Exercise, PEM or PENE, and general medical research

[anciendaze]

Here is an article which explicitly states some things I had deduced, but had not found in print.
Dangerous Curves : A Perspective on Exercise, Lactate, and the Anaerobic Threshold

Jonathan Myers; Euan Ashley
Chest. 1997;111(3):787-795. doi:10.1378/chest.111.3.787

Blood lactate during exercise and its associated ventilatory changes maintain useful and interesting applications in both the clinical exercise laboratory and the sport sciences. However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science.

My bolding.

Those changes in lactate levels are particularly significant for ME/CFS patients because we appear to have defects in the mechanisms that clear lactate. Even when it is cleared from peripheral blood it can persist in muscles or cerebrospinal fluid, where it has been found by magnetic resonance spectroscopy (MRS). Other papers suggest that lactate levels are the least reliable of the indicators discussed in this paper. This could be an indirect indication that some researchers had encountered patients with problems clearing lactate.

 

[Mark]

I did take half of a free statistics course from Coursera, focused on exactly for that sort of thing, before getting floored by ME. We're currently working on getting a proper database set up for the 23andMe data, which is finally done more or less, and the next step is getting R talking to that database, so I can easily determine p values, generate scatterplot graphs, and maybe even determine how much each variable is contributing to things.

Great stuff Valentijn, that sounds really exciting. I do think this work you're doing has the potential to evolve into something really quite significant in terms of hypothesis-generation, and the maths of all this stuff rather appeals to me so I'm watching with interest. So thanks for what you're doing, and good luck!

 

[MeSci]

I'm finally getting round to typing out my one-off exercise results from a student self-experiment at my Open University summer school carried out in the year that I became ill. I haven't got a detailed health diary for that year - only snippets - but one entry reports a resting pulse rate of 100 in the late evening, prior to the summer school test. Yet I was told that my results indicated excellent metabolism! There is no 'VO2 max/peak' etc in there but hopefully someone can pull something useful out of it.

I'm having to type it in small bursts due to the annoying effects of ME causing my eyes and brain to pack up after a short spell of concentration.

I think I will be posting the results in my blog for people to see if there is anything useful there if they want.

I have posted my 1995 step-exercise test results along with early symptoms here.

 

[anciendaze]

Just wanted to bump this topic because I still have not found or been given anything to indicate that the deficits in VO2 max and anaerobic threshold seen in ME/CFS have previously been reported in medical literature for any condition, (with the possible exception of overtraining syndrome, which takes place in presumed healthy athletes at a much higher level of performance. )

In the process of investigating the literature I have been struck by the persistent confusion about fundamental physiology of exercise in sick people. It seems incredible that most doctors have been trained to promote exercise even in people who exhibit "flu-like symptoms", with only specialists in myocarditis and cardiomyopathy giving warnings. (These warnings overlap those given in the case of cardiac problems resulting from Lyme disease. Considering the trouble patients and doctors both have in confirming that a patient actually has Lyme disease this situation seems absurd. If it often takes six weeks for a patient to develop antibodies which will reveal infection, and if levels fall off in chronic infection, it would seem there is only a small window in which a doctor following current guidelines can give useful advice about a life-threatening complication.)

This leads me to ask broader questions about the value of medical advice. A visitor from another planet might conclude that prolonged contact with medical doctors is a stronger predictor of morbidity and mortality than smoking.

Just as we need research distinguishing the cause and effect of exercise and health, so we don't confuse "exercise is the result of health" with "exercise is the cause of health", when we observe the fact that "healthy people exercise more", we also need research to distinguish the results of medical treatment from the presumed intent of that treatment. Once the profession decides some treatment is a good thing, or at least the best option available, it becomes hard to find patients who have not been subjected to that treatment, even if it is known to be seriously flawed. This makes true "evidence-based medicine" nearly impossible.

 

[alex3619]

Anecdotally I have heard that the Ampligen studies used it for ME in the 80s, and Jay Goldstein in the early 90s, but nothing much was publicly reported.

 

[MeSci]

I just found this 2008 study in the ME Research UK database while looking for something else. I can't find the study mentioned on PR from a quick search so thought I'd better post it somewhere before I forget.

Abstract:

Clin Physiol Funct Imaging. 2008 Nov;28(6):364-72. doi: 10.1111/j.1475-097X.2008.00822.x. Epub 2008 Jul 29.
Prefrontal cortex oxygenation during incremental exercise in chronic fatigue syndrome.

Patrick Neary J1, Roberts AD, Leavins N, Harrison MF, Croll JC, Sexsmith JR.
http://www.ncbi.nlm.nih.gov/pubmed/18671793#
Abstract

This study examined the effects of maximal incremental exercise on cerebral oxygenation in chronic fatigue syndrome (CFS) subjects. Furthermore, we tested the hypothesis that CFS subjects have a reduced oxygen delivery to the brain during exercise. Six female CFS and eight control (CON) subjects (similar in height, weight, body mass index and physical activity level) performed an incremental cycle ergometer test to exhaustion, while changes in cerebral oxy-haemoglobin (HbO2), deoxy-haemoglobin (HHb), total blood volume (tHb = HbO2 + HHb) and O2 saturation [tissue oxygenation index (TOI), %)] was monitored in the left prefrontal lobe using a near-infrared spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE) were recorded at each workload throughout the test. Predicted VO2peak in CFS (1331 +/- 377 ml) subjects was significantly (P < or = 0.05) lower than the CON group (1990 +/- 332 ml), and CFS subjects achieved volitional exhaustion significantly faster (CFS: 351 +/- 224 s; CON: 715 +/- 176 s) at a lower power output (CFS: 100 +/- 39 W; CON: 163 +/- 34 W). CFS subjects also exhibited a significantly lower maximum HR (CFS: 154 +/- 13 bpm; CON: 186 +/- 11 bpm) and consistently reported a higher RPE at the same absolute workload when compared with CON subjects. Prefrontal cortex HbO2, HHb and tHb were significantly lower at maximal exercise in CFS versus CON, as was TOI during exercise and recovery. The CFS subjects exhibited significant exercise intolerance and reduced prefrontal oxygenation and tHb response when compared with CON subjects. These data suggest that the altered cerebral oxygenation and blood volume may contribute to the reduced exercise load in CFS, and supports the contention that CFS, in part, is mediated centrally.

 

[anciendaze]

I had not seen this paper, and will have to read carefully. I am unfamiliar with the method of measuring oxygenation in the prefrontal lobe using near-infrared spectrophotometry, and will need to read some background on it.