Aware she was treading into treacherous waters Dr. Klimas quickly reminded everyone as she began her talk on ‘Exercise and CFS’ during a recent CDC sponsored tele-webinar that she’s been at the forefront of biological research into chronic fatigue syndrome.
That was a good idea because what she said wasn’t easy to hear. Deconditioning, Dr. Klimas said, is a significant problem in the ME/CFS community and if you’re unlucky enough to be deconditioned you’re going to suffer, and, she feels, probably needlessly.
Strong words but it’s really no surprise that deconditioning would be prevalent in such a debilitated community; if you’re bedbound you’re deconditioned whether you have ME/CFS or cancer or a spinal injury or whatever and the consequences are not good.
Getting to the Heart of Post Exertional Malaise (???)
Dr. Klimas noted that time sensitive gene expression studies have revealed the fascinating and possibly absolutely pivotal finding that during exercise the autonomic nervous system tanks first in ME/CFS and then it takes down the immune system. That ANS ‘tank point’ occurs when the body changes over from aerobic to anerobic metabolism, a switch that occurs all too early for many people with ME/CFS.
The ANS/Immune system cascade in ME/CFS suggests that if you can stop the autonomic nervous system from blowing up you may be able stop the immune cascade with all the nasty inflammation that follows; ie you might be able to stop the post-exertional malaise that whacks patients after exercise.
The autonomic nervous system (ANS) is showing up in spades in ME/CFS research right now. A major component of the stress response, the autonomic nervous system controls our breath, blood flows, blood pressure, heart rate, gut motility and is an important immune regulator. Dr. Klimas asserted the ANS/immune system interface plays a major role in how you feel from day to day.
Dr. Klimas is currently using gene expression tests to see which genes turn on and off in her patients as they go through her exercise program. If she can pinpoint which genes start flaking out as ME/CFS patients exercise she may be able to grab this disease by the horns. We are, after all, possibly talking about getting at the heart of post-exertional malaise..
The promise of gene expression – real time data on the processes happening in the body – has never been fulfilled in ME/CFS but it sounds like researchers are getting closer. The problem has been poor consistency and miserable validation across studies but the gene expression field is a young one and much improvement has been made over time.
Given the ANS trigger it was no surprise to hear that Dr. Klimas, an immunologist by training, focuses on getting the autonomic nervous system back on track first.
Deconditioning A Big Player in Chronic Fatigue Syndrome
Dr. Klimas statement (paraphrased) that “Deconditioning can explain much of the dysautonomia (autonomic nervous system problems) present in CFS” definitely raised eyebrows.
This is going to be a tricky subject. For one thing the symptoms of deconditioning do closely mimic those of chronic fatigue syndrome in general, and orthostatic intolerance, in particular. Problems standing, rapid heart rates, low cardiac output, low blood volume, reduced VO2 max have all been associated with prolonged bed rest and all are present in ME/CFS.
On the other hand, virtually everyone with ME/CFS struggles with post-exertional malaise prior to becoming deconditioned or bedbound and, of course, many people with ME/CFS are not deconditioned now. My 30-40 minute walks 4 or 5 times a week easily preclude that but even that amount of mild exercise is often too much.
I don’t know if I have POTS, low blood volume, low cardiac output or any of the other problems associated with deconditioning but I do know that one of the consequences of over-exertion for me is, ironically enough, increased problems with orthostatic intolerance… I start getting dizzy spells when I stand.
It may be that deconditioning does cause considerably symptomology in a chunk of ME/CFS patients but something else is causing many of the same symptoms in other ME/CFS patients.
The good news, though, is that something Dr. Klimas is doing is working…
The Next Big Moment – Exercise and Chronic Fatigue Syndrome ‘Recovery’
Eyes must have popped open across the US and elsewhere when Dr. Klimas briefly stated that some of the patients on her exercise protocol had returned to work and to their normal exercise routines (ie; resumed their prior ‘athletic life’).
We’ve heard that these exercise programs increase fitness, resilience and quality of life but people fully exercising again is new.. That implies, as the title of the talk suggested, a true reconstruction of their aerobic system had occurred with normal VO2 max scores, no quick entry into anerobic energy production and normal aerobic functioning. This is exciting and its new and there’s obviously a lot more to learn….How many people gotten this far? How ill were they? Do they fit a certain subset? How important were other treatments?
We’ll get more information on these patients during a panel discussion with then on Dr. Klimas NSU Conference on the Jan 26th. The first 200 people to register for the webcast will be able to view it.
With that information in hand let’s take a look at the Klimas/Sol exercise program.
The Klimas/Sol Exercise Program
Connie Sol, Dr. Klimas’ exercise physiologist briefly went over the highlights of the exercise program used at the clinic. Noting that post-exertional malaise is also common in multiple sclerosis, Connie emphasized that understanding your personal aerobic and anerobic limits is very important and offered some general guidelines about how to do that.
