Swimming inhibits autoimmunity

Is swimming beneficial in MS?

As part of our remit the UK government wants us to discuss animal experiments, and as this is a blog about good and bad research news, we will defend animal experimentation when it is useful.

However, I think we need to be bold and say “Not in my name” when it is not. 

Yes this goes against the norm on science reporting where “every thing is amazing” and “we are all made out of stardust”. 

OK it does not make me any friends.

Xie Y et al. Effects of moderate- versus high- intensity swimming training on inflammatory and CD4+ T cell subset profiles in experimental autoimmune encephalomyelitis mice.J Neuroimmunol. 2018;328:60-67.

Multiple sclerosis (MS) is an inflammatory neurodegenerative disease of the central nervous system (CNS). Evidence about experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, has been shown to modulate disease parameters within exercise intervention. However, these initial studies weren’t carried out intensity of exercise in mice. This study explored the impacts of different-intensity swimming training on EAE mice. Female mice were given access to swimming with predetermined weight (moderated-intensity (ME) group is 0% body weight; high-intensity (HE) group is 4% body weight) for 6 weeks, were immunized to induce EAE and then continued swimming until sacrificed. Compared to non-exercise mice, ME training didn’t affect EAE clinical symptoms and neuropathology. However, HE swimming attenuated EAE clinical scores, reduced infiltrating cells and demyelination of spinal cords. Analysis of CD4+ T cell subsets from CNS of EAE showed the reduction of Th1 and Th17 populations and an increase of Treg in HE, not ME mice. Accordingly, HE training lead to a decrease of IFN-γ and IL-17 and an increase of IL-10 and TGF-β. Of note, HE, not ME, swimming induced an increase of brain derived neurotrophic factor in the CNS of EAE. Moreover, HE training upregulated Treg and downregualted antigen-specific T cell proliferation and Th1 and Th17 populations from draining lymph node cells. These results suggest that HE swimming training might have benefits on attenuating the progression and pathological hallmarks of EAE, thus representing an important non-pharmacological intervention for improvement of chronic inflammation or T-cell mediated autoimmunity.

So mice were given access to swimming (they were chucked in a tank full of water) and if they have to do alot of swimming, they do better and you have reduced Th1/th17 and increase IL-10 and Tregs (Standard Mechanism of EAE control…Yawn). 

So does this mean swimming will be beneficial in MS?  

Maybe, swimming is a good low impact exercise… but I have to say studying mice is not a worthwhile way to find out. You can do it in humans and ask them. 

I suspect if you asked the mice what they were thinking…you may get an answer like “Some guys tried to kill me, they kept me swimming without a break for ages and I thought I was going to drown. It was so, so  stressful!” 

Yep, we know that stress is immunosuppressive in animals. Stress inhibits EAE!

We call it the “building site effect”. There is so much noise the mice get stressed and their EAE goes away. 

If we put humans in a building site would it stop their MS…probably not, and you say it is not a relevant experiment worth doing.

We have to request permission to do such experiments and they must go through ethical review committees to get approval to do them. This study will have done the same but it shows that the level of ethical review varies from country to country.

The UK is quite strict and it is getting harder and harder to do animal research on MS. It just gets moved Eastward and Westward..This is what you get:-(.

“Not in my name”.

We could ask our paralympian swimmers if high intensity swimming gets rid of MS, I would think the answer is no. Stephanie Millward one of our MSer Olympians was S9 at London 2012 and S8 at Rio 2016, so there was seeming deteriortion.

Has swimming limited MS? who knows without a trial?

Oh I forgot to say they has been some already (click)…So why do mouse studies?

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  • Incredibly cruel and pointless.

    There are no useful parallels. Humans are not mice, EAE is not MS, and these mice were not doing "high intensity exercise". They were fighting for their lives, struggling not to drown.

    I'm glad to read your take on this, MD.

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