry shirts warmed up under the covers so I don't have to get up at all. My sleep is disrupted, but once I get into dry warmer clothing I am able to fall back asleep for the most part of the night.

 

Totally spitballing but could this by why people often report weirdness around dreams. “ie. vivid dreams, constantly wake up after dreaming, fever dreams etc”

 

I've made a poll about sleep changes due to exertion:

[Poll] How does exertion affect sleep?

 

So this study looked at the same 33 participants as the other 2010 study linked above.

I'm not sure it's good to exclude those with restless leg syndrome, since that may be an effect of ME/CFS.

For the below "traditional" sleep variables, the most significant effect seems to be sleep latency (how long it takes to fall asleep). Healthy controls fell asleep significantly faster after exercise (about 15 minutes, p<0.01), while sleep latency change was not significant in ME/CFS (about 3 minutes faster).


And it looks like ME/CFS there might be an effect of more REM sleep and less non-REM sleep in ME/CFS after exercise compared to controls.

There were a few other findings, but the other main one that is interesting to me is that they found that in ME/CFS, the higher a person's probability of transitioning from REM to wake (I think this is the night after exercise), the more their fatigue, sleepiness, and pain worsened the morning after exercise compared to the evening after exercise but before sleep. In controls, there was no such correlation. (After removing an outlier, sleepiness and fatigue were still significant, but not pain.)

Since this study used Fukuda, it's unclear if everyone had PEM. But asking about how much fatigue, sleepiness, or pain worsened the morning after exercise may be a useful indicator of PEM. So using a correlation may be showing that this variable is actually associated with PEM severity, or only high in those patients who have PEM, if not all do.

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Edit: I'm not totally sure what night the correlation stats are based on, or if they averaged the two nights, or something else.

Edit 2: Okay, I think they used both nights, but controlled for which night it was. I was worried they treated different nights from a single person as independent samples.

 

What do you class as genuine ME then? Also which pre-Covid prevalence figures do you believe because the 250,000 figure often cited is derived from the criteria you disqualified? https://meassociation.org.uk/2024/05/how-many-people-have-me-cfs-in-the-uk/

 

I don't know if there's a "genuine" ME/CFS since all the criteria are mostly just arbitrary groups of symptoms that happen together often. I'm interested in these studies because I think whatever is harmful about exercise in people with PEM might show up on before/after exercise tests. There's not as obvious a reason to include people without PEM and I think it's likely to just dilute the effect, if there is one.

I don't know much and am not overly concerned about prevalence. If 250,000 is based on Fukuda, it's based on Fukuda.

 

If people who previously would have fulfilled Fukuda, but are not considered ME/CFS any longer because they don't fulfill newer criteria with PEM, feel like the science is moving on without them and they're stuck with something like "idiopathic chronic fatigue" that doesn't have the momentum of "ME/CFS", well, that's a tragedy. And I'm sure there are very, very many of those people.

With long COVID, what is it 50% have PEM, and the rest are chronically ill in other ways? I have little doubt there are similar percentages for triggers of similar pre-COVID illnesses. But the non-PEM people don't have the massive COVID pandemic everyone else is experiencing as their trigger to unite them, and they don't fit ME/CFS criteria. They might not even know if there was a viral trigger so can't say they have post-viral fatigue. They're just sick and don't know who's going to help, and that's awful.

It may be a bit insensitive of me to say some people have no reason to be in a study when not many others are including them in studies either. It's definitely something for me to think about.

 

Wide definitions lead to more heterogenity in the studied population. This added noise makes it more difficult to find patterns and results.

When we have limited resources, it makes sense to study only the strictest definitions first, and then expand the inclusion criteria once we have something specific to target.

I understand that «being studied» might have some value for the patients, but I don’t think that warrants the cost.

 

Would you want to hear "we need to study the people with IBS but without PEM first and once we figure something out, we'll include the ones with PEM as well"?

While the best solution probably isn't to spend $100 of available research funds on a study that globs everyone together, I don't think it's fair to use all $100 on PEM and tell everyone else to be patient.

There are 8500 papers on PubMed that mention "chronic fatigue syndrome". For "post viral fatigue" (or similar terms)...344. "Idiopathic chronic fatigue"...84.

 

It makes sense to seperate into subgroups and prioritise the more disabling ones. It also makes sense to study strict definitions and see if anything can be found there, then see if it holds in less strict definitions.

It obviously does not make sense to only study one subgroup or definition. Because in that case people are left behind.

 

If the objective is to figure out IBS, then yes.

I have had IBS for over ten years. It changed after I got Covid and PEM as a result of that.

If the objective is to figure out ME/CFS, being strict about having PEM makes sense. The effort preference NIH study did not make sense because they excluded all co-morbidities, even POTS. So it depends on the specifics.

 

As far as I've seen, I don't think this is the case. Most people that applied for the study didn't get in because they failed had been ill for longer than 5 years or didn't have an infectious onset (or one that couldn't be documented). Of course the sickest are never going to be able to participate in the first place. Diseases such autoimmune diseases, cancers, Lyme diagnosis etc were an exlusion criteria but I think it can be argued that, that is very sensible given the scope of the study. We shouldn't forget that even after people had passed screening and medical records reviewed, in person evualations still revealed things such as cancer, Parkinson etc. I haven't seen POTS mentioned as exclusion criteria, where did you see that?

I'm afraid we cannot have it both ways. We can't criticise the intramural study, that is one of the only studies to have ever rigorously recruited patients, whilst accepting other studies that pay little attention to recruitment and yet at the same time criticise the BPS lobby for being too little attention to recruitment criteria.

IMO recruitment is one of the few things they got right!