It’s official. My body and brain have officially divorced. It feels like my body is becoming closer & closer to normal (when the air is good) whereas my brain’s progress is glacial.

A few weeks ago, Lisa suggested that climbing was huge for Erik. When he was still really sick, apparently climbing 300 ft up the hill from his driveway made him feel better — hard to relate to that story but I didn’t quite shelve it either. I was starting to hit a wall somewhere around 4 miles of hiking, which I know sounds ridiculous, but my goal isn’t to hike the longest but to continue pushing my body with exercise as a primary form of detoxification.  I knew that at some point I would do what Erik did, but the time had to be right.

Well my family visited me a few weeks ago, and probably due to nothing short of raging machismo and feeding on the fuel that was my family’s happiness that I appeared normal from the outside again, I decided to do a 400 ft ascent as part of a 3 mile hike with them.  Yeah logic went out the window here, but then again, the discovery that I could hike 40 minutes within touching down in the desert didn’t happen “logically” either.  If all attempts to test our bodies happened logically, Erik would’ve gotten to Mt Whitney when he was 80 years old.  Well, imagine my surprise when I started feeling better as I really got into the ascent, almost like my body felt like it could run up the hill. I thought I’d crash for sure, but I didn’t. In fact, my legs weren’t even much more noodly than they were from hiking 4 miles flat. It seems that the noodly legs are a function of exertion and time, not just exertion. Therefore, my body seems to be able to exert more if I cut short the time a little bit, and vice versa. That’s my hypothesis for now anyway.

After my family left, I rolled with it. I went on another 400 ft ascent.  This time, my lungs felt like they used to feel when I did 7-mile mountain runs in college, or cross-country races in high school: winded and heaving, but not swollen.  At night however, I developed this scary sharp pain I’ve never had before, where I could notice the swelling whenever I swallowed or took a deep breath. Very disconcerting, but Erik told me he has the same acclimation issues when he first started clmibing. I thought it made sense actually, that this was due to deconditioning and would thus improve with conditioning, since only a month ago I was struggling to walk 40 minutes at a very measured pace and now I feel like my body actually wants to go running rather than hiking. Maybe mostly rationalization, but I knew I wasn’t gonna go the ER so I might as well test the theory out, feeling comfortable that this wasn’t serious enough to be fatal.

Well I hate to sound like a broken record, but Erik was right. A few days later, I did a 350 ft ascent followed by immediate 300 ft descent and roundtrip back (750 ft total ascent) as part of a 3-mile hike. This time I don’t think I had any lung issues during the hike or at night, or the next day.

The crazy part is: this was the second-to-last hike I made in college right before i got sick, and I remember how difficult this hike was at that time because I had bronchitis. How surreal that I now, after 6 years of ME/CFS and still with it, have an easier time physically doing the same hike that I had trouble with during the months leading up to ME/CFS? I was in denial for so long, and my body is actually improving from pre-cfs.

Today, I did another 500 ft ascent in super windy conditions at sunset (hiked a fourth of the way in pitch black–stupid timing!) and right now I feel great.  On the way down from the mountain I felt like making a run for it, but I rationalized that there’s no benefit to running at this point versus the type of hiking I’m already doing right now, so why fix what ain’t broken?  Yes even on endorphins highs I rationalize.  That must prove I’m still a ME/CFS patient (jk)

On the anaerobic side, I’m continuing to max out upper-body plus abs workouts as I do on all non-hiking days, and I seem to be getting what feels more like the soreness I used to get after working out rather than screaming total-body burn and intractable pain in my left chest I was getting a few weeks ago. Thus it seems that even my heart is improving with exercise, which I didn’t expect at all.

I started famvir 2 weeks ago, and I don’t think that’s playing much of a role in what I’ve  described so far, because the two things I was told to expect it to do in the near-term (lower reactivity and help my cognitive abilities) haven’t really been helped at all. Therefore, I’m inclined to think all the improved exercise capacity is just due to the other R&R, rehabilitation and reconditioning. I had some nausea when I first started the drug but it’s more or less worn off now, so I don’t feel much at all from taking the drug. I’ll be starting Valcyte shortly.

Now the ugly: my body is still as sensitive to bad air quality as usual, and I don’t foresee that changing for another few months. Changing oxygen metabolism and anaerobic capacity is clearly an easier game for me than changing immune reactivity.  All my friends ask me if that means I’ll be staying in the desert forever.  Well of course I’d rather not! But if my reactivity never goes away, then really it’s a no brainer since living in the desert beats the crap out of feeling sick 24/7.

About CityChanger

This blog is about my participation in a clinical trial for ampligen, an experimental immunomodulatory and antiviral drug, for ME (Myalgic Encephalomyelitis).

2 responses »

  1. Glad to hear that you’re still making progress!

    While Famvir did help my reactivity a _little_, it did not help my cognitive function at all.

