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. 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. 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. 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 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. You develop the aerobic system by doing aerobic exercise. A healthy body can tolerate lots of aerobic exercise. 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 (https://www.healthrising.org/blog/2015/09/25/walking-marathon-me-cfs-case-study/). 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 https://philmaffetone.com/the-overtraining-syndrome/ (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: Pace yourself by staying under your MAFHR. 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 (https://www.ncbi.nlm.nih.gov/pubmed/20185614). 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 (https://www.stevehoggbikefitting.com/outcome/recovering-from-cfs/). This person used milnacipran along with the Maffetone method. (http://www.healingwell.com/community/default.aspx?f=15&m=3700103). Caveats 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. Summary 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.