Wednesday, March 5, 2014

Conditioning For Athletes: Does Your Program Condition You To Win?

Anaerobic training is far superior to aerobic training for almost every athlete.  There, I said it.

I'll say up front that this article will probably come across as anti-aerobics.  Actually, I kind of hope it does, because I see way too many coaches out there shooting their athletes in the foot by having them waste their time and energy on dedicated aerobic training.  I'll probably end up trashing on conditioning methods I know plenty of coaches still use, and I'm sure I'll hear all about it, but it is what it is. 

I'll also cover myself by saying that this article deals with athletics. I won't discuss the general health implications of aerobics vs anaerobics.

With that, let's get to it.

Some Vocab
The terms "aerobic" and "anaerobic" literally mean with oxygen and without oxygen.  In the context of exercise, these terms are used to describe activities that supposedly either utilize oxygen, or do not.

There's no such thing as a purely anaerobic or aerobic activity (more on that in a bit), so the entire subject is full of misnomers.  We're going to define anaerobic exercise as anything that could not be sustained for more than 2 minutes straight without performance changing.  For example, an all-out sprint cannot be maintained for more than 2 minutes without turning into a run, for reasons we will discuss.  Note that the exercise doesn't have to be done for 2 minutes to be anaerobic, it just has to be intense enough that you could never do it for more than 2 minutes all out.  Anything less intense than this is going to be called aerobic in this article.  Cues I use when I want anaerobic work done are "do it at a sprint pace" or "go balls out".

Some examples of anaerobic conditioning include all types of sprinting, jumping, explosive/athletic movements, gymnastic activities, most interval training, and any other high intensity burst activity.  Conventional resistance training is largely anaerobic, but this article focuses entirely on conditioning.  Some examples of aerobic conditioning include running more than ~800 meters ( a mile, 5k, etc.), biking, jogging, most group exercise classes (zumba, step, most yoga, etc.) cross country skiing, and anything else at low to moderate intensity that can be performed for more than 1-2 minutes without the distinct sensation that your heart is going to explode. 

A Brief Discussion Of Energy Systems
Every activity in life is powered by a particular energy system. This subject has a lot of labels including energy systems, metabolic pathways, bioenergetics, etc. but they all deal with the usage of various molecules for energy production.  This is a quick peek; we're skipping over lots of intermediaries and subsystems. They break down as follows:

ATP Stores
Anaerobic, lasts <2 seconds of intense effort.

Going back to high school bio, adenosine triphosphate is the "energy currency" our bodies use to power activity. Every time you move, ATP is being hydrolyzed to fuel that movement. Unfortunately, ATP is very heavy and we don't store much of it (~250g). Once a high intensity activity starts, ATP stores will be depleted within ~2 seconds.

Phosphocreatine (PCr) System
Anaerobic, lasts < 8-10 seconds of intense effort

As ATP (TRI, 3 phosphate) is broken down, remnant ADP (DI, 2 phosphate) are recycled to form new ATP molecules to power more activity. A single phosphate is cleaved from phosphocreatine and combined with ADP to form new ATP. This system produces no negative byproducts, and therefore does not require any compensatory mechanisms. In other words, the only thing that really governs this system is how long the phosphocreatine stores hold out.  ATP recycling happens constantly, but under intense activity it will be overwhelmed within about ~8-10 seconds depending on training status (creatine supplementation extends this threshold a bit).

When phosphocreatine levels dip, the body immediately begins to resynthesize them. It uses the phosphate released from ATP hydrolysis and combines it with creatine to make new phosphocreatine.  This process takes time.  Full PCr regeneration from a maximal activity can take 3+ minutes of rest.  While we're on the subject, creatine supplementation comes into play here by increasing the intramuscular pool of phosphocreatine to pull phosphates from, thus allowing the PCr system to be used for a longer duration. If creatine interests you, see Everything You Ever Wanted To Know About Creatine.

Glycolytic Systems - Anaerobic Glycolysis/Lactic Acid and Aerobic Glycolysis
Anaerobic glycolysis lasts < 2 minutes of intense effort, aerobic glycolysis system lasts until glycogen runs out.

At this point, muscle glycogen is broken down through glycolysis, producing pyruvate-->lactate to form new ATP, hence it often being called the lactic acid cycle.  Anaerobic glycolysis occurs when ATP must be made rapidly, IE during intense activity.  It is less efficient, yielding much less ATP, but requires no oxygen and provides fuel much more rapidly.  This system is often referred to as fast glycolysis.

Aerobic glycolysis starts in the same way, but grabs those pyruvate molecules before they turn into lactate, runs them through the Krebs cycle, and finishes with oxidative phosphorylation.  These extra steps yield a lot more ATP, but make the process slow enough that it cannot meet the fuel demands of intense activity.  The term "aerobic glycolysis" is actually inherently wrong since glycolysis is always anaerobic - the process doesn't become aerobic until oxygen enters the equation during subsequent cycles, but oh well.  This system is often referred to as slow glycolysis. 

The obvious question is, "Why don't we just use anaerobic glycolysis indefinitely until glycogen runs out?".  The limiting factor is that glycolysis generates H+ ions, which gradually acidify the blood.  The formation of lactate from pyruvate buffers some of these ions, but intense activity eventually overwhelms buffering capacity.  As [H+] increases, muscle burn and fatigue also increase .  This is why no one, no matter how trained, can sustain a dead sprint for long - waste products eventually overwhelm the system, forcing intensity to decrease.