- Slow as You Go – first be patient. This ‘exercise’ program hardly resembles exercise as we know it. For instance it takes three months of very, very gentle exercise before you start to notice the benefits.
- No ‘Burn’ No Nothing – Connie Sol’s exercise program requires that you not only don’t ‘feel the burn’ but that you don’t feel anything afterwards. In this very gentle nudging of your aerobic system you shouldn’t notice that you did anything afterwards. (Now that’s a gentle exercise program :))
- Exercise Laying Down or in a Gravity Reduced Environment Is Important - removing the burden of exercising and standing at the same time is very important. Doing pool exercises and yoga positions – which often occur seated or lying down as well – are recommended as well.
- Watching Your Heart Rate During Exercise Is Critical – maintaining a heart rate during exercise that does not push you into your anerobic zone is critical. The Klimas Clinic uses sophisticated tools to determine exactly where your anerobic threshold is but here Connie provided a very basic method; 220 – your age x .60 ((220 – age) x.6 ). Heart rate monitors can be purchased rather cheaply online.
- Take Frequent Breaks – Such as two minutes exercise (under your targeted heart rate) then two minutes rest; two minutes exercise/two minutes rest.
That’s it. It boggles the mind, quite frankly, that such a mild, mild program could ultimately achieve a return to aerobic health for some people. This ‘less is more approach’ might just be better, though, at turning a turned off aerobic system back on than the usual hit it over the head with strenuous exercise approach.
In response to a question Dr. Klimas suggested that the problem is not a damaged system so much as a system that’s been turned off. Gene
expression studies suggest that systems are turned off in ME/CFS, not damaged and that includes the mitochondria. She proposed the mitochondria may have switched themselves off during bed rest and then, for whatever reason, have not been able to turn themselves back on again. Dr. Julia Newton has referred, rather obliquely, to a process of aerobic relearning in one of her studies.
Why these systems wouldn’t turn themselves back on is unclear since they seem to be able to do that in astronauts or in other people who become bedbound for other reasons. Answering that question, of course, is what those real-time gene expression studies are all about.
There’s also the question of subsets. Some people may be able to respond to exercise better. A small group of patients, do after all, respond well to GET. Check out a study which suggested that some postural tachycardia syndrome ( POTS) patients respond well to a pretty intensive exercise program.
A Deconditioned POTS Subset ?
Postural tachycardia syndrome (POTS) is present in some people with ME/CFS and indeed the symptoms of the two disorders are very similar. The theory behind Levine’s small 2010 and 2012 studies was that if you reverse the deconditioning and boost blood volume, you’ll get rid of POTS. It didn’t quite work that way but the POTS patients did improve.
(Levine believes that the increased heart rates found in POTS patients are an attempt to make up for the reduced stroke volume (reduced cardiac output) present which, in turn, is caused by deconditioning. )
The 2010 study included a 3 month exercise program consisting of 30-45 minutes of recumbent exercise, 2-4 times a week at 75-85% of maximum heart rate. Short weight lifting periods (15-20 minutes) occurred once a week at the beginning and then twice a week later. Increased salt and liquid loading (6-8 grams/salt/day; 3-4 liters/water/day).
The use of ‘recumbent exercise’ ; exercise while sitting or lying down (with a recumbent bike, rower or swimming) was described as ‘critical’.
By the second or third month participants were starting to exercise standing. By the third month most participants were doing 5-6 hours of exercise a week.
At the start of the trial blood volume levels in POT’S patients were approximately 20% lower than in sedentary controls and heart size was approximately 15% smaller. By the end of the trial blood volume had increased significantly but was still significantly reduced relative to the sedentary controls. Heart size increased significantly and SF-36 (quality of life) scores increased significantly.
With it’s small size, no control group and the rudimentary SF-36 scoring this was not a particularly strong study but most participants finished the study and significant improvements were seen. The authors asserted that over half the participants no longer met the criteria for POTS at the end of the trial.
While the group as a whole still suffered from blood volume and other issues this group appeared to tolerate rather strenuous recumbent exercise well. Participants in small studies like this are often cherry-picked to produce results and validation in larger studies is needed but it does appear that some people with POTS can improve significantly with the right kind of exercise.
But, but, but…….A blogger, Liz at Potsrecovery.com who’s been promoting Dr. Levine’s drug-free, fluid loading and exercise intensive approach to POTS disappeared from the web early last year after experiencing an unexpected blood pressure crash while working out.
In her first blogs in about a year she recently reported that not only did had she been diagnosed with Ehlors Danlos Syndrome but with progressively worsening Mast Cell Activation syndrome as well(MCAS). (An MCAS attack had caused her crash) While she still believed Levine’s program was helpful she still suffered from orthostatic intolerance and POTS…..Exercise and fluid retention therapy only went so far for her and she ultimately lost some of her gains.
This is a complex subject….
There’s a lot more to learn about Dr. Klimas’s success and the presence of subsets (or not). We’ll find out more about recovery and exercise in the Conference on the 26th.