пятница, 23 января 2015 г.

Gender Differences in Training and Metabolism

http://www.strengtheory.com/gender-differences-in-training-and-diet/

What you’re getting yourself into:

2700 words, 8-12 minute read time

Key Points

1. Most of the major differences in performance and metabolism between genders can be explained by size and body composition, not gender itself.

2. Of the true gender differences, the most important ones have to do with differences in sex hormones and fiber types.

3. Additionally, womens’ fat and muscle tissue is better equipped than mens’ for handling both carbs and fat.

4. All of these differences make women better metabolically suited for… just about everything related to health and performance except for short, intense bursts of activity that rely on glycolytic capacity.

5. If you prefer pictures to words, the highlights of this article are presented in an infographic at the bottom.

Woman Squatting
It’s no secret that most strength, fitness, and nutrition content out there is by men, for men.  That’s shifting somewhat, but powerlifting, bodybuilding, and sports science have traditionally been, and still are, male-dominated pursuits.
So, just for starters, how much of a difference IS there between men and women?  Or at least, how large are the physiological differences in major parameters that relate to strength and performance?
Not very large at all.
For starters, men and women are very metabolically similar, at least when looking at metabolic rate.  About 90% of daily energy expenditure can be explained by fat-free mass, fat mass, and activity level.  Women *do* tend to have slower metabolisms than men, but the difference is primarily a function of muscle mass and body size, not gender.
In terms of muscle mass differences, women tend to have about 2/3 the muscle mass men do, with a larger difference in upper body muscle mass (about 1/2) than lower body muscle mass (about 3/4).  And although men tend to be stronger than women, that difference is explained *almost* entirely (97%) by muscle mass differences.  That means if a man and woman have the same size muscles, they should have roughly the same strength.
On the aerobic side of things, men tend to be slightly faster than women with equivalent levels of training.  However, the difference is almost entirely explained by body composition differences (men tend to be leaner), hematocrit differences (higher levels of testosterone lead to slightly higher red blood cell counts), and differences in heart size.
So, just to get this out of the way early, the VAST majority of the differences between men and women that are relevant to performance aren’t necessarily gender differences, but rather can be primarily explained by differences in body composition.  A woman and a man with similar training and similar amounts of muscle and fat will perform similarly.  The point of this article is to delve into those differences that DO exist and talk about the difference they can make in training and diet.

Metabolism

To discuss metabolic differences, the main source for this article is this recent (absolutely fantastic) review article.
The article starts out with an interesting quandary.  Women tend to have about 2/3 the muscle mass and 2x the fat of men, but tend to have substantially better metabolic health.  On the surface, you’d expect someone with more muscle and less fat to be more metabolically healthy.  However, the numbers tell a different story.  In men, depending on the study, rates of elevated fasting blood glucose are 50-100% higher, whole body blood glucose clearance is ~15% slower, and the rate of glucose uptake in muscle is ~30-50% slower.
image
So the obvious question:  Why the difference?
Short answer:  Women are more metabolically equipped for just about everything.
Longish answer:  Keep reading.

The Role of Estrogen

When discussing gender differences in just about any realm, the first place most people think to look is sex hormones, and for good reason.  The majority of the difference is muscle mass is attributable to mens’ higher testosterone levels, and a lot of the difference in metabolic characteristics can be explained by womens’ higher estrogen levels.
Your muscles have estrogen receptors, and, in fact, there’s good reason to believe that estrogen plays a major role in the beneficial adaptations that occur with aerobic training.  When compared to sedentary men, endurance-trained men have 3-5x as many estrogen receptors in the muscles (suggesting they become more sensitive to the effects of estrogen), and it’s been found that, at least in mice, estrogen receptors on mitochondria increase the rate of glucose uptake into the muscle when activated.
Now, I’m sure men reading this are starting to get a little uneasy.  The last thing you’d want is estrogen affecting your muscles, right?  Isn’t this just another reason to avoid cardio forever?  Wrong.  Men who are born with abnormalities in the estrogen system (faulty aromatase enzymes or mutated estrogen receptors) are more prone to insulin resistance and diabetes.  As long as your estrogen levels are normal, the only major thing that happens due to increased muscle sensitivity to estrogen is improved glucose uptake into your muscle and improved metabolic health.
Another major reason to believe that estrogen is a major player in womens’ superior metabolic health is that gender differences in insulin sensitivity don’t arise until puberty (at which time, it decreases in men and increases in women per kg of lean body mass).  Furthermore, womens’ insulin sensitivity declines again after menopause, but is often improved when they go on estrogen replacement therapy.
However, as with most things, too much can be just as bad as too little.  Some studies have shown that women using oral contraceptives have about 40% lower insulin sensitivity than women not on the pill, when matched for BMI, body composition, and physical activity.
(Note: HRT and hormonal contraceptives don’t follow those trends in all cases, and the literature isn’t unanimous.  As always, don’t base medical decisions on blog posts.  Ask your doctor about your options and the potential risks and benefits)
So the major takeaway:  Estrogen is a good thing for metabolic health, within the normal physiological range.  It’s a major reason women are more metabolically healthy than men (and increased sensitivity to estrogen is one reason metabolic health improves in men with endurance training).  When it’s too low (like after menopause), when something in estrogen system is out of whack (like nonfunctional aromatase or estrogen receptors), or when it’s too high, metabolic health suffers.