Similar to how creatine supplementation improves the PCr system, beta alanine is a supplement with the purported ability to improve fast glycolysis.  Beta alanine has been fairly well confirmed to increase intramuscular concentrations of carnosine, which is a powerful buffering agent.  This, in turn, delays blood acidosis and allows for more time in the fast glycolysis system.  Beta alanine is fairly well studied, but if it's something you've never heard of, check out Effects of Beta-Alanine on Muscle Carnosine and Exercise Performance:A Review of the Current Literature.

Fat Oxidation System
Aerobic, takes place at all times, lasts indefinitely.

Activity past 2 minutes of high intensity will be regulated by slow glycolysis and fat oxidation, and the longer the activity goes, the more energy production will shift towards fat oxidation.
For very long events where glycogen will eventually deplete, (that nasty point in a marathon where heavy fatigue sets in, known as "bonking out") activity is fueled almost entirely by fat and some protein degradation.  It's beyond the scope of this article, but I should mention that this does not implicitly make steady state aerobics better for fat loss.

To recap:
  •  Energy systems
    • Anaerobic
      • ATP-PCr - Very high power, very short duration
      • Fast glycolytic - high power, short duration
    • Aerobic
      • Slow glycolytic - moderate power, long duration
      • Fat oxidation - low power, very long duration

The Bioenergetic Continuum
The bioenergetic continuum is just a fancy way of saying that energy systems do not work independently, and this is where most people get it all wrong.

The PCr system is a rocket ship - massive power, burns out quick, needs a ton of time to refuel.  Anaerobic glycolysis is an F1 car - tons of power, terrible fuel efficiency, needs frequent pit stops to keep working.  Aerobic glycolysis is a 4-cylinder hatchback - meh to good power, great fuel efficiency, super reliable.  Fat oxidation is a Geo Metro running on vegetable oil (get it?!  They both run on fat ahahahaha!!!) - garbage power, goes forever, tons of fuel just laying around all over the place. 

The amazing thing is that our bodies have this incredible metabolism which can seamlessly use all of the above at the same time, however much or little as needed, to best fit the demands of activity.  Need 100% power for a short period?  You're a rocket ship.  Need 95% power for 6 seconds? ?  You're half rocket ship and half V12 sports car.  Need 80% power for ~1 minute?  You're mostly a rocket ship and a V12, some Ford Focus, and even a little bit Geo Metro.  Need 25% power for 10 minutes?  You're some V12, mostly hatchback, and a good bit of Metro.  Distance runner?  You're pretty much all 4-cylinder and grease car.

It's vital to understand that though we generally use the term "anaerobic" to describe intense activity lasting less than 2 minutes, and "aerobic" to describe anything over that, the fact that every energy system is at work to some extent at all times. This is especially true of most game conditions where athletic demands are constantly shifting - you've got periods of all out activity where ATP/creatine is being depleted, high intensity periods where glycogen is the primary fuel source, intermittent relative rest periods that allow for creatine stores to at least partially replenish, and all the while, aerobic systems are contributing to a varying extent.

Duffield et al, 2004 directly measured the metabolic contributions for the 100m and 200m sprint. They found that it was right around 75%/25% and 70%-30% anaerobic to aerobic respectively, with a slightly higher ratio of anaerobic to aerobic for males. Gastin, 2001 indicates that aerobic metabolism contributes significantly even at durations/intensity classically considered purely anaerobic, and that anaerobic and aerobic energy systems reach a 50/50 contribution split between 1-2 minutes, likely at ~70 seconds. Losnegard et al, 2012, did a similar study on elite cross-country skiers skiing at maximal effort for ~3 minutes. They found that overall contribution was 25%/75% anaerobic to aerobic.  Case in point, aerobic contribution starts a lot earlier than we previously realized.

Furthermore, it seems aerobic metabolism can up it's game when anaerobic fuel is depleted. Bogdanis et al, 1996 indicates that in repeat-bout sprinting activity, anaerobic fuel contribution is lower on subsequent sprints (this is always going to be true unless enough rest for full PCr resynthesis occurs, very unlikely in a game unless a player is benched). Once this happens, aerobic systems kick in to help cover the gap. The study cited a 41% decrease in anaerobic fuel in the repeat bouts, but only an 18% performance drop due to aerobic systems sharing the load.

It is clear that aerobic contributions occur much earlier than previously assumed.  The bottom line is that the aerobic systems do contribute a significant amount of energy to what we always considered "anaerobics".  Doesn't this imply that we should be spending a significant amount of effort improving these systems?  Well, maybe not so much.

This graph summarizes energy systems nicely (note that PCr=ATP-PC, fast glycolytic=lactic acid, and aerobic system=slow glycolysis and fat oxidation):

What About Game Time?
Every major sport has been analyzed for it's metabolic demands. Various methods have reported slightly different contributions, but the general trends have long been established. Really, they're only estimates anyway since even within a sport, every athlete and every game is different.

  Figure 5.1 Essentials of strength training and conditioning (3rd ed., p. 95)

Some sports make it very easy to approximate energy demands - a short distance track athlete, for instance, is going to sprint a set distance for a more or less fixed duration, and we can predict with relatively high accuracy what energy systems are needed for that activity. Similarly, football and baseball/softball are fairly simple as well; short bursts of all out activity, high ratios of activity:rest, no real active recovery - all rocket ship and formula 1.  The tricky part is doing it with a field athlete in constant play, or a combat athlete.

