Talking about taking research into your own hands. Mark Vink is a physician in the Netherlands who suddenly fell ill with chronic fatigue syndrome (ME/CFS). He wasn’t just your typical physician; he also happened to have a brown belt in judo, was the former captain of a Dutch national field hockey championship team and was a marathoner and triathlete.
In other words, the guy was a stud who loved to test himself physically – the last person anyone would ever expect to get ME/CFS. Or end up bed bound. Or end up using a six yard tramp from his bed to the bathroom to test his exercise capacity.
But that’s what happened. Mark Vink’s ME/CFS story – like many stories – is so striking in its suddenness and so devastating in its comprehensive that it beggars the mind to think that anyone could believe his downfall could have other than a physiological cause.
After a patient of his with pneumonia coughed in his face, Vink’s energy and endurance quickly tanked. He estimated that from one day to the next he lost 70-80% of the power in his legs. Very quickly this former marathoner was unable to walk 30 yards without having to rest for 15 minutes. He also experienced severe dizziness, headaches (for the first time in his life) and problems sleeping. Graded exercise therapy (GET) caused him to relapse further and he ended up bedridden.
For those who are wondering what psychological disasters lurked in his background – there were none. He stated he’d had a very happy childhood, had no childhood traumas, was not a perfectionist, did not suffer from anxieties and that a psychiatrist found no mental health problems. He also had no history of an autoimmune disorder, MS, pyschosis, major depression, heart disease, thyroid-related disorders or any other chronic illnesses apart from ME. He did not smoke and rarely drank.
Prior to becoming ill he was running 3-4 times a week and doing a long run of 20 to 25 km on weekends. He was probably in the upper tenth percentile in health, education and overall achievement.
All of which helped not at all when it came to getting struck down by ME/CFS. Mark’s story suggests that if you’re beating yourself up over working too hard, or not taking care of yourself you may be missing the point. Mark Vink appears to have been doing everything right and he still got very, very sick.
A Severely Ill Patient Does a Case Study of 1
Mark Vink is a not a typical ME/CFS patient. He is severely ill. It takes him twelve hours to recover from a walk from his bed to the bathroom. While he’s not typical he may not be that uncommon, though. Some estimates suggest that about 25% of ME/CFS patients are home bound or bedridden. Few ever make it into research studies.
Mark Vink obviously was never going to make it into a research study so he decided to do one himself. He did an N of 1 case study – of himself.
The Aerobic Energy Production and the Lactic Acid Excretion are both Impeded in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Mark Vink. Family Physician/GPwSI, Soerabaja Research Center, The Netherlands. Journal of Neurology and Neurobiology.
Noting that the pain he experienced in his legs was similar worse than he’d experienced during strenuous exercise Vink set out to capture the ‘bioenergetic” problem occurring in his muscles.
Vink measured his creatine kinase (CK), inorganic phosphate (Pi) and lactate before and after exercise. A finger prick, using pediatric sized tubes, was used to take the blood samples. The blood was then centrifuged and samples send via overnight express to the head of the Deventer Hospital Laboratory in the Netherlands.
He used a handheld blood lactate analyzer called the Edge to check his blood lactate levels frequently. The Edge was the winner in a contest of six hand held blood lactate analyzers – all of which performed reliably and accurately.
The exercise stressor he used? His 5-6 yard walk from his bed to the bathroom.
Vink’s normal CK levels suggested no muscle damage had occurred and his inorganic phosphate levels were normal. His lactate levels before his little walk were normal as well, but five minutes later they were high – in fact, they were so high that Vink reported they were beyond the level at which healthy people would stop exercising.
|Patient with severe ME||1 minute before theExercise||5 minutes after theExercise||30 minutes after theExercise||Std. Deviation|
|Creatine kinase (CK)||96||110||—||9.90||N= – 200 U/l|
|Inorganic phosphate (Pi)||1.45||1.15||—||0.21||N= 0.90 – 1.50mmol/l|
|Lactic acid||1.6||8.0||11.8||5.15||N= – 2.2 mmol/l|
Minute by minute testing showed his blood lactate levels initially peaked at five minutes (as expected) and then shot up again about thirty minutes later. The thirty minute peak was completely unexpected and apparently is not found in the literature. It suggested that either
- a) Vink’s short walk had overloaded his muscle cells with so much lactate that they were still trying to dispose of it thirty minutes later or
- b) that his cells were so poor at removing lactate that even 30 minutes later they still had not gotten rid of it or
- c) both.
Vink chose thirty minutes because he’d observed that the pain and symptoms in his legs usually receded around that time. That observation was apparently explained by the large dump of lactate out of his tissues and into his bloodstream.
