Dat een bezoek aan de WC al een topprestatie is voor mensen met ernstige ME

bewijst een studie van Mark Vink (huisarts en voormalig top-hockeyer).

Hij onderzocht 1 minuten vóór en 5 en 30 minuten na zijn WC-bezoek de bloedconcentraties

Pi (dat vrijkomt bij de omzetting van ATP naar ADP: energieverbruik),

creatinekinase (dat ontstaat bij de aanmaak en verbruik van energie via het ATP–CP-systeem) en

lactaat (dat in grote hoeveelheden vrijkomt bij zuurstofloze energieproductie via glycolyse).

Hij ontdekte dat het lactaat-niveau na ca. 5 minuten sterk steeg,

maar dat die na ca. 30 minuten opnieuw steeg en dan naar een nog hoger niveau.

Dat betekent dat de (tweede golf) lactaat pas na een half uur uit de spieren vrijkomt

en verklaart volgens de schrijver de spierzwakte/spierpijn na een minimale inspanning.

Ook kwam Mark erachter dat als hij niet lang voor zijn WC-bezoek at,

de (tweede) stijging van het lactaat-niveau nog veel later tot stand komt,

mogelijk omdat de spijsverteringskanalen de beschikbare zuurstof verbruiken,

waardoor er voor de spieren nog minder zuurstof beschikbaar is.

Je vraagt je af: zou gedragstherapie ook hier niet de oplossing zijn...

The aerobic energy production and the lactic acid excretion

are both impeded in Myalgic Encephalomyelitis/chronic fatigue syndrome.

J Neurol Neurobiol, 2005 Sep 10; 1(4). doi: 10.16966/2379-7150.112

Vink M.

Background:

In this study

the muscle bioenergetic function in response to exercise in severe ME was explored

to see if the underlying metabolic problem in ME,

responsible for the severe difficulties with trivial exercise, and

the severe loss of muscle power, could be discovered.

Methods:

Inorganic phosphate, creatine kinase and lactate were measured

in a former Dutch National Field Hockey Champion,

who is now a patient bedridden with severe ME,

before and 5 minutes after very trivial "exercise",

from which his muscles needed 12 hours to recover.

Results:

Inorganic phosphate and creatine kinase were both normal,

however, lactate after this trivial exercise was very high, and

further testing showed that

a second batch of lactic acid was excreted after the same exercise with a 6-fold delay,

showing that the lactic acid excretion was impaired and split into two.

And this was delayed up to 11-fold by eating closer to the exercise.

Conclusion:

This study found that

in severe ME,

both the oxidative phosphorylation and the lactic acid excretion are impaired, and

the combination of these two is responsible for the main characteristic of ME,

the abnormally delayed muscle recovery after doing trivial things.

The muscle recovery is further delayedby immune changes,

including intracellular immune dysfunctions, and

by lengthened and accentuated oxidative stress,

but also by exercise metabolites,

which work on the sensitive receptors in the dorsal root ganglions,

which in severe ME are chronically inflamed, and

are therefore much more sensitive to these metabolites,

which are produced in high quantities in response to trivial exercise,

which for ME patients, due to the underlining metabolic problem, is strenuous exercise.

And a similar problem is most likely responsible for

the abnormally delayed brain recovery after doing trivial things.

This study also shows that the two metabolic problems

are the result of an impaired oxygen uptake into the muscle cells or their mitochondria and

in combination with the Norwegian Rituximab studies,

which suggest that ME is an autoimmune disease,

it is suggestive that

antibodies are directly or indirectly blocking the oxygen uptake

into the muscle cells or their mitochondria.

Keywords

Myalgic encephalomyelitis; Chronic fatigue syndrome; Exercise; Muscle fatigue; Muscle pain;

Lactate; Lactic acid; Immune dysfunction; Inorganic phosphate; Creatine kinase

https://www.sciforschenonline.org/journals/neurology/article-data/JNNB-1-112/JNNB-1-112.pdf

Met dank aan Manja, die me attendeerde op de studie.