Anabolic Steroids – Doping For Climbers

Intra-Workout Performance Enhancement (testing methodology for 17α alkylated anabolic steroids)

Ok so let’s remind ourselves of the point to PED use in climbing: maximising training results and enabling maximal opportunity for progression, all while avoiding weight gain via hypertrophy of large muscle groups, or excess retention of either subcutaneous or intramuscular fluid. Training, drug use, and climbing practice itself should synergistically work together to optimise strength to weight ratio while, obviously, not impacting overall health.

Hopefully I’ve already put myself in an optimal or at least enhanced hormonal environment in the day to day sense via my weekly administration of Testosterone and Nandrolone. There’s still some tweaking to do with this and it’s not something I can point to as leading to immediate benefits; it’s more likely I’ll be able to look back in a few years and see a clear delineation between pre and post PED use when it comes to my climbing progression. The injectable esters I’m using (nandrolone decanoate and testosterone undecanoate) are perfect for this long-term outlook, but is there anything I can do to help with specific, short term training objectives and performance goals which will be noticeable over the period of days and weeks, rather than months and years?

I’ve already discussed Anavar and Winstrol in a previous post and these are both 17α alkylated steroids, which is a term that probably needs explaining. The next two paragraphs are a bit technical. Please feel free to skip them if you don’t care about the science.

If you swallow testosterone, nandrolone, or masteron nothing will happen because the liver metabolises the molecule before it can exert any performance enhancing effect. So these compounds need to be injected intramuscularly and the addition of an ester group (decanoate, enanthate, etc), at the 17th carbon allows a larger dose to be administered less frequently where it will sit in the “injection depot” and dispense itself slowly over time. The longer the attached ester (or more specifically the higher it’s molecular weight), the slower the release rate and this is something we’ve already been through in some detail in a previous post.

An alternative way to fiddle with a given steroid molecule is to add a methyl or ethyl group to the 17 position instead of attaching an ester there. This makes it harder for the liver to break the drug down and you end up with an orally active compound with a serum half life, usually, of about 9 hours. However, unlike esterified steroids, 17α alkylated compounds have different characteristics from their parent molecule. For instance Superdrol is 17α methylated version of Masteron and the two have very different effects indeed. Contrast this to testosterone undecanoate and testosterone enanthate which have essentially the same effect, just with different pharmokinetics.

Welcome back those who skipped the chemistry. Where were we?

There is a downside to using these orally active steroids. It’s not particularly healthy to feed the liver something that’s intentionally designed to be difficult to metabolise. Thus 17α alkylated steroids can cause stress approximately equivalent to getting drunk, and as most climbers have realised by the time they get to be serious about the sport, chronic alcohol abuse isn’t particularly conducive to living clean, staying light, and all the other lifestyle choices which make us better at what we do. I’m sure that many of us are happy to spend the occasional weekend on the piss, but very few of us will be seen in the pub 5 nights out of 7 downing pints and knocking back shots. It’s the same with 17α alkylated steroids. They can be used for short periods without much concern but they’re not suitable for year-round, long term use.

There are essentially two reasons why I’d pop a pill to help with a short-term performance objective. The first is probably the easier to get across: let’s call it acute activity. Say I’m going out, conditions are good, and I’m planning to finally finish a project I’ve been working on for a couple of sessions. A drug which gives me immediate gains in strength and mental drive might lend the edge necessary to stick that hard, scary crux move at the top of the boulder. And if it acutely boosts work capacity, it will allow me more attempts during the session, therefore maximising my chances of sending. It doesn’t really matter if this drug is at the higher end of the hepatotoxicity spectrum because I’m only likely to use it once or twice a month.

That hard scary crux move at the top of the boulder

The other reason why I might want to pop a pre-workout pill is to take advantage of progressive strength gains over a number of weeks: let’s call this chronic activity. In this case I may want to select a drug which builds in effect over repeated doses, rather than one which delivers an immediate and extreme boost in performance up front. This strategy would be useful if I wanted to work on a specific, defined weakness; say I want to improve my left hand half-crimp for a certain boulder I’m working on. In this scenario I might train the position every day for a few weeks before going back and trying the project again, and the drugs might increase the gain in crimp-strength I’m able to achieve in a given timeframe. I’d want these drugs to be at the lower end of the hepatotoxicity spectrum because I’m taking them daily for a few weeks.

Ok. So we’re splitting orally active anabolic steroids into two categories, those to aid with training and those for performance-day use. How do we decide which drug is suitable for which application? The first task is to list all the 17α alkylated compounds available to me and then narrow it down by applying the criteria which I discussed in a previous post. That only really leaves me with four compounds: Anavar, Winstrol, Halotestin, and Superdrol. Out of the four I’m expecting Anavar and Winstrol to be more suitable for chronic assistance over a weeks-long training block, and Halotestin and Superdrol to be more suitable for acute use on a per-session basis. The only way to know for sure though is to test them, so I’m going to standardise as many variables as possible into a protocol I can use to compare each of them directly.

