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Maffetone, Mitochondria; CFS and Overtraining Syndrome (OTS)

Discussion in 'General ME/CFS Discussion' started by FieriBrandon, Apr 29, 2017.

  1. FieriBrandon


    Because many people (myself included) observed that their CFS started during a period of intense exercise, I eventually found myself reading the reports of people who developed OTS. Just as CFS is a recognized but poorly understood syndrome in medicine, OTS is a recognized but poorly understood syndrome in athletics. Although they're probably different syndromes, there many similarities between OTS and CFS, both in their presentations and in their underlying causes. There's a very brief summary at the bottom of the page. Here are some of the symptoms of OTS
    • Washed-out feeling, tired, drained, lack of energy
    • Mild leg soreness, general aches, and pains
    • Pain in muscles and joints
    • Sudden drop in performance
    • Insomnia
    • Headaches
    • Decreased immunity (increased number of colds, and sore throats)
    • Decrease in training capacity / intensity
    • Moodiness and irritability
    • Depression
    • Loss of enthusiasm for the sport
    • Decreased appetite
    • Increased incidence of injuries
    • Hormone imbalance includes elevations of cortisol with secondary lowering of testosterone and DHEA levels
    • Premenstrual syndrome and menopausal symptoms may be secondary complaints for women, but amenorrhea is a common problem
    • Sexual dysfunction may be a problem for both sexes, typically producing reduced sexual desire and sometimes infertility
    • Mental and emotional stress, including mild or clinical depression and anxiety is not uncommon
    There are many theories regarding what kind of activity leads to OTS, and and many theories regarding the underlying biological mechanisms of OTS. The most compelling conceptualization of OTS I've found is Phil Maffetone's. Maffetone is a coach who trains endurance athletes (eg marathon runners, triathlon competitors). His view is that the basis of good health is a well developed aerobic system, and that anaerobic exercise is physiologically stressful and wears down the aerobic system. Thus OTS results from some combination of insufficient aerobic capacity and excess anaerobic activity. His treatment for OTS is rest and low intensity aerobic exercise.

    I've found discussions of these subjects to be hampered by muddled thinking, largely due to ambiguously defined terms, so let me make some definitions and take a moment to discuss aerobic/anaerobic metabolism. There will be a lot of information in this post that is already well understood by people on this forum, but I've included it anyway for those who don't know much about these topics.

    Energy Metabolism

    The energy currency of cells is adenosine triphosphate or ATP, a molecule of adenosine attached to three phosphates. When ATP is used for an energy consuming reaction, one phosphate is removed and the result is ADP (adenosine diphosphate). Thus regenerating energy amounts to converting ADP back into ATP. There are three energy systems most cells use to generate energy.
    1. Creatine phosphate in cells is a form of stored energy; it can rapidly donate phosphate to convert ADP back into ATP. Creatine phosphate runs out quickly (after a few seconds of sprinting), and requires on the order of minutes to recover.
    2. Glucose, fatty acids, and amino acids can be degraded into H2O, CO2, and ammonia to generate ATP; this process generally consumes oxygen, many of its steps occur in mitochondria, and it is called aerobic metabolism. This process generates most of the body's energy needs. Aerobic metabolism is why animals breathe in oxygen and breathe out CO2.
    3. The first step of glucose degradation in aerobic metabolism involves cleaving it into two molecules of pyruvate, which are then further broken down; this splitting of glucose (glycolysis) actually generates a small amount of ATP on its own, so if the cell needs energy to be produced faster than aerobic metabolism can supply it, glucose will be split faster than pyruvate can be degraded. The pyruvate is converted to lactate, which accumulates in the tissues and, if enough lactate is being produced by enough cells, in the blood.
    Here are some examples (assuming you're healthy): when sprinting ten yards, your muscles uses mostly 1; when walking, your muscles use mostly 2; when running a mile fast (for you), your muscles use 2 and 3. Someone with a well developed aerobic system can run a fast mile (say, 7 minutes) without their muscles using much of 3. In general, if you're using 3 you must be revving 2 pretty fast.

