The MastAttack 107: The Layperson’s Guide to Understanding Mast Cell Diseases, Part 41

50. How does mast cell disease affect hearing?

For readers who don’t know, I lost the majority of my hearing in 2009. I am profoundly deaf in my left ear and have moderate to severe hearing loss in my right. This happened years before I was diagnosed with systemic mastocytosis or Ehlers Danlos Syndrome.

Mast cell disease affects hearing in multiple ways. Some related diagnoses also affect hearing.

Mast cells are involved in sensorineural hearing loss. The exact role of mast cells is still being researched but hearing loss is not an unusual complaint for mast cell patients. Mast cell disease can also cause auditory processing disorder. This condition makes it difficult to understand speech. Ringing in the ears (tinnitus) is also a symptom of mast cell disease.

Many mast cell patients also have Ehlers Danlos Syndrome (EDS), a disease in which the body makes defective connective tissue. EDS patients are vulnerable to both sensorineural hearing loss, in which the nerves don’t correctly transmit sound from the ear to the brain, and conductive hearing loss, in which the ear is not able to carry the sound waves correctly to the inner ear. Having both types of hearing loss, sensorineural and conductive, is called mixed hearing loss.

Many mast cell patients are deconditioned. This means that their body has undergone lots of changes as the result of not being active. Sensory processing is affected in deconditioned patients. In particular, sounds must be louder to be heard correctly. POTS patients sometimes experience something similar.

Having certain autoimmune disorders can increase the risk of autoimmune inner ear disease, resulting in hearing loss. Many mast cell patients also have autoimmune disease.

Skinny

My body is my adversary. I hardly remember a time when that was not the case. Even before I got sick, I struggled to make my body do the things I wanted it to. You can only do that so much before you begin to resent these shells we live in.

I was a small child, very small. I wasn’t four feet tall until eighth grade. That year, I grew a foot, and never again. Throughout elementary school, people commented on how small I was and how little I weighed. I was limber and very nimble; together with my lack of height, these characteristics gave me the body of a gymnast. I did splits and back handsprings and aerial cartwheels in my living room and backyard. I threw tricks during recess. I weighed so little that very little strength was required.

In seventh grade, I acquired the body of a woman overnight. I took ballet classes at that point in a small brown building around the corner from my house. One day, I caught my reflexion in the wall mirrors. I was rounder, with thick legs, breasts and a forming hourglass figure. I was still short but I wasn’t small.

I lamented the loss of my tiny frame but I wasn’t overly concerned with toning or losing weight. I walked a lot and was active if not athletic. In 2000, I started getting a three month birth control injection. In the months that I followed, I gained 26 lbs. I went from being thicker to being fat.

I was very unhappy with my body throughout college and grad school. I worked more than full time and carried a full course load. I picked up better eating habits when I got an apartment but I didn’t have time to exercise.

In 2007, I woke up in the middle of the night and while walking across my living room carpet to the bathroom, I realized my ass was jiggling. It actually stunned me awake. The next morning, I signed up to walk the Breast Cancer 3-day, 60 miles in three days, largely for the fitness aspect of the event. For the next six months, I walked increasing distances 3-4 days a week and did short workouts on the other days. I didn’t change my diet at all except for not drinking coke. I lost 25 lbs and gained a lot of muscle.

The summer of 2007 stands out for me as a time when I was happy with my body. I was still bigger than I wanted to be, but I was actively losing weight and felt much stronger and more able. I went backpacking in Scandinavia and was on strenuous mountain hikes without trouble. I took up rock climbing. I completed the 3-day and continued with the training schedule. Over the next three years, I would walk four more 3-days.

In 2009, I lost most of my hearing. I ended up on high dose oral steroids for a few weeks and quickly gained 20 lbs. My face was squishy and I was swollen everywhere and nothing fit anymore. At the same time, my disease was also accelerating. I still walked and tried to make time for yoga class but I was in a lot of pain and often too exhausted to work out. I gained more weight. And more.

