Endurance Training and Thyroid Function

Sweat Science take on a new study, and the short take is worth a read.

http://www.runnersworld.com/health/endu ... d-function


Key finding that in Amateur (female) masters's athletes there was no significant impact of just about any reasonable training parameter to hypothroidism. 12.2% of the runners were taking medication for the problem.

The only statistically significant differences were that the hypothyroid group was marginally older on average (47.1 vs. 45.3), and they were more likely to report having started running before the age of 10 (4.7 percent vs. 1.5 percent).

However, the standard cautionary note at the end:
Whether the same applies to athletes training at Olympic-finalist level is another question – one that we'll need data, not just anecdotes, to answer.



The one glaring flaw Alex didn't address is the population issue

12.2% taking medication is by far and away higher than is typical for a population.
That is in and of itself worthy of further examination.
 
Sep 29, 2012
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Not your fault at all. They broke link functionality - I posted a msg to the devs in the appropriate forum.
 
Mar 13, 2009
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Catwhoorg said:
Sweat Science take on a new study, and the short take is worth a read.

http://www.runnersworld.com/health/endu ... d-function


Key finding that in Amateur (female) masters's athletes there was no significant impact of just about any reasonable training parameter to hypothroidism. 12.2% of the runners were taking medication for the problem.

The only statistically significant differences were that the hypothyroid group was marginally older on average (47.1 vs. 45.3), and they were more likely to report having started running before the age of 10 (4.7 percent vs. 1.5 percent).

However, the standard cautionary note at the end:
Whether the same applies to athletes training at Olympic-finalist level is another question – one that we'll need data, not just anecdotes, to answer.



The one glaring flaw Alex didn't address is the population issue

12.2% taking medication is by far and away higher than is typical for a population.
That is in and of itself worthy of further examination.
Ask Digger, but 99% sure Landis had this
but the anecdotally-reported high incidence of thyroid problems in elite runners raises the question of whether extreme levels of training might affect thyroid function.
 
Sep 29, 2012
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Hypothesis:

I think there's a natural attenuation that your body will go through when placing stress on it through training and racing. Your body will reach a certain point and then start shutting down - this is in line with the central governor theory.

As a simplified example, when you do weight training, your muscles get bigger, but when you have natural muscle development, your tendons and ligaments also increase in strength, typically matching the increase in muscular strength.

Sure, you can still injure yourself in both scenarios, but when you add steroids and their increased effect on muscle development, and EPO / testosterone / cortisone, etc for endurance aerobic athletes, where you push your body beyond what it would naturally be capable, you reach the following scenario far more rapidly:

* strength trainers: ligament and tendon damage
* endurance aerobic athletes: hormonal imbalances and breakdown

Situations of prolonged stress such as those faced by endurance athletes force the adrenal glands to work overtime to meet the metabolic demands.
IMO: even more so when said athletes are pushing their bodies beyond natural capacity thanks to artificial assistance.

But if we look at the thyroid function:
The thyroid hormones, in particular tri-iodothyronine (T3), facilitate the input of nutrients into the cells and increase the production of energy within mitochondria, allowing to body to meet energy demands.
it becomes immediately apparent to me why you would take thyroid boosting drugs, and just as body builders lose their nuts when taking testosterone, no doubt your body seeks equilibrium on thyrod supplementation and shuts the thyroid down. Go off those meds and yeah tough luck buddy.
 
Mar 13, 2009
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Wiggo, you know that the white tissue, bones/ligaments/tendons, do not increase in strength IN PROPORTION to the red tissue.

the white tissue scaffolding can now not manage this new demand
 
May 19, 2010
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blackcat said:
Catwhoorg said:
Sweat Science take on a new study, and the short take is worth a read.

http://www.runnersworld.com/health/endu ... d-function

Key finding that in Amateur (female) masters's athletes there was no significant impact of just about any reasonable training parameter to hypothroidism. 12.2% of the runners were taking medication for the problem.

The only statistically significant differences were that the hypothyroid group was marginally older on average (47.1 vs. 45.3), and they were more likely to report having started running before the age of 10 (4.7 percent vs. 1.5 percent).

However, the standard cautionary note at the end:
Whether the same applies to athletes training at Olympic-finalist level is another question – one that we'll need data, not just anecdotes, to answer.