Here’s a pretty brief rundown of my plan for testing these compounds. I’ll go into more specific detail in the next post, in the interest of stopping this one from becoming too unwieldy.

Each compound will be assessed for a period of two weeks. If they don’t show their utility over this period they’re not suitable for my purposes (although they still may be a perfectly efficacious drug to use in other situations). Calorie intake will be kept consistent during the tests, between days and from test to test. I’ll leave at least three weeks between each test to allow time for the drugs to clear and for my body to recover.

Dosage will remain the same between compounds for sake of comparison although some are slightly more potent than others. 15mg per day seems like an effective compromise dose between all four compounds while hopefully avoiding muscle hypertrophy associated with taking the doses higher. In addition to keeping the dose relatively low, I’m hoping that the short two week cycles might be another factor helping to mitigate unwanted mass-gain.

The dose of 15mg isn’t exactly pulled out of my arse my the way. The study “A quantitative expression for nitrogen retention with anabolic steroids” compares intravenous doses of Anavar and concludes that the mimimum effective dose is 2.5mg whereas no further nitrogen retention (their proxy for measuring anabolic effect), occurs after 30mg. Obviously I’m not planning on taking any of these compounds intravenously so let’s say that an oral dose, with it’s different pharmokinetics and bioavailability is half as active; this means that the dose range we’re looking at is 5-60mg with 5mg being minimally effective and 60mg blowing me up like a balloon. Say, (and this is the point I *am* pulling a figure out of my arse), I want to be a quarter of the way up that scale. That lands me at around 15mg. I’m sure a bodybuilder would scoff at that dose, but I’m specifically trying to avoid the gain in muscle mass which they seek.

So this is the protocol I’m going to use. I’m going to take the dose on an empty stomach two hours before I begin the workout. Then one hour before the workout I’m going to take a standardised portion of carbs (porridge, flapjack, something like that). I’m going to start with a standardised warmup/strength and conditioning session lasting one hour, followed by the the testing protocol which will also an hour in length. The purpose of the testing protocol is to assess the maximum one-arm half crimp for each side followed by how many pull-ups in total I can do over 5 sets.

I’ll graph total number of pull-ups achieved each day and the maximum half crimp weight for each hand as a percentage of a baseline measurement taken on the day before the test begins. I’ll also record my daily weight in kg and water content (as a percentage of body weight, measured by the hand-to-foot bioelectrical impedance machine in my gym).

This is where I’m going to leave this post for now; on a bit of a cliff hanger (excuse the pun). My laptop is broken and I’m tired of typing on my phone. I’ll continue after I’ve tested the first compound which will probably be Anavar, and go into specific detail on methodology at that point. Now I’m heading out to climb.

EDIT 1/4/2022: a quick addendum… I started programming the test protocol and realised that I could seriously irritate a nagging elbow injury I’ve had for a few months by doing pull-ups every day. Because of this I’m changing the plan a bit. I’ll be testing my left hand half crimp strength only. While I do this I’ll use the opportunity to rehab my right arm on a larger edge; I won’t be recording this as it will be about recovery rather than strength and there’s not a useful metric I can think of to codify the improvement.

EDIT 21/4/2022: this project is now on hold until summer. The exact timing when spring and autumn bouldering seasons start in the UK is always a bit difficult to predict. When it dries out and gets warmer (but not too warm) I spend as much time as I can on rock, and training takes a back seat to actual climbing. This has been the case for a few weeks now. Obviously with a potentially short window when rock is in ideal condition and climbing is good, this isn’t a time when I’m willing to devote two weeks at a time to daily training in the gym. No doubt when it starts getting too hot to climb hard I’ll be raring to go again with this research (I’m particularly curious to try Halotestin). Until then if I dabble, I’ll report back with my thoughts and findings.

Weight Gain, Training, and Tendon Health (anavar vs winstrol)

Over the winter I tend to train inside rather than climb outside. This was an ideal opportunity to run some “phase one trials”, and the first compound I was really interested in trying was Anavar (Oxandrolone). I ran it for about five weeks at dosages between 20mg and 40mg per day. Bear in mind that this was only my second experience with performance enhancing drugs (after Ostarine), so my ponderings in this case are obviously coloured by my inexperience, and inability to subjectively compare it’s effects to previous anabolic steroid use.

Later in my winter training season I had a quick go at Winstrol (Stanozolol). This was a shorter duration experiment, lasting only about two weeks as my objective was mainly to confirm that the effects (both desired as well as side effects) justified future experimentation. As it happened I did learn some important lessons even though the exposure wasn’t really long enough to get a particularly accurate idea on how the effect felt compared to Anavar, particularly as I was more cautious with dosing Winstrol. However this is what I’ve got.