A review by Spencer et al, 2005 looked at average sprint distance, number of sprints, and time to rest between sprints for elite level field sports such as soccer, lax, field hockey, etc. The review indicated that the average sprint time for these sports is a very consistent 2-3 seconds or 10-20 meters across many trials. Similarly, the average maximal sprint (the longest an athlete would have to sprint during a game) is 4.1 +/- 2.1 seconds. The average rest time between sprints was 20-60 seconds. The studies reviewed all resoundingly stated that while the player was in the game, 95% of rest was active, meaning that "rest" between sprints equates to moving around the field at a jog pace.  

The same review reports that for these sprinting activities, the contributions are 10% stored ATP, 55% PCr, 32% anerobic glycolytic, and 3% aerobic. This makes complete sense given the demands of a 3 second sprint, but what about when an athlete is forced to repeat this over and over as a game progresses?

Gaitanos et al, 1993 tested for energy contributions on a sprint protocol consisting of 6 10 second sprints followed by 30 seconds of rest. They found that after the first sprint, PCr stores had fallen to 57% of baseline, and that by the 10th sprint, PCr stores had fallen to only 16% of baseline. Given a full 3 minutes to recover, PCr had climbed back to 84% of baseline. It should be obvious that full PCr resynthesis will never take place in a game unless an athlete is benched.

It is well established that glycogen stores fall with activity. Somewhat surprisingly, using the same protocol, Gaitanos et al found that rate of glycogenolysis (how fast new sugar can be made) fell 11 fold, and rate of glycolysis fell 8 fold. Take home point - not only do glycogen stores fall, an athlete's ability to even utilize and make new glycogen falls as well.  I don't know why this occurs, but my guess would be that it's a self-limiting control to prevent acidosis.  The same review by Spencer et al reported that a single soccer game played at an elite level burned through 80-90% of glycogen stores. It also stated that those with lower starting glycogen sprinted less, walked more, had reduced running speed, and covered an average of 1800m less distance over the game.

In that same Gaitanos et al protocol, sprint performance from first to last only dropped by 27%. That's very significant over 6 repeat sprints (and would obviously continue to degrade past that point), but it should be much lower given the PCr and glycolytic degradations. The explanation? The aerobic systems pick up the slack, but don't do anywhere near as good a job.  The aerobic systems are a lot like that industrial-size can of Folgers you keep around for when the good coffee runs out.  It may not be the greatest, but it's there when you need it, it gets the job done, and it seems to never run out.

Energy Demands and Conditioning Strategies
I've spent the better part of this article illustrating that many sports have a large aerobic component. I've also used a good deal of it showing that what we always considered to be "anaerobic" work, actually has a very large aerobic component. You might be asking yourself at this point why I would ever say that aerobic training is a waste of time. Many coaches in the past have taken the standpoint that if sports have an aerobic component, then we need to train "aerobically".

Understanding that anaerobic conditioning actually involves a huge contribution from the aerobic system essentially invalidates this notion. Remember that over a SINGLE bout of maximal intensity sprinting, aerobic and anaerobic contributions match each other at ~70 seconds. Aerobic contribution only increases over repeat bouts, depending largely on rest periods used. This means that practically every form of known anaerobic training with any kind of reasonable rest period gives all the aerobic training most athletes ever need, while also maximally training the anaerobic systems. This is especially true if active rest is used.

Then again, why not just throw in more aerobic work, just to be safe and cover our bases? Put simply, excess aerobic training detracts from sports performance. Aerobic and anaerobic training have wildly different, diametrically opposed physiological adaptations; this is well documented and understood, and it's why distance runners can't sprint or jump to save their lives. An athlete simply cannot be highly conditioned in all systems. In this regard, I take the standpoint of "do as much aerobic work as necessary, and not a single bit more." Given the confirmed aerobic crossover of traditionally anaerobic work, for many athletes this means zero dedicated aerobic training. This is especially important when dealing with athletes that have precious little time to devote to S&C.

In a nut shell, aerobic performance is crucial, yet usually requires no dedicated improvement if anaerobic training is performed.

Plenty More Than Energy Systems
Beyond considering which energy system each sport utilizes, we also need to examine other adaptations that occur. *note: I'm not going to bother with references in the following section because frankly, it's all common knowledge that can be found in any textbook or reliable website and I'm too lazy to regurgitate.

Skill Practice
Ask any coach, and they'll tell you that sprinting/jumping/explosive movements are among the most difficult to teach. One major benefit of incorporating high intensity anaerobic training is that it allows for a lot of practice at the actual skill of being fast/jumping high/performing explosive movements. This is absolutely critical because of the huge skill component involved in sprinting quickly and efficiently.

A major mistake many coaches make is assuming that if athletes spend a lot of time running, then they'll become good at sprinting. In reality, sprinting mechanics and jogging mechanics are worlds apart. Sprinting for conditioning isn't going to confer the same benefits as dedicated speed work (done fresh, never to fatigue, with mental effort going towards optimal, smooth form), but it does give athletes a chance to get a whole lot of repetitions in under the physical demands of a game situation.

Substrate Storage
Athletes need glycogen, and plenty of it. As indicated by reviewed studies, athletes who carry submaximal loads of glycogen take a major hit to their game performance. Luckily, there's a way to essentially over-stuff muscle tissue with extra glycogen by utilizing a principle known as glycogen supercompensation.

The glycogen supercompensation window opens in response to an activity which depletes a large portion of stored glycogen. We can create this window by conditioning with activities that heavily tax the glycolytic system. It can be done with aerobic training as well, but it takes quite a long time to deplete glycogen enough to open a supercompensation window with low intensity activity.

