Trial Report The impact of bed rest on human skeletal muscle metabolism, 2024, Wüst

Dolphin

Dolphin

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https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(23)00601-8#

ARTICLE| VOLUME 5, ISSUE 1, 101372, JANUARY 16, 2024
The impact of bed rest on human skeletal muscle metabolism
  • Moritz Eggelbusch
  • Braeden T. Charlton
  • Alessandra Bosutti
  • Bergita Ganse
  • Ifigenia Giakoumaki
  • Anita E. Grootemaat
  • Paul W. Hendrickse
  • Yorrick Jaspers
  • Stephan Kemp
  • Tom J. Kerkhoff
  • Wendy Noort
  • Michel van Weeghel
  • Nicole N. van der Wel
  • Julia R. Wesseling
  • Petra Frings-Meuthen
  • Jörn Rittweger
  • Edwin R. Mulder
  • Richard T. Jaspers
  • Hans Degens
  • Rob C.I. Wüst


    Highlights
    • •
      Muscle glycogen build-up in bed rest reduces insulin sensitivity and further storage
    • •
      Muscle lipid overload, lipotoxicity, and inflammation develop during bed rest
    • •
      Bed rest shifts muscle metabolism from fatty acid to glucose oxidation
    • •
      Intrinsic mitochondrial alterations occur after long-term bed rest





      Summary
      Insulin sensitivity and metabolic flexibility decrease in response to bed rest, but the temporal and causal adaptations in human skeletal muscle metabolism are not fully defined.

      Here, we use an integrative approach to assess human skeletal muscle metabolism during bed rest and provide a multi-system analysis of how skeletal muscle and the circulatory system adapt to short- and long-term bed rest (German Clinical Trials: DRKS00015677).

      We uncover that intracellular glycogen accumulation after short-term bed rest accompanies a rapid reduction in systemic insulin sensitivity and less GLUT4 localization at the muscle cell membrane, preventing further intracellular glycogen deposition after long-term bed rest.

      We provide evidence of a temporal link between the accumulation of intracellular triglycerides, lipotoxic ceramides, and sphingomyelins and an altered skeletal muscle mitochondrial structure and function after long-term bed rest.

      An intracellular nutrient overload therefore represents a crucial determinant for rapid skeletal muscle insulin insensitivity and mitochondrial alterations after prolonged bed rest.

      889E5150-EACD-4777-8EB0-E2C9A1814977.jpeg
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Not sure why the poster on Twitter is saying the participants didn’t develop ME/CFS. I skimmed through the paper and I don’t see where they assessed if participants developed clinical symptoms of PEM, fatigue, cog dysfunction etc.
 
Compare with their Long Covid study —

Healthy bed-rest said:
Daily reduction in muscle size was largest in the first 6 days of bed rest, while a marker for mitochondrial density (succinate dehydrogenase activity) was only reduced after long-term bed rest.
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Long Covid post exercise said:
Succinate dehydrogenase (SDH) activity, a marker for mitochondrial density, was not different between groups (p = 0.06) and only reduced (p = 0.0083) after induction of post-exertional malaise in long COVID patients (n = 25) compared to healthy controls (n = 21).
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Healthy bed-rest said:
Notably, no change in fiber type composition was observed at any time point of the bed rest
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Long Covid post exercise said:
Patients with long COVID (n = 25) had a higher percentage (p-value: 0.036) of glycolytic type IIx compared to healthy controls (n = 21).
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Sid said:
Not sure why the poster on Twitter is saying the participants didn’t develop ME/CFS.
Click to expand...

in collaboration with the German Aerospace Center, the European Space Agency and the National Aeronautics and Space Administration. All participants gave written informed consent prior to the study. The study was conducted in accordance with the declaration of Helsinki and was registered at the German Clinical Trials Register under number DRKS00015677. The protocol was approved by the ethics commissions of the Medical Association North Rhine (number 2018143) and NASA (Johnson Space Center, Houston, United States).
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Development of ME/CFS would have constituted a serious adverse event that would be required to be reported. NASA and the ESA have been doing these types of bed-rest studies for decades.
 
SNT Gatchaman said:
Development of ME/CFS would have constituted a serious adverse event that would be required to be reported. NASA and the ESA have been doing these types of bed-rest studies for decades.
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That’s quite a leap.

Anyway, the metabolic changes observed here are very similar to those reported in obesity studies. What they inadvertently looked at here is the effect of a hypercaloric diet.
 
NelliePledge said:
was wondering what exactly was meant by bed rest. I couldn’t find an explanation by a quick skim of the study.
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This press release by their university gives some brief info:

All experiments, meals, and leisure activities took place lying down. Participants were restricted in their movements, reducing the strain on muscles.​

"The beds were inclined at an angle of 6 degrees, with the head lower than the feet to simulate the displacement of body fluids that astronauts experience in a microgravity environment. For the first time, the potential of artificial gravity was investigated (centrifugation at about 1G at the level of the navel) as a preventive measure against the adverse effects of weightlessness on the human body", says Wüst.
​
Source: After 6 days of inactivity, people develop the first symptoms of type 2 diabetes - Vrije Universiteit Amsterdam (vu.nl)

Sid said:
I skimmed through the paper and I don’t see where they assessed if participants developed clinical symptoms of PEM, fatigue, cog dysfunction etc.
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Could not find anything either. Suspect that people are using the info Wust shared on Twitter earlier rather than the info in this paper. I hope that they will directly compare this deconditioned group and ME or LC patients in a future paper.
 
So it isn't deconditioning. Who knew?

Identify and interrogate the assumptions is the first step in assessing any hypothesis.

The deconditioning assumption is critical to the psychosomatic hypothesis of ME.

Its proponents have never interrogated that assumption.

How much time and resources and cruelly wasted patients' lives could have been saved if they had done their job properly at the start and robustly tested just that assumption alone?
 
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I wonder how many of them developed OI or POTs and if so, for how long? It's something I was told when seeing Cardiologists re: POTS or low BP. Was told being bedbound for ME was causing this.
 
Sean said:
So it isn't deconditioning. Who knew?

Identify and interrogate the assumptions is the first step in assessing any hypothesis.

The deconditioning assumption is critical to the psychosomatic hypothesis of ME.
Click to expand...
It was never a reasonable hypothesis, whatever they might say. Deconditioning doesn't fluctuate, doesn't vary on the order of hours or even minutes. That's why they added the "illness beliefs" nonsense, because it's not deconditioning and they couldn't account for that but they sold their cake, ate it, and had it too because reasons.

And that's on top of how it affects people who were very active mere weeks before, or people who were recovered, resumed their activities, then crashed. And on top of how it's only a minority who ever go through extensive bed rest. And how the symptoms don't necessarily change from early onset, where some people were very active shortly before, compared to months later, when deconditioning could be argued, if there was excessive bed rest.

This is why falsification is critical in science. These quacks never used scientific reasoning, because it proved them wrong. Their arguments amounts to "people with red hair don't exist, if you don't look for them or count them" while dismissing people with red hair saying otherwise as activists, or whatever. It's the excessive level of lying and making stuff up that makes it especially hard to kill. It was always so blatantly fake and wrong.
 
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