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muscled absby: Kelly Baggett

Mention the term ‘ectomorph’ and most people think of the naturally ripped guy who can put away 10,000 calories per day and never put on an ounce of body-fat. Often cursed in the ‘natural’ amount of muscle they carry yet blessed in the leanness department, the ecto is both revered and scorned by his peers for his ability to put away food like a human garbage disposal unit while never losing his abs or gaining an ounce of fat.

However, based on my observations I’ve identified two different types of ectomorphs. One is the naturally ripped ectomorph I described above. The other is what you might call the ‘skinny-fat’ ectomorph. Both groups are naturally thin and tend to have long limbs, long tendons, and small muscle bellies. Both groups have super fast metabolic rates. Yet that is where the similarities end. One group tends to be fast twitch dominant while the other group wouldn’t know what a fast twitch muscle was if it jumped up and bit them in the ass. One group RARELY if EVER gains fat and they put on muscle and strength very easily as long as they eat enough. The other group really struggles to put on any semblance of muscle and strength and they also tend to have a much softer appearance.

For every one of the what could be called, ‘genetically gifted’ ripped ectomorphs, you’ll find plenty of guys that are built like an 80’s rock star – a rake covered in a veneer of lard.

I’ve heard it called ‘scrawny white boy syndrome’, ‘pure hardgainer genetics’ and a few other things; yet regardless of what you call it, the song remains the same. Bodybuilding is difficult for these people. Not only do these folks not have any tendency whatsoever to build muscle, but they don’t have a whole lot of tendency to be lean either. In contrast, the ripped ectomorph is ALWAYS lean and usually very solid and strong for his size. Providing he eats well, he actually has excellent bodybuilding genetics.

The skinny-fat ectomorph is well, just skinny. This type of ectomorph has an entirely different set of problems then the ripped ectomorph. Ever since I first heard Dan Duchaine say, “There’s a big difference between being ‘lean’ and being ‘skinny’, I’ve always been curious about the difference. Now, after about 12 years of observation and a little education I think I’ve pretty much got it figured out. Dealing with the physiology and problems of the skinny-fact ectomorph is what I want to talk about today. But first let’s talk about the physiological differences between the lean ecto and the skinny ecto.

What Causes the Differences and Problems?

You see, the outward appearance of a person (such as the amount of muscle they tend to carry and how easily they build muscle and shed fat), is largely controlled by what internal messages the body is sending to the external parts, such as the muscles, and what those external parts are ‘being told’ to do by the internal signals. Your body has an entire ‘signaling’ network in place that allows various parts of the body to communicate and send messages to other parts, that ‘tell’ the body what to do and how to behave. A hormone is nothing more then a signal or messenger. Your brain releases signals that communicate with your muscles and other peripheral tissues while your muscles release signals that communicate back to your brain and tell it what’s going on. Increase this, decrease that. From a bodybuilding standpoint, what those messages are saying largely determines how well you build muscle and fat.

What’s the difference between a male and female? It’s all hormonal, and hormones are nothing but internal signals. How about a boy and a man? Again, all internal signaling. Someone with good genetics and bad genetics? Mostly all hormonal. When you see a physical characteristic demonstrate itself ‘outwardly’, such as a scrawny ass hardgainer, what’s often causing that characteristic is often somehow related to the overall message carried out by the internal signaling. In the case of the skinny fat ectomorph the message screams, “Stay scrawny and weak!”

Understanding the ‘Ripped’ Ectomorph

The only real problem the true ripped and lean ectomorphs have is that they have a fast metabolism. Many professional athletes in popular American sports are naturally in this class. They start off skinny as rakes but end up being powerhouses. The limiting factor for them is eating enough food. If they eat and train with any type of consistency they will gain pure muscle without any fat gain.