I won't go too far into glycogen loading here - I will say that lot of people get it wrong by trying to do it a few hours before a game (there's nothing wrong with getting carbs in before a game, but that isn't supercompensation). The window is open after the taxing event, so get the carbs in then.

Substrate storage improvement isn't limited to glycogen.  Creatine phosphate, enzyme concentration, and even ATP stores are all subject to supercompensation induced by anaerobic training.

Power Generation and Muscle Composition
I probably don't need to tell you that athletes require the ability to generate power. Practically every athletic movement a player makes is the direct result of their ability to develop force rapidly and efficiently over a particular motor pattern.

There's mountains of studies indicating the negative relationship between aerobics and force production. This is largely due to neurological adaptations, over training, and hypertrophy inhibition (from the catabolic nature of aerobics). Its been shown conclusively that combining aerobic training with strength training and/or anaerobic conditioning reduces strength and power output. Furthermore, this relationship is unidirectional; aerobic training impairs anaerobic performance, but anaerobic training does not impair aerobic performance.

Injury Resistance
Bone and connective tissue adapt to stress just as muscle tissue does. High intensity training results in the growth and strengthening of bone and connective tissue, to better withstand the forces the body is subjected to during intense activity. This style of training also causes tendons to stiffen, making them more efficient at transferring muscular force.

These adaptations makes the body more resistant to injury and more efficient at force production. They occur as a response to high intensity anaerobics, but do not occur with low intensity aerobics.

Trade Offs and Risks
Is there anything to be lost by ditching aerobic training? Purely from a performance standpoint, and assuming the athlete is focused on only one sport or activity, then no. There are, however, other factors to consider.

First off, aerobic training increases VO2 max more than anaerobic training. This is well known and well documented. Whether or not this matters is up to the individual coach/athlete. There are still many coaches who strongly associate VO2 max and overall athleticism or fitness. I'm of the opinion that an athlete really needs no higher a VO2 max than what their sport demands, but it is what it is. Aerobics will definitely improve VO2 max more than anaerobics.

Secondly, the risk of over-training is considerably higher with anaerobic training. Burning an athlete out on anaerobic conditioning, especially when it's combined with resistance training, is a very real concern that isn't present with aerobic training. This concern ultimately falls on the shoulders of coaches. Implementing anaerobic conditioning into a complete training protocol requires much more skill, observation, and attention to detail on the coaches' part. Same goes for whoever handles the nutrition (which is usually the coach at most levels). Athletes, especially younger ones, must be strongly encouraged to consume enough calories/carbs and get enough rest, or they will burn out on a resistance exercise/anaerobic conditioning program.

Similarly, there's risk of injury to consider. It isn't necessarily higher with anaerobic conditioning, as aerobic conditioning has a whole set of chronic injuries and conditions that go along with it. Risk of acute injury is, however, certainly higher. Again, this is on the coach to make sure kids are adequately warmed up, neurologically primed, have no serious flexibility/mobility issues, and that his/her athletes have a decent of strength (debatable, but if your athletes can't squat/dead their body weight, they have no business sprinting).

One of the worst things a coach can do is dump a bunch of anaerobic work on a group of novices. The best way to handle anaerobic sessions is to treat the same way you'd treat strength training sessions - with attention to technique, fatigue, and recovery. 

Summary and Implications
The primary objective of any conditioning program is to prolong time to fatigue from game conditions. Baseline ATP storage is relatively immutable, so don't expect much improvement there. Some studies suggest that a well trained individual might carry more ATP, but considering the very short supply of local ATP stores (~2 seconds), it's unlikely that this would offer much actual performance increase.

The PCr system, and by extension fast ATP recycling, is limited by intramuscular creatine pools. The system itself can't really be significantly improved - once the fuel is gone, the system is done providing ATP until phosphocreatine is resynthesized. Some studies suggest that well trained athletes do resynthesize phosphocreatine more rapidly, but there's very little data to be found. That being said, there's piles of data to be found on oral creatine supplementation dramatically improving time to fatigue of the PCr system and resynthesis of phosphocreatine. In this regard, one of the best ways to improve the PCr system's conditioning is simply to supplement with creatine.

The fast glycolytic system is a different story. Because glycolysis creates negative byproducts, conditioning in the 10 second - 2 minute area depends largely on how well H+ ions can be buffered, and how much a person can tolerate the drop in blood pH (and the pain that comes with it). Conditioning above the lactate threshold has been shown to result in a 16-38% increase in blood buffering, as well as a higher tolerance to the physical discomfort of being above the lactate threshold.  In the real world, this means more time in fast glycolysis, AKA more time in a high energy system before fatigue.

Nutrition, and to a lesser extent supplementation, are paramount for high intensity endurance.  Creatine supplementation can offer a lot of benefit to the PCr system, and beta alanine to the slow glycolytic system (perhaps to a lesser extent) but nothing will ruin on field performance like starting a game with depleted glycogen.  We've all heard the adage "Strength is built at the gym, size is built at the dinner table. " - you could easily add in "conditioning is built at both."
The take home points:  though there is an aerobic component to plenty of sports, it is the anaerobic activity that wins or loses games.  Furthermore, classically "anaerobic" conditioning generally covers these aerobic needs, as there's actually plenty of aerobic work being done - especially when anaerobic work is combined with active rest.  Lastly, glycogen availability, and to a lesser extent supplementation, are huge factors in sports conditioning.  