I’m already learning that the use of anabolic steroids in climbing is of limited benefit. These compounds are unfortunately not the holy grail and other than bio-identical hormones used at physiologically relevant dosages, it’s beginning to become clear that androgens should only be used in a climbing context acutely, at very conservative levels, and for specific defined aims.

The reason for using these two particular compounds would be to achieve increased strength, neuromuscular efficiency, and an energy boost during discrete short training blocks. As well as augmenting the anabolic effects of my testosterone/nandrolone base, this will hopefully lead to the ability to work harder, and therefore increase training stimulus during the timeframe of the block. As both these compounds are quick acting, the best time to take it them is an hour or two before training so that peak effects are experienced at the most useful time. I’ll go into more detail in a future post about how this whole strategy can be slotted into an overall framework for climbers.

I really need to work on body tension.

Anavar is an orally active anabolic steroid with a serum half life of about 9 hours. On paper it’s the perfect performance enhancing drug for climbers and it was my first choice of compounds to try. It has a reputation for being mild; for me it was nothing of the sort (more on that later).

These are the reasons why I initially thought Anavar would be highly suitable for climbers.

It’s has less liver toxicity than most other orally active anabolic steroids. Therefore it can be run for longer without issues
It promotes collagen synthesis so it may help keep tendons healthy during intense training
It’s the only anabolic steroid that’s been observed to reduce both subcutaneous and visceral fat
It doesn’t aromatise into estradiol so there’s no oestrogen related fluid retention or gynecomastia symptoms to worry about

Winstrol is structurally similar to Anavar and its effects are often seen as comparable. It’s available in both oral and injectable forms; I used the oral form at 25mg a day. Anecdotal reports suggest it’s a bit less potent than Anavar milligram for milligram, so this dose may work out to be lower, in terms of therapeutic effect than my minimum Anavar dose. The serum half life of the oral version is a little shorter than Anavar’s and the half life of the injectable version is about a day. It’s known as being “stronger” than Anavar but in actuality this claim usually refers to the fact that it possesses a higher likelihood of undesirable side effects. It is also quite a bit more toxic for the liver so it shouldn’t be run for as long a duration as Anavar.

Winstrol has a diuretic effect that Anavar doesn’t. It’s clinically prescribed in low dosages to cure hereditary angioedema and this could obviously be beneficial for a climber who wants to carry minimum water weight. However this same effect can manifest as reduced synovial fluid in the joints which can cause pain and increases the potential for injury. There’s also some differences in Winstrol’s effect on collagen synthesis compared to Anavar which I’ll go into at the end of this post.

So how do the two drugs compare subjectively? A good start would be to examine the way I felt during the first exposure to each compound, as both of them had significantly psychoactive effects. I’m going to use the following vocabulary very loosely as a way to describe “feels” rather than suggesting that this is actually what’s happening chemically in the brain. I’m hoping that anyone who has had sufficient experience of “party drugs” may be able to take away some sort of meaning from a phenomenological experience which doesn’t translate very well into language. Anavar felt serotonergic, like MDMA, whereas Winstrol felt dopaminergic like cocaine. There! Told you it would be fuzzy. I’m obviously not suggesting that these compounds share anything in common or can be used as a substitute for each other. OK?

With repeated use, Anavar retained a level of background stimulation which could be rather annoying, whereas Winstrol faded into the background and it was possible to forget that I had taken it. Neither compounds felt in any way recreational or euphoric after the initial, virgin dose. Presumably the sympathetic drive experienced from Anavar could be leveraged for performance enhancement by playing with dosage and timing while avoiding it interfering with sleep (it did a few times), and general day to day well-being.

Although Winstrol fit in to daily life better, to the extent that it wasnt annoyingly psychoactive/stimulating, I did notice a couple of cognitive downsides to using it. Firstly, my memory of the whole cycle is a little fuzzy; this it turns out has been established as a known side effect of the drug. Secondly I felt a lack of motivation and get-up-and-go. If these effects end up translating to less “psyche” for climbing and training then there’s literally no point in running the compound as enthusiasm is what makes me want to climb in the first place. More self experimentation is required before I make a decision on this but it’s potentially a show stopper.

I know, I still really need to work on my body tension

One last subjective difference: with Anavar, I felt constantly on the verge of “bonking“. I could negate this feeling by increasing my carbohydrate consumption and it felt as if this extra energy was being shuttled directly into my muscles which became full and rounded. This impressive loading of glycogen (and probably creatine too) was responsible for a sudden and noticeable weight gain. Muscular fullness was far less of a concern while taking Winstrol and this can definitely be seen as a pro in its favour. If I was a bodybuilder looking for a visual effect I’d have loved Anavar but as a climber on a calorie deficit, being in a state of borderline hypoglycaemia which can only be addressed by consuming more food, isn’t helpful.