Characteristics of the Ripped Ectomorph

The ripped ectomorph may appear docile, yet inside, energy runs full bore. The sympathetic nervous system of the ripped ectomorph is geared for sport. They may have characteristics such as increased leptin sensitivity in the brain, (which means their appetite tends to shut off even at a relatively low body-fat), good nutrient partitioning (which means their physiology shuttles nutrients easily into the muscular department), and a low number of fat cells; yet I believe what separates them from the other group is that most of the increased metabolism and nervous stimulation existing in them occurs due to greater production and better CNS sensitivity to androgens like testosterone and DHT. I believe this is the case, rather than greater stress hormone production and sensitivity that occur in the other group, which I’ll cover in a minute.

Sensitivity to androgens like testosterone and DHT can vary considerably, an estimated 4 to 5 times according to some sources, which is probably a big reason why sprinters and other track athletes get superior results using anabolic dosages most bodybuilders would laugh at. As anyone who has ever been on any type of androgen will tell you, the effect on metabolic rate is considerable. Now, what happens if you take a young teenager full of testosterone or put a normal aged guy on steroids and they don’t eat enough? They don’t get any gains whatsoever. What happens when they start eating? They EXPLODE. Same type of deal with the naturally ripped ectomorph.

The effect of anabolic hormones on the muscular characteristics such as fast twitch expression and relative strength is also significant as well; and nobody can deny the existence of those qualities in this ‘group’ of ectomorphs.

The Skinny-Fat Ectomorph – Summarizing the Problems

From a bodybuilding perspective, the problems for the skinny-fat ectomorph are much greater. Not only do they have a less then optimal structure and a lack of positive muscular characteristics (such as lack of total muscles cells and lack of fast twitch muscle cells), but they lack the naturally good anabolic hormone production of the first group. The metabolism and sympathetic nervous system runs very much on high gear but it seems to be dominated by more of a cortisol (worry-wort) dominated stimulation. This group definitely seems to have an increased sensitivity to stress and not only does stress impact virtually every system of the body, but it also negatively influences androgen production. Not only does this stress sensitivity interfere with muscle growth, but it can also make recovering from life itself difficult. When you add more stress in the form hard training, things can get a lot worse, as you will see in a minute.

Running through the Problems

Now let’s go through the problems of the skinny-fat ectomorph and see how they relate to the internal signaling:
1. Poor Endocrine Status (Overproduction of cortisol);
2. Body Structure;
3. Lack of work capacity (overtraining); and
4. Lack of fast twitch muscle

Poor Endocrine Status – Overproduction of Stress Hormones

From a growth standpoint, the easiest way to get as big as humanly possible is to maximize your endocrine status. If you take steroids or have good genetics a lot of that is automatically taken care of for you. Endocrine status depends on the level of anabolic (muscle building) hormones like testosterone, DHEA, IGF-1, and growth hormone, and their relationship to the level of your catabolic (muscle eating), hormones like cortisol.

The absolute numbers of those various hormones doesn’t really mean jack, but the relationship between them does. In other words, you might have the testosterone level of a Gila monster but it won’t mean a damn thing if you also have the cortisol level of a guy getting ready to jump in a pool with sharks to test out a shark repellent. Or you could have a low to moderate testosterone level, but if your cortisol is as low as a male porn star, you will probably tend be in a good anabolic state for muscle growth.

1. Besides influencing muscle growth and paritioning, your anabolic status also influences how fast you recover.
2. Anything that ‘creates’ stress, tends to increase catabolic hormones and decrease anabolic hormones. Anything that alleviates stress, like sleeping, eating, meditation etc. tends to decrease catabolic hormones and increase anabolic hormones.

From an endocrine perspective, the body does not differentiate much between stressors. Which means that emotional stress, a lack of sleep, a bad relationship, a shitty job, dealing with stupid people, training, and even THINKING about something stressful all add up to create more catabolic hormones; and negatively influence your endocrine status, and wreak havoc on your ability to train and progress.