By 2012, I weighed about 165 lbs. I started doing advanced yoga several times a week and was able to lose 10 lbs in about nine months. The following year, I had my colostomy placed and lost 10 more lbs. I was stably 145 lbs until the end of 2013 when I started high dose steroids again along with several other meds known to cause fluid retention and weight gain. I gained 30 lbs in six weeks and then gained a little more. My abdomen was so swollen that I looked nine months pregnant. I had to wear maternity clothes to accommodate my belly.

Decreasing steroids took off some weight but I was still much bigger than I wanted to be. In 2015, I had another GI surgery. I again lost 10 lbs almost immediately. Following the surgery, I was able to do a reconditioning program before I returned to work in order to build up my stamina and physical tolerance for exercise. I was less inflamed than before the surgery and reacting less. I was able to address several smaller concerns that had been on the back burner like vitamin D levels. Together, these changes allowed me to recondition effectively. I could exercise again, making it easier to manage my fitness. (For those interested, I describe my reconditioning program here.)

Over the next 18 months, I lost another 10 lbs. I found long, flat muscles in places I never expected to see. Even as I cursed my body for having this disease, I was happier with how it looked. I had to buy new clothes because even my smallest clothes, saved from previous years, were too big.

Last fall, I started dropping weight, much faster than I should have been. At the same time, I was having fevers, night sweats, and a slew of other symptoms I have written about. I countered the weight loss by eating more but I eventually developed gastroparesis and started throwing everything up. I am now getting some of my calories through 2L of IV fluids daily. I am now getting most of my calories from “nutritional drinks”. (My homemade version is Orgain chocolate protein powder, organic maple syrup, and almond milk.) I am tolerating it but I can’t drink it fast without getting nauseous. I’m not getting much fat in my diet and my body is now showing that.

I took a picture of myself tonight. For the first time, I was unsettled by how I looked. I am getting very thin. I am the smallest I have been as an adult. I can certainly lose more weight before I’m in danger but it was seriously jarring to see myself. I am leaving “you don’t look sick” territory.

So here I am at 3am thinking of ways to gain back weight that I spent years trying to lose. A different kind of adversary.

 

29 Jan 2017

29 Jan 2017 2

 

 

 

My exercise program for POTS and deconditioning

I designed the following schedule for myself after being medically cleared to return to exercise following surgery. This routine is not appropriate for everyone. Please speak with your medical provider regarding safe ways to exercise.

I put together this routine for myself by integrating POTS/dysautonomia exercise programs and my own personal exercise history. Even on my most miserable days, I walk for 20-30 minutes, so walking is something that I can trust to not raise my heart rate. I also have been practicing vinyasa style yoga for over fifteen years and started with very easy seated poses and progressed to more fluid sequences (Sun Salutation A 3-5x, Sun Salutation B 3x, followed by whatever sequences I felt were reasonable for that day.)

For the first few weeks, I timed my exercise for about an hour after taking antihistamines. For weeks 1-3, I performed all of my allotted exercise for the day consecutively over about an hour. For weeks 4-8, walking was often broken up over the course of the day as this included walking I did as part of my commute. My first walk of the day occurs within an hour of taking my morning medications and I take meds about an hour before leaving work for the day to cover my commute home.

Slow walking: about 2.5-3 miles/hour
Moderate walking: about 3-3.5 miles/hour

For seated cardio, I just looked around online for some seated cardio that I could do at home. I found a few routines.

For standing cardio, I did various things like jumping jacks and high knees. I usually incorporated bodyweight exercises that I could modify, like squats and planks.

Walking was all done outside. Some was done at night and some during the day. I tried to limit walking during the middle of the day to the extent that it was possible because heat and sunlight trigger me. All other exercises were done in my air conditioned apartment.

If I felt like I needed a break while exercising, I took a break. So ten minutes of cardio does not always represent ten consecutive minutes, but rather a total of ten minutes performing cardio exercise.

As I added in more exercise, I increased to exercising four days a week, which means that sometimes I exercise twice in one day. Walking is also split up over the course of the day, as I previously mentioned.

