Article: The Test: Part I of the Heart Rate Based Exercise Video Series with Dr. Klimas on ME-CFS Co

Article: VO2 Max Exercise Video Series with Dr. Klimas on ME-CFS Community Center: Pt

You can view the page at http://forums.phoenixrising.me/content.php?462-VO2-Max-Exercise-Series-klimas-Begins-on-ME-CFS-Community-Center-moricoli

 

I have to disagree or maybe I would just alter the emphasis. The fact that 'reduced aerobic capacity' can be proven using validated instruments to the medical community is huge. The fact that researchers can or are proving that it is not the result of deconditioning is immense. That places ME on a whole new playing field. It may be obvious to us that we have reduced aerobic capacity but not to the research community (ie CFS is not called 'reduced aerobic capacity disorder' .) If that could REALLY be be established imagine the difference in emphasis. Showing that symptoms occur more readily when patients push themselves outside of their (relative) energetic cardiovascular safe zone - should shift the conversation.

I'm looking forward to the rest of the series.

In the meantime I Googled 'reduced aerobic capacity' and within the first two pages found the following conditions associated with reduced aerobic capacity :

The elderly
Older HIV patients
Systemic sclerosis
Thyroid deficiency
obesity
heart disease
liver transplant

and this with respect to hepatitis B :

Any illness tends to decrease your aerobic capacity. However, you can gain back the capacity lost in the acute phase of an illness if you work with your doctor to come up with the safe program for you. According to the Hepatitis B Foundation, getting regular exercise can benefit patients with chronic Hepatitis B.

Read more: http://www.livestrong.com/article/346395-hep-b-reduced-aerobic-capacity/#ixzz1ThCdaYc2

In many cases the reduced capacity is due to deconditioning.

So yes reduced aerobic capacity can be objectively measured but it is not by any means unique to ME/CFS and is often the result of deconditioning arising from chronic disease.

Could you elaborate on how it has been proven IN ME/CFS to not result from deconditioning (not that I believe it does)?

I would imagine that you would need either a large scale prospective study or (perhaps using the new international criteria that don't require a 6 month delay before diagnosis) identify new onset cases that were previously aerobically capable and now show measurable reduced capacity.

Even then I would expect continued skepticism from the general medical community who are accustomed to dealing with reduced aerobic capacity in the chronically ill as a matter of course.

Alternatively, and much more convincing, not to mention useful to us, would be to identify the mechanism that reduces our aerobic capacity and demonstrates beyond any argument that it results from pathology.

The potential for rehabilitation can then be realistically gauged.

 

So yes reduced aerobic capacity can be objectively measured but it is not by any means unique to ME/CFS and is often the result of deconditioning arising from chronic disease.

According to Staci Stevens and Dr. Snell at the Pacific Fatigue Lab the metabolic abnormalities; ie the reduced VO2 max seen in ME/CFS patients during the repeat exercise tests are not seen in any other disorders. Here's something from Cracking the Foundations - an article on their work I did earlier

http://aboutmecfs.org.violet.arvixe.com/News/PRJan09Pacific.aspx

According to modern medical science this shouldnt occur. For decades researchers have shown that human beings, under virtually all conditions and in a variety of disease states, can take an exercise test to exhaustion, recover and return the next day and score the same the next day. It doesnt matter if she/he has heart failure or end-stage kidney disease again and again researchers have shown that the human body even in extremely poor health - has an amazing ability to quickly return to a baseline level of energy. That is until now.

But its not just that chronic fatigue syndrome (ME/CFS) patients are failing these tests, its also the unique way theyre failing them thats raising eyebrows. Decades of research have shown if you a take a female of W age and have her do X amount of exercise at Y heart rate she will exhibit Z levels of oxygen consumption. Researchers have believed these algorithms are set in stone but theyre not holding up in chronic fatigue syndrome (ME/CFS) patients. That theyre not suggests that something has gone awry in the basic physiological processes the body uses to produce energy in this disease.

Even after 20 years in the field Staci Stevens excitement was palpable. The implications of her findings are profound not just for ME/CFS patients but for the field of exercise physiology. She said We are charting waters that have never been charted before. Its an exciting time to be involved in CFS research!