    Here are the key points to take away.
    • Processes 1 and 3 don't require oxygen, so they're both described as anaerobic; you can see that the use of the term anaerobic to describe an activity is thus pretty ambiguous, especially since processes 1 and 3 are physiologically very different. For example, doing a low rep weighlifting workout with lots of rest between sets, and running a 5 minute mile, both involve anaerobic metabolism, but they're very different exercises.
    • The term anaerobic is ambiguous for a second reason. Suppose I do bicep curls with a 10lb dumbbell to failure; at a certain point my bicep muscle cells will run out of creatine phosphate and will start relying on glycolysis and lactate will accumulate in my biceps muscle cells. However, the biceps is a relatively small muscle, so any lactate it produces will enter the blood, travel to other tissues, and be metabolized there; in other words, blood lactate will probably not accumulate. Thus we need to distinguish between activities that cause only tissue lactate accumulation somewhere, vs activities that cause both tissue lactate accumulation somewhere and blood lactate accumulation.
    The point is this: saying that an activity is anaerobic or aerobic is vague, and is not enough to predict what kind of physiological effect it will have. In what follows, it's crucial to be precise with language, so I'll define the following terms (again, the examples below are for healthy people)
    • An activity is globally anaerobic (GA) if it causes blood lactate to rise. The aerobic capacities of enough cells have been exceeded by a large enough margin that enough pyruvate is being produced and converted into lactate to exceed the body's ability to metabolize lactate. For example, a fast mile, or a full out sprint farther than ~60m.
    • An activity is locally anaerobic (LA) if it causes tissue lactate to rise somewhere but doesn't cause blood lactate to rise. For example, high rep bicep curls with low weight, high rep calf raises. GA activities must be LA (the lactate in the blood must be coming from some tissue), but LA activities in general aren't GA (eg high rep bicep curls).
    • An activity is brief if in theory the creatine phosphate system has enough stored energy to supply all of the activity's energy demands. For example, a golf swing, a jump, calf raises or bicep curls for a few moderate reps. These activities should in theory not cause any lactate accumulation anywhere, and in theory should not even require much increase in aerobic metabolism.

    Maffetone's Theory

    One of the reasons I buy into Maffetone's ideas is that they are well grounded in the established biochemistry above. Maffetone's basic idea can be boiled down to three premises
    1. The aerobic system is how cells obtain energy for maintenance and repair, so the aerobic system is the foundation of health. Since the aerobic system relies heavily on mitochondria, good health requires to having a lot of well functioning mitochondria.
    2. You develop the aerobic system by doing aerobic exercise. A healthy body can tolerate lots of aerobic exercise.
    3. Globally anaerobic (GA) exercise is physiologically stressful and among other things wears down the aerobic system. Recovery from GA exercise (or any stressor really) relies on the aerobic system. A combination of excess GA exercise and insufficient aerobic capacity results in overtraining; in other words, OTS results in part from a combination of excess training stress and insufficient recovery.
    Note the the proposed underlying problem in OTS involves a damaged aerobic system, and that many CFS researchers believe the same to be true of CFS. For example, Mark Vink, a Dutch physician with severe CFS, has shown that his lactate rises to well above normal when he walks back and forth from his bed to the bathroom ( For severely overtrained people and for some people with severe CFS, walking to the bathroom is in some ways like doing a 400m sprint. Maffetone believes that exercise programs that are popular these days lead to overtraining, even many of the routines followed by endurance athletes. But endurance athletes do a lot of cardio, and doesn't that build up the aerobic system?

    Notice the language used here: "cardio". Cardio is a vague term that includes both aerobic and GA exercise. Most people who start doing cardio pay little attention to whether they're actually functioning primarily aerobically. Here is a typical example, taken from the comments section of this article (many other stories can be found in the comments).

    Even the American Heart Association's recommendations for exercise don't respect these biochemical principles:

    If Maffetone is correct, these recommendations are counterproductive for many people or even overtly dangerous.​

    I believe that me and many people on this forum have CFS induced by an excess of GA exercise, perhaps with other factors (eg infection) as contributing stressors. I think that severe OTS can become or can appear similar to CFS.