Week One:

Three days:
Twenty minutes of slow walking
Ten minutes seated cardio
Twenty minutes stretching/seated yoga
Ten minutes slow walking

Week Two:

Three days:
Thirty minutes of slow/moderate walking
Ten minutes seated cardio
Ten minutes yoga
Ten minutes stretching

Week Three:

Three days:
Forty minutes of moderate walking
Twenty minutes yoga
Ten minutes stretching

One day:
Sixty minutes of walking

Week Four:

Two days:
Fifty minutes of moderate walking
Twenty minutes of yoga

One day:
Fifty minutes of moderate walking

Week Five:

Two days:
Fifty minutes of moderate walking
Twenty minutes of yoga

One day:
Fifty minutes of moderate walking
Ten minutes of standing cardio

One day:
Sixty minutes of moderate walking

Week Six:

Two days:
Sixty minutes of moderate walking
Twenty minutes of yoga

Two days:
Fifty minutes of moderate walking
Ten minutes of standing cardio

Week Seven:

Two days:
Sixty minutes of moderate walking
Twenty minutes of yoga

Two days:
Fifty minutes of moderate walking
Fifteen minutes of standing cardio

Week Eight:

Two days:
Fifteen-twenty minutes of standing cardio
Twenty minutes of yoga

Three days:
Sixty minutes of moderate walking

 

Edited on 29 Jan 2017 to include weeks 9-12 of this program:

Week Nine:

Two days:
Twenty minutes of standing cardio
Thirty minutes of yoga (intermediate)

Three days:
Sixty minutes of moderate walking

Week Ten:

Three days:
Twenty minutes of standing cardio
Forty minutes of yoga (intermediate)

Three days:
Sixty minutes of moderate walking

Week Eleven:

Three days:
Fifty minutes of yoga (intermediate/advanced, pace moderate/fast)

Three days:
Sixty minutes of moderate walking

Week Twelve:

Three days:
Sixty minutes of yoga (intermediate/advanced, pace moderate/fast)

Three days:
Sixty minutes of moderate walking

Independence Day

I live my life as a series of wagers. A lot of these wagers involve my health. I bet that I can fly if I take enough steroids. I bet that I will get better if I get an ostomy. I bet that I will be more stable if I use IV hydration. I bet that taking this med or that will make me less tired. Sometimes I win. Sometimes I don’t.

The last 18 months of my life have all been one large scale bet. It has been many months of moving the pieces around and trying to shove them into place. It has been emotional and stressful and scary.

I slept through the four weeks following my surgery. I did some other things too, but mostly I slept. One day while I was resting in bed, it occurred to me that all of the strength and stamina I had lost was perhaps for the best. There are few opportunities to reset your body and this was one of them. I wasn’t reacting because I was heavily medicating and resting most of the time. I realized that this might be an opportunity to rebuild my body in a calculated way.

Once I was cleared by my surgeon to exercise, I started an exercise program designed for POTS patients. It was pretty detailed (I’ll do a separate post about this) but involved cardio exercise 3-4 days a week. I haven’t been able to do cardio in years. But I figured it was worth a shot.

The first two weeks were brutally hard. Then it got easier. I am now on the sixth week of a twelve week program. For the first time in many years, I can do cardio (with premedication in a controlled environment) without having a reaction.

I went back to work last week. I took the train to and from work on Monday, Wednesday and Thursday, which also involves about a mile and a half of walking each day. It was pouring torrentially on Wednesday and hot as hell on Thursday. I was exhausted when I got home but I managed to get through each day without napping. I slept every night last week. Getting myself to and from work is a level of independence I have not achieved in a year.

I very rarely drive anymore because I can’t use some of my medications if I need to drive and I have been so reactive that that might have been dangerous. But I made a huge wager on Saturday: I drove myself an hour away to New Hampshire to celebrate the Fourth of July with my friends and nieces. I stayed overnight and went swimming today, deaccessing and reaccessing my port. I drove myself home after being in cold water and direct sunlight for over an hour, stopping at Whole Foods and doing my grocery shopping on the way. I cleaned my apartment, did laundry, made lunch for tomorrow, ironed my work clothes, and watched Shark Week. I did all these things without any help.

The Fourth of July is Independence Day in the US. As I watched the fireworks, it felt like I was celebrating my own personal Day of Independence. I don’t know how long this will last.  But I got this one great week and this one Fourth of July.  And maybe I’ll get more.

Deconditioning, orthostatic intolerance, exercise and chronic illness – Part 7

A number of studies have investigated whether loading with intravenous hydration solutions (saline, etc) or with a volume expander such as dextran can ameliorate symptoms associated with deconditioning. These studies have found that volume expansion (also called fluid or volume loading) can improve a number of symptoms in deconditioned patients, but does not improve exercise capacity. Multiple studies have found the best effects from intravenous saline in conjunction with exercise.

Shibata investigated whether orthostatic intolerance could be mitigated following bed rest with exercise and/or fluid loading (Shibata 2010). This study found that OI could be dextran solution (IV fluids) given after twenty days of bed rest was insufficient to control OI symptoms, but that it was successful when used in conjunction with a daily exercise program. This finding was important, as it indicated that low blood volume was not the exclusive factor in orthostatic intolerance.

Figueroa et al looked at the relationship between blood volume and exercise capacity in POTS patients (Figueroa 2014). They found that acute volume loading with IV saline reduces heart rate and improves orthostatic tolerance and other symptoms in POTS patients. Importantly, IV saline significantly increased the stroke volume, cardiac output and reduced systemic vascular resistance. However, IV saline did not affect peak exercise capacity or improve cardiovascular markers during exercise. So while IV saline does help symptoms in these deconditioned patients, it does not improve exercise capacity. The author notes that for this purpose, acute infusion may not be sufficient and may need to undergone chronically to see benefits on exercise physiology.

Whole body heating is known to increase cardiac output, constrict the blood vessels in the abdominal cavities, increase sympathetic nerve activity in the muscles and decrease vascular resistance in the skin. Taken together, these factors stress the regulatory mechanism of the cardiovascular system. One study (Keller 2009) found that acute expansion of blood volume (with dextran) completely mitigated the impact of heat stress on orthostatic tolerance. In short, receiving an infusion that increased the blood volume allowed the cardiovascular system to function properly in the face of a known stressor.

One study looked at the effect of fluid loading on orthostatic intolerance and blood flow in the brain (Jeong 2012). They found that following bed rest, volume loading alone prevented larger reductions in cerebral blood flow, but did not prevent orthostatic intolerance. Exercise and volume loading prevented orthostatic intolerance but did not affect cerebral blood flow. Importantly, aerobic or resistance exercise before bed rest did not prevent development of decompensation.

A 2000 paper notes that POTS symptom scores improved significantly following administration of IV saline (Gordon 2000). Additionally, a 2013 study evaluated the frequency and characterization of “brain fog”, a common term for the cognitive deficits associated with this (and other) conditions (Joyner 2013). 86% (56/66) of patients reported that IV saline was the most effective treatment for brain fog.

In summary, bolus IV fluids or volume expanders have been found to improve a number of symptoms in deconditioned patients, although they have not been found to improve exercise capacity. For this metric, a graded exercise program is recommended. 

(Author’s note: I have recently been made aware that the data supporting use of graded exercise for chronic fatigue patients was hugely flawed. I retract this statement at this time. For details on this topic, please refer to this Lancet article: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60686-7/fulltext)

A 2008 paper compared POTS and deconditioning (Joyner 2008). The author pointed out that a number of parallels existed between the physiological changes seen in POTS patients and those seen in deconditioned patients. Additionally, he made note of the parallels between POTS, chronic fatigue syndrome and fibromyalgia and the fact that exercise training had seen benefits in all of them. Given the significant relationship between mast cell disease and POTS, and the large overlap in CFS, fibromyalgia and mast cell populations, it is a comfortable assumption that an effective treatment modality for CFS, POTS and fibromyalgia may also be effective for mast cell disease. It is my belief that this is the basis for the frequently discussed finding of mast cell patients that intravenous fluids ameliorate a number of symptoms.