The labs findings are so unusual that their peers sometimes cant believe what theyre hearing. Since decades of research have indicated theres no need to do repeat exercise tests, they are simply not done. Until recently the Pacific Fatigue Lab may be the only lab in the world that regularly does them. I asked Staci Stevens how her colleagues across the country were reacting to this data were they excited? She said some of them say, Its just not possible, they think we must have imputed the data wrong but others are enthralled. She said one colleague on the east coast whos doing the tests said that after 30 years in the field, Id never seen anything like this.

There's a big difference as well. I imagine, between the kind of reduced aerobic capacity found in many of these disorders and in CFS. Note that with hepatitis B that quote stated the aerobic capacity could be regained. Nobody has suggested that in CFS - or even close to it. It may be that some people can start to exercise above their 'safe heart rate' in CFS at some point but that is not the expectation. The expectation is that they will be able to increase their level of endurance at a specific heart - increasing their level of fitness. Really moving the bar - and returning to their former level of fitness -is another matter indeed.

I think over time with more research going into this area - we will learn more about the pathologies associated with exertion. Broderick has a 4 million dollar exercise study grant to look at a large variety of factors...Throw in the Lights, Newton, Klimas, Stevens/Snell and others interest I think we are moving forward to better understand the pathology that is causing the heart rate based exertion problems in ME/CFS.

 

Part 2 is out.

http://vimeo.com/27073084

 

My resting heart rate was 160 bpm last week and took along time to go down. Exercise is highly dangerous for someone with ME. I have also been confirmed to have a new human retrovirus.

 

My experience is very similar to DAnnFL's. I also did VO2Max testing about 5years ago at Hunter Hopkins and discovered that virtually all my daily activities put me over my AT. The heart rate monitor with the alarm was a real eye-opener, not just for me, but for my family and my students.

I cut back HUGELY on my activities based on the feedback from the heart rate monitor. I also kept very careful logs for a couple a weeks that included AT for certain daily activities, and avg HR over the day and how I felt. Moderating my activities based on staying below my AT was one of the best things I've done for my ME.

Once I moderated my activities based on that info, I had fewer flares/relapses -- especially ones with muscle pain. But it means that I have to dawdle in bed in the morning, sit to shower (or do much of anything) and walk v-e-r-y s-l-o-w-l-y.

I'd like to add some points from my experience that I'm not hearing from Dr Klimas or anyone else (so far). For several years I managed my behavior and activities to stay just below my AT. I didn't have as many pain flares and I think I maintained my level of (ill) health during that time. However, I didn't get better, either. I was happy to be doing as much as possible (even if it wasn't much) without making myself worse.

When I caught H1N1 and had a major infection-induced relapse (the whole bag of worms -- pain, exhaustion, terrible brain fog), I couldn't recover.

Some time after that I started on Valcyte, which has given me big improvements so far (bedbound to housebound), but I've found that in order to really make progress, I have to rest way more than I would if I was staying just below my AT.

So, for me, at least, staying below my AT seemed to moderate my pain-type flares, but didn't do much for the more immune-type ones (exhaustion, sore throat, swollen lymph nodes). And I wasn't getting better, I was just not getting worse.

While I've been on Valcyte, it's been clear that if I do as much as I can without going over my AT, a make some, but small, progress with lots of slide-backs. If I force myself to uber-rest, I improve faster and don't have the regressions.

I have to question, for me, anyway, the wisdom of maintaining activity near the AT limit until I'm in the "mild" range -- which looks to me like a recovery phase where we are probably not dealing with serious infections (or only intermittently).

In conclusion, for me, moderating my activity to just below my AT educated me and those around me to what was needed to stop getting slowly worse. That was amazingly useful. But in order to get better, I have had to stay well below my AT.

Just my experience, YMMV.

PS I'm wondering if Dr Klimas' exercise experience/recommendation is based on people who are routinely taking the immune modulators she often recommends. That may alter how the patients react to exercise. Just a thought....

Thanks for sharing your observations, that's an interesting distinction. It pretty much jibes with my trial-and-error experience, that carefully paced activity is good most of the time, but when I'm having one of the flu-like periods (feeling feverish, sweats & chills, etc), the best thing is bedrest.

 

So yes reduced aerobic capacity can be objectively measured but it is not by any means unique to ME/CFS and is often the result of deconditioning arising from chronic disease.

Could you elaborate on how it has been proven IN ME/CFS to not result from deconditioning (not that I believe it does)?