    Note that in Maffetone's view, even many endurance athletes have surprisingly poorly developed aerobic systems, even if they have competitive race times. These people are heavily globally anaerobic even at relatively slow paces. Being fit and healthy are two different things. In theory a fit and healthy person should be able to run pretty fast without becoming globally anaerobic.

    Treating CFS and OTS

    In order to fix OTS it is necessary to develop the aerobic system by doing aerobic exercise. The higher your heart rate during a given exercise, the more energy you're consuming. So we can expect heart rate to correlate with how hard you're pushing your aerobic system and more generally how much you're stressing your physiology. We can use heart rate as a guide to determine which training intensities will develop the aerobic system and avoid overtraining.

    Maffetone recommends the following formula for healthy people to determine that heart rate: 180 - Age; this is called the maximum aerobic function heart rate (MAFHR). For example, he recommends healthy people undergo an aerobic base building period during which they train at just under this heart rate, carefully avoiding exceeding it. A typical example would be maybe 90 minutes per day, 5 days per week, for 6 months. During this time one should see improvements in their performance at the MAF HR. For example, a 20 year old might go from running an 10 minute mile at a HR of 160 to running an 8 minute mile at the same HR.

    For people who are in the earlier stages of overtraining, he recommends the formula 170 - Age. Now, the question is what heart rate should someone with severe overtraining or CFS use? This is going to depend on the individual - for one person it may be 95, for another 120 - but the point is that HR monitoring should play a central role in guiding pacing and exercise. For pacing, you should in theory stay under your anaerobic threshold. But for exercise, in order to improve your aerobic function, you need to regularly approach your MAFHR (without exceeding it).

    In summary we have the following two recommendations:
    1. Pace yourself by staying under your MAFHR.
    2. Exercise regularly by approaching - but not exceeding! - your MAFHR.
    The question is, will this work for CFS? Obviously the crude heart rate formulas will not work well for PWC just as they don't work for people with severe OTS, but in theory there is a MAFHR for everyone. Point 1 has already been articulated and tested a little bit by the Workwell Foundation, which does research on CFS. Workwell and the idea of HR based pacing has been brought up on on this forum before.

    What's interesting to me is Workwell's exercise recommendations. They advise against aerobic exercise and instead recommend repeated brief exercise (recall the definition of "brief" above) with rest to allow creatine phosphate to regenerate ( Now, from a pacing point of view this makes complete sense, since in theory PWC have well functioning creatine phosphate systems, so repeated exercise using only this energy system might be well tolerated. But this almost completely avoids stressing the aerobic system, so their protocol might not adequately stimulate aerobic development.

    In other words, Workwell's recommendations are good for management of CFS, but they're no cure.

    The reason I made this post is because there are a lot of similarities between Maffetone's ideas and what is known about CFS, but neither group seems to know much about the other. It seems that Maffetone's ideas and the success of his method are not well known in the CFS community, and similarly CFS is not well known in the endurance or athletic community. I think it would help if both groups know about each other. I think there should be some experimentation with low HR exercise among PWC, particularly those whose CFS may have been caused by exercise.

    Finally, here are a couple of people I've found who used Maffetone's ideas to recover from CFS (

    This person used milnacipran along with the Maffetone method. (


    With all this said, these strategies may not work for most or even many PWC. For example some people who are bedridden with CFS may not have enough reserve to do exercise without becoming GA. Other people may not recover until some underlying problem like a chronic infection is addressed (although as the story above illustrates, chronic infection like EBV certainly does not preclude recovery). I also think that many of us may benefit from avoiding LA exercise as well as GA exercise, and that it may be necessary to limit total daily energy expenditure ("spoon theory"); the autonomic system is involved in OTS and CFS for many people, a point which I haven't addressed. That said, I do think this could work for many of us, particularly those of us whose CFS may have been caused in part by exercise.