Difference in Fat

Though women tend to have more fat, there are differences in where that fat is stored, and also the characteristics of that fat.
For starters, men tend to have more visceral fat (fat stored around the organs in the abdominal cavity), and women tend to have more peripheral subcutaneous fat (fat stored between the muscles and the skin).  This gives rise to the “apple” and “pear” shaped, or android and gynoid fat distribution patterns.
android gynoid obesityThis is a very important difference.  Visceral fat is the particularly nasty kind that increases your risk of heart disease, diabetes, and all sorts of nastiness.
A major reason that visceral fat is particularly nasty is that it’s more sensitive to catecholamines (adrenaline and noradrenaline), meaning more of it gets broken down and released into the blood stream.  Subcutaneous fat goes directly into general circulation, but visceral fat is sent first to the liver.  Your liver and your pancreas are the major organs that regulate blood glucose, and the increase in fatty acids sent to your liver from visceral fat can decrease your liver’s insulin sensitivity, which can throw off glucose homeostasis.
Since women tend to have less visceral fat, they’re less prone to fatty acid-induced hepatic (liver) insulin insensitivity.
Visceral fat is also more active in producing inflammatory cytokines as well.  Inflammation (and how it’s affected by and interacts with fat tissue) is a big topic, so for the purposes of this article, just be aware that that’s also not a good thing, and we’ll leave it there.
So the fat distribution pattern in women is a more beneficial one, and the fat itself also helps women metabolically.
Fat produces two hormones that positively impact metabolic health:  leptin and adiponectin.
Leptin helps suppress appetite and improve insulin sensitivity.  Interestingly, although women have up to 4x higher leptin levels, they have greater central leptin sensitivity than men, largely due to the effects of estrogen.  However, its effects seem to be mainly central (i.e. altering hunger), at least in humans.  Resting leptin levels don’t seem to affect metabolic rate in humans the same way they do in animal models.
Adiponectin is associated with better insulin sensitivity.  Depending what study you look at, women have somewhere between 34% (obese women vs. obese men) and 127% (lean young women vs. matched men) higher adiponectin levels.  Adiponectin works by activating AMPK (the AMPK pathway is implicated in many of the positive effects of aerobic training), increasing glucose uptake and fat oxidation in muscle.  However, women have fewer adiponectin receptors than men, and a strong correlation between adiponectin level, AMPK activation, and glucose uptake is only seen in men.
Taken as a whole, though women DO have higher levels of leptin and adiponectin, they probably only play a minor role in the metabolic differences between men and women.
One last little tidbit before we move on from fat differences:  Fat tissue absorbs glucose from the blood at roughly 40% of the rate of muscle tissue, meaning that although muscle is a more important factor for glucose disposal, fat tissue does play a non-negligible role.  When you culture male and female fat cells in a petri dish, the rate of glucose uptake is higher for female fat cells than male fat cells, which could (potentially, though you shouldn’t put too much faith in in vitro research) also play a role in womens’ superior glucose handling.

