Oxidative stress in exercise training: the involvement of inflammation and peripheral signals, 2019, Francesca et al

Andy

Andy

Retired committee member
Note: abstract mentions chronic fatigue syndrome but I'm not convinced that they are referring to CFS as we understand it.
The evidence about the health benefits of regular physical activity is well established. Exercise intensity is a significant variable and structured high-intensity interval training (HIIT) has been demonstrated to improve both whole-body and skeletal muscle metabolic health in different populations.

Conversely, fatigue accumulation, if not resolved, leads to overwork, chronic fatigue syndrome (CFS), overtraining syndrome up to alterations of endocrine function, immune, systemic inflammation, and organic diseases with health threat. In response to temporary increases in stress during training, some athletes are unable to maintain sufficient caloric intake, thus suffering a negative energy balance that causes further stress.

The regulation of the energy balance is controlled by the central nervous system through an elaborate interaction of the signaling that involves different tissues such as leptin, adiponectin and ghrelin whose provide important feedback to the hypothalamus to regulate the energy balance. Although exercise-induced reactive oxygen species are required for normal force production in muscle, high levels of ROS appear to promote contractile dysfunction. However, a high level of oxidative stress in may induce a rise in inflammatory markers and a disregulation in expression of adiponectin, leptin and grelin.
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Paywall, https://www.tandfonline.com/doi/abs/10.1080/10715762.2019.1697438
Scihub, https://sci-hub.se/10.1080/10715762.2019.1697438
 
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I do believe oxidative stesss is a problem for us, but so is it in many other diseases as well. That overexercising can induce flares in autoimmune diseases is not uncommon.

Some years ago there were someone who looked at oxidative stress and heat shock proteins (HSP) in CFS patients (I think using Fukuda criteria). I thought it interesting and whish someone could look at it again. The HSPs didn't act as they should which means the cells aren't protected from the stress of exercise as they should be. But of course, small study, Fukuda, did they measure something useful (this is not my area so I have no idea, but I think it also sounds interesting).
 
Mij said:
I had high oxidative stress on tests, the problem was that my antioxidant levels were very low/below normal.
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Which could be caused by the high oxidative stress, the system becomes overloaded. Low glutathione (our strongest antioxidant) is also not uncommon in diseases, it gets used up at a higher rate than normal. This is why I wish dieticians would be more involved with the chronically ill, our bodies need nutrients to deal with whatever goes on inside us. Like cysteine for synthesizing glutathione, or vitamin c to reactivate glutathione if it's been used in some reaction.

Never mind all the other nutrients that do important work. There's been talk on here about red blood cell deformability, which can also be affected by high oxidative stress and lack of vitamin E (an antioxidant that protects cell membranes).

I'm not advicing people to take cysteine or vitamin supplements, I'm just frustrated that a lot of doctors keep telling patients diet doesn't matter. It's not about diet being a "cure", but about damage control.

Then again, I'm studying to become a dietician so I am of course biased to the importance of diet :P Together with how sleep, activity, pain etc. affects both metabolism and diet.
 
I have never really understood what is meant by 'oxidative stress'. Chemistry is normally a subject that does not include the word stress, just things like acid and base and oxidation and unsaturated bonds and the like. Stress is a word mostly used in psychology. Selye introduced it into pathology but those of us who worked on such things later on found his concept a bit confusing.

And having worked in inflammation most of my life I never found a connection to oxidative stress. But maybe I missed something.
 
Markers never detected inflammation in my case. So oxidative stress status was high (when tested), but no inflammation.
 
Mij said:
I had high oxidative stress on tests, the problem was that my antioxidant levels were very low/below normal.
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As Midnattsol suggested, how do you know it was due to low antioxidant levels, rather than low antoxidant levels due to depletion by elevated oxidative stress?

Jonathan Edwards said:
I have never really understood what is meant by 'oxidative stress'. Chemistry is normally a subject that does not include the word stress, just things like acid and base and oxidation and unsaturated bonds and the like. Stress is a word mostly used in psychology. Selye introduced it into pathology but those of us who worked on such things later on found his concept a bit confusing.

And having worked in inflammation most of my life I never found a connection to oxidative stress. But maybe I missed something.
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That is because it is a biochemical phenomena, relating to the viability of cells when subject to elevated peroxides and oxygen radicals. The origin of the word stress long predates it's appropriation by psychologists and originally meant under pressure/tension.