    CFS and Maffetone's ideas about OTS both seem to involve a damaged aerobic system. Pacing and low intensity aerobic exercise guided by heart rate may help in recovery for some PWC, particularly those whose CFS seemed to be caused in part by exercise.​
    Last edited: Apr 29, 2017
  2. CFS_for_19_years

    CFS_for_19_years Hoarder of biscuits

    I came down with ME/CFS in 1990. During the period of about 1995 to 2010 I was able to increase my aerobic capacity by walking at about 3 to 4 miles per hour. This is somewhere between a comfortable stroll and a brisk walk. When using a HR monitor during the earliest years I had no problem reaching HR of 140-150 and keeping it there near the end of the walk for about 10 minutes, then doing a cool down. I may have been walking for up to 25-40 minutes at a time.

    In later years I focused on not going over 105 or 120 bpm, depending on the year, and then walking for up to 35 minutes at a time. My best performance during the later years was being able to walk briskly for 35 minutes twice a day. Every so often I might swim for half an hour. Today I'm unable to exercise at all, unless you call bathing "exercise" because that will bring my HR up to 115-120 for a sustained time.

    I used to be a competitive swimmer, gym rat and casual cyclist. I might have overtrained at some time. I know I pushed myself tremendously because it felt good! I recall feeling a bit washed out, lack of enthusiasm, increased resting heart rate. This is pretty much how SLIGHTY overdoing with ME/CFS feels now, i.e., PEM.
    Mij likes this.
  3. keenly

    keenly Senior Member

    Aerobic exercise is terrible for CFS patients. It is very damaging and does not help.
    Art Vandelay likes this.
  4. FieriBrandon


    This seems to be false in general. There probably are some or even many PWC for whom aerobic exercise is as a rule harmful, but in my OP I linked to two cases of PWC who used aerobic exercise to significantly improve or cure their CFS.

    I suspect that the reason aerobic exercise gets such a bad rap in CFS is because people who think they are just doing aerobic exercise are actually becoming globally anaerobic. Keep in mind the distinction between aerobic activity and cardio. This is why I was so compulsive about the definitions and biochemistry. There are many fit people who cannot run aerobically, no matter how slow their pace.

    Similarly, there are probably PWC who cannot walk at a normal pace while staying aerobic. These people may have tried walking, only to have it trigger PEM; they're likely to conclude "aerobic exercise is bad for me" even though what they were doing was not primarily aerobic.
    Last edited: Apr 30, 2017
    pattismith, Learner1 and HowToEscape? like this.
  5. keenly

    keenly Senior Member


    Do you work with PACE team?

    That is not possible. You can NOT cure CFS with exercise.
  6. Valentijn

    Valentijn Senior Member

    There have been dozens of studies of exercise therapies in ME/CFS patients, all of which show no objective improvements. These therapies typically focus on gradually increased aerobic exercises, such as walking. Some of the early ones used heart rate monitors to set limits.

    Very large surveys also show that most ME/CFS patients have found exercise therapies to be harmful. In some cases, the harm is permanent.

    I'm afraid the theory you're presenting has already been resoundingly disproven. If there's one thing that we know will not cure ME/CFS, it's exercise. It's been studied to death.
    Last edited: Apr 30, 2017
  7. Snowdrop

    Snowdrop Rebel without a biscuit

    Hi @FieriBrandon

    You're new here. First of all the term cfs is a mislabel. It was chosen to denigrate this disease by turning into not only a syndrome but a syndrome of a symptom (chronic fatigue is a symptom of many illnesses).

    It would be more accurate to say that a large subset of people got sick after a viral infection. Although there are some people here who were athletes at the time.

    Here is some correct info on the disease that many prefer to refer to as ME (cfs is used but often because it is felt no one knows the term ME).

    Biology of ME:

    explained here:


    Here is a link to diagnostic criteria that define the disease ME: Consensus Primer -2012-11-26.pdf

    I noted your list does not include cognitive exhaustion. It's also useful to note that many people with ME have multiple diagnosis and often associated either with the gut (IBS) or allergy (MCAD) as well as Orthostatic Intolerance issues. This may be a large point of deviation between the two.