So how to use these two compounds? Seeing as my winter training activities can broadly be categoirised into two types: power and strength, why not use each compound in a way which plays to their strengths and circumvents their weaknesses? Because multiple studies show that Anavar upregulates collagen synthesis (and therefore stimulates tendon repair), it’s an obvious candidate for power training blocks focussed around dynamic loading where injury is a considerable risk. I’m thinking specifically about campussing and large dynamic moves requiring contact strength.

Winstrol’s effect on collagen synthesis is a little more complex than Anavar’s. Studies have shown that although it does promote tendon growth via enhanced collagen synthesis it also results in a “stiffer tendon that absorbs less energy and fails with less elongation”. This is due to the architecture of the new tissue and the fact that it’s more highly cross-linked than tendon tissue grown under natural conditions (which tends to retain more elasticity and flexibility). Furthermore Winstrol increases procollagenase expression which can potentially lead to connective tissue breakdown; although this has only been demonstrated in the skin and not in the tendons so it’s a little uncertain whether the phenomenon is a concern to us or not. Because of the suboptimal effect on tendon health in addition to the synovial fluid issue caused by it’s dietetic effect, it would suggest that Winstrol is more appropriate for static training such as finger-boarding.

Anecdotal reports from bodybuilders suggest that a great deal more muscle bulk can be gained with Winstrol compared to Anavar, although it is uncertain whether there is much research to substantiate these claims. If there is any truth to these anecdotal reports, it would be a further reason to limit the use of Winstrol to training blocks focussing on static hanging exercises designed to develop the finger flexors only. This way hypertrophy would be limited to the forearm and rotator cuff muscles which tend to be small in size and their increase in volume would be unlikely to have a great effect on the overall weight of a climber.

To summarise, neither of the two compounds are perfect. Winstrol carries the risk of injury in addition to some weird cognitive effects. Anavar causes fuller (heavier), muscles and a distractingly stimulated mental state. Hopefully all of these effects can be mitigated by running the compounds at more appropriate doses for sports performance (I’ll go into more detail on dosing in a future post).

A final note: if you’re a cis man, IE you own testicles and require them to produce male sex hormones for you, both these compounds will shut down your natural testosterone production. It’s not a good idea to be on either of these unless you’re also on testosterone replacement. If you have an oestrogen-dominant body, Winstrol may cause you to develop secondary male sex characteristics such as a deepened voice, increased body hair, and male pattern baldness; Anavar will do this to a lesser degree and is the most common anabolic steroid to be used by women (but at smaller doses than a man would use).

Shortlist Selection (which drugs should I try)

I thought I’d briefly outline a strategy I’ve been using to come up with a shortlist of potentially useful compounds. The issue is that there’s an extensive catalogue of performance enhancers and I can’t try everything; if I attempted to it would be forever before I’d likely have much of use to report. So I needed to implement some ways of thinning down the list.

Here are a number of reasons why potential drugs aren’t on my list to assess at this point, along with examples:

Because I’m looking at this from a bouldering perspective where explosive power and short bursts of strength are the name of the game, I’ve excluded a number of compounds from consideration which would be more appropriate for endurance athletes. A sport climber may benefit more from compounds such as Turinabol or Boldenone. A “trad” climber might benefit more from a fag and a pint of ale. For me though, there are drugs better suited to my objectives so they’re the ones which have made it into the shortlist.

Oxymetholone is a widely used and extremely effective pre-workout performance enhancer. It’s know to impart instant strength gains and obviously this could be very beneficial for bouldering sessions. However it is also associated with rapid weight gain and is totally counterproductive for a bodyweight-dependent sport such as climbing. There are many, many other compounds which fail to make the shortlist for similar reasons (Trenbolone is another example).

I’m obviously also limited by my ability to source the compounds in question. Stenbolone acetate for example seems, on paper, to be a potentially ideal compound for climbing performance. It might give me the strength enhancement I experienced with Masteron but without the muscle cramps and rapid fatigue. However I cant find it from a reputable, trustworthy source so there’s no point in considering it until that situation changes. Similarly Increlex is prohibitively expensive, even if I could find a trustworthy source for it.

Lack of proven efficacy is another concern and this is the case with many of the peptides and “sports supplements”. This is more of a grey area than an absolute criteria for me. For instance BPC-157 has pretty scant evidence in the form of clinical trials but there’s a large number of of positive anecdotal reports regarding it’s use. This could obviously be a placebo thing and I’ll attempt to control for that if I ever experiment with it. The price and other factors play a role here too; if it’s cheap and there’s no reason to worry about safety or side effects (as happens to be the case with BPC-157), I there’s a better case for considering it. A great rule of thumb turns out to be “is it banned by WADA?”. Strange as it seems, anti-doping institutions are the only funding bodies who have enough interest in performance enhancement to commission studies. If it’s not on the banned list then it either doesn’t work or hasn’t been fully assessed yet, in which case it probably will be on the watch list.