 Here's how it breaks down in the real world:
  • Field sports
    • dominated by those who have well conditioned and prepared fast glycolytic system combined with an adequately conditioned aerobic system
      • anaerobic training will drastically improve buffering ability and performance
      • muscle glycogen should be as close to full as possible or performance will be severely impacted
      • creatine supplementation can benefit conditioning
      • beta alanine likely also beneficial
    • have a significant slow glycolytic component
      • anaerobic training with active rest covers this aerobic demand, no more aerobic training is needed
  • Football/short track/comp lifters
    • played almost entirely anaerobically
      • rest periods long enough/complete enough to stay anaerobic
      • should be conditioned purely with anaerobic training 
      • well conditioned and prepared fast glycolytic system is make or break
      • creatine supplementation can be hugely beneficial
  • Combat sports 
    • harder to predict given the chaotic nature of each match 
    • energy requirements largely dependent on pace of match
    • shorter play time, but much longer average bouts of maximal intensity
    • glycogen stores key, creatine and beta alanine beneficial
      • harder to manage due to water retention and weight gain 
    • K1/Thai Boxing
      • 3 minute round times push demands more towards aerobic conditioning
        • aerobic conditioning will become a larger factor in later rounds
    • MMA
      • 5 minute round times require a greater emphasis on aerobic conditioning, especially in the later rounds
      • high intensity nature + long duration necessitates more aerobic conditioning
      • carb loading should begin as soon as the weigh in is over
    • Wrestling
      • 2-3 minute round times and fewer rounds mean greater emphasis on anaerobic conditioning 
        • conditioning can be done at maximal intensity with little to no need for active rest
    • Boxing
      • potential for high intensity over large amount of rounds
        • aerobic conditioning necessary for late rounds, especially if early rounds have been very active
Energy system interaction and relative contribution during maximal exercise. Gastin, P. Sports Medicine. 2001, 31(10):725-741, 2001. Retrieved from

Human muscle metabolism during intermittent maximal exercise.

Gaitanos GC, Williams C, Boobis LH, Brooks S. J Appl Physiol (1985). 1993 Aug;75(2):712-9. Retrieved from

Baechle, T. R., & Earle, R. W. (2008). Adaptations To Anaerobic Training Programs. Essentials of strength training and conditioning (3rd ed., p. 95). Champaign, IL: Human Kinetics.

Energy system contribution to 100-m and 200-m track running events.
Duffield R, Dawson B, Goodman C. J Sci Med Sport. 2004 Sep;7(3):302-13. Retrieved from

Metabolic Limitations of Performance and Fatigue in Football. Abdullah F. Alghannam. Asian J Sports Med. Jun 2012; 3(2): 65–73. PMCID: PMC3426724. Retrieved from

Anaerobic capacity as a determinant of performance in sprint skiing. Losnegard T, Myklebust H, Hallén J.2012 Apr;44(4):673-81. Med Sci Sports Exerc. doi: 10.1249/MSS.0b013e3182388684. Retrieved from

Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise. J Appl Physiol (1985). 1996 Mar;80(3):876-84. Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK. Retrieved from

Physiological and metabolic responses of repeated-sprint activities:specific to field-based team sports. Spencer M, Bishop D, Dawson B, Goodman C. Sports Med. 2005;35(12):1025-44. Retrieved from

Wednesday, January 22, 2014

Yohimbine HCl: A Fat Loss Aid?

There's been one burning question on the lips and minds of dieters around the world: can yohimbine HCl help me lose stubborn fat? 

In my usual fashion, I've crafted a painstakingly thorough and long-winded answer to that question, full of sciency crap no one but me and like five other people care about.  Even so, this article should provide you with everything you ever wanted to know about yohimbine HCl supplementation. 

Note: If you've Googled yohimbine, there's a 99% chance you've read what Lyle McDonald has to say on it - if not, you'll probably want to take a look at his website,, and/or his book The Stubborn Fat Solution, where speaks to greater depths on the supplement.

What is Yohimbine?

Yohimbine hydrochloride (HCl) is the standardized extract of the active ingredient found in yohimbe bark, which grows natively in western Africa. Yohimbe bark has been used for generations as a holistic aphrodisiac, but supplement companies have recently begun to tout yohimbine HCl as both an ergogenic and fat loss aid. Right now, there's a relatively healthy body of research involving Yohimbine HCl as treatment for erectile dysfunctions and certain neurological conditions, but very little data on it's efficacy as a fat loss agent.

So, from a body composition perspective, what's this stuff actually supposed to do? Depending on who you ask, the supposed benefits of yohimbine HCl supplementation include heightened metabolic rate, appetite suppression, and preferential lipolysis (targetted fat loss) in “stubborn” adipose sites. 

Is there any merit to these claims? Let's dive right in and find out. 

*please note, yohimbine HCl is NOT the same supplement as yohimbe. Yohimbe supplements are generally uncontrolled, unstandardized, ground up tree bark. The dosage of active ingredient, yohimbine HCl, can vary wildly. If you're considering supplementation, get a quality yohimbine HCl extract.

A Very Condensed Endocrine Primer
To understand yohimbine, you must have at least a rough understanding of adrenergic receptors and catecholamines.  The endrocrine system can get a bit messy, so we'll try to keep this fairly simple.   


The word "catecholamine" is used to describe a number of plasma bound hormones, but it usually just refers to adrenaline (epinephrine) and noradrenaline (norepinephrine).  These hormones play a number of roles in the body, but it's common knowledge that adrenaline is a potent stimulant which increases heart rate, vasoconstrictor (closes blood vessels -> increases blood pressure), bronchodilator (opens airways -> increases airflow).  Most importantly for us, it also suppresses hunger, and increases blood sugar via inhibiting insulin (which normally mediates sugar from the blood, into cells) and signaling sugar release from the liver.  The net result is an increase in metabolic rate.  (Barth et al, 2007).  From an exercise physiology standpoint, some of these effects are not unlike what occurs as a result of aerobic training.  