Muscle Differences

The most important muscular difference is that women tend to have a greater proportion of Type 1 fibers (roughly 27-35% greater Type 1 fiber area relative to total fiber area) and greater capillary density.
Those are two major factors.  More Type 1 fibers and greater capillary density mean better tissue perfusion (ability to get more blood to the muscle to provide oxygen and clear metabolites) and greater capacity for glucose and fatty acid oxidation (because Type 1 fibers are the ones with more mitochondria and aerobic enzymes).  Insulin resistance and type 2 diabetes are negatively correlated with Type 1 fiber percentage and capillary density in both lean and obese people.
(As an aside, that’s a major reason why black people – particularly of West African descent – tend to do exceptionally well in power-dependent sports like football and basketball, but also suffer from higher rates of diabetes and heart disease.  On average, they have a higher proportion of Type II muscle fibers, which are awesome for explosive sport performance, but not so great for metabolic health.  Just one example here.)
So women have a greater proportion of Type 1 fibers and the assistance of higher estrogen levels, which largely explains how their muscles handle glucose better.  However, it doesn’t end there.  Female muscles also handle fat better, even when comparing female Type 1 fibers to male Type 1 fibers.
Women have roughly 40% higher plasma fatty acid concentrations than men, and they’re able to put those fatty acids to good use.  FAT/CD36 is the most important protein for bringing fatty acids into muscles and transporting them to the mitochondria.  FAT/CD36 concentrations increase in both genders as a result of aerobic training, but they’re higher in women regardless of training status.
This is a great thing for cardiac risk factors.  After you eat, triglycerides and VLDL (very low density lipoprotein, which primarily functions as a transport vessel for fat) levels increase.  They return to baseline faster in women because their muscles can absorb more fat, and do so quicker.
Building off that, women have greater stores of intramuscular triglycerides than men.  Now, these aren’t the nasty sort described in the last article, but rather the beneficial sort I briefly mentioned in the footnote.
Just a little aerobic physiology 101 – the greater the proportion of fat you can burn at any given exercise intensity, the better.  It spares glycogen, reduces rate of perceived exertion (which is strongly related to glycogen levels), and pushes back how long it takes to “hit the wall.”  Most importantly, there’s a strong relationship between how much fat is stored in the muscle (not independent fat cells interspersed with the muscle tissue as the last article mainly dealt with, but fat stores within the muscle fibers themselves) and how readily available it is to use during exercise.
What’s more, it’s not just that women have more intramuscular triglycerides than men, but those fatty acids are also more accessible.  Men tend to have a few large lipid droplets, and fewer perilipins (proteins on the outside of the lipid droplets that break down the triglycerides and help transport them to the mitochondria).  Women, on the other hand, have more numerous, smaller lipid droplets, and more perilipins.  Smaller lipid droplets have a higher surface area to volume ratio, meaning they’re more accessible to perilipins and lipases to break down the stored fat to be oxidized in the mitochondria.
Going a bit further down that rabbit hole, women also have higher levels of the protein Stearoyl CoA desaturase 1, whose role is to (as the name implies) convert saturated fatty acids into unsaturated fatty acids.  There is some data to suggest that muscle lipases have a higher affinity for less saturated fats.
So now to the important stuff:  how all this actually affects training.
Regardless of training status, women use more fat at any given exercise intensity than men do, meaning that, all other things being equal, they’re more resistant to fatigue.
Conversely, men have a higher glycolytic capacity than women.  That means that they can burn through more glucose in the absence of oxygen, which lends itself to better performance for short-intense bursts of effort, but which also means more lactate accumulation and longer recovery times after all-out efforts.  This is related to both the higher percentage of Type II fibers, and also higher levels of glycolytic enzymes (glycogen phosphorylase, pyruvate kinase, phosphofructokinase, and lactate dehydrogenase in particular).
More on this later.

Differences in Substrate Use

There are some interesting differences in the proportion of fat and carbs men and women use at different times.
In the fasted state, men and women tend to burn about the same proportion of fat and carbs.  However, after eating, women tend to preferentially store more fat and oxidize more glucose immediately, relative to men.  When eating isocaloric, high-carb diets (increasing from 55% to 70% over the duration of the study), glycogen concentrations increased in men, but not in women because the additional carbohydrate was immediately used as fuel instead of stored.
In the fasted state, plasma triglyceride levels increase in both genders, but after a 48-hour fast, muscle triglyceride storage increases in women, and liver triglyceride storage increases in men.
During training, as previously mentioned, women burn a greater amount of fat relative to glycogen at any exercise intensity.  However, after training, that reverses.  Women then tend to burn an increased proportion of carbs, whereas men burn an increased proportion of fat.