Based on the above criteria, an overall framework is starting to fall into place and this is something I’ll definitely go into in more detail in a future post. There are whole classes of compounds though, which just don’t fit into the emerging framework. This isn’t to say that I won’t look into them in the future, just that they aren’t currently my area of focus. SARMS (Selective Androgen Receptor Modulators) are the obvious exclusion from my current shortlist and in fact I have experimented with Ostarine already. There’s definitely space for consideration down the line but for now I have to limit myself to a manageable list of candidates so compounds which potentially show promise (LGD-4033, YK-11, S4, RAD-140, etc) will have to wait for now. This is no bad thing as they’re fairly new and could do with a few more years of clinical research and anecdotal reports.

Finally, for me to want to experiment with a compound, I don’t want it to be potentially dangerous. Most compounds have side effects which need to be managed and all can be assigned some level of risk. However if it was dropped from clinical trials, as happened to Cardarine because “animal testing showed that the drug caused cancer to develop rapidly in several organs”, I’m just not interested. Similarly DNP has caused multiple deaths, so count me out.

Now, onwards with experimentation…

The Benefits of Nandrolone (with evidence)

This is going to be more of a pondering than a report into self experimentation. So far I’ve taken a few small doses of Nandrolone Decanoate to judge its tolerability, and I’m about to start adding 50mg to my weekly testosterone injections. This is a quick explanation as to why I might want to do this.

After about 7 weeks of taking Testosterone Undecanoate at 250mg a week, I took a blood test as a quick interim check to see what my levels were. I didn’t do a full blood panel, I just checked total testosterone so I can adjust up or down accordingly before re-testing estrogen levels and all the other stuff that I’ll need to keep in range over the long-term. As you can see from the image below, my levels had doubled since the last blood test but were still a little lower than I was expecting from the dose. Ideally I’d want it to be into the “borderline high” area of the reference range: IE optimised without being supra-physiological.

This unexpectedly low value could be caused by one or more of the following factors:

It could be that with such a long ester of testosterone, my levels hadn’t fully had a chance to stabilise. 7 weeks wouldn’t usually be long enough to achieve stable blood serum levels from such a long-acting ester but I had “front loaded” in the first few weeks and calculated that I’d have reached saturation by this point. However it’s possible that regardless of my diligence that dose by dose, week by week, the drug was still accumulating in my system
The “underground lab” I was using to supply the testosterone may have under-dosed the product leading to me taking a smaller dosage than I had intended
There’s some evidence to show that intramuscular injections into the medial deltoid might provide suboptimal bioavailability compared to administration into the ventrogluteal muscle. As I was rotating between these two muscle groups, half my shots might have had a less potent effect than the other half
The dose might have just been too low. There’s considerable variation from person to person regarding the relationship between dose administered and resulting blood serum levels. Maybe I excrete the drug faster than the average person or maybe my body cleaves the ester off the parent molecule less efficiently.

I decided to take the following actions and test again in 15 weeks:

I switched to a supplier who provides traceable batch numbers and publishes lab test results for each batch
I’m standardising my injection site protocol: one week in the left ventrogluteal, one week in the right ventrogluteal, and repeat
I’m upping the dose from 250mg to 300mg per week

Anyone who’s familiar with scientific standards will have immediately spotted a red flag; the first rule of experimentation is to change one variable at a time. However two of the three changes I’m making to my protocol are more about standardisation than optimisation so will provide a good base to gain maximum insight into the next round of blood test results.

My new supply of testosterone is provided in handy 1ml, single use ampoules, each containing 250mg of testosterone undecanoate (providing 157.9mg of testosterone once the ester has been cleaved off by biological processes). The issue is that unlike drawing a dose of one’s choosing from a 10ml vial (how my previous supply of testosterone was packaged), I’m now stuck with dosing in multiples of 250mg.

One easy strategy to circumvent the ampoule size issue is to keep the dose the same and change the administration frequency instead. So if I want to increase my levels I can inject every 6 days instead of every 7. Conversely if I want to reduce my levels I can inject every 8 days. But there’s actually something else I can do which kills two birds with one stone in a particularly elegant way: I can top up the weekly dose with 50mg of Nadrolone Decanoate.

So why might I want to do this? Anecdotal reports from generations of athletes who dope with Nadrolone have made a pretty clear case that it has a significant effect on reducing joint pain. This has been backed up by clinical trials and the results are very convincing. As a 49 year old climber, my fingers are continually achey, creaky, and a bit crackly. Nadrolone might be the perfect remedy and I get the benefits for free as a result of tweaking my year-round testosterone protocol.