Hell, some people are so stress sensitive they can’t even recover from life itself much less hours per week of hardcore lifting. This tends to be the problem many skinny-fat ectomorphs suffer from. Note the number of stress related disorders such as anxiety, depression, etc. suffered by people in this group. These dudes are often so stressed out that adding balls to the wall training to their already stressed out state is like beating a dead horse. No matter how hard you kick him, that sumbitch ain’t getting up. No matter how hard you train some ectos, ain’t nothing happening until they first get to where they can recover from their daily stressors.

If having stress sensitivity wasn’t a big enough problem, with each subsequent stressor the body becomes even more stress hyper-responsive. In someone who is very ‘over-reactive’ to stress, they tend to have a hard enough time staying in homeostasis even without any other external influences trying to knock them out of it. I’ve likened the hardgainer physiology similar to what most people only experience after a bad breakup, a divorce, or some really emotional upsetting event that throws their entire physiology off kilter. Only they don’t have to go through a divorce, a bad breakup, or whatever, to experience the same type of effects. Muscle gain is difficult when recovering from life itself is difficult. For more info on stress, stress sensitivity, and its effects in general, I highly recommend Robert Sapolsky’s book, “Why Zebra’s Don’t Get Ulcers”.

Body Structure

Ectomorphs tend to have less then an optimal structure for bodybuilding. That observation itself should be worth of some sort of prize. What do I mean by ‘structure’? Well, length of the bones and natural number of muscle cells. Someone with naturally round and full muscle bellies tends to carry a lot of muscle cells in those muscles and thus they more growth potential. Chances are pretty damn good Ronnie Coleman was born with more muscle cells then Pee Wee Herman. Those with long bones and long tendons tend to have short muscle bellies and a lack of muscle cells, and thus not a whole lot of growth potential.

If that weren’t bad enough, long limbs can make it difficult to get tension on key muscle groups because the bones get in the way. That’s why some guys can squat and have trouble developing their quads while others can bench and have trouble developing their pecs. ‘Getting to’ the muscle is more difficult for the ectomorph due to those structural reasons and also because of what is often poor neuromuscular coordination. Thus, while a bench press may work fine for a mesomorph, the ectomorph will often find flyes develop their chest more effectively and so forth. Whereas freaks like Mike Mentzer, Dorian Yates, and other HIT freaks are ‘capable’ of totally exhausting a muscle with one hardcore set, many ectomorphs are gonna need a slightly different approach to get the same amount of stimulation.

Variations in limb lengths and body structure can change leverages, weak links, and even the type of injuries people get. For example, the lower back is usually more of a limiting factor for tall athletes when it comes to doing squats. In fact, even in the absence of any acute injury, most D1 basketball players already have a degree of degenerative disk disease simply because of the way they’re built. Additionally, if you survey 100 successful short limbed bodybuilders and 100 successful long limbed bodybuilders and ask them what exercises they benefit from the most, I’m sure you’ll see a disproportionate amount of long limbed guys preaching flyes, laterals, and hack squats; and a disproportionate number of short limbers preaching benches and military presses. The only explanation is that people tend to gravitate to what works for them.

Body Structure and Internal Physiology

Now, is their any relationship between the body structure and internal signaling? Sure. The relationship between body structure and various anomalies related to psychology and physiology is fairly well documented. For example, if you take a look at people with a benign heart condition called mitral valve prolapse (MVP) it is well documented that many of them suffer from an imbalance in the autonomic nervous system totally unrelated to the valvular abnormality that causes the body to overproduce fight or flight hormones like epinephrine and cortisol. (2-5)

The term “MVP syndrome” (MVPS) is used to refer to symptoms due to endocrine or autonomic dysfunction that occur in these people MVP and that cannot be explained on the basis of valvular abnormality alone. It is believed that while the fetus is developing in the womb, certain parts of the nervous system are also developing, so while the mitral valve abnormality and the enhanced sensitivity of the SNS have nothing to do with each other, they are associated. Several studies have shown that patients with MVPS have high urinary epinephrine and norepinephrine excretion, high plasma catecholamine concentrations, and hyperresponse to adrenergic stimulation.