Takeaways

Just to reiterate, gender differences related to acute performance aren’t that huge, and are less a function of gender per se, and more a function of body composition.  Furthermore, be aware that everything in this article is representative of trends, but may not hold true when comparing individual men and women, obviously.
Of the differences that do exist, the largest contributing factors are fiber type differences and sex hormone differences.  And, in essence, they set women up to be more metabolically suited to just about everything.  They clear VLDL and triglycerides better, have better insulin sensitivity, have a more favorable fat distribution, and burn a greater proportion of fat at any given exercise intensity, making them less fatigueable.  The only place where men have the edge is in glycolytic capacity and explosive (but not maximal strength) performance (both related to Type II fiber proportion).
So what do we do with all that?
For starters, ladies, do not be afraid of carbs.  Not only are they delicious and awesome, but you have better insulin sensitivity, and the more of them you eat, the more of them you burn.
Second, you do not have a harder time losing weight because you’re a woman.  Yes, you’ll probably have to eat fewer calories than a man who weighs the same amount you do, but the primary factors in determining your calorie needs are body size, body composition, and activity level, with gender playing little to no role.  If you’re more jacked and/or more active than a guy who weighs the same as you, then you can eat more than him.  If not, you can’t.
Finally, as far as training goes (though we’ll get more into training as this series progresses), odds are pretty good that you can do more work and benefit from more work than a guy can.  Your muscles are inherently more glycogen-sparing and fatigue-resistant.  You can probably do more reps with a given percentage of your 1rm before fatigue sets in, and do more total work (relative to 1rm) before you hit a wall due to higher proportion of Type 1 muscle fibers, greater proportion of fat being burned instead of glycogen, and lower glycolytic capacity.
So with that, I’ll put a bow on Part 1 of a (planned) 4-part series.  This article was to set a basic groundwork with metabolic differences, Part 2 will cover structural differences and delve into training implications much more, Part 3 will mainly be about the menstrual cycle and contraceptives, and Part 4 will cover the female athlete triad.
Sources:
Gender Differences in Metabolism

Chubby Muscles? What You Need to Know About Intramuscular Adipose Tissue

http://www.strengtheory.com/chubby-muscles-what-you-need-to-know-about-intramuscular-adipose-tissue/


Fat mouse

What you’re getting yourself into:

~4000 words

12-15 minute read time

Key Points

1) the same satellite cells that can repair muscle can be turned into fat cells within the muscle sheath given the right environment

2) the main factor in the creation of intramuscular adipose tissue is inactivity

3) intramuscular adipose tissue can decrease insulin sensitivity, increase inflammation, reduce recovery from training, and decrease strength

