Are Asthma Inhalers Ergogenic Aids? By Jerry Brainum 9/25

 

When I was 12 years old, just as my nascent bodybuilding activity began, I was diagnosed with asthma. Before that, I had hay fever as a child. I recall visiting a doctor's office, with the physician confirming that I had asthma and warning me that I would need to curtail my physical activity to prevent undue strain on my heart. He then prescribed the primary oral medication to treat asthma back then, a drug called theophylline, which is found naturally in coffee. Along with the theophylline, he prescribed an asthma inhaler drug used at the start of an asthmatic episode. Such inhalers were called "rescue inhalers" because they helped to curb an existing asthmatic episode. The drugs to treat asthma in those days were crude and tended to overstimulate the heart. The reason for that was that the drugs work by interacting with adrenergic receptors in the lungs. By activating beta-2 adrenergic receptors in the lungs, the drugs, especially the inhaled ones, caused dilation of the bronchial tubes, which had become constricted due to asthma, thereby limiting breathing. 

The main problem with those early asthma drugs was that they weren't specific for beta-2 adrenergic receptors in the lungs but also overlapped with beta-1 receptors in the heart. The stimulation of beta-1 receptors in the heart caused it to beat faster and harder, a sensation I often experienced when using the inhaler. Theophylline, the leading oral drug, also tended to stimulate the heart. Back then, asthma was considered an allergic disease, where the lungs were exposed to specific allergens or proteins, and they would react by immediately constricting the bronchial tubes, which was the cause of asthma. The problems with the standard asthma therapy were not only the overlapping heart stimulation but also that they weren't that effective in either preventing or stopping an asthma incident or "attack." I was susceptible to cat exposure. When I was near a cat, I soon developed an asthma attack within about 20 minutes. Many of those attacks were so bad that I was gasping for breath and had to get to an emergency room for immediate treatment. In the ER, I was given an injection of epinephrine that caused a rapid dilation of my bronchial tubes, thus relieving the asthma. In some instances, the asthma attack was so intense that it required hospitalization for a few days. 

With further research over the years, it became apparent that asthma, while having some allergenic components, was essentially an inflammatory disease. The constriction of breathing, a cornerstone of asthma, was primarily caused by excess lung inflammation. Inflammation may have originated from a localized allergic reaction in the lungs. However, the knowledge that asthma was more . . .