    And lastly, VIROLOGY the blog of Vincent Racaniello hosted a series of articles by David Tuller (Uof C Berkeley Public Health/Journalism)
    on why the PACE trial was wrong in it's findings regarding exercise and ME: (there are many other papers I can direct you to on this) see also:

    Admittedly it's a lot to digest. But it might help you consider your hypothesis a little more fully with the additional data.
    trishrhymes likes this.
  8. FieriBrandon


    Walking is not aerobic for many PWC.

    Exercise is a vague term. I don't know of any studies that used laboratory evidence to guide exercise intensity and keep participants at primarily aerobic intensities. Programs like GET are quite different from what I'm proposing. In GET, HR pacing plays only a partial role in guiding pacing, and is based on crude formulas without using laboratory evidence to guide exercise intensity. Patients are encouraged to increase exercise heart rates over the course of the program, again without any rationale or laboratory evidence to justify this. They're also encouraged to push through PEM. None of this respects the apparent underlying problem in CFS. Contrast this with one of the examples I linked, where the individual was eventually able to walk miles but nonetheless continued exercising at under 107bpm.

    I doubt such a broad statement will ever be true for such a heterogeneous syndrome as CFS.
    Learner1 and HowToEscape? like this.
  9. keenly

    keenly Senior Member

    If you can exercise at under 107bpm you are doing very well. I am at 110 with 2 steps in house.

    If exercise makes you well again, you never had CFS. You were unfit.
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  10. jpcv

    jpcv Senior Member

    SE coast, Brazil
    Interesting topic. When I got sick in 2015, I had no idea what was going on. After some research, I came to the conclusion that I had Overtraining.. At the time , I had never heard of ME. I realized that I had ME more than a year after, because my Overtraining symptoms wouldn´t go away.
    I remember I talked to an instructor with experience in caring for athletes with overtraing . He said something like "you don´t have overtraining now, you had it one year ago"
    That´s when I started to study again what was happening and that was the first time that I read something about ME.
    I agree with @FieriBrandon , Overtraining has lots of similarities with ME. And I also firmly believed that my ME was caused or triggered by exercise; right now I´m not so sure.
    Was it OTS leading to ME because it was not treated properly?
    Or was ME since the beggining?
    CFS_for_19_years likes this.
  11. Mij

    Mij Senior Member

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  12. Wishful

    Wishful Senior Member

    The theory seems to be based on 'the metabolic effects of exercise are the culprit'. An alternative is that the immune system activation caused by exercise triggers changes that result in CFS. My CFS started with immune activation due to type IV food sensitivity; no overexercising involved. I think Maffetone's going down a false trail.
    Learner1 and Runner5 like this.
  13. Silencio

    Silencio Senior Member

    @FieriBrandon Hi, this is so so interesting, and thank you for sharing. It's the best description of energy systems I've come across!

    I got sick after getting really into road biking, but at the time, I didn't connect the two. Now, I think it may have been the cause. I was a runner previously, but road biking and doing hills really puts you into anaerobic with your quads working so hard, and my body responded very differently to how it felt running and hiking.

    I have been sick 4 years. The first 2, I spent in push / crash cycles and not understanding much about ME. The last 2, I've spent housebound, sometimes bedbound and aggressively resting, although I could move around the house a little. I was pacing and doing workwell style anaerobic exercises, but not progressing at all w these.

    Then I had to unpack some boxes over a two week period, so I would walk around upstairs for about 3 mins, push up to my AT, rest a while, and do it a few more times. This gave me confidence to try to walk further and have been testing out gradually increasing from 1 to 3 four min walks (.2 miles) every other day going right up to my AT (from ithaca CPET). I have noticed that this gradual increase seems to be working this time, my HR isn't going above AT. It stays in a safe zone of 100 - 114 while I'm walking. My AT was 115 when I did the test two years ago, and I don't know what it is now. My OI / Pots has improved since I've been doing this and I can be upright longer without feeling that awful weakness, like I must lie down.