Catecholamines are responsible for jacking up the sympathetic nervous system, and in fact you have a basal flow of these hormones at all times.  A large release of catecholamines occurs during the well documented fight-or-flight response, triggering a very noticeable manifestation of these effects.  You already know this though - think about what happened the last time you were in a fight-or-flight situation; your heart rate and blood pressure went up, you lost your appetite, and you got warm.  

A large release or infusion of catecholamines would be undesirable, as you'd basically be "on 11", and the effects would wear off shortly - so don't go sticking yourself with an epi-pen to try and lose weight.  That being said, it is well documented that an increase in plasma concentrations of these hormones does increase metabolic rate. 

Lastly, there is an important effect of catecholamines that, for some reason, always seems to fly under the radar: catecholamines increase tissue lactic acid and reduce muscle tissue's ability to use it as a gluconeogenic precursor (how we get sugar from non-sugars when more is needed for exercise, a very important factor in anaerobic endurance) (Hamann, et al. 2001).  Not only does this effect reduce time until fatigue under heavy anaerobic work, it also means that that blood will acidify more rapidly because there's less lactic acid being shunted into muscle tissue.  I won't get any further into lactic acid because it's a whole other can of worms, but these are potentially serious implications for exercise performance.

Adrenergic Receptors

Adrenergic receptors are the the body's way of monitoring and making use of catecholamines.  They come in two main flavors - alpha, α, and beta, β.  There's a number of subgroups with a huge host of varying hormonal implications between them, but we're only going to examine a few of the effects and keep it specific to fat loss and exercise performance:

Effects of Agonizing (Activating) Each Receptor:

  • α-1
    •  Blood vessel constriction, notably in the gastrointenstinal tract. Sphincter contraction in the gastrointenstinal tract
  • α-2
    •  Can increase or decrease blood vessel diameter based on agonist type and dosage. Reduced force of heart contraction. Inhibition of lipolysis. Inhibition of noradrenaline secretion
  • β-1
    •  Heart rate/force of heart beat increase.  Lipolysis (fat loss).  Dilate skeletal muscle vessels.  Increased sugar production and metabolism in liver and muscle tissue.
  • β-2
    •  Bronchodilation (opening of the airways)
  • β-3 
    •  Lipolysis
Again, this is a very limited list of what these receptors do, and I encourage you to look more into them if you plan on taking any sort of receptor agonist or antagonist (which yohimbine HCl is).
File:Adrenoceptor-Signal transduktion.PNG
Ripped straight off of Wikipedia
These receptors are found all over the body, and though their downstream effects vary, they all share one common trait -they are the targets of catecholamines.  Greatly simplified, upstream structures produce catecholamines, some event(s) happen, the catecholamines are released, and they make their way to the adrenergic receptors.  At this point the catecholamines either agonize (boost the effects of) or antagonize (diminish the effects of) whatever the function(s) of that receptor may be - again, this varies greatly depending on the type and concentration of receptors, the tissue they're located in, the type and amount of catecholamines, and a lot of other variables.  

Yohimbine: A Strong α-2 and Weak α-1 Antagonist

Yohimbine HCl is a non-selective alpha antagonist, but has a much higher affinity for alpha-2 receptors compared to alpha-1 receptors, meaning that it antagonizes α-2 receptors to a much greater extent. It's a little tricky to understand the noradrenaline inhibiting function of the α-2 receptor, so pay attention to the following: as catecholamines diffuse across the synaptic cleft, they bind to pre and postsynaptic terminals. When catecholamines pass the presynaptic terminal of an α-2 receptor, a negative feedback loop activates, which inhibits release of additional catecholamines.   In this regard, α-2 receptors essentially act as a “flow check” for upstream catecholamine secretion (Philipp et al. 2002).  

It's a lot like how the heating system in your house works; you have a set point controlled on your thermostat, the furnace (those upstream functions which release the catecholamines) fires up, heat is applied to the water in the pipes (catecholamines enter the blood stream), the hot water reaches the space you want heated and sensors determine that no more hot water is required (receptors determine that the tissue doesn't need any more catecholamines, and the negative feedback loop is activated, stopping further release upstream).

Antagonizing this receptor reduces this function, which is to say that it reduces the receptor's effect on reducing the upstream flow of catecholamine secretion. In other words, it's like tricking those sensors in your heating system to not work as well, making your furnace release more hot water than it needs. Heat goes up in the room, more catecholamines are delivered to tissues (actually a decent analogy since heat increases in both examples).

Take another look at this graphic:

File:Adrenoceptor-Signal transduktion.PNG
Ripped straight off of Wikipedia
You'll see that agonizing (the regular line) the α-2 receptor inhibits (the checked line) transmitter (norepinephrine) release. The important thing for us to keep in mind is that yohimbine HCl essentially inhibits the inhibitor, which actually increases transmitter release. Through this mechanism, Yohimbine HCl should ultimately increase noradrenaline release. 
To summarize, yohimbine HCl acts as a non-selective α receptor antagonist, having a high affinity for α-2 receptors and a moderate affinity for α-1 receptors (Millan, 1999).   The potent α-2 blocking effect of yohimbine HCL downregulates the catecholamine-inhibiting action of the α-2 receptor. This, in turn, causes upregulation of norepinephrine secretion (Okamoto et al, 2012, Shibao et al. 2010).