The one glaring flaw Alex didn't address is the population issue

12.2% taking medication is by far and away higher than is typical for a population.
That is in and of itself worthy of further examination.
Ask Digger, but 99% sure Landis had this
but the anecdotally-reported high incidence of thyroid problems in elite runners raises the question of whether extreme levels of training might affect thyroid function.
Landis took medication for a thyroid problem. They tried using it as explanation for the T/E reading, the thyroid medication had somehow messed with his testosterone level. Takeing testosterone and HGH is known to mess up the thyroid, it could be the reason he needed thyroid medication in the first place.
http://www.scienceofrunning.com/2013/04/thyroid-madness-everything-you-need-to.html
 
Apr 20, 2012
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Re:

blackcat said:
Wiggo, you know that the white tissue, bones/ligaments/tendons, do not increase in strength IN PROPORTION to the red tissue.

the white tissue scaffolding can now not manage this new demand
Growing pains equals doping pains.
 
Re:

Taking thyroid medication causes your normal level to suppress to a new equilibrium level. Taking more, and you can finally find a point where your TSH is zero, that is the amount of thyroid hormone which will suppress your natural level and cease production entirely. Hence, you take an amount of thyroid hormone to lower the TSH to the level where you feel the best and don't have symptoms of hypothyroidism.

Thyroid hormone is one hormone, unlike testosterone, where you can stop it, and your levels will always return to your natural level. There is not shutdown like steroids often cause in the feedback loop.

Bodybuilders take T3 to burn/cut fat. I would assume these athletes are taking these meds for a variety of reasons, 1) to burn fat, 2) they are likely to seek medical/aging doctors who are likely to treat them for thyroid disorders, perceived or real, to find a youthful level of thyroid/hormone...nature of athletes often.

And lastly, if they think there is some perceived competitive advantage, they will do it.

The general population is though to have a higher level of thyroid disorder than what your average jackass idiot doctor things, having a TSHh of 4.5 out of 5 on a scale, and they think you fall within the range of normal, although you are hypothyroid. It is though an ideal level is really between 1.0-2 on the scale of 0-5 TSH.

Not to mention, FT3/FT4, Reverse T3 etc...these all play an important part...just having thyroid meds in your body if you can't convert it to T3, the usable form of thyroid, doesn't mean much taking it.

excuse typos, on cell phone at airport
 
Some good info here: http://www.scienceofrunning.com/2013/04 ... ed-to.html

The author writes with a bias that can't understand the disregard dopers have for their body's natural function and feeling. And, he doesn't grasp the possibility of unethical doctors. But here are the good starting points

Genuine Hypothyroidism:
Hypothyroid is the condition. It is not the disease.

That’s a major distinction that should be noted.

The large majority of hypothyroidism occurs because of an autoimmune disorder (Hashimoto’s) which essentially means that your body is attacking itself. SO, your antibodies essentially attack the thyroid and if nothing is done, the thyroid is eventually “destroyed.” This would be called primary hypothyroidism because there is something wrong with the thyroid itself. Other forms include secondary hypothyroidism and tertiary hypothyroidism. Secondary refers to when the Pituitary gland is messed up and doesn’t create enough TSH (Thyroid Stimulating Hormone), and tertiary is when the hypothalamus doesn’t release enough Thyrotopin-releasing hormone (TRH) which doesn’t stimulate the pituitary to produce TSH, and so on.

That’s hypothyroidism in a nutshell. The symptoms of it are unpleasant. You can look those up yourself, but just so people understand, it goes beyond the idea of just “fatigue”. For example, hair loss, impaired cognition, inability to focus, inability to tolerate cold, depression, and on and on. In fact, occasionally, clinical depression is found to be due to a thyroid problem and not the traditional route. Bottom line, is it kind of sucks. And it’s an every day suck. If you have overt hypothyroidism you lose ability to go through your normal everyday life, so in those cases it’s medically necessary.
Clinical diagnostics of hypothyroidism:
When it was first introduced, Normal range was about .5 to 5.0, with treatment not starting until you were over 10.0. So if you were in that middle ground of 5-10, you may or may not get treatment depending on other signs.