    Suffice to say, I will continue to try this and I agree that ME is going to be a bit different for everyone. it could be that some people can use training their aerobic system to get out of this -- I have read accounts of this before.
    jpcv likes this.
  14. JollyRoger

    JollyRoger Senior Member

    Does the famous hallmark of Post exercise malaise also exist in overtraining?
    I mean the "do sports and have no problem and collapse after 24h for a few weeks" thing.
    Many diseases have the same pattern.
    A friend of mine for example had burnout and was unable to speak and was bedridden.... but he had a remission due to stress reduction and psychotherapy.
    Its important to find the cause.... that's the problem in cfs.
  15. Learner1

    Learner1 Forum Support Assistant

    Pacific Northwest
    Interesting discussion. I was in the best shape of my life at 52 doing HIIT and exercising 7 days a week, when I was diagnosed with cancer (now resolved) followed by ME/CFS.

    I also have a child who got a serious mental illness after competing at state and national levels at an endurance sport who is well now after replenishing her body and brain over a long time.

    Intense activity over time can damage the immune system's ability to fight off infection and the immune system can malfunction, so that's the likely link between CFS and overtraining.

    However, what's not included in the above is the nutrient depletion in overtraining which can dramatically affect metabolic processes. Standard bloodwork may look normal, but a detailed nutrient test, like a NutrEval will show severe deficiencies.

    There's a lot of oxidative stress in intense training which can stress glutathione recycling and damage mitochondrial membranes. And many athletes are taught to eat carbs - foods with lower nutrient density, when they need amino acids, lipids, and micronutrients to replenish their bodies.

    Its no wonder they crash...

    As for exercise with ME/CFS, it seems that encouraging recycling and proliferation of healthy mitochondria should be a goal. Exercise is key to doing this.

    For some, exercise means very simple movement to support life. I've read all the debate about the PACE study and the horror stories about CPET. Its obvious that exercising over one's threshold is damaging.

    With that said, it has made sense to me throughout my cancer treatment, recovering from major abdominal surgery, and now with CFS, that exercise at some level is a survival strategy.

    Doing what we can, as we can, in small increments, while closely monitoring our responses, heart rate, etc. and carefully adjusting amount of exercise up or down is important. Feeding the body to support exercise is important, too. And having a pragmatic attitude.

    I've found that weight training with light weights, small amounts of cardio while monitoring heart rate, and frequent 10 minute naps on the gym floor is sustainable 4-5 days a week, without pushing me into PEM. Some days I can't do anything at all, but I listen to my body and do what I can when I can.

    It strikes me that the problem with GET is its arbitrary and pushes people past their personal limits, which is not good. We need a personal approach.

    I'm in pretty good shape even though I do a fraction of what I once did, and I've had to realize that NOT losing functionality or muscle mass is a valid fitness goal, along with not pushing hard enough to produce PEM. It takes patience and discipline and it can be very frustrating at times.
    Last edited: Jun 12, 2017
  16. HowToEscape?

    HowToEscape? Senior Member

    I wonder if the subject even fits within the few simple points that we've staked out. Let me throw or two half thoughts and then I'll float back into my brain fog:
    A: The right amount and type of exercise may not cure the underlying disease but it may move one into a better phase of it.
    A': The same exercise as above in the same person but done at a different time in a different phase of the disease may knock them down further.

    B: GET or anything similar is the wrong thing for us. That was designed to hammer the patient into the treatment, rather than finding a treatment that fits the patient.
    B': even when lack of exercise is necessary, it isn't good. If we can figure out when what kind and how much exercise to do, we need to do it. The right amount might be one minute and then immediately back to bed, it may be past the 20 minute aerobics threshold or it may be a half hour weightlifting. Then for the same person it may later be back down to five minutes. Right answers are elusive with this disease.

    D: what we call exercise now is simply a slice of what was normal activity throughout most of humanity's existence. When we needed water we have to get and carry it, when we wanted to eat we had to go chase something, once we had anything worth taking the neighboring tribe would come and attempt to beat it out of us, or vice versa. We would not have survived during most of history.

    In my experience I found the worst thing is simply being out of my apartment for too long, doing anything other than lying flat in a quiet place. Standing in line at the post office or sitting and talking in the social occasion with background noise would knock me out for a minimum of a week, usually over a month ( I don't do either now). Walking a 1 km would also give me a crash. Those aren't what most people consider exertion.