4) it can be reduced via diet and exercise

Adipose tissue functionality and distribution
Adipose tissue was originally thought to be inert tissue used as storage for excess calories and thus was only of importance to the body’s energy balance. This is not the case however, due to adipose tissue’s ability to secrete hormones and pro-inflammetory cytokines. Rather than being inert; adipose tissue influences a number of systems including the cardiovascular, musculoskeletal, metabolic and central nervous systems (Stehno-Bittel 2008, Fischer-Posovsky et al. 2007, Sepe et al. 2010).
There are several important types of adipose tissue located throughout the body, the location (Goodpaster et al. 2010, Gallagher et al. 2005) and type of adipose tissue (Wronska & Kmiec 2012) is a significant predictor of a number of conditions associated with obesity (Wronska & Kmiec 2012). Whilst some researchers have expressed that whole body adiposity is not as important as local adipose tissue when predicting disorders associated with adipose tissue (Addison et al 2014) it should be considered that whole body adipose will largely predict local adipose tissue.
There are two clearly distinguishable compartments of the adipose organ in the body, these are subcutaneous adipose tissue (SAT) and also visceral adipose tissue (VAT). More recently, increasingly sensitive technology such as magnetic resonance imaging (MRI) scanners have enabled the identification and measurement of other deposits of adipose tissue which contribute to whole body adiposity (Bernard et al. 1996, Thomas et al. 1998).
One such deposit of adipose tissue is intermuscular adipose tissue (IMAT), which previously has been referred to in the literature by a number of names including myostasis, intermuscular fat, intramuscular fat, as well as low density lean tissue. IMAT is considered to be the broadest definition when referring to the infiltration of the muscle by lipids (Addison et al. 2014) and for the purposes of this article “IMAT” is inclusive of adipose tissue accumulated between muscle groups, beneath the muscle fascia and intramuscular adipose tissue which is located within individual muscles (Vettor et al. 2009, Addison et al.2014). This compartment of fat also includes most of the intramyocellular lipids (IMCLs) as well as the adipocytes present between muscle groups and between muscle fascicles (Vettor et al. 2009).
Causes of IMAT
The causes of IMAT are observed on a pathophysiological level as beginning with the stem cells, or satellite cells (SC) (Vettor et al. 2009).
Satellite cells on a muscle fiber.
Satellite cells on a muscle fiber. From Vettor (2009).
The regeneration of muscle tissue is controlled largely by SCs, specifically a number of SCs committed to the task of muscle regeneration located adjacent to the plasma membrane of myofibers. These particular SCs are self-renewable (Fuchs & Segre 2000, Oreffo et al. 2005) and have the ability to differentiate into different types of cell (Asakura et al. 2007, Collins et al. 2005, De Coppi et al. 2006, Shefer et al. 2004).
Satellite cells can be used both to repair muscle, or add to IMAT.  From Vettor (2009)
Satellite cells can be used both to repair muscle, or add to IMAT. From Vettor (2009)
In vivo SCs are typically in a dormant state (Hawke & Garry 2001, Schultz et al. 1978) however they can be activated by an increase in muscular work or muscular damage; for example prolonged exercise, or similarly they can be activated by myotrauma (Vettor et al. 2009). When activated SCs express myogenic transcription factors (such as Myf5, MyoD, MRF4) which in vivo promote muscle tissue formation (Tapscott et al. 1979). However SCs have been shown to be able to differentiate into adipocytes given a sufficiently adipogenic environment (Vettor et al.  2009).
New adipocytes (fat cells) from satellite cells.
New adipocytes (fat cells) from satellite cells. From Vettor (2009)
Moreover, it has been shown by Shefer et al. 2004 during clonal analysis of SCs that Adult Mouse SCs could spontaneously differentiate into adipocytes, and that in the progeny from an individual clone myogenisis and adipogenesis were mutually exclusive. It is believed that the molecular cause of this shift from myogenic to adipogenic SC progenitors is due to an ectopic expression of peroxisome proliferator-activated receptors (PPAR), specifically PPARδ which in turn causes an upregulation of PPARγ (Vettor et al. 2009).
So what constitutes an Adipogenic Environment?
As previously mentioned, SCs will not differentiate into adipogenic cells without a change to the muscular environment. A number of conditions have been examined with regards to IMAT accumulation in vivo, spinal cord injury (SCI) was shown to increase thigh IMAT by an average of 26% on the three months following a complete SCI, which also accounted for a 70% reduction in glucose tolerance (Gorgey & Dudley 2007). The change to the muscular environment appears to be primarily down to inactivity, a number of causes have been identified for IMAT which are as follows; partial and complete SCI (Gorgey & Dudley 2007), whiplash associated disorder (Elliot et al. 2006), sporting injuries such as torn hamstring (Slider et al. 2008) and torn rotator cuff (Goutallier et al. 2003) as well as in the elderly and young-but-sedentary (Addison et al. 2014). All of these causes share a common characteristic which is an amount of time generally spent with limited mobility, partial local immobility or complete immobility, which was shown by Manini et al. (2007) to cause 15-20% increases in IMAT in the timespan of 30 days.
The effects of IMAT
Muscle structural composition is one of the most important factors which contributes to muscle function (Goodpaster et al. 2001). In older adults, muscle mass deterioration declines at a slower rate than strength, implying that factors other than decreased muscle mass contribute to the loss of strength (Kallman et al.1990). A direct effect of IMAT on muscular strength has been shown in single limb experiments by Manini et al. (2007) and Tuttle et al. (2012) showed decreases in performance across a number of physical performance measures including a power test with increased IMAT. These decreases in strength, power and other physical performance measures are likely due to changes in the muscle form caused by IMAT. These changes in form include an increase of Muscle-Tendon unit stiffness caused by IMAT (Faria et al.2009) which would cause decreased compliance, decreased elastic energy storage and more energy required to contract the muