He came up with it after years of studying steroid users in Boston-area gyms and comparing them not just to non-steroid users in the same gyms, but also to bodybuilders from different eras. For a 1995 study, Pope and his coauthors estimated the FFMIs of Mr. America winners from 1939 to 1959, before steroids were readily available. The group includes future B-movie star Steve Reeves, whose physique was so iconic that he was name-checked in The Rocky Horror Picture Show . The average FFMI was . (One of the highest was George Eiferman, Mr. America 1948, with a FFMI. His upper body was later the model for George of the Jungle, a 1960s cartoon character.) Even today, with all we’ve learned about training and nutrition, an FFMI in the mid 20s is still considered the ceiling for natural bodybuilders. Anything above 26 or 27 is suspect.
Myopathy due to steroids can be acute or chronic  and in some instances may involve the respiratory muscles . The chronic form occurs after prolonged use with a more insidious onset whereas the acute presentation, if present, may be associated with rhabdomyolysis and abrupt onset . Myopathy secondary to steroid may predispose patients to osteoporosis and sedentary life style which exposes to risks of contractures, deep venous thrombosis (DVT) and pressure sores. Stopping the administration of steroids results in insidious response; however, complete recovery may take weeks to months . The laboratory findings are generally non specific [11, 12]. Creatinine kinase (CK) and lactate dehydrogenase (LDH) levels may be within normal limits; however, before development of myopathy the urinary creatinine excretion may specifically rise . Acute myopathy shows increased CK levels with myoglobinuria which is absent in cases of chronic use of steroids . EMG and NCS remains normal in chronic phases but some case reports of acute onset have indicated abnormal spontaneous activity (positive sharp waves and fibrillation potentials) . There is no definite treatment for reversing steroid-induced myopathy; however, stopping the administration of steroids or, in cases where it is essential to be given, administer low doses on alternate days or offering non-fluorinated forms may minimize the risk with improvement in weeks to months. Our patient sufficently showed improvement on withdrawal of steroids and had been ambulatory in the ward three to four weeks after appropriate dose reduction.
During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.