2. The standard for almost all labs then shifted to the .5-5.0 as the one true range for normal.
3. In 2002, it all changed.
a. The American Association of Clinical Endocrinologist changed their reference range to .3-3.0 (Baskin et al. 2002)
b. In 2003, The National Academy of Clinical Biochemistry- changed their suggested range to .5 to 2.5. (Balloch et al. 2003)
c. (http://www.worldhealth.net/pdf/WhitePap ... ns-HRT.pdf) “In2003, the consensus panel (Endocrine Society, American Association of Clinical ndocrinologists, and American Thyroid Association) recommended a target TSH range of 1.0 to 1.5 mI U per liter in patients already receiving thyroxine”
d. In 2007, Endocrine Society changed their recommendations for labs
e. In 2010, more research came out that suggested individual assessment of TSH values based on age, sex, and race…
f. Lastly, just go do an internet search for different labs reference ranges. Go to the Mayo Clinic site and you get .05-5.0. Go to UNC health care and you get .6-3.3. And those are just the first two that popped up…. (http://labs.unchealthcare.org/labstesti ... ts/tsh.htm)

Hopefully you see that the consensus is all over the place. The point isn’t to call into question the TSH value, but instead to show that defining what is clinical and what is not is hard based off only TSH.
Training induced changes?
Can you fool the test? Can someone simply overtrain and make it appear like there is a thyroid problem?

The answer is maybe and no.

Maybe, if a doctor doesn’t actually diagnose you and instead relies solely on a TSH number.
If a doctor does that then manipulations of training, stress, taking certain medications, etc. can all alter TSH.
If the doctor is competent at all and goes through a full diagnosis, it’s much harder to create a “false” hypothyroid. The problem though goes back to what is hypothyroid, since endocrinologists can’t quite define it.

Focusing first on TSH, if we look at the research TSH changes acutely immediately after hard workouts. So if you went and did a hard workout then an hour later went and got your blood drawn, you’d see changes in TSH levels most likely. It’s not surprising. You just stressed your body and it needs time to come down to normal. A relatively short time after the workout a normal persons TSH levels are normalized. Even with a very hard workout, the swing isn’t terribly large.

In a study by Schmid et al. (1982 TSH, T3, rT3, and fT4 in maximal and submaximal physical exercise) they found that after maximal exercise in runners, TSH actually dropped before starting to return to normal. During submaximal, there was a gradual increase from 1.35 to around 1.5 at the end of exercise. So a subtle shift. Similarly, a 1971 study by Terjung found no changes in TSh, 30min, 3hrs, and 24hrs after 30min at 61%VO2max. Similarly (Dessypris et al. 1980) found no change in TSH after a marathon. A more recent(Ciloglu et al. 2005) study found that during exercise TSH levels changed from 1.69 at 45%, 1.78 at 70%, and 1.89 at 90% HR max. So again, exercise changes things acutely, but not a ton.
On the other hand, certain types of exercise has actually been shown to decrease TSH temporarily!
Given that, I would recommend getting blood work on an easy day, not following a hard workout.

What about over the long haul? It’s hard to study over months and months, but here’s the best the research gives us.

1. One study tracked TSH changes in 16 professional cyclists during the Vuelta a Espana in 1998 (which maybe means these dudes were on EPO?...) Anyways. Over the 3 week T4, free T3, and free T4 changed, which is what you’d expect, but there was no change in either TSH or free T3. Hoyos et al. (2001) http://www.karger.com/Article/FullText/48112

2. Barron et al. 1995 – Took 6 marathon runners and followed them for 4 months until 2 showed signs of overtraining which was defined as having all physical symptoms (heavy legs, fatigue, etc.), mental symptoms (apathy), and decrease in performance that lasted at least 3 weeks. In these athletes, no change in TSH occurred. (Hypothalamic dysfunction in overtrained athletes)

3. Lehman et al.1999, 1993 performed a series of studies where they tried to over train 8 runners. They took one group and increased their volume for 5 weeks, and another and increased their intensity for 4 weeks. In the volume study they went from their normal average of 86km/wk to 177km/wk. In the intensity study, they increased interval volume from 9km/wk to 23km/wk. What they found was no change in TSH whatsoever.

4. In recreational athletes, they took them and had them do 4 “units” per week of high intensity endurance running (90% of threshold) and 2 units of interval workouts (3-5x3-5min segments at 110% of 4mmol level) on a bike for 6 weeks. They then checked hormone levels and found that there were no significant changes in TSH, among other hormones (Gastmann et al. 1993)

Does this mean TSH does not change over the long term or due to overtraining? No, but it does mean that it’s more difficult than just go train hard and have your TSH change.

The reason I mention this is because there’s this concept that if you just go train hard you can make your thyroid appear hypothyroid. We will touch on this a bit more later.

But, with TSH levels, there is a big distinction to make. If you killed yourself in training and did manage to elevate TSH, with time off it would normalize if you have no problem. If you have a legit hypothyroid issue, if you took 3 months off, your TSH would still be elevated. If you have a legit problem, no amount of rest/time off will normalize things.

