No Power to Your Punch?

Why do your muscles feel weak yet they appear normal when examined? Could it be that you just don’t get enough quality sleep to revitalize your body each night? Or, is there something going on within the muscles and other cells of people with fibromyalgia that leaves you in a constant state of exhaustion? Although sleep is likely to be an important factor, Mario D. Cordero, Ph.D. and Placido Navas, Ph.D., biochemists in Spain, have identified an enzyme abnormality that might shed light on your energy drain.¹

Coenzyme Q10 is produced by the mitochondria inside your cells and is a key enzyme for producing the energy required by each cell. In other words, coenzyme Q10 (CoQ10) is essential for powering up your muscles and giving you that “get-up-and-go” feeling. CoQ10 also neutralizes toxic substances and waste products that may damage your cells, potentially producing pain. In addition, CoQ10 can be transported outside the cells into your plasma (the nutrient-rich liquid portion of your blood) to neutralize toxic substances. These nasty chemicals can be measured and their total quantity is often referred to as the reactive oxygen species (ROS) content.

Given that fatigue and muscle pain are primary symptoms of fibromyalgia, Cordero and Navas reasoned that patients might have some abnormality with their CoQ10. Blood was drawn from 40 fibromyalgia patients for measuring CoQ10 and ROS, and the results were compared to 30 healthy control subjects (matched for age and gender). Keep in mind that the blood cell findings tend to mimic what is happening in the muscles.

Looking at the level of CoQ10 inside the cells and outside the cells in the plasma fraction of the blood, Cordero and Navas made two interesting observations:

• the cell content of CoQ10 in the fibromyalgia group was 40% less than that of the control group
• the amount of CoQ10 in the plasma of fibromyalgia patients was double that of the healthy controls

Despite the high enzyme content in the plasma, the concentration of ROS was substantially greater in the patient group.

At first it may seem odd that patients have an abundance of CoQ10 in their plasma (the liquid portion of their blood) and an inadequate amount in their blood cells. However, Navas confirmed this imbalance by another method. The blood cells were isolated in a dish and the ROS content within them was measured. The ROS of the fibromyalgia group was significantly higher compared to the controls. Then CoQ10 was added to the dishes of isolated blood cells. Those from the fibromyalgia group sucked up the enzyme and the ROS content dropped to the level of the control group. This experiment demonstrated that the cells are deficient in CoQ10 and offers at least one explanation for why your muscles have no power to their punch.

“There is a contradictory situation in these patients,” says Navas, referring to people with fibromyalgia. “Clearly the cells need more CoQ10, but the high content in the plasma is not working.” What could this possibly mean? CoQ10 should be able to travel back and forth across the cell membrane so that it can be where it is most needed. Yet, there is an imbalanced distribution with too much CoQ10 in the plasma and a serious deficiency within the cells. As a result, your cells (particularly those in your muscles), cannot produce the energy that they need to power up your body’s activities.

Referring to the accumulation of CoQ10 in the plasma, Navas offers an analogy. “The picture is similar to that observed in patients with CoQ10 deficiency syndrome treated with CoQ10. If the enzyme is dissolved in oil before administering, the levels in the plasma are normal, the cells properly incorporate it, and the muscle pain/fatigue symptoms decrease significantly. However, if CoQ10 is provided as a powder, the plasma content becomes very high and no benefits are observed.” The ability of CoQ10 to travel across the cell membrane depends upon the presence of fat-containing carrier molecules in the plasma.

It’s possible that the carrier molecules in the plasma are defective or that CoQ10 is somehow tied up with another molecule that renders it useless. There are also multiple reports in the literature of genetic glitches that can alter the way CoQ10 functions in the body, producing a variety of symptoms such as fatigue, muscle pain, shortness of breath, gastrointestinal problems, etc.² Cordero and Navas plan to study the chemical condition of CoQ10 in the plasma and skin cells of fibromyalgia patients to gain a better understanding of why the enzyme imbalance exists and how it can be corrected.

In the meantime, you should know that the more you exercise, the more mitochondria your cells will make. An increase in the number of mitochondria per cell could possibly raise the CoQ10 level within your cells and this might be one of many ways in which gentle, aerobic exercise improves physical function in people with fibromyalgia.³ Studies also show the best way to ease into a fitness program is to begin with a warm water exercise routine because you are less likely to strain your muscles.⁴ You may want to sit in a hot tub afterwords (if available) to help relax your muscles after exercising in a heated pool.

Cordero’ s and Navas’ research may also help explain why beginning or restarting an exercise program is so difficult. The initial activity may further drain your cells of CoQ10 and energy, but once you make more mitochondria, you may slowly start to feel better. Of course, the moment you stop exercising for any reason (such as a bad cold), your muscles will quickly decondition, so you may not be able to pick up where you left off.

As an aside, medications that lower cholesterol, called statins, also reduce the availability of CoQ10. Based on Cordero’s and Navas’ findings, fibromyalgia patients may be more susceptible to the muscle-pain enhancing side effects of statins. You will need to discuss alternative therapies with your doctor, such as adding CoQ10 to your treatment regimen along with the statin.

1. Cordero MD, et al. Clin Biochem 42(7-8):732-5, 2009.
2. Quinzii CM, et al. FASEB J 22:1874-1885, 2008.
3. de Andrade SC, et al. Rheumatol Int 29:147-52, 2008.
4. Evcik D, et al. Rheumatol Int 29:885-90, 2008.