Stanford Medicine study details molecular effects of exercise

Mij

Senior Member (Voting Rights)
Researchers at the School of Medicine have shown how exercise changes the body at a molecular level and have identified blood markers of fitness.

A flurry of change
Snyder’s team set out to better understand the molecular shifts that underlie changes in physical fitness. The gold standard of medical fitness assessments is a peak VO2 test, which measures a person’s peak oxygen consumption during intense exercise and uses the score as a proxy for aerobic fitness. But Snyder and his team wanted more detail — specifically, about the ways in which exercise initiates change at the molecular level.

They performed VO2 testing for 36 individuals, including Snyder, on a treadmill. Participants, both male and female, had an average body mass index of 29 kilograms/meter squared, and their age range was from 40 to 75 years old. Before the treadmill test, the researchers drew a baseline blood sample. Participants then donned an oxygen-measuring mask and ran at a slight incline until they reached peak oxygen consumption, at which point they stopped and got off the treadmill. The researchers took blood samples from participants 2 minutes, 15 minutes, 30 minutes and 60 minutes after they had reached their peaks.

“All of these measurements allow us to describe a choreography of molecular events that occur after physical exercise,” Snyder said. “We know that exercise causes an array of physiological responses, such as inflammation, metabolism and hormone fluctuation, but these measurements allowed us to characterize those changes in unprecedented detail.”

It turns out that in the first two minutes post-exercise, the body experiences an intense flurry of molecular activity. In most participants, molecular markers of inflammation, tissue healing and oxidative stress, a natural byproduct of metabolism, spiked sharply shortly after hopping off the treadmill, as their bodies began to recover. Molecular markers of metabolism varied, Snyder said. At 2 minutes, blood samples revealed evidence that the body was metabolizing certain amino acids for energy, but it switched to metabolizing glucose, a type of sugar, around 15 minutes. “The body breaks down glycogen as part of its exercise recovery response, so that’s why we see that spike a little later,” Snyder said. Glycogen is a form of stored glucose.

As part of the study, Snyder also compared the molecular response in individuals who were insulin resistant, meaning they’re unable to process glucose properly, with the response in individuals who could process glucose normally. “The main difference we see is that insulin resistant individuals have a dampened immune response post-exercise,” he said.

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Does this include measuring molecular changes pre and post-exercise for pwME? I mean, delayed PEM is what I would be very interested in knowing more about.
I'm not up to it right now as having to wear my specs, and not a biology expert, but I am thinking similarly that perhaps the really interesting stuff is the tools and methods here. In particular given they seem to be being specific on timings for taking these measures whether they can develop protocols that for example could provide data over the days following exertion - in order to compare eg pwme vs controls of varying types.
 
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We are continuously vetting and adding new treatments based on the latest research and treatment profile. Here is a list of our range of low-risk medications available immediately: Low Dose Naltrexone, Propranolol, Pyridostigmine, Ketotifen, Metformin

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As a doctor, I don't consider any of those medications low risk! Many have significant side effects and can cause a variety of serious health problems.

I looked up their website, it looks like a on-line physician site especially aimed at providing prescriptions for pwLC, ME/CFS, MCAS.

Confined to some states in the USA but hoping to extend their reach to other states.

I am not sure they can really say that all these meds are supported by (good) research. Maybe some but not all.

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Creating a baseline of data on what healthy and unhealthy bodies do under exercise is going to be really useful.
The timeline they have there is maybe not long enough to capture PEM. But that doesn't mean differences won't be present in the early phases.

Hanson's data seems to suggest that pwme don't react to exercise much at all, i.e. all the appropriate adaptations don't happen. That might be notable.

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I just want to mention a medical device that can be used for pretty intensive longitudinal blood sampling, it's caled the Edwards Vamp, it was used in some ongoing research in South Australia. I'm not sure how good the research hypothesis was but the repeat longitudinal sampling seemed useful.

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Study 1: Cytokines and clinical symptoms
Following a half day of clinical evaluation, participants were waited on hand and foot as blood samples were collected at 7 minute intervals over eight hours. Warmly known as the Vampire Study, the original plan was to look at Leptin and Interleukin-6. Samples from the resulting ME/CFS biobank have since been analysed for additional cytokines based on emerging research. It is anticipated that the biobank will later be used for genetic studies.
 
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