But for sake of thoroughness, a ton of things can alter TSH. Just perusing through the research, here’s a few:

Can potentially depress TSH:
Birth control, glucocorticoids, aspirin, anti-depressants, depression itself, pregnancy, aging, fasting, exercise

Can potentially increase TSH:
Stress, emotional arousal, cold exposure, sleep deprivation, severe illness, iodine, lithium, and high high doses of anti-histamines.
So, a thorough analysis will be able to see past overtraining, but we also know that team doctors may already have their diagnosis before the patient walks into the room.

What happens if you take too much thyroid medication?

Well if you actually have a thyroid disease, you feel horrible.

You actually take your body from a normal state, to a hyperthyroid state. What does hyperthyroid entail?
It’s basically like you are hopped up on adrenaline or caffeine all the time. Which may sound like performance enhancing, but it’s not. It’s to the extreme, not a short jolt of energy, but instead like you are the verge of a breakdown. You have crazy anxiety, inability to sleep, weight loss, increased appetite, nervousness, heart racing, your hands shake, your muscles are weak, and you generally feel like crap. And for those who know anything about overtraining, you overstimulate your sympathetic nervous system. For those who don’t know about overtraining, overstimulating your NS is one of the ways in which people theorize overtraining occurs.

So, it’s a generally unpleasant state. Thyroid is an interesting conundrum in that if you have too much or too little you get many of the same symptoms.

...

But for sake of due diligence, what if someone with a normal functioning thyroid took just a bit of synthetic thyroid and became slightly hyperthyroid. Would it help?

We can sort of investigate this by looking at subclinical hyperthyroid patients. This gives us the ability to look at patients who aren’t quite full blown hyperthyroid. It’s not a perfect comparison but it’s the best you’ll get:

1. In this study, they looked at the cardiovascular effects of subclinical hyperthyroidism. They found that it caused abnormally high resting HR (82 bpm) and increased systolic contractility and decreased diastolic relaxation. http://www.thyroid.org/wp-content/uploa ... pdf#page=5

2. In this one, they looked at patients who were Hypothyroid and took just a bit too much synthetic thyroid, so that they were now slightly hyper (so it’s the perfect model for our question). What were the results? There was a 9 percent reduction in bone density.http://www.sciencedirect.com/science/ar ... 4387902191

3. This one looked at muscle performance in subclinical hyperthyroidism. What they found was that muscle strength and muscle size were reduced in subclinical hypothyroidism, and if they were put back in a normal state, it improved back to normal. http://online.liebertpub.com/doi/abs/10 ... 006.16.375

Is that a definitive analysis? Nope. The exact studies haven’t been done. But it does give a good idea of what happens when you go slightly over.
Up until now, I’ve gone over the traditional route to thyroid disease. Now I want to delve into the 'what if' scenario. What happens if you take thyroid and you don’t need it and how could athletes potentially abuse it?

But I heard bodybuilders use it, so it must enhance performance!?

In the bodybuilding world they apparently use thyroid to cut weight because of the effects it has on metabolism.(How’d I learn bodybuilders use it…google) They essentially put themselves in a hyper state for a short time to cut fat. I have no idea why/how, but again this seems like a horrible idea. First off a runner would be sacrificing recovery (you recover worse in hyper state), and most runners are lean enough.

But the REAL reason bodybuilders and people use it is simple. It’s NOT to enhance performance.

It’s because taking Testosterone and/or HGH severely impacts the thyroid, making you temporarily hypothyroid.

You can see that in the two studies below.
http://ajs.sagepub.com/content/15/4/357.short
http://psy2.ucsd.edu/~mgorman/Daly.pdf

Both studies found that with taking either testosterone or HGH, your TSH levels were elevated. So in order to keep order in their hormonal systems they took thyroid. In fact, look towards Major League Baseball and you can find an incidence of this in 2010.

http://www.nydailynews.com/sports/baseb ... e-1.174940

(Also, note in that article that in 2010 WADA already looked into thyroid as performance enhancers. It’s 2013. It’s safe to say at that time they found just what they said in the WSJ article.)

So, that’s the reason your local steroid junky football player might take thyroid…because testosterone or HGH made him hypothyroid.

Interestingly, if you followed the Floyd Landis case, you know he was taking synthetic thyroid. I don’t know the details, but it makes sense because he was also on a drug program that included EPO, testosterone, and who knows what. My bet is his drug taking knocked him into hypothyroid status.