It’s not entirely clear why nandrolone has such a demonstrable effect on joint pain but there are two commonly cited hypotheses (yes I had to look up the pleural of “hypothesis”):

It may potentiate collagen synthesis leading to cartilage deposition in the joints
It’s a rather “wet” compound so the effect might be the result of increased synovial fluid production.

It would be great if point one was the case because increased collagen synthesis would also aid in tendon health, and therefore reduce the likelihood of a training-induced finger injury. Point two would suck because fluid retention (as we’ve discussed so many times so far) is bad for climbers who care so, so much about strength to weight ratio. The likelihood is that both hypotheses (I looked it up a second time to double check that it actually is the pleural of “hypothesis”) are correct and contribute to the beneficial effects on joints.

I shouldn’t have tried to pull the label off but I wanted to remove the unique verification QR code.

So if I’m upping my dose by adding a second compound, how do I know if I’ve reached my desired hormone level when I do my next blood test? Conveniently the ECLIA test employed by the service I use actually can’t tell the difference between nandrolone and testosterone, so the serum level i get back from them will actually be a combined serum level of testosterone and nandrolone. Convenient eh?

At this point everything seems to be falling conveniently into place. The half life of Nadrolone Decanoate is long enough that the two drugs can be administered with the same frequency, and therefore together in the same injection. Also nandrolone is actually present in small concentrations in both the male and female natural endocrine environment, so my protocol can still be classed (if anyone cares), as bio-identical hormone replacement.

There are however potential downsides to using nandrolone year-round: there are plenty of anecdotal reports of the drug causing depression, anxiety and increasing incidents of jealous, possessive ideation, and this has be backed up by research. These mental effects are usually reported at much higher doses than I’m planning to run, but it’s certainly something I’m going to be diligently looking out for. There is research to show that nandrolone messes with dopamine transport proteins and monoamine oxidase function. I don’t want to be fiddling with my brain chemistry in that way. Also as I alluded to earlier, nandrolone is notorious for promoting fluid retention in a dose dependent manner. Both of these issues are a good reason to stay around 50mg which is a very low dose in comparison to that taken by most athletes. Which brings me conveniently on to…

How do I know that the 50mg dosage necessary to top up my weekly testosterone protocol is enough to lubricate my finger joints? In short, I don’t. The Tatem, Holland, Lipshultz paper I linked to above presents evidence that “Deca” (as nandrolone Decanoate is colloquially known) was efficacious at reducing joint pain at a median dose of approximately twice that which I’m planning on taking. I have three grams of the stuff so I might as well give it a go. It may require some future fiddling, or my plan might not be feasible at all. I’ll start at 50mg a week because it fits into my protocol and play around with things if I need to. I think it’s more probable though that if I don’t get what I’m looking for at 50mg, or I experience depression or water weight, I’ll chalk it up to an interesting experiment and revert to testosterone only.

A quick note: many if not all of the anabolic steroids discussed in this blog have the effect of suppressing or “shutting down” natural testosterone production, but nandrolone particularly so. I wouldn’t have chosen to use it unless I was committed to long term hormone replacement. Restarting ones testicular production can be a lengthy and difficult process.

The Pump (problems with masteron)

You’re going to have to excuse another comparison to bodybuilding but we’ve already established that as a group they have a monopoly on available information when it comes to performing enhancing drugs. If gymnasts or swimmers created a similar volume of blog posts, YouTube videos, and podcasts about the compounds they use I’d be all over it. But no, it’s just bodybuilders. Wall to wall bodybuilders.

With that said, I’m not sure whether bodybuilders and climbers mean exactly the same thing by “pump”.

For a climber, being “pumped” is usually described as a build-up of lactic acid in the forearm muscles although this is an oversimplification of the physiological processes involved. I don’t want to divert this post to one on metabolism, so here’s a video from someone who seems to know what he’s talking about.

For climbers, pumps are awful but for bodybuilders they’re seen as a positive thing. The muscles fill with blood and look fuller, harder, and more defined. As bodybuilding is about optics, this is presumably desirable.

Whether this effect on muscle volume is a different aspect of the same physiological process or a separate phenomenon entirely, named identically, I’m not really sure. And that actually matters too because it’s possible that certain compounds might produce pumps from the point of view of a climber but not a bodybuilder, and visa versa.

This brings me to Drostanolone. On paper it seems like a perfect PED for climbers.

Seeing as a low to moderate dose of Testosterone should already have me covered terms of enhancing post-exercise recovery, really what I’m looking for is an add-on which will help with strength. I could just use more testosterone but this comes with the potential of increased water retention not to mention muscle gain. Both of these are counterproductive when it comes to my goal of remaining as light as possible.