The term inflammation is also used in a different way, referring to localised damage within cells, rather than a widespread stimulation of the immune system.

To find a connection between inflammation and oxidative stress, you'd need to specifically study a disease that is primarily caused by oxidative stress.
 
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Snow Leopard said:
That is because it is a biochemical phenomena, relating to the viability of cells when subject to elevated peroxides and oxygen radicals. The origin of the word stress long predates it's appropriation by psychologists and originally meant under pressure/tension.
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Yes, the word stress has a long-standing meaning in physics but it does not appear in either chemistry or biochemistry. I don't think the use in 'oxidative stress's anything to do with pressure or tension. The relevant measure is presumably relative concentrations of various species of molecule or radical.

There is vast literature suggesting that reactive oxygen species are 'bad' and involved in disease. Oxidative stress is almost always mentioned as if it were a 'threat'. But in the right compartments these species are presumably part of normal adaptive mechanisms. In themselves they have nothing in particular to do with cell viability one way or another.

Snow Leopard said:
The term inflammation is also used in a different way, referring to localised damage within cells, rather than a widespread stimulation of the immune system.
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I did my doctorate in the pathology of inflammation - I don't think either of these counts as inflammation to be honest. Inflammation is all about compartments and in the last forty years people have forgotten that and built theories that ignore crucial compartmental issues.
 
Jonathan Edwards said:
Yes, the word stress has a long-standing meaning in physics but it does not appear in either chemistry or biochemistry. I don't think the use in 'oxidative stress's anything to do with pressure or tension. The relevant measure is presumably relative concentrations of various species of molecule or radical.
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In my studies it's been used in cell biology and biochemistry mostly, and somewhat in microbiology. Stress in this case means a type of pressure, but it's not measured in mmHg. It's more along the lines of stressing a system with too much heat, cold, poor nutrient medium (but unlike a cell culture we don't grow in petridishes, which means diet again comes into play), reactive oxidative or nitrosative reactive species to name a few. If the system can adapt, great! If not, well then damage is likely to occur.

A common measure used for oxidative stress is the relationship between oxidized and reduced glutathione.

Jonathan Edwards said:
There is vast literature suggesting that reactive oxygen species are 'bad' and involved in disease. Oxidative stress is almost always mentioned as if it were a 'threat'. But in the right compartments these species are presumably part of normal adaptive mechanisms. In themselves they have nothing in particular to do with cell viability one way or another.
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Oxidative stress is a threat. Under normal circumstances the amount of reactive oxidative species are neutralized by antioxidants and the cell goes about its business. The "stress" part is when there (for some reason) is a lack of antioxidants, and these reactive species instead react with other cellular structures and cause damage to them.

Jonathan Edwards said:
I did my doctorate in the pathology of inflammation - I don't think either of these counts as inflammation to be honest. Inflammation is all about compartments and in the last forty years people have forgotten that and built theories that ignore crucial compartmental issues.
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I don't think compartments was mentioned at all when I took immunology.. except "Naive B-cells are kept here, T-cells are kept here, these cells move from the blood and into tissue like this" but I'm not sure that's what you meant. We also used the term "inflammation" when talking about muscles recovering after a work-out.
 
Midnattsol said:
It's more along the lines of stressing a system with too much heat, cold, poor nutrient medium
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Indeed, it seems to have become a value-laden concept, like in psychology. I prefer to keep my biology free value-laden terms.

Midnattsol said:
Oxidative stress is a threat. Under normal circumstances the amount of reactive oxidative species are neutralized by antioxidants and the cell goes about its business. The "stress" part is when there (for some reason) is a lack of antioxidants, and these reactive species instead react with other cellular structures and cause damage to them.
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That is what people keep saying but I have seen precious little evidence fit being relevant to health and disease. It is one of the memes that has grown up since people stopped dealing with facts and started telling value laden stories!

Midnattsol said:
I don't think compartments was mentioned at all when I took immunology.
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That sounds like post-1980 immunology after which compartments got forgotten. Microcompartments are essential to all immunological processes. Complement does opposite things in intravascular and extravascular compartments. B cells do completely different things in half a dozen micro compartments within a lymph node. Reactive oxygen species do quite different things in different intracellular compartments.