    In contrast, resting for a while, until I get a break from the feeling half-dead sensation (which might be over a month), and then running that same distance would knock me out for a couple days, but then I'd feel better after that. Walk the the same route same weather, and days later I feel worse. Short bursts of exercise, at the right time, improve my condition. They did not prevent a relapse when the next stressor came by; they were managing but not curing the disease. They were also the only thing that improved quality-of-life.

    I apologize for my flailing, stuttering writing style, cognitive functions seem to be the first thing to go.
    Learner1, Isaiah 58:11, jpcv and 2 others like this.
  17. Learner1

    Learner1 Forum Support Assistant

    Pacific Northwest
    I think you might be onto something.

    There are a lot of variables in the equation, and it's sort of a "your mileage may vary" at any given point in time.

    Seems that it's in our best interest to have as many mitochondria as we can. Exercise is the one best way to promote their proliferation.

    We recycle them, too, so having the proper ingredients laying about to make healthy ones rather than dysfunctional ones is important, so feeding with mito cocktails and encouraging toxins out of the body and not into the mitochondria is important. (Movement, sweat, and a healthy gut help with this.)

    On the risk side, more exercise than our mitochondria can make ATP for, or having them run so fast making ATP throws off increasing amounts of free radicals. Without the ability to defang them, mitochondrial membranes become damaged and leaky, wasting ATP. If membranes are not replenished, we have unhappy mitochondria, which is counterproductive, and we have to wait for them to recycle and hope for the best.

    Then there's the stress of exercise on the immune and endocrine systems. And every other system. More than these systems have the capacity to deal with can deplete resources and cause inadvertent damage, which the body must work hard to repair.

    My layman's view... but there's a lot of science behind what I've described.

    The game is to exercise below our threshold (which may be almost nil) at any given point in time, which may vary dramatically and erratically over time. Ideally, we slowly increase capacity on our own terms, just like an athlete would train for a competition...
    HowToEscape? likes this.
  18. lnester7

    lnester7 Seven

    I have exercise my most CFS years. I measured my AT w a CFS exercise specialist so I know for sure my AT was 115BPM. I also Have POTs,
    Here is the thing. for 10 years I have tried to make it better, I hit a plateau and I do not get any better, it is as if my capacity to repair my aerobic system is gone. I HAVE TRIED IT ALL.

    I am at a 7 of 10 this days. I go from 3 (which I do not exercise much then) to a 7. The only reason I exercise is because in MY CASE i]I can only get better when I work slowly towards it (could be because in my case I avoid getting my POTs worst making the CFS better). Not sure.

    So I followed the prescription: work under AT, and build a Set slowly every 2 weeks. I can do that and I have gotten now myself out of bed more times that I can count (I walk a mile a day now), I have it down to a science now (do not recommend this to anybody). Also the 3 bad relapses (outside of my regular Fall season ones) have been due to exercise. So I have to be careful and I have learnt my lesson. BUT 10 years later I cannot increase my AT. I do get better when bed ridden if I exercise slowly building it up, but then hit a wall and that is as good as I get.
    HowToEscape? likes this.
  19. lnester7

    lnester7 Seven

    Usually is advised 2 weeks before increasing since our PEM tends to be delayed.
    You can measure your resting heart rate before you get out of bed. If your RHR went over 8% from day before, you know you over did it! just a tip to keep it safe. Please forgive me for the unrequested advice in advance!
    jpcv, Murph and CFS_for_19_years like this.
  20. SmokinJoeFraz93


    United Kingdom
    Wow! How relevant is this article for myself. My symptoms started when I started exercising intensely 5 days a week. Hard boxing sessions with HIIT training and weights. The weight was dropping off me and I wasn’t eating enough.

    The silly thing is, I was declining month by month, but I continued to push through it until I could no longer lift my arms up during a session, and my lungs felt like they had no oxygen. I did this solidly for around one year.

    I had to stop everything (work included), and now I’m 23 years old and practically House bound.

    And not mention, I discovered an eating disorder during this time, so now I’m getting treated for that. What a shit 3 years!!
    pattismith likes this.

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