Many people with MVP experience panic attacks, nervousness, low blood pressure, insomnia etc. (how many hardgainers also experience those symptoms?). Many also have a VERY thin and frail ectomorphic type build with often a flat breast plate. Since the heart valve irregularity evidently has nothing to do with the nervous system effects experienced and plenty of people experience that same imbalanced nervous system in the absence of MVP, I believe a natural lean towards that same hyperactive sympathetic nervous system is present in many others and probably contributes a lot to the typical ecto problems as well.

What other evidence is there linking structure to neural and endocrine factors that could influence things from a bodybuilding standpoint? Keep in mind the skinny-fat ecto is inherently gonna have a natural tendency to overproduce stress hormones. Now, what do stress hormones do? Well, one thing they do is negatively impact testosterone levels.

Look at the effects of stress on growth. Stress has a direct negative effect on testosterone. (10-14) Not only does lower testosterone obviously lead to less muscle mass, but lower testosterone levels can actually lead to delayed puberty and longer limbs as is evident if you look at castrated individuals from the earlier part of the 20th century and people with genetic conditions like Kallmans syndrome. Stress also impacts growth hormone levels. In one study done on children in a hospital setting, the impact of positive relationships on growth hormone was enough to cause a doubling of growth over short durations of time.

Next Problem – Overtraining

Anyone who observes ecto’s on a consistent basis will realize they do have a tendency to overtrain. A given amount of volume in a skinny-fat ecto takes more time to recover from. What causes them to have such a tendency towards overtraining? Well, in addition to the above ‘stress sensitivity’ factors, they are also probably more sensitive to the inflammatory cytokines released by the body in response to muscular damage. (15)

What the hell is an inflammatory cytokine? Well, it’s just a chemical messenger. The main chemical messengers I’m concerned about are the ones that send messages related to ‘overtraining’. Recent evidence indicates systemic overtraining is actually caused by the following process:

When a muscle is damaged, the cytokines IL-6 and TNF-Alpha are released in response to that damage. These cytokines then go up and stimulate parts of the brain and the CNS that, in addition to creating more whole body inflammation, also ‘signa’” overtraining type symptoms which tend to negatively impact energy, motivation, and strength levels. Get enough of this and it leads to overtraining. One that ‘overexpresses’ inflammatory cytokines would likely tend to have a low muscular work capacity and a tendency towards overtraining. They would not tolerate much muscle damage and when they did create microtrauma they would get large systemic effects from the microtrauma response.

Being ultra sensitive to the stress of training makes it difficult to make strength gains and train with any sort’ve frequency. The end result is thiat skinny-fat ectos have to really watch their training volume.


One other factor that likely separates the ‘ripped’, lean and strong ecto from that of the skinny-fact ecto is the angiotensin converting enzyme. Angiotensin converting enzyme (ACE) contributes to blood flow, blood pressure, vascularity, glycogen storage, and host of other things. In humans ACE _expression is dependent on what’s called insertion (I) or deletion (D) genes. Three phenotypes exist, I/I, I/D and D/D.

One specific ACE genotype, called II (insertion/insertion), is linked towards performance in aerobic events and has a cardioprotective effect. Those with the II ACE gene have less ACE, tend towards lower blood pressure, more Type I fiber, higher degree of vascularization, higher levels of interstitial glucose, less visceral fat accumulation and more subcutaneous fat accumulation. This is good if you want to be a marathon runner or live to be 100. Not so good if you wan to be a fast twitch dominant strength athlete or build a lot of muscle.