It is extremely important to understand that this increase occurs upstream, meaning that noradrenaline secretion is increased at the sites of production. This means that plasma concentrations will increase and all downstream receptors will experience an increased flow of noradrenaline, not just the α-2 sites.

This noradrenaline will then go on to agonize all α and β receptors to a varying extent based on affinity, and that's where this situation gets interesting.  Noradrenaline is a strong agonist of α-1, α-2, and β-3 receptors, but a weak agonist of β-1 and β-2 receptors.  What happens when these receptors are agonized all at once, to different extents?  The answer is obviously dose-dependent - in theory, more yohimbine hcl taken, the more upstream norepinephrine secretion occursIt stands to reason, then, that supplementing with yohimbine HCl essentially causes all of the effects of increased noradrenaline discussed in the catecholamine section. 

In reality, this begs more questions than it answers.  How does this increase in noradrenaline effect each receptor in each tissue? How would each receptor respond to having noradrenaline flow increased relative to adrenaline flow? Does the answer to that question change depending on the dosage, or perhaps some other variable we aren't aware of? And so on and so forth. The answers to these questions matter, because each receptor has different affinities for and responses to each type, ratio, and quantity of catecholamine - and when you're dealing with mechanisms that control functions like cardiac output and airway tone, it's kind of important to know these things. 

Yohimbine HCl and Stubborn Fat
As mentioned, catecholamines have a well documented effect on lipolysis (fat loss).  The efficacy of catecholamines’ ability to induce lipolysis varies between adipose sites, primarily because of differences in blood flow and the ratio/number of  α and β receptors (Arner, 1999).  Historically “stubborn” fat sites, particularly those around the hip and butt, have a higher concentration and ratio of α-receptors, where fat in the abdomen tends to have a higher concentration of β-receptors. Sites with high α-receptors also tend to have less blood flow compared to abdominal fat (Millet et al., 1998). 

Does yohimbine HCl target "stubborn" fat? There's a few studies done on supplementation and overall fat loss, but there's no clinical data or research that I'm aware of which tested for fat loss in specific areas - so for now, its a guessing game. That being said, since one of the primary functions of α-2 receptor agonism is the inhibition of lipolysis, then anything which antagonizes α-2 receptors should in turn promote lipolysis. This is especially true of areas where there is a high concentration of α-2 receptors and a low concentration of β receptors (again, typical of "stubborn" fat sites). Though unsubstantiated, yohimbine HCl should indeed help bust stubborn fat. 

Performance Enhancement and Hunger Suppression
Yohimbine HCl has not shown any capacity for improving physical performance measurements whatsoever.  It might be logical to assume that anything which triggers what is essentially a very low grade fight-or-flight response would improve performance. Alas, this is not the case. Ostojic, 2002, and McCarty, 2002, both found that yohimbine failed to improve exercise performance, and there's more studies out there with similar results. The lack of performance enhancement coupled with it's catabolic properties makes yohimbine HCL entirely unsuitable as a pre strength training supplement.

The hunger suppression question is an interesting one.  One of the functions of α-2 receptors is to block hunger and decrease stomach motility. It stands to reason that anything which antagonizes α-2 receptors should actually increase hunger. 

There's no studies I'm aware of which polled for hunger suppression, but many users anecdotally report that it does reduce appetite.  Perhaps the overall increase in noradrenaline agonizes receptors which elicit hunger suppression potent enough to override the hunger boosting effect of directly antagonizing α-2 receptors. Or maybe not, and it's all in people's heads. In either case, the reported hunger suppression effect is mild at best, so we can deem yohimbine HCl ineffective as an appetite blocker. 

A Look At Some Existing Research
A study by Bharucha et al., 2008, administered an acute dose of 0.125 mg/kg body weight followed by an infusion of 0.006 mg/kg body weight in 55 healthy human adults.  Blood pressure, heart rate, and plasma catecholamine levels were measured both before and after a 300 kcal liquid feeding.  The study found that the yohimbine HCL dose increased serum catecholamine levels by 2-3 fold.  Heart rate remained unchanged, but blood pressure increased significantly.

Similarly, a study by Galitzky et al, 2001, administered a 0.4 mg/kg acute dose to 13 healthy adult male dogs following an 18-20 hour fast.  All 13 showed significant increases in catecholamine levels, as well as blood pressure. Resting metabolic rate was also increased by an average of 16%.  It must also be noted that restlessness and anxiety were all significantly increased as well, though no change to alertness was found.
Another study by Kucio et al, 1991, placed 20 obese females on a 3 week, 1,000 kcal/day diet.  They were kept on the same diet for another 3 weeks, but half were given 5 mg of yohimbine HCL 4 times a day, while the other half were given placebo.  The yohimbine HCL group lost an average of 3.55 kg, while the placebo group lost an average of 2.21 kg.  

A study by Sax, 1991, had half of a 47 health adult male cohort take up to 43 mg yohimbine HCL per day for six months, while the other half took placebo.  No differences in BMI, body weight, and body fat change were measured between the two groups.  It must be noted that caloric intake was not addressed or monitored during this study.   

Similar studies by Ostojic, 2002, and McCarty, 2002, both found that a moderate pre-exercise dose of yohimbine HCL increased serum FFA concentrations both during and after exercise, and that fat loss was significantly higher amongst the yohimbine HCL group compared to placebo.  Blood pressure was increased, but not heart rate.  Both studies noted no increase in exercise performance markers between the groups.  

