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
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.
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.
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
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.
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.
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