The lactate levels at the 30 minute mark were much higher, though. They higher, Vink said, than most professional athletes including marathoners reach during their most strenuous exercise efforts.
Vink attributed the high lactate levels to an almost complete breakdown of his ability to produce energy aerobically and his need to rely on anaerobic energy production. The downside of anaerobic energy production is the accumulation of hydrogen ions and lactate and metabolites that cause pain and impair muscle efficiency. Vink’s finding suggested he has an extremely small almost non-existent window of available aerobic energy production.
Using the Edge, Vink tested his blood lactate levels again and again and found that eating a meal an hour before his “exercise” (his trip to the bathroom) caused his muscle pain and weakness to last longer and delayed the “lactate dump” into the blood for another 25 minutes (55 minutes total).
Vink’s study had an N of 1 – himself – and therefore cannot be assumed to reflect what happens in the ME/CFS community at large. It may give us an insight, however, into the exercise problems of the severely ill. People as severely ill as Vink rarely participate in research studies (and certainly never in an exercise study). While Vink’s finding of two significantly increased lactate events after trivial exercise is highly unusual, Vink’s isn’t the first highly unusual finding to show up during exercise in ME/CFS. Nor is it the first time lactate has been highlighted.
The inability of many ME/CFS patients to maintain energy levels over a two-day exercise test has been described as unprecedented by exercise physiologists. Jones’ found a jaw dropping 50 times increase in levels of acidosis (h+) in people with ME/CFS. As with Vink, Jones found that it took ME/CFS patients much longer (4 x’s longer) to clear the lactate levels from their tissues as well.
An exercise model predicted high lactate levels will occur in people with ME/CFS during exercise. A 2003 study found high lactate levels in almost 60% of ME/CFS patients after a submaximal exercise test. The study suggested that enterovirus infections were common in the high lactate producing patients. (Lane called what he found an “enterovirus related metabolic myopathy: a postviral fatigue syndrome”).
A 2005 study finding greater energy output, lactate production, oxygen uptake and heart rate in healthy controls than ME/CFS patients had an opposite finding. (Further studies, however, indicated that that study’s conclusion – that reduced effort and avoidance behavior are responsible for the reduced oxygen uptake in ME/CFS – are invalid.)
Studies finding increased brain lactate levels and D-Lactic acidosis in the guts of ME/CFS suggest that a breakdown in aerobic functioning could be system-wide.
Increased lactate levels have popped up in several comorbid disorders associated with ME/CFS as well. Increased brain lactate in a subset of GWS patients was associated with reduced exercise capacity. That finding appeared to fit well with Hue’s finding that increased muscle pH was associated with reduced cerebral blood flows in ME/CFS. Studies have found increased lactate in the brains of fibromyalgia patients and their trapezius muscles and blood and in the brains of people with migraines.
There’s little doubt that aerobic energy production is decreased in a considerable number of people with ME/CFS. Staci Stevens, an exercise physiologist, has reported that almost any activity can put very severely ill patients such as Vink into anaerobic energy production. (The first “exercise” Stevens, teaches, by the way, involves deep breathing techniques to provide maximum oxygenation of the blood without raising the heart rate.)
Some ME/CFS patients find that using aerobic testing to determine the maximum (usually very low) heart rates they should attain very helpful not just in improving their symptoms but improving their health and activity levels as well.
Heterogeneity Probably Present
The two-day exercise study findings suggest, however, that considerable heterogeneity exists in the ME/CFS population. Some people with ME/CFS may not have aerobic energy production problems while others that do have breakdowns in different aspects of their aerobic energy production pathways. My guess is that increased lactate production during exercise is probably simply one of several different energy production issues found in ME/CFS.
Mark Vink was a doctor, not a researcher and he writes like one. His long and at times wandering paper would not have passed muster in most journals, and in fact, it was not published in a reputable journal. (Citations from that journal, for instance, do not show up in PubMed. Citations from the now defunct Journal of Chronic Fatigue Syndrome were not found in PubMed either.)
Vink’s do finding about himself, do however, fit what we know about ME/CFS. While Vink’s findings obviously aren’t statistically relevant for the ME/CFS population at large, his innovative approach should be lauded. Like any case study his results don’t point to a conclusion but to a possibility to be explored.
The Edge and other home monitoring tools like it present intriguing possibilities for patient centered research. Portable lactate monitoring devices appear to be fairly expensive ($3-400) but given that post-exertional malaise virtually defines ME/CFS their potential for providing insights into it could be high.
If CDC’s ME/CFS program survives the next year we should know more soon about lactate production during exercise in the next couple of years. The CDC is interested enough in the issue of lactate production during exercise in ME/CFS to be measuring it in the second phase of their large multisite study.
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