Why We Have Low Energy and How to Fight It
Something fibromyalgia (FMS) and chronic fatigue syndrome (ME/CFS) have in common is a lack of energy. That’s different from fatigue or the lack of motivation that can come with depression. We can want to do something yet be physically unable to do it.
First, it’s not like being tired and needing to sleep. It’s more of a bone-weary, can’t move a muscle feeling. If you’ve ever worked out to the point that you can’t do anymore, no matter how much you want to, that’s what we’re talking about.
If you’ve ever come out of anesthesia with your limbs feeling too heavy to lift, you get it. You may want to sleep, but you absolutely need to rest your muscles before you do anything else.
With FMS and ME/CFS, though, that lack of energy can strike suddenly and last for a long time, regardless of how much we rest. It might happen in the middle of a shopping trip, at work, or ten minutes after getting out of bed. It might also just be there first thing in the morning and keep you from getting up at all.
We don’t fully understand this symptom or why it’s part of these illnesses, but research suggests that it is, at least in part, due to low levels of something called adenosine triphosphate, or ATP.
What Is Adenosine Triphosphate?
ATP stores the energy in your body. Biologists often call it “the energy currency of life.” It’s the main source of energy in all living cells. It’s what the energy in your food is turned into so it can fuel all of your body’s processes.
ATP is produced by the mitochondria in your cells. Your cells need it to function, your muscles need it to contract, everything in your body needs it in order to perform like it’s supposed to.
Adenosine occurs naturally in your body and, among other things, deals with the regulation of blood flow to some of your organs.
When it comes to ATP, though, it’s the triphosphate part that’s more important.
To form ATP, adenosine joins with three groups of phosphates. When energy is needed somewhere and ATP is sent, one of those phosphates is broken off, releasing energy. Then your body replaces the phosphate to once again create ATP. It’s an endless recycling process.
When the building blocks of ATP aren’t available to your body or something interferes with the recycling process, ATP levels can become low and result in energy deficiency.
ATP Deficiency in Fibromyalgia
We don’t have a ton of research on the role of ATP in FMS, and the studies we have are pretty small. Fortunately, they’re pretty consistent in suggesting that ATP levels are low in this condition.
A European study published in 2013 showed a correlation between lowered muscle capacity in the hands and feet in FMS and significantly lower concentrations of ATP and phosphocreatine, which is like a bag of phosphate that’s your body uses to keep that recycling process going as it burns energy.
Earlier work found significantly low ATP levels in platelets of participants with FMS along with other abnormalities suggesting that the body was unable to maintain consistent amounts of ATP.
So while the body of work appears to identify a deficiency, and that deficiency is assumed to play a role in the lack of energy, that’s really all we can say for now.
ATP Deficiency in ME/CFS
In ME/CFS, ATP has received a bit more attention from researchers, possibly because the lack of energy is more of a distinguishing feature in ME/CFS than in FMS, where the focus is generally on pain.
A handful of ME/CFS studies looking at mitochondrial function in the cells has supported the growing belief that low ATP production steps from mitochondrial dysfunction, meaning that the very building blocks of the cells are not functioning properly.
One of the hallmark symptoms of ME/CFS is post-exertional malaise, which is an abnormal and extreme upswing in symptoms after exertion. The amount of exertion it takes varies by person, but it leaves them unable to do the same amount of activity the following day, which is unusual and unique to this disease.
A 2015 paper links post-exertional malaise to critically low levels of ATP due to inadequate adenosine, suggesting that the prolonged recovery period exists because the body has to catch up first on adenosine, and then on ATP.
A review article published in 2014 supports this hypothesis, with researchers linking defects in ATP production to not only post-exertional malaise, but possibly the onset of the disease itself and several metabolic abnormalities associated with it. The authors of this paper also have put forth the possibility that low ATP production in ME/CFS may lead to autoimmunity via an influence on the death of cells.
Treating ATP Deficiency
The pharmaceutical treatments that are generally prescribed for these illnesses don’t address possible mitochondrial dysfunction or ATP deficiency. However, some doctors report success with supplements believed to improve these underlying problems. Some of these supplements do have research offering at least some evidence of their effectiveness.
You’ve probably heard of coenzyme Q10 (CoQ10), which occurs naturally in your body and also can be taken as a supplement. It’s popular among people with FMS, ME/CFS, and many other conditions, as well as for general health. In part, that’s because your body needs CoQ10 to make ATP.
Several studies involving FMS and/or ME/CFS link low ATP levels with CoQ10 deficiency. Several studies also suggest that CoQ10 supplements do improve energy in these conditions. CoQ10 supplements may:
- improve energy
- alleviate post-exertional malaise
- alleviate fatigue
- relieve the pain amplification (hyperalgesia) of FMS
Other supplements sometimes suggested for mitochondrial dysfunction include:
Your doctor may be able to recommend other treatments for boosting your energy by raising ATP levels.
Remember that even natural substances can have side effects and negative interactions with other things you’re taking. Be sure to talk to your doctor about any treatments you’re interested in before you start, and make sure you know how to safely start a supplement regimen.
Gerdle B, Forsgren MF, Bengtsson A, et al. Decreased muscle concentrations of ATP and PCR in the quadriceps muscle of fibromyalgia patients—A 31P-MRS study. European journal of pain. 2013 Sep;17(8):1205-15.
Lengert N, Drossel B. In silico analysis of exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome. Biophysical chemistry. 2015 Jul;202:21-31.
Morris G, Anderston G, Berk M, Maes M. Coenzyme Q10 depletion in medical and neuropsychiatric disorders: potential repercussions and therapeutic implications. Molecular neurobiology. 2013 Dec;48(3):883-903.
Morris G, Berk M, Galecki P, Maes M. The emerging role of autoimmunity in myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs). Molecular neurobiology. 2014 Apr;49(2):741-56.
Morris G, Maes M. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immune-inflammatory, oxidative and nitrosative stress pathways. Metabolic brain disease. 2014 Mar;29(1):19-36.