Those at the opposite end of the spectrum would have the DD (deletion/deletion) ACE gene and have more ACE. They have poorer endurance oriented performance but greater muscular strength and muscular hypertrophy, more type II fiber and more cellular glucose stores. They also appear to have a much greater risk of heart disease, high blood pressure, stroke, and a lean towards visceral fat accumulation. (17,18)

The distribution of these phenotypes among Caucasian males is 25% II , 50% ID and 25% DD. That means if you fall in the former or latter category, you have a genetic tendency to become better at endurance or strength sports. (16)

Not all that surprisingly, african americans tend to express the “D” allele with a much greater frequency then whites. (19) Those with more of a natural soft marathon runner type physique such as our skinny ecto would likely lean towards the opposite “I” allele.

Summarizing the Problems

So, to summarize we have this big circle. A naturally hyperactive person naturally geared towards overproducing stress hormones. A person naturally geared towards over-reaching and overtraining. A person that has a hard enough time recovering from life itself. A person that doesn’t have a lot of testosterone. So what are we gonna do about it? Well, that’s what I’ll talk about next time.



1. “Why Zebras Don’t Get Ulcers”. Sapolsky, Robert. Owl Books
2. Association between idiopathic mitral valve prolapse and panic disorder. Tamam, Ozpoyraz, San, Bozkurt. Department of Psychiatry, Cukurova University Faculty of Medicine, B. Blok No.15, 01130 Adana, Turkey
3. Mitral valve prolapse: causes, clinical manifestations, and management. Devereauz, Kramer, Kligfield. New York Hospital-Cornell Medical Center, New York
4. Boudoulas, J. (1992). Mitral valve prolapse: Etiology, clinical presentation and neuroendocrinefunction. Journal Heart Valve Disease, 1, 175188
5. Coghlan, H., Phares, P., Cowley, M., Copley, D. & James, T. (1979). Dysautonomia in mitral valve prolapse. American Journal of Medicine, 67, 236244
6. “Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?” Smith. Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, NC 28608, USA.
7. “Elucidating the unexplained underperformance syndrome in endurance athletes : the interleukin-6 hypothesis.” Robson. UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, Sports Science Institute of South Africa
8. “Tissue trauma: the underlying cause of overtraining syndrome?” Smith.
Tshwane University of Technology, Pretoria, South Africa
9. “Somatomedin and growth hormone in psychosocial dwarfism, Saenger, Levine, Wiedemann, Schwartz, Korth-Schutz, Parera, Heing, New. Padiatrie und Padologie (1977): supp. 5, 1.
10.“Lower sex hormones in men during anticipatory stress,” NeuroReport 7 (19996): 3, 101.
11.“Suppression of plasma testosterone levels and psychological stress,” Archives of General Psychiatry 26 (1972): 479.
12. “Acute suppression of circulating testosterone levels by cortisol in men,” Journal of Clinical Endocrinology and Metaboism 57 (1983): 671
13. “Direct inhibitory effect of glucocorticoids upon testicular uteinizing hormone receptors and steroidogenesis in vivo and in vitro,” Endocrinology 108 (1981): 2142
14. “Testosterone dose-response relationships in healthy young men.” Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81. Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
15. Rodney Johnson’s Laboratory of Integrative Biology.
16. Jones A, Woods R. Skeletal muscle RAS and exercise performance. Int J Biochem Cell Biol. 2003 Jun;35(6):855-66.
17. Effect of angiotensin-converting enzyme insertion/deletion polymorphism DD genotype on high-frequency heart rate variability in African Americans. Thayer, Merritt, Sollers, Zonderman, Evans, Yie, Abernethy. Nation ional Institute on Aging Intramural Research Program, the National Center on Minority Health and Health Disparities, National Institutes of Health, Bethesda, Maryland, USA
18. Elevated mortality rates from circulatory disease in African American men and women of Los Angeles County, California–a possible genetic susceptibility? Henderson, Cotezee, Ross, Yu. Departtment of Emergency Medicine, University of Southern California School of Medicine, Los Angeles, USA.
19. Frequencies of the angiotensinogen gene and angiotensin I converting enzyme (ACE) gene polymorphisms in African Americans. Rutledge, Browe, Ross. University of Florida, College of Pharmacy, Department of Pharmacy Practice, Gainesville 32610, USA.


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