Exercise is highly recommended as an adjunct therapy in Fibromyalgia. When we’re talking about exercise and FM, however, we’re not talking about pounding the pavement.
A 2010 review of exercise studies that ‘slight to moderate’ intensity aerobic exercise sessions done two to three times a week worked best and that appropriate levels of exercise result in improved fitness but only modestly improved pain. Another review warning not to overdo stated that “the latest findings concerning the neurophysiology of nociception indicate the fundamental importance of assigning workloads that do not exacerbate post-exercise pain.”
Something is stopping many FM patients and almost all ME/CFS patients from participating in intense exercise. Four studies suggest that “something” in ME/CFS involves a damaged aerobic energy production process. We haven’t covered exercise in FM before but guess what – some FM studies suggest the same. Aerobic energy production – which relies on the consumption of oxygen by the muscles -is where we get most of our energy. In fact, when it comes to exercise the study results are very similar.
Déjà vu All Over Again – the Fibromyalgia Exercise Studies
A 2013 study found reduced oxygen consumption in FM patients both during a submaximal and a maximal exercise test. . A 2011 finding of reduced oxygen consumption (VO2 max), reduced heart rates during exercise, and delayed heart rate recovery suggested a familiar pattern of autonomic nervous dysfunction (increased sympathetic nervous system activation/decreased parasympathetic nervous system activity) was responsible.
The authors pointed out that 57% of FM patients met the criteria for chronotropic incompetence (an inability to get the heart up to speed during exercise), which may also be found in ME/CFS.
They also noted FM patients demonstrate ‘sustained sympathetic hyperactivity’ during rest (the stress response is on during rest) but a hypoactive or poor response to stress. This suggests that the stress response in FM is on when it should be off (at rest) and it tends to poop out when faced with work (such as intense exercise). People with lupus have a similar response to exercise.
A 2002 study finding of reduced oxygen uptake (VO2 max), ventilatory anaerobic threshold, and heart rate during a maximal exercise test in FM again suggested problems with aerobic energy production were present. These authors proposed that dysregulation of the autonomic nervous system (dysautonomia) was behind the exercise issues in FM. They also noted that resistance training was able to improve some aspects of autonomic nervous system functioning.
These findings suggest that, whatever the differences in their ability to exercise, FM and ME/CFS patients have very similar problems with aerobic energy production and autonomic dysfunction. Now on to the present study…
Pain severity is associated with muscle strength and peak oxygen uptake in adults with fibromyalgia. Hooten WM, Smith JM, Eldrige JS, Olsen DA, Mauck WD, Moeschler SM. J Pain Res. 2014 May 3;7:237-42. doi: 10.2147/JPR.S61312. eCollection 2014.
These researchers wanted to know if reduced aerobic energy production (low VO2 max) was associated with reduced strength and increased pain, so they had their FM patients exercise to exhaustion while measuring their oxygen uptake and then did a separate muscle strength test.
It turned out that the FM patients with reduced aerobic energy production were significantly weaker and in more pain than FM patients with higher aerobic energy production.
The Triad: Energy Production, Strength and Pain
What’s causing this energy production-pain association? Studies have illuminated a number of possibilities.
Simply the presence of pain could be reducing muscle contractions during exercise. It turns out that activated pain receptors in the joints tell the motor neurons in the brain not to turn on the muscles. Even the anticipation of pain can reduce the efficiency of motor neuron activity. Pain is designed to make us stop using/help heal the affected tissue, and the brain is happy to participate in having us exercise less efficiently if that will help achieve that goal. (An April 2014 study indicating that trigger point injections increased handgrip strength in women with FM and/or myofascial pain syndrome suggested pain may be reducing strength. )
- Indeed, some research suggests the normal muscle recruitment is not occurring in FM.Because stimulating the same muscle unit again and again puts it into a contracted painful state, more and more muscle units need to become activated as we exercise. Reduced muscle recruitment, then, could contribute to the painful, contracted feeling of muscles found in FM. Neither of these possibilities tell us anything about the energy production-pain link. The next one does.
- Blood flow is critical not just to meet the oxygen demands of exercising tissues but to remove the toxins created during exercise. Both reduced capillary density and blood flow have been found in FM. At least as early as 2006, researchers were suggesting that muscle ischemia (low blood flow) both during and after exercise was causing pain in FM and driving the central sensitization found. Problems with the microcirculation could, therefore, be contributing to the aerobic energy problems, pain, and weakness found in FM.
The authors argued that next step is to determine associations between VO2 max and capillary flow during exercise. Being able to associated reduced capillary blood flow with low VO2 would point an arrow at the capillaries and the microcirculation, particularly if flows in larger blood vessels are normal. Given the overlap in both exercise and muscle study results in ME/CFS and FM, those results could very well apply to ME/CFS as well.
This study also suggests finding an appropriate exercise regimen could be helpful. FM studies have suggested that greater muscle strength is associated with better mental and emotional well-being and reduced oxidative stress , but not improved heart rate variability.
ME/CFS and FM
What an interesting jumble of energy production and muscle studies have occurred in these two disorders. Low blood volume – obviously potentially a critical factor in getting blood to the tissues – is acknowledged in ME/CFS but is hardly considered in FM. Four repeat exercise studies have been done in ME/CFS but none in FM. Still, the FM exercise studies show similar abnormalities without the need to do that second exercise test. (Aerobic energy production (VO2 max) also takes a hit in several autoimmune disorders (lupus, rheumatoid arthritis and polymyositis)).
Increased levels of oxidative stress, mitochondrial problems, muscle fiber issues, increased muscle levels of the toxins pyruvate and lactate, and reduced microcirculation in the muscles have all been found in FM.
Newton’s studies finding poor pH handling and increased muscle acidosis suggest something similar is happening in ME/CFS. Reduced muscle ATP production has also been found in ME/CFS. Studies have suggested both ME/CFS and FM have reduced oxygen uptake at the level of the muscles.
A 2014 study finding normal blood flows but increased muscle and blood glutamate and lactic acid levels in the people with chronic widespread muscle pain suggested normal blood flows may not be enough to remove toxic byproducts from dysfunctional muscles.
The ME/CFS and FM fields remain stubbornly separate with few studies incorporating both types of patients. For most part FM researchers research FM and ME/CFS researchers research ME/CFS. Rarely, do the twain meet. The energy production and muscle study results appear to be strikingly similar, however, and findings from either disease could end up informing the other. With neither disorder getting much in the way of federal funding working together might be a good idea.
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