British tennis player with 'chronic fatigue' wins 2020 Aus Open doubles

Sounds like the real headline should be about the inadequacy, or lack of use, of the decent diagnostic criteria available for this illness in the medical profession.

I do wish him well though and I'm he's glad pulling through whatever it is he has.

 

Can't read it because The Times has been playing up for a week or 2 on my computer, but I think one of the other British tennis players has had CFS as well - was it Katie Boulter? (There does seem to be a higher-than-average incidence of glandular fever among tennis players - it's been suggested that all the flying may have something to do with it, I think - several have even had their careers cut short by it)

 

To me these sorts of cases illustrate that the 50% functioning cutoff for diagnosing ME/CFS is ultimately arbitrary (of course there should be criteria for research and clinical diagnosis).

There's a spectrum from people who are severely ill, bed-bound and tube-fed, to those who have mostly bounced back to a level of function that we wouldn't call 'ill', but still experience an impactful reduction in stamina.

 

High performance tennis may be correlated to hypermobility, which of course we know has a relationship with ME (and a basket of other conditions). A world of overlapping Venns.

One of Britain's leading paediatric rheumatologist specialising in hypermobility once explained to us that a number of sports are apparently led by people who are hypermobile, tennis in particular. Benign hypermobility with sufficient strength can be an advantage. He demonstrated using photographs of specific manoeuvres, bent joints and hands holding pens while signing autographs. It was quite striking, albeit observational and not quantitative.

 

There is a limit to how much aerobic capacity a cell can have. Aerobic exercise, when the cell switches to anaerobic respiration, increases fitness because the mitochondria die which is a signal to the cell to make more of them so there will be a greater capacity for aerobic respiration. We call this getting fitter. Sedentary people can increase their fitness a lot but athletes can't because they are close to the limit of possible capacity.

In ME the aerobic system is broken so we rely on anaerobic respiration whereas in athletes, they get burnout because they exceed their aerobic capacity by making too high a demand on their bodies by over exercising and begin to use anaerobic systems for everyday living instead of emergencies just like we do.

This would make it seem like ME but their systems are not broken and can recover.

 

Aerobic fitness is more about the heart and cardiovascular system than it is about peripheral mitochondrial numbers. It is the increased volume of oxygen that is able to be pumped to the muscles that leads to increased numbers of mitochondria to take advantage. The oxidative capacity of major muscle groups (for example, leg muscles during running or cycling) always exceeds that of what the cardiovascular system can deliver, unless the individual has a severe mitochondrial disease (in which case, more mitochondria won't help much).

 

See Nick Lane's books on mitochondria. Sports physiologists are not so knowledgeable about biochemistry and cell bioenergetics.

 

Many sports physiologists don't know the fact I stated in my previous post either. Likewise, most biochemists lack knowledge of exercise physiology.

But for the sake of argument, the equilibrium of mitochondria is when the rate of death is equal to the rate of new mitochondria being formed. What is the limiting factor?

If hypothetically, the major cause of mitochondria death is anerobic metabolism and mitochondria subsequently multiply to recover numbers when this occurs, then what happens at the point at which insufficient oxygen is delivered to the cell? Excess mitochondria would die due to insufficient oxygen, reaching an equilibrium.

We then say, hang on, the oxygen partial pressure is dynamic, not in a constant equilibrium. So perhaps during the 'rest' phase when there is sufficient oxygen for the mitochondria, excess mitochondria can survive. Hence excess oxidative capacity for a given oxygen supply.

Then we say, hang on, muscles are made up of tens to hundreds of motor units, each with their own sets of muscle fibres with variable levels of force generation, variable levels of (neurological) sensitivity, variable capillarisation and so on. Hence why fitness should be considered primarily a physiological, rather than biochemical phenomena.

 

When the Kreb's cycle is saturated so it cannot take in any more of the pyruvate being produced by the anaerobic chemical reaction it builds up and damages the mitochondrion. The waste products from this destruction signal the cell to produce more mitochondria.

The different levels of organisation in the body each have their role to play. Ultimately everything depends on the cell biochemistry but even now we do not know enough about how it all works (which makes the claim that everything is down to our emotions very dubious).