...and so on. Most of the studies corroborate the same results; when used with a hypocaloric diet, yohimbine HCl increased the secretion of catecholamines and thus increased lipolysis.

Multiple studies have shown that yohimbine HCL increases blood pressure, though seems to have little, if any, effect on heart rate.  This is likely just how the change in catecholamine levels pans out in regards to vascular tone.  Yohimbine HCL supplementation is contraindicated for anyone with conditions, diseases, or risk factors impacted by an increase in blood pressure. In a similar vein, yohimbine HCL can reverse the vasodilative/blood pressure lowering properties of certain medications, most notably clonidine (Smet and Smeets, 1994). Yohimbine HCL is contraindicated for those on antihypertensive medications.

In studies which polled for it, an increase in anxiety was reported with high frequency after yohimbine HCL dosage (Galitzky et al, 2001). The reports are almost always more severe for those with preexisting symptoms of depression or anxiety. This is a well-documented effect with a large body of evidence from studies testing yohimbine HCL on mood and anxiety disorders. While not necessarily a contraindication, users may expect some minor to moderate mood alteration and increase in anxiety.  

Lastly, there appears to be a synergistic, cascading effect from taking yohimbine HCl with other stimulants such as caffeine (McCarty, 2002). Considering the well-documented increase in smooth muscle tone and thus blood pressure caused by yohimbine HCL supplementation, it is logical that any substance which further increases either smooth muscle tone or heart rate would potentially lead to tachycardia or hypertensive crisis.  Many other supplement, especially those used as thermogenics/performance enhancers, also affect adrenergic receptors. The moderate dosage of caffeine most users usually coingest with yohimbine HCl is fairly benign, but you wouldn't catch me taking it with ephedrine HCl or any other more potent stimulants. If you chose to take an ECY (ephedrine, caffeine, yohimbine) stack or any other combination of yohimbine HCl and other substances shown to increase cardiac output/vascular tone, you're taking a significant risk. If you wind up in the ER with hemorrhaging eyes and a pulse so high you're gettin friction burns on your heart, don't tell the ER doc I didn't warn you.


Dosage has always been done in the 0.2 mg/kg body weight range; some study started this (I forget which) and the trend has just sort of continued. This dosage has proven effective and relatively safe for eliciting lipolysis. Up to 20 mg a day, split into two 10 mg doses, has improved lipolysis in healthy adult males. I wouldn't go any higher than that in any circumstance, and it's probably best to just stick to the 0.2mg/kg body weight range. Within a normal range, it really comes down to stimulant sensitivity and your own personal mental stability - as mentioned, for many with existing depression/anxiety, yohimbine HCl has exacerbated these conditions. Pushing the dosages higher than this will likely result in some nasty and potentially serious side effects of the cardiac and psychological nature. 

While we're on the subject, an effective dose requires keeping insulin to a minimum. A function of pancreatic α-2 receptors is to block insulin release, so antagonizing them will increase the effect of anything which triggers an insulin spike. The effects of yohimbine HCl don't dissapear in the presence of insulin; it actually boosts the release of insulin thereby negating any lipolytic effects it may otherwise have provided. Many will tell you that yohimbine HCl has to be taken while fasting - that's a sure way to avoid an insulin spike, but it can also just be taken with a non-insulinogenic meal (basically a keto style, medium-low protein, high fat meal with little to no carbs).

Odds and Ends 
A study by Keller et al., 1989, indicates that norepinephrine boosts th effects of ketosis - but the study didn't use yohimbine HCl, rather a direct infusion. Glucagon and insulin levels were also regulated via infusion. Yohimbine HCl may increase norepinephrine which may intensify ketosis, but that is not what this study tested for directly. Food for thought. 

I'm going to go out on a limb and say that it wouldn't surprise me if supplementing with yohimbine HCl would A) lead to some measure of blunted catecholamine response once you come off , and B) lead to acutely reduced catecholamine secretion once you come off. I have absolutely no evidence for this. It's a phenomenon seen with other supplements/medications which alter the natural production or secretion of something the body produces. The body often grows accustomed to an exogenous substance doing some of the work it usually does, and when that substance goes away, there's usually lag time until the body adapts to not having that substance anymore. Again, no evidence, just something to consider.

Conclusion and the Cliff Notes
So, what can we ultimately say about yohimbine HCl as a fat loss agent?  Based on mechanism of action alone, the supplement should increase norepinephrine levels, which should enhance lipolysis.  Likewise, it should also antagonize α-2 and α-1 receptors, increasing lipolysis specifically in classically stubborn fat sites. It is probably not particularly effective as an appetite suppressant at nominal dosages.

In regards to the research, its pretty clear that in studies where yohimbine HCl was used in conjunction with a hypocaloric diet, the supplement appeared to be an effective fat loss aid. In studies where calories were unaccounted for, yohimbine HCl itself did not cause fat loss. This should be a no-brainer to anyone with a basic understanding of how fat loss works. 

We can say with a fair degree of confidence that yohimbine HCl:
  • Antagonizes α-2 receptors
  • Increases upstream secretion of noradrenaline
  • Increases amount of noradrenaline received by all adrenergic receptors
  • Improves overall lipolysis
    • Improve lipolysis specifically in stubborn fat sites
  • Increases vascular tone, blood pressure
  • Likely exacerbates preexisting psychological conditions
  • Is not an effective performance enhancer or appetite suppressor
  • Is effective at a dosage of 0.2 mg/kg body weight 
  • Should be taken fasted or with non-insulinogenic, keto-style meals 
  • Is a suitable pre aerobics supplement, but not a suitable pre strength training supplement

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