    Valcyte helped my cognitive function for brief spurts within a month or two (with increasing consistency in subsequent months), but it took about six months for the increased reactivity from the drug to turn into decreased reactivity.

    Good luck!

    • Here is an article by Jacob Teitelbaum about the issue of small heart size in CFS.

      http://www.ei-resource.org/expert-columns/dr.-jacob-teitelbaums-column/special-report:-small-heart-size-common-in-cfs/

      >Surprisingly, this finding is good news for those with CFS and POTS. Here’s why:

      >You weren’t born with a smaller heart. If you were born with a smaller heart, your POTS/NMH symptoms would have started around age 18, when your body was full-grown. You wouldn’t have had the sudden onset of POTS/NMH symptoms that are common in CFS.

      >The smaller heart is a symptom of CFS. The study suggests that CFS causes a smaller heart. How does that happen? CFS causes a decrease in the number and size of energy-generating mitochondria within muscle cells, shrinking muscles — including the heart muscle. When the heart and other muscles shrink, exercise becomes a strain and a drain. You exercise less and your muscles become deconditioned. Once the heart muscle is both smaller and deconditioned, blood pressure is compromised — and you develop CFS/POTS.

      >Natural cures can improve and even reverse the condition. We’ve seen many CFS/POTS patients strengthen and condition their hearts and improve their symptoms, often without drugs.

      >Light-intensity exercise (exercising at a level that is comfortable, and never beyond) helps the problem. And many nutrients can improve heart function in about six weeks, as discussed in my article “Heart Disease.” With this combination of exercise and nutrition, symptoms can improve within six to 12 weeks. And I suspect that heart size and function often return to normal within a year or so.

      Miwa, the author of the Japanese studies looking at the small heart size, wrote to me a couple of months ago with a related comment, below.

      Of course, both Miwa and Teitelbaum are ignoring the fact that CFS sufferers typically get worse as a result of exercise, due to the inflammation in the disease. For many severely ill sufferers, any amount of exercise is too much. For details, see this link:

      https://docs.google.com/viewer?a=v&pid=explorer&chrome=true&srcid=0B7A3lHR1hqW5ZTk5YjEzNjQtN2E0NC00NmQ3LThiZGMtZmYyOThjYjBmOWU0&hl=en_US

      A good goal thus may be to try to do an “override” of the inflammatory limitations by damping down the system (e.g. through extreme avoidance). Insofar as the resulting exercise may allow the issue with the small heart to be addressed, improvements in POTS may occur.

      Good luck to you in making it happen!

      *

      I would like to comment on the controversial issue of the therapeutic effects of exercise on the symptoms in patients with chronic fatigue syndrome (CFS). Recently we reported that a considerable number of CFS patients have a small heart. Small heart may contribute to the development of CFS as a constitutional factor predisposing to fatigue, and may be included in the genesis of CFS. Small left ventricles in patients with small hearts have limited preload reserve resulting in limited reserve of cardiac output. Habitual exercise can improve preload reserve and enlarge the left ventricular cavity. In addition, exercise can cause muscle development. Leg muscle development can enhance muscle pump activity during upright position, improving orthostatic intolerance, which is important orthostatic component of symptoms in CFS patients, by augmentation of venous return leading to increase in cardiac output and cerebral blood flow.

      Although CFS patients are limited by the discomfort of an increased perception of exertion, an appropriately designed exercise program is probably beneficial. We recommend graded exercise therapy to our CFS patients expecting late improvement even in spite of initial worsening.

      Kunihisa Miwa, MD/PhD
      Doctor-in-Chief
      Miwa Naika Clinic

      References
      Miwa K, Fujita M. “Small heart syndrome” in patients with chronic fatigue syndrome. Clin Cardiol 2008; 31: 328-33

      Miwa K, Fujita M. Cardiac function fluctuates during exacerbation and remission in young adults with chronic fatigue syndrome and “small heart”. J Cardiol 2009; 54: 29-35

      Miwa K, Fujita M. Cardiovascular dysfunction with low cardiac output due to small heart in patients with chronic fatigue syndrome. Inter Med 2009; 48: 1849-1854

      Fu Q, VanGundy TB, Galbreath M, et al. Cardiac origins of the postural orthostatic tachycardia syndrome. J Am Coll Cardiol 2010; 55:2858-2868.
      Miwa K, Fujita M. Is small heart syndrome a “heart” disease or low output syndrome? Int J Cardiol 2011; 146 : 95-96

      Hurwitz BE, Coryell VT, Parker M, et al. Chronic fatigue syndrome: illness severity, sedentary lifestyle, blood volume and evidence of diminished cardiac function. Clin Sci 2010; 118:125-135

      Miwa K, Fujita M. Small heart with low cardiac output for orthostatic intolerance in patients with chronic fatigue syndrome. Clin Cardiol in press

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