On to the next claims.


Red Blood Cell production

This is the one everyone is talking about. There are several studies out there that show a link between Thyroid and EPO. It’s easy to get distracted and start yelling blasphemy because anytime the word EPO is involved, the first thing that comes to mind is drugs! Let’s take a look:

First study:Thyroid hormone induces erythropoietin gene expression through augmented accumulation of hypoxia-inducible factor-1]

We’ll use this study as a starting point to the discussion.

First, in simple terms, EPO production essentially occurs when oxygen levels within the cell get low. The main regulator to this process is HIF-1a. If you want the full details of how this works go read my literature review from grad school as there is a section on how this works. But all you really need to know is: Low O2 triggers HIF-1a which eventually results in EPO production IF HIF-1a is activated long enough.
So this study took cell cultures, put them in hypoxic or normoxic conditions for ~4hrs, and soaked them in either T3 or T4 for the whole time. The amount of Thyroid hormone used is also significant because I have no clue what that translates over to in terms of clinical amounts.

What’s interesting is that if you look at the study T3 + hypoxia caused an increase in EPO production in the cell. T3+normoxia caused a slight bump.. And T4+ either normoxia/hypoxia didn’t cause a bump. Just as an overview, T4 is what is prescribed to almost all hypothyroid patients. Very few people use direct T3.

The issue at hand is whether this translates from a cultured cell or isolated tissue to the whole body?
It shouldn’t be surprising that putting T3 into a cell causes EPO increase. Partly because T3 is a metabolic regulator, so it acts as a stimulant to increase Oxygen demand. In a single tissue, if O2 demand is stressed, then EPO production increases. The 2nd part of the equation though is that Thyroid hormones may increase HIF-1 synthesis. That’s the issue that needs to be looked at.

The question is would that same effect occurs in a full organism? The O2 demand wouldn’t be shifted much at all in a complete organism via taking thyroid. You’d shift the O2 demand way more by jogging for a minute. So to me, that eliminates that part of the equation, but still leave the thyroids direct effect on red blood cells and RBC production. The question that needs to be answered is whether clinical amounts of T4/3 is enough, and is present in the tissues long enough. Because if we look at studies like these it’s hard to translate over.

Studies like these are essentially used to figure out cellular pathways. SO it’s important to remember in studies like this, it’s generally a non-therapeutic dose given (meaning way more than you could safely take as a human), and the exposure time is different (taking a pill vs. soaking in it for 4 hours).

So we’re back to square one, and I’m not well read enough to know what the exact mechanism would translate to in a functioning person. I dig around through all the research I could find, and to my knowledge there have been no studies looking at EPO increase via thyroid medication. The only studies I found showed that hypothyroid people who were anemic had an increase in RBC content once both were fixed (which shouldn’t be a surprise...)


If someone smarter than me wants to delve into this, they are more than welcome. I’ve reached out to a few expert scientists who have done the research and am waiting to hear back.

Recovery

Another big one being batted around is what if I take synthetic thyroid to recover.

First, the question needs to be asked is what role does the T4/T3 play in the recovery process?

Secondly, you have to understand the dynamics. If someone is in medical need of the substance that means there own thyroid isn’t producing T4. So they rely on the pill for T4. In this circumstance, recovery is impaired. Why? Because you essentially take a pill once a day that diffuses and gives you a stream of T4. If you have a normally functioning thyroid, it doesn’t work this way. You get spurts of T4 when needed. The body knows when to secrete it and when not to. It functions and works better.

So, if you were to abuse thyroid hormones for recovery what would it take? You’d need to time it so it helps you maximally, and you’d probably take T3 instead of T4 because T3 is generally going to give you a more rapid effect. This would be pretty dang difficult.
If the author had more wherewithall of the culture of doping, he'd realize that the bolded should be the entire post. Athletes that are doping don't take anything in isolation. The performance enhancers of thyroid medication in isolation are not relevent to the discussion.

The rested of the quoted bits show that it is easy to appear hypothyroid, between acute manipulations via a hard training session, bad guidelines for diagnoses, and doctors with an agenda.

The other parts show that thyroid medication is not the performance enhancer, but an intervention to the side effects of other substances. The effects of over training aren't fixed by thyroid; it's not anti-overtraining medicne. It is a masking agent's cousin, limiting the collateral damage of everything else.

And this should frame the discussion: that thyroid issues can be an indicator of being on a bigger program.
 

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