Our previous post deals
specifically with asthma. Please read
previous post. Let’s see what
hypothyroidism treatment can do for us.
Remember, Galen Rupp has been treated for asthma and hypothyroidism:
Last week, the Wall Street
Journal profiled Jeffrey Brown, an endocrinologist to star
athletes and a medical consultant for Nike. His roster of patients includes
nine-time Olympic gold medalist Carl Lewis, and athletes treated by Brown have
won 15 Olympic gold medals combined, according to the doctor.
We can believe that confined variables exist to the fact that gold medalists taking thyroid hormone won
gold; they are more focus, they take care of details, etc. but we still have other problems.
Thyroid hormone is known to affect sex
hormone-binding hormonal globulin (SHBG) concentrations. Men with hyperthyroidism have
elevated concentrations of testosterone and SHBG. Thyroid hormone therapy in
normal men may also duplicate this elevation.
This knowledge about thyroid
hormone elevating the concentration of testosterone is well known by
endocrinologists, even Floyd Landis knew about it:
In 2006, bicycle racer Floyd Landis blamed his
hypothyroid medication for the illegally high testosterone levels detected in urine
samples taken during his Tour de France ride, according to the New York Times. An overactive
thyroid gland does seem to coincide with higher levels of testosterone, so it seems
feasible that an increase in thyroid hormones from medication could cause a
similar reaction. Race officials, however, were not swayed, and Landis was
stripped of the yellow jersey that summer.
We have a history of using performance
enhancing methods for years, at one point valid methods; Lasse Viren injecting
his own blood for example. Emma Snowsill running with a Ventolin puffer. If we want a clean sport, TUEs should be
transparent. Who has one and how he/she
is monitored by WADA should be available to the public.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2658979/
Our results add to the growing body of evidence that salbutamol mediates anabolic effects, and we report a mechanism by which salbutamol might promote such effects. Salbutamol has a short plasma half‐life (3–6 h).4 Following a recommended dose of inhaled salbutamol, the compound is only transiently detectable in the plasma,4 and salbutamol reaches levels up to 2.5 ng/ml or 1.04×10−8 M.27 These levels are considerably lower than effective concentrations in our in vitro experiments, which were above 10−6 M with an (IC50 value of 8.93×10−6 M). Whereas anabolic properties have been demonstrated in several species after systemic use of some beta‐2 agonists,11,20,21 salbutamol possess anabolic activity only after intravenous administration,22 and no potent anabolic effects have been reported after oral administration in animals.11,21 In addition, in humans, oral administration of therapeutic levels of salbutamol increases maximal anaerobic power,24,25,26 irrespective of the subjects' training status, without changing the body composition.25,26 Similar improvements in performance have been shown in two other studies, using a comparable daily salbutamol dose.9,23 Of note, there is no evidence that inhaled beta‐2 agonists have ergogenic effects at therapeutic doses.28 Although it is too early to draw final conclusions, based on these studies we hypothesise that the agonistic activity we observed at the androgen receptor might play also a role after intravenous administration of salbutamol.
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