Among bodybuilders Masteron (as Drostanelone is more commonly known), is not known as a “mass gainer”. They call it “mild” and mention that rather than being beneficial for muscle accrual, it has a “hardening” and “drying” effect. I’m not exactly sure what this means (I do find it difficult to relate to those who are in the game for aesthetics), but it sounds like it doesn’t just lack water retention it actually counters it.

OK, so this sounds good so far. We know what it doesn’t do, but does it increase strength? Anecdotal reports are mixed and seeing as there hasn’t exactly been any clinical trials on it’s use as a performance enhancer, that’s all I have to go on.

There are definitely other compounds better renowned for their neuromuscular enhancement capabilities. Anadrol, Halotestin, and Trenbolone all spring to mind, but they are also renowned for both side effects and toxicity. Masteron may hit a sweet spot in this respect. A relatively benign compound with some strength gains which will either keep me light or actually make me lighter than running Testosterone alone.

So, what about the dose? Bodybuilders (bodybuilders again), are fairly unified in suggesting that a 400mg/week is appropriate whether you’re at a beginner, intermediate, or advanced level. Less results in reduced effects, but more doesn’t help. So (will I ever learn?), in the face of such a consensus from the bodybuilding crowd, 400mg administered over two 200mg injections a week is where I started. And… at this dose I have never felt such incredible, stinging, crippling pumps.

A couple of weeks in, once the drug had time to take hold, campussing was near on impossible. Three sets in I’d had enough, and gritting my teeth (and gripping each forearm with the opposite hand), I called it a day. The troubles didn’t stop there either. I woke up at night with shooting pains in whatever muscles I’d worked that day, and even holding a climbing guidebook as I walked through the forest of Fontainebleau made my hand ache.

As you can imagine being the sensible sort that I am, I stopped taking it immediately and waited for it to work it’s way out of my system… did I fuck?!

Seeing as I did notice an obvious if not profound increase in my strength in the days leading up to my forearms exploding, I decided to play with the dose to see what would happen. At 140mg a week, I didn’t notice much of anything. Raising up to 300mg a week and the pumps were a problem again but (thankfully) to a lesser extent. At this point the bottle ran out so I’m left at least with a question: is there a dose between 140mg and 300mg a week where I can find the strength gains I’m after but with tolerable pumps?

Testosterone Replacement (part one)

A quick note at the beginning. This article is really only relevant for cis men. I will be publishing content in the future which is more suitable for women, enbees, trans people, etc; in short you probably want to avoid androgenic hormones and focus on other performance enhancers such as peptides, SARMS, and weird-arse agonists of non-androgenic hormones.

I’ve been conducting what I cynically refer to as “phase one trials” with various performance enhancing compounds. Like the more organised and curated pharmaceutical namesake, the aim of my experiments have not been too fully understand the nature and effect of each compound – that takes time. It’s been more about ascertaining the approximate dose I may want to run in the future, noting tolerability (any obvious side effects for instance), and a getting rough “feel” for each drug. Let’s say it’s been about taking a shortlist of candidate compounds and making it shorter, and as I revisit each of them I’ll record my experiences here.

Many, if not all of the drugs I’ve been experimenting with have the effect of suppressing natural testosterone production. This is one of two reasons why I’ve been administering a weekly “base” of testosterone undecanoate throughout the whole venture. I’ll elaborate in a future post on the necessity of using testosterone while running synthetic anabolic steroids, but meanwhile let’s talk about the other reason as its a bit more considered and a bit more applicable to athletes.

When I decided to begin this journey the first thing I did was to test my natural levels of a bunch of hormones, liver enzymes, cholesterol biomarkers, and anything else that can potentially be effected by anabolic steroids. I’ve always found it pretty easy, if not too easy to put on muscle mass, so I was a little surprised when I found out that my testosterone levels were on the low side of normal.

This is what’s probably been happening: when you’re reliant on natural testosterone production your testicles (assuming you own testicles) squirt small amounts of the hormone into the blood stream throughout the day. Levels are highest in the morning and lowest in the late afternoon. The daily volume of hormone produced is reliant on many factors: BMI, age, diet, sleep, stress levels, and most importantly in my case how hard you’ve been training.

To a point, exercise increases natural testosterone levels but hard training sessions deplete natural production, leading to a kind of bell curve. Climbing five times a week at the age of 49 is almost as counterproductive to maintaining natural testosterone levels as sitting on the sofa watching daytime tv and eating pizza for breakfast. If you’re interested in maximising natural production a moderate load of exercise with frequent rest days is the way to go. This is something that Lattice Training (for instance), spend a lot of their time trying to convince their customers: less is more. Bit it’s something I want to push beyond.