Furthermore, there are special considerations for mast cell disease that make intravenous fluids likely to cause a positive change in symptom profile. The first is that mast cell degranulation can induce systemic effects on arterial tone, hypotension and vasodilation (Willingham 2009). The next is that hypotension is characteristic of systemic mastocytosis, and that hypotension and syncope may occur due to cerebral hypoperfusion (Ozdemir 2010). Lastly, it is well known that mast cell mediators, including histamine, serotonin and tryptase, can induce capillary leakage leading leading to edema, and that they can increase vascular permeability (He 1997). Taken together, these points indicate that a mast cell patient may lose volume from the bloodstream into the surrounding tissues, which can exacerbate an already existing tendency toward hypotension, in turn made worse by orthostatic intolerance.

Fluid loading in the form of intravenous fluids may decrease symptoms in mast cell patients due to deconditioning, orthostatic intolerance and the capillary leakage often seen as a result of mast cell disease, which is especially present following mast cell attacks and anaphylaxis.

 

References:

Gordon VM., et al. Hemodynamic and symptomatic effects of acute interventions on tilt in patients with postural tachycardia syndrome. Clin Auton Res. 2000 Feb; 10(1): 29-33.

Ross, Amanda J., et al. What is brain fog? An evaluation of the symptom in postural tachycardia syndrome. Clin Auton Res 2013 Dec; 23(6): 305-311.

Raj, Satish R., et al. Postural orthostatic tachycardia syndrome (POTS). Circulation 2013; 127: 2336-2342.

Rocío A. Figueroa, et al. Acute volume loading and exercise capacity in postural tachycardia syndrome. J Appl Physiol 117:663-668, 2014.

He, Shaoheng, Walls, Andrew F. Mast cell activation may be all that is sufficient and necessary for the rapid development of microvascular leakage and tissue edema. European Journal of Pharmacology 1997; 328(1): 89-97.

Ozdemir, D., et al. Hypotension, syncope and fever in systemic mastocytosis without skin infiltration and rapid response to corticosteroid and cyclosporine: a case report. Case Reports in Medicine, Volume 2010 (2010), Article ID 782595.

Willingham DL, et al. Unexplained and prolonged perioperative hypotension after orthotopic liver transplantation: undiagnosed systemic mastocytosis. Liver Transpl 2009 Jul; 15(7): 701-8.

Keller, David M., et al. Acute volume expansion preserves orthostatic tolerance during whole body heat stress in humans. J Physiol 2009 Mar; 587(5): 1131-1139.

Sung-Moon Jeong , Shigeki Shibata , Benjamin D. Levine , Rong Zhang. Exercise plus volume loading prevents orthostatic intolerance but not reduction in cerebral blood flow velocity after bed rest. American Journal of Physiology – Heart and Circulatory Physiology 2012 Vol. 302 no. 2.

Shizue Masuki , John H. Eisenach , William G. Schrage , Christopher P. Johnson , Niki M. Dietz , Brad W. Wilkins , Paola Sandroni , Phillip A. Low , Michael J. Joyner. Reduced stroke volume during exercise in postural tachycardia syndrome. Journal of Applied Physiology 2007 Vol. 103 no. 4, 1128-1135.

 

 

 

 

 

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 6

Exercise can be very effective in treating deconditioning due to orthostatic intolerance or other conditions. Exercise can exacerbate symptoms in deconditioned patients even when it is mild, and this effect will be more pronounced if exercising in hot weather or after eating. Recumbent exercise, rather upright, is ideal for deconditioned patients at the beginning of exercise regimens, as being upright more stress on the body.

There are some physical maneuvers that can be helpful in avoiding OI episodes or in managing them when they do occur.   A sustained hand grip will activate the sympathetic nervous system and raise blood pressure for a short time. This can be helpful when changing position or following triggering activities, such as eating a meal or exercising. Leg crossing while tensing muscles can also prevent blood from pooling in the leg veins. This is recommended when an OI episode first occurs, and for vasovagal syncope patients to prevent fainting.

One study regimen prescribed POTS patients to engage in recumbent exercise 2-4 times a week for 30-45 minute sessions. In this study, they attempted to keep heart rate at 75-85% of maximum heart rate. As patients continued and became more fit, upright exercise was added in slowly in the second or third week. The length of training sessions increased and sessions of maximum intensity was added gradually until there were two maximum sessions per week. Weight lifting started once a week as a 15-20 minute session and increased to twice weekly 30-40 minute sessions. At the end, patients were exercising 5-6 hours/week. The duration of this study was twelve weeks.