I just don't think 'oxidative stress' has anything much to do with inflammation or indeed damage in real life medicine.

Midnattsol said:
We also used the term "inflammation" when talking about muscles recovering after a work-out.
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That is fine because within 24 hours of unfamiliar levels of exertion, and especially eccentric contraction, muscles fill up with macrophages and can be painful and even swollen and that is good old fashioned inflammation.
 
Snow Leopard said:
As Midnattsol suggested, how do you know it was due to low antioxidant levels, rather than low antoxidant levels due to depletion by elevated oxidative stress?
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What I meant was that low antioxidant levels might lead to oxidative damage to the mDNA if I continue exercising.

I don't understand why I had the profile of someone who was malnourished when I following a healthy diet.
 
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This is interesting. I'm not sure if it was already posted.

Purpose: Oxidative stress has been proposed as a contributor to pain in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/ CFS). During incremental exercise in patients with ME/CFS, oxidative stress enhances sooner and antioxidant response is delayed.
 
I emaied the corresponding author:
I am a sufferer of CFS, and I read with puzzlement the line in the abstract of the paper to which you are corresponding author:

"Conversely, fatigue accumulation, if not resolved, leads to overwork, chronic fatigue syndrome (CFS".

I am keeping up with the literature on CFS, and do not recall any such paper.

Are you referring to the sentence in reference 19 which merely states "Overtraining syndrome has... also been known as CFS"?

Or is this an uncited reference to the use of extremely questionable models of forced swimming in mice as a CFS model?

I note the recent NIH explanation of the diagnostic criteria that should be used for CFS research -
https://www.ncbi.nlm.nih.gov/books/NBK284910/box/box_7_1/?report=objectonly

To sum up - are you aware of any research linking CFS and overexercise alone ?
Thanks.
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I had not seen the paper mentioned immediatey above before doing so.
Reference 19 was a paper that dealt with overtraining and was immediatey after the comment on CFS.
 
Is there a theory or evidence that 'overexercising' may cause ME in the first place? Or perhaps it could be a contributing factor with a patient catching a virus?
 
Cornwall13 said:
Is there a theory or evidence that 'overexercising' may cause ME in the first place? Or perhaps it could be a contributing factor with a patient catching a virus?
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It seems there are some similarities but we're talking about high-level athletes, the kind who train intensely 8-10-12 hours per day for months and months. But the similarities are not exactly solid and we are talking about a level of overtraining that is ridiculously beyond normal.

Otherwise I think it's just used as a crude attempt to justify the stupid boom-and-bust thing, nevermind that it's basically comparing the fittest people in the world at the peak of super high-intensity training with... microwaving a meal instead of eating a protein bar, or something. Not that this kind of absurdity has ever stopped someone arguing for their psychosomatic beliefs but that's where we are.
 
I think that athletes who continually push their bodies beyond their energy production capabilities experience what we do when we push our bodies beyond our energy production capabilities. The difference is they push a healthy system to its limits while we struggle with an energy production system inadequate to daily living.
 
The reason i ask is because people often say that their trigger in getting ME was a virus, but often said they had busy lives/stress of some kind whether it's physical or mental before they got ill and this contributed to getting ME in the first place.

I don't know if there is evidence for this or people would have got ill anyway regardless of their circumstances or is there an increased risk?, but it was a virus which was the trigger.
 
Cornwall13 said:
The reason i ask is because people often say that their trigger in getting ME was a virus, but often said they had busy lives/stress of some kind whether it's physical or mental before they got ill and this contributed to getting ME in the first place.
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I think on that it's pretty much the same thing as with eating fast-food or something like that, it's just so common that you'll find it easily within any population. I think most people would say they're constantly busy in their adult lives, especially parents. I had a pretty easy life and I would have said that as well because I was doing many things I enjoyed. That's busy, but completely different from stressful to the point of being detrimental to health.
 
Cornwall13 said:
The reason i ask is because people often say that their trigger in getting ME was a virus, but often said they had busy lives/stress of some kind whether it's physical or mental before they got ill and this contributed to getting ME in the first place.
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How often? I know of plenty of people who didn't lead busy/stressful lives in the year or so before becoming ill. All of this suggests that either the stressful life kind is a different illness, or a stressful life is merely a secondary factor that increases the risk.
 
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