You might find this article interesting:
http://circ.ahajournals.org/content/110/4/e27.full - especially under the section of "Etiology of Dyspnea" and the Fig 2 chart. While the info is for heart patients, I had the report on hand for my Social Security disability hearing as the chart clearly showed that my low VO2Max was NOT from deconditioning, rather what they would classify as circulatory impairment. Whether this is true in most ME/CFS cases, I don't know.

 

GET and ME - a mechanism?

In a recent article, Hollingsworth et al. found "Impaired Cardiac Function in Chronic Fatigue Syndrome measured using Magnetic Resonance Cardiac Tagging." See PR thread here.

I'd like to comment on the first sentence of the last paragraph in the conclusions section as it relates to GET and the author's conclusions that the specific type of impaired cardiac function is consistent with hypovolemia:

"Potentially these findings suggest that therapies which can correct the low cardiac blood volume may be helpful: this might include graded exercise therapies, which might improve cardiac blood volume."

If GET can correct low blood volume (I did not explore the mechanisms cited in the paper cited by Hollingsworth et al. - increased vascular tone?), it is my personal belief that it does not directly address the problem and that based upon numerous accounts and personal experience, desmopressin is more direct and exceedingly effective in severe cases.

If a defect in ADH production is the underlying cause of hypovolemia in ME patients (hypothalmic/pituitary dysfunction?), is it wise to prescribe exercise for ME patients?

Are ME patients particularly susceptible to the negative impact of "too much" activity in the form of a chronic low grade infection that is repeatedly and easily exacerbated?

ETA - I just checked the article cited by Hollingsworth et al. There is no reference in that article to a relationship between GET and hypovolemia (Can pacing self-management alter physical behavior and symptom severity in chronic fatigue syndrome? A case series, Journal of Research and Rehabilitation Development,Volume 46 Number 7, 2009, Pages 985 996).

 

I have tremendous respect for Nancy Klimas so I am trying this activity program suggestion. Even though I blame activity for increasing the severity of my M.E. to the point of impending heart failure. I also credit 'uber rest', 'aggressive resting' for bringing me back from the brink to a stable yet totally dysfunctional state.

The body needs energy to heal itself. Getting a wheelchair and doing almost nothing allowed me to use the tiny energy I had to heal enough to become stable again. To heal any further requires energy I currently do not have. Assuming 97% of the energy loss is from M.E. the other 3% from deconditioning (maybe 99% and 1% who knows exactly?), then reconditioning theoretically could give me another tiny boost of energy. Any extra energy improves the odds of the body healing itself.

The difference between now and when activity caused a worsening of my M.E. is I have a heart rate monitor and check my morning resting heart rate and also monitor it during activity. I also know that anything mental/physical that triggers PENE lowers my baseline so the energy envelope needs to be strictly respected.

TL;DR
"Activity can make M.E. much worse" and "activity can slightly improve M.E." are not contradictory statements if the activity in the latter case is strictly tailored/monitored to respect the energy envelope.

 

I'm looking for an effective , strapless, HRM watch, with real time HR alarm. I don't mind having to touch to get the HR digital reading, but having a real time HR alarm is essential. If it has no alarm, and I have to press the watch to get the pulse, I don't see the difference between doing that and just manually taking my own pulse for free.

Any suggestions?

 

Early morning pulse rate warning protocol. This is cited from one of the Phoenix Rising sites. Alas I've mislaid the exact site:


> "The Key Measure - Perhaps the key activity management tool, however, is something called ‘resting heart rate’, which is measured after you get up in the morning. Your resting heart rate is measured by obtaining a cheap heart rate monitor (@$30 – Amazon.com) getting up in the morning for a bit and then lying down and taking the reading (before taking any stimulants such as coffee).
>
> Pushing through fatigue only leads to more fatigue…You can’t beat it – but you can go around it. Dr. Connie Sol works with Dr. Klimas.
>
> Doing this over 10 days or so and keeping a simple activity and symptom log should help you notice how changes in your morning resting heart rate are associated with your symptom and energy levels that day. If you engaged in too much activity/stress over the day or two before – it will probably result in an increased morning resting heart – and a more symptomatic day. Connie Sol stated that if your RHR rises as much as 8% above your baseline level then you need to cut back on your exercise/activities. If you ignore that warning, you’re going to crash.
> (This means you can use a heart rate monitor to manage your activity levels without doing the VO2 max testing. The VO2 max test can pinpoint the point at which exercise/activity level becomes dangerous but there are ways for the less well off of us to get some an idea of the maximum heart rate we should achieve during exercise/activity without doing the expensive testing…"