Of the 29 patients who completed this study, a number of cardiovascular markers were improved. Blood volume and plasma volume were both expanded. The peak oxygen uptake during exercise, usually low for POTS patients, was increased by 11%. The muscle in the left ventricle of the heart, often smaller than usual in POTS patients, increased by 8%. Both laying down and standing heart rates decreasing significantly. Quality of life improved significantly and at the conclusion, almost half of the patients who completed the training no longer met the criteria for POTS.

Another study had POTS patients begin exercising twice a week in recumbent exercise, such as rowing or swimming, for 30-45 minutes. They increased to four times per week. After three months, plasma and blood volumes were both increased, as well as total hemoglobin mass and red blood cell volume. Systolic and diastolic pressures were lower while standing. Standing heart rate was lower and the amount of blood pumped out of the heart was stable.

Multiple papers have noted that OI patients are motivated to exercise, but often exert themselves too much in the beginning and trigger symptoms that make it difficult to continue. Going slowly and building up your tolerance is critical here. It is the factor that will make this successful. As an example, when I was very POTSy last year after several days of bed rest, I was advised that I could only stand for 10 minutes a day for an entire week. I could increase by ten minutes every week until I got to sixty, at which point I could resume normal activity. It was incredibly frustrating and drove me crazy, but I was able to get my orthostatic symptoms under control. Gradually increasing activity for OI patients is tried and true.

For severely disabled patients, it may not be practical to begin with recumbent aerobic exercises. If this is the case, gentle stretching and very low impact moves are good to start.

Following this, short workouts preceded by 5-10 minutes of stretching can be added. Target heart rate of 75-80% has been cited as desirable in some publications. Of utmost importance is the use of recumbent exercises, like rowing, swimming or recumbent cycling. Start slow. Dysautonomia International has a great breakdown on their site for how long you should workout at this stage.

Following several weeks of success, normal weekends can be introduced. Some patients are able to recover significant capability, running marathons and so on. It is recommended that POTS patients who are significantly conditioned exercise for at least 45 minutes three times a week.

While OI is a prime example of deconditioning as so many of its patients are deconditioned (95% of POTS patients and 91% of OI patients in one study), it is not the only condition associated with deconditioning that can be significantly improved with exercise.

In various studies with chronic fatigue syndrome patients, 60-84% said they felt better or much better after a graded exercise program. A study with fibromyalgia implemented three times a week workouts of sixty minutes, which included 10 minutes of slow walking, 20 minutes of aerobic exercise at 60-70% max heart rate, 20 minutes stretching and strength training, and 10 minutes cooling down. This program was highly successful for a number of patients.

Given the variety of illnesses which produce secondary deconditioning, and the success achieved by their patient populations with graded exercise, it is reasonable to assume that graded exercise may provide conditioning benefits to the mast cell population. Mast cell patients have the addition concerns that mast cells can be mechanically degranulated by the motions associated with vigorous exercise and that heat and sweating may be triggering, so exercise should be undertaken carefully and never alone. Some patients find utility in premedicating with H1 and H2 antihistamines before exercising. Please consult with your healthcare provider prior to beginning an exercise regimen.

 

References:

De Lorenzo, H. Xiao, M. Mukherjee, J. Harcup, S. Suleiman, Z. Kadziola and V.V. Kakkar. Chronic fatigue syndrome: physical and cardiovascular deconditioning. Q J Med 1998; 91:475–481.

Hasser, E. M. And Moffitt, J. A. (2001), Regulation of Sympathetic Nervous System Function after Cardiovascular Deconditioning. Annals of the New York Academy of Sciences, 940: 454–468.

Mathias, C. J. et al. Postural tachycardia syndrome – current experience and concepts. Nat. Rev. Neurol. 8, 22–34 (2012).

Parsaik A., et al. Deconditioning in patients with orthostatic intolerance. Neurology 2012; 79; 1435.

Benarroch, Eduardo E. Postural tachycardia syndrome: a heterogeneous and multifactorial disorder. Mayo Clin Proc 2012 Dec; 87(12): 1214-1225.

Shizue Masuki , John H. Eisenach , William G. Schrage , Christopher P. Johnson , Niki M. Dietz , Brad W. Wilkins , Paola Sandroni , Phillip A. Low , Michael J. Joyner. Reduced stroke volume during exercise in postural tachycardia syndrome. Journal of Applied Physiology Published 1 October 2007 Vol. 103 no. 4, 1128-1135.

Sung-Moon Jeong , Gyu-Sam Hwang , Seon-Ok Kim , Benjamin D. Levine , Rong Zhang. Dynamic cerebral autoregulation after bed rest: effects of volume loading and exercise countermeasures. Journal of Applied Physiology 2014 Vol. 116 no. 1, 24-31.

 

 

 

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 5

Deconditioning and physical inactivity are risk factors for atherosclerosis and cardiovascular disease. The cardiovascular impact of deconditioning is very well characterized and has been described in my previous posts. However, there are also a number of other system deficits induced by deconditioning.

Musculoskeletal system has the most obvious decline in response to deconditioning. A person can lose 10-20% of muscle strength in one week or bed rest. Thigh muscles can lose 3% of mass within seven days. Muscle loss is greatest in the lower back and weight bearing muscles of the legs.

After three days of continuous bed rest, contractures can form. This is the result of connective tissue and muscles being kept in a shortened position. After three weeks of bed rest, the connective tissue around joints changes to stabilize the joint in a shortened position.

Osteoporosis can occur in deconditioned patients. This is called “disuse osteoporosis” as it occurs because the bones are not bearing weight. When the bones are not bearing weight, the pressure of the body and gravity is not applied to the bones. This causes the bone cells to be resorbed at an abnormal rate, with liberated calcium entering the blood stream. After twelve weeks of bed rest, bone density can be almost 50% less. This effect is most pronounced in the long bones. Cartilage degeneration and osteoarthritis can also occur, along with a variety of other bone specific complications.

Frequent episodes of bed rest can also increase the risk of blood clots forming. This in turn can cause pulmonary embolism, in which a blood clot blocks one of the arteries in the lungs.

Bed rest causes a number of pulmonary concerns as well. Over time, reduced muscle strength and endurance causes less movement of the diaphragm, intercostal and abdominal muscles. Mucous becomes trapped in the airways and impaired cilia are unable to move it out. This can cause a cough and eventually develop into pneumonia.

Deconditioned patients often experienced decreased appetite, lower gastric secretion, constipation, impaired absorption and atrophy of the mucosa and glands in the GI tract. Excretion of water and salt is increased. 15-30% patients on bedrest develop kidney stones and urinary tract infection is not uncommon. Deconditioned patients have less lean body mass and develop more fat. Nitrogen metabolism becomes disordered and minerals and electrolytes are excreted more quickly than appropriate.

Frequent bed rest can compress peripheral nerves, especially the perineal and ulnar nerves. Cognition is also affected. These patients find focusing difficult and judgment and problem solving impaired. Pain threshold becomes lowered, making pain worse. Anxiety, fear and depression are more commonly found in deconditioned patients than in the general population. Sensory processing is affected, increasing the auditory threshold so that sounds must be louder to be heard correctly.

Bed rest can also affect the patient’s circadian rhythm, temperature and sweating response and provoke glucose intolerance. A number of hormones, including thyroid, adrenal and pituitary hormones, undergo altered metabolism and regulation. After two weeks of bed rest, two weeks of resumed activity is needed before glucose behavior returns to base line.

 

References:

Bleeker, Michiel W.P., et al. Vascular adaptation to deconditioning and the effect of an exercise countermeasure: results of the Berlin Bed Rest study. Journal of Applied Physiology (2005); 99(4); 1293-1300.

Parsaik A., et al. Deconditioning in patients with orthostatic intolerance. Neurology 2012; 79; 1435.

Sung-Moon Jeong , Gyu-Sam Hwang , Seon-Ok Kim , Benjamin D. Levine , Rong Zhang. Dynamic cerebral autoregulation after bed rest: effects of volume loading and exercise countermeasures. Journal of Applied Physiology 2014 Vol. 116 no. 1, 24-31.

