Exercise: Use it and Lose it

by Dr. Richard L. Bruno
 I read that you don't recommend exercise for polio survivors who are getting weaker.  But if I stop exercising and do nothing, won't I lose muscle tone, get flabby and become deconditioned and become weaker still?

You're asking a good question but are using buzzwords that Americans hear on infomercials.  It's vital that polio survivors understand what the research really says about exercise for newly weakened muscles and know the definitions of "muscle tone" and "deconditioned."

We never tell polio survivors to "do nothing."  Both The Post-Polio Institute and Warm Springs long-term follow-up studies find the same thing.  All PPS symptoms, fatigue, pain and muscle weakness, decrease when polio survivors stop exercising and follow The Golden Rule: If anything causes fatigue, weakness or pain, DON'T DO IT! (Or do much less of it.) 

Unfortunately, those who recommend strengthening exercise to polio survivors quote from the conclusions of a half-dozen small studies of leg muscle strengthening, apparently without having read them critically. The studies' conclusions say that exercise programs "lead to significant gains in strength."  However, when you look at the responses of individual subjects the "significant gains in strength" are hard to find.  Just over half of the studies’ subjects had an increase in upper leg muscle strength of about 26%. One quarter had no change in strength while 21% actually had a decrease in strength of about 10%.  So almost as often as not exercise either had no effect or actually decreased muscle strength. 

What's more, only two studies asked whether exercise affected polio survivors' fatigue and their ability to function in their daily lives.  In one study, strength increased by 36% but muscle fatigue also increased by 21%.  In the other study, although muscle strength increased by 30%, there was no improvement in polio survivors' ability to do daily activities, and muscle fatigue increased as much as 300%!  You have to ask what good comes from any small percentage increase in muscle strength that is not related to improved functional ability and that actually increases muscle fatigue more than strength. 

And what of "muscle "tone"? Most people think that muscle tone means muscles that are firm and have a nice shape.   Muscle tone actually means that muscle fibers are ready to contract. Muscle tone is lost when motor neurons are damaged and can't turn on muscle fibers.  Loss of tone can happen when polio survivors exercise too much and muscles become weaker when poliovirus-damaged motor neurons fail.  Remember, PPS researcher Alan McComas found that polio survivors who have muscle weakness lose at least 7% of their motor neurons each year (see PPS Forum June 2001). This is why he concluded that "polio survivors should not engage in fatiguing exercise or activities that further stress metabolically damaged neurons that are already overworking."   

Polio survivors' muscles get smaller lose tone if they're overused and the motor neurons that turn on the muscle fibers die.  Arms and legs get flabby because of increased fat deposits, not a loss of muscle tone. Exercise does burn fat and at first causes muscles to increase in size. But polio survivors don't want bigger muscle fibers because they "further stress metabolically damaged neurons that are already overworking." The best way to prevent flabby arms and legs is to stop overusing and abusing your motor neurons and to follow the higher protein, low fat and lower carb Post-Polio Diet (see PPS Forum July, 2002).

And what does "deconditioned" mean?  Many polio survivors believe that there are only two ways to live: overusing and abusing or being a couch potato and becoming "deconditioned." Deconditioning is something that happens when astronauts live in space or you put someone to bed for weeks, removing the pull of gravity and causing a decrease in blood volume and blood pressure.  Deconditioning can only happen if polio survivors never leave the couch, not if they take two daily rest breaks on the couch, take a ninety minute nap, stop strengthening exercising or use a power wheelchair. 

However, polio survivors may need to "condition" their hearts, especially if they have had a heart attack.  Cardiopulmonary conditioning" uses exercise to strengthen the heart muscle (which was not affected by polio) and make it work more efficiently.  However, there is no benefit to running on a treadmill or riding a bicycle to exercise the heart if you thereby stress and kill off poliovirus-damaged motor neurons. Many polio survivors can do heart conditioning by using their less affected limbs, usually their arms, in a carefully monitored program of paced and non-fatiguing exercise (see PPS Forum May 2001).

Dr. Richard Bruno is Chairperson of the International Post-Polio Task Force and Director of The Post-Polio Institute and International Centre for Post-Polio Education and Research at Englewood (NJ) Hospital and Medical Center. His book, THE POLIO PARADOX: UNCOVERING THE HIDDEN HISTORY OF POLIO TO UNDERSTAND TREAT "POST-POLIO SYNDROME" AND CHRONIC FATIGUE, is published by Warner Books. (AOL Keyword POLIO PARADOX.) E-mail questions to him at PostPolioInfo@aol.com. 

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Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno




A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

Figure 1

The patient's legs, showing massive enlargement of the right calf and wasting on the left


What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?



An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.


A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3


Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

Figure 2

Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition


The differential diagnosis of the progressive calf hypertrophy is given in the box.

Causes of calf muscle hypertrophy

Chronic partial denervation

  • radiculopathy

  • peripheral neuropathy

  • hereditary motor and sensory neuropathy

  • spinal muscular atrophy

  • following paralytic poliomyelitis

    Neuromyotonia and myokymia

  • Isaac's syndrome

  • generalised myokymia

  • neurotonia

  • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

    Muscular dystrophies



  • tumours

  • amyloidosis

  • cysticercosis

    Link here