So what’s so special about testosterone anyway? In the male body, as the primary anabolic hormone its responsible for promoting protein accretion in the muscle tissue, and this results in increased rates of recovery from exercise. As such, crashing your testosterone levels by over-training leads to reduced recovery rates and that’s an issue that can be hacked by supplementation with an exogenous source of hormone.

One important aspect to understand is that supplementing exogenous testosterone has the effect of shutting down your natural production. Your Hypothalamic–pituitary–gonadal axis (if you’re a cis male), senses that there’s enough testosterone floating around and doesn’t bother making more. So if administered intelligently (we’ll get into the details of that in a minute), you’ll replace the diurnal, pulsatile production of endogenous testosterone with a steady, constant source which remains optimal regardless of how often you train, if you’ve managed to have enough sleep, or if you couldn’t resist eating all 5 of those donuts in one sitting.

So what about the dose? The obvious assumption to make when supplementing testosterone would be to push into supra-physiological levels, IE somewhere above the 32.63 nmol/L cutoff that the blood testing service I use considers the upper end of their natural reference range (see diagram at top of page). After all if a moderate dose helps increase work capacity a little, then a less moderate dose must help a lot, right? Actually in climbing as in many other sports where power to weight ratio is a consideration, this isn’t actually the case.

In the a study titled “Testosterone dose-response relationships in healthy young men”, the researchers gave varying amounts of testosterone to men and measured their resulting weight gain. Higher doses led to more weight gain so if you’re trying to stay light then you want just enough testosterone to replace your natural level. That way, morning or evening, whatever your allostatic load, you’ll recover at a rate that’s optimal for you. Or if you already have a problem with recovering optimally, you can dial in your testosterone levels to near the top of the “normal” range to optimise recovery, and if you start putting on weight drop the dose until you reach a happy balance. This obvious requires regular testing, which you should be doing anyway if you’re taking exogenous hormones.

There are various esters of testosterone available. Different esters have different serum half lives. For instance if you inject testosterone propionate today, in 4.5 days time you’ll have half of it left in your system. If you inject testosterone cypionate, it will take around 8 days.

If you’re a competitive athlete concerned about the possibility of drug testing, a shorter acting ester may be more appropriate because it can be out of your system with minimal planning. A bodybuilder who goes on and off cycle might use a medium acting ester; that way when they’re finished with the cycle they don’t have to wait months for the drug to clear out of their system. But for me, as someone who’s planning to dial in the right dose and stay on it, it makes sense to use a long-acting ester as this will lead to the most stable levels. Seeing as what’s most important to me is unvarying levels, morning and evening, whatever I’m doing, the longer the half life the better.

The longest acting ester I have access to is testosterone undecanoate so that’s what I use. With a half life of around 21 days it takes quite some time for serum levels to stabilise so it’s a long-term endeavour to test, tweak, test, etc. The plus side however is that it’s leads to extremely stable and unvarying hormone levels which is the point of the whole exercise.

Above are three screenshots from steroidplotter.com comparing blood serum concentrations of three different testosterone esters administered at 100mg once per week. As you can see the short-acting ester (testosterone propionate) takes no time to reach maximum blood serum concentration but by the end of the week there’s nothing left in the system. The long-acting ester (testosterone undecanoate) takes the full 12 weeks to reach stable blood serum concentration but is the most stable of the three showing similar levels at the beginning and end of each week. The medium acting ester (testosterone cypionate) is a compromise between the two extremes.

Regarding administration frequency, I was going to go into detail about the considerations around this but the post is already pretty long and detailed. I’m going to split the subject into a separate post and put it up when I’ve had more time to thoroughly research how changing administration frequency can be used to manipulate SHBG levels.

Many users administer testosterone undecanoate once every 8-12 weeks and although this is possible it leads to the same yo-yoing of hormone levels you’d get from more frequent administration of a shorter acting ester. Conversely I don’t love needles so injecting every day wouldn’t be preferable, in fact it would be a massive pain (quite literally) in the arse. Once a week seems to me to be a good compromise between convenience and stability, and leaves room to tweak up or down if necessary.

In summary, exogenous administration of testosterone, particularly frequent administrations of a long acting testosterone ester like undecanoate as a means of keeping testosterne at a pre-planned level at all times of the day, no matter what else is going on has significant effects on ability to recover. Which means you can train harder, wake up the next day with optimal levels, and do it again.

On a final note, it occurred to me while I was writing this post that it’s actually possible to use testosterone for the purpose of reducing hormone levels if needed. Why would you want to though? Say your natural levels were abnormally high and you had a problem with putting on muscle weight when you didn’t want to. Well, taking exogenous testosterone shuts down your natural production, so you could dial it in at a lower level than that which your tesicles would have produced and avoid the problem. Very hypothetical I know but fun to think about.