 

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 1

Deconditioning (also called cardiovascular deconditioning) is the acclimation of the body to a less strenuous environment and the decreased ability to function properly under normal conditions. This basically means that when you have less physical stress on the body for a certain period of time, like seen in bed rest, the body adapts to that level of functioning, so when you want to engage again in normal physical activities, it is difficult for your body. Deconditioning makes multiple systems of your body less functional.

Bed rest is the typical situation associated with deconditioning. Patients on bed rest lose muscle mass and strength rapidly.  1-3% of muscle strength is lost per day, with 10-20% decrease in a week’s time. If completely immobilized for 3-5 weeks, a patient can lose up to 50% of their strength. Loss of muscle mass is also a problem. Upper legs can lose 3% mass within a week of bed rest. The lower back and weight bearing muscles in the legs are most affected by loss of mass.

Within 24 hours of bed rest, your cardiovascular system is changing. In this time, your blood volume decreases 5%. In less than a week, 10% is lost; in two weeks, 20%. Resting heart rate also increases 4-15 bpm within the first month of bed rest. Laying down for so long means that blood that is normally in the lower part of your body is moved to the trunk. This causes excretion of water and salt, resulting in less plasma and blood volume.

In healthy controls, when you change position, your body rapidly moves fluid from one part of the body to others. This phenomenon is called fluid shifting. Normally, when moving from a laying position to standing, 500-700 ml of blood are moved from the trunk to the legs. This movement of fluid is called “functional hemorrhage”. Special nerve clusters called baroreceptors (which measure pressure in the blood vessels) tell the nervous system that there is less blood in the chest.   Your body then increases the heart rate, the force with which your heart beats, tightens up vessels so that they are less “leaky” and tells your body not to make urine temporarily. All of these functions allow your body to keep a normal blood pressure and adequate blood supply despite this large movement of fluid.

In healthy controls, when you lay down after standing, the reverse happens. 500-700 ml of fluid is rapidly transferred from the lower body to the trunk. This is called a “central shift”. This increase in fluid in the chest results in the veins returning more blood to the heart, increasing blood pressure. When the baroreceptors feel more pressure than usual from this added fluid, the heart rate and force with which the heart beats decrease, the vessels are relaxed so that fluids can move out of them more freely and your body begins to make urine again.

When you are deconditioned, your body does not make these changes correctly when you change position. The hallmark of deconditioning is reduced orthostatic tolerance. This means that when you change position, your body does not compensate correctly to maintain necessary blood pressure and adequate blood supply to the brain. Deconditioned patients often do not have sufficient blood volume to maintain blood pressure when standing. When they stand, their heart pumps out less blood than normal, so the heart starts beating faster to compensate. When it beats too fast, it is called tachycardia.

In addition to inability to maintain blood pressure correctly when changing positions, deconditioned patients also exhibit decreased blood volume pumped out by the heart, atrophy of heart muscle and decreased maximum oxygen consumption. These patients often have other forms of vascular dysfunction, diminished neurologic reflexes and reduced ability to exercise. A number of other systems are affected by deconditioning.

Though prolonged bed rest is the model with which deconditioning is most often associated, there is significant evidence that chronically ill patients may often be deconditioned, including those with chronic lower back pain, chronic fatigue syndrome, and rheumatoid arthritis.

References:

Munsterman et al. Are persons with rheumatoid arthritis deconditioned? A review of physical activity and aerobic capacity. BMC Musculoskeletal Disorders 2012, 13:202

Eric J. Bousema, Jeanine A. Verbunt, Henk A.M. Seelen, Johan W.S. Vlaeyen, J. Andre Knottnerus. Disuse and physical deconditioning in the first year after the onset of back pain. Pain 130 (2007) 279–286.

De Lorenzo, H. Xiao, M. Mukherjee, J. Harcup, S. Suleiman, Z. Kadziola and V.V. Kakkar. Chronic fatigue syndrome: physical and cardiovascular deconditioning. Q J Med 1998; 91:475–481.

Hasser, E. M. And Moffitt, J. A. (2001), Regulation of Sympathetic Nervous System Function after Cardiovascular Deconditioning. Annals of the New York Academy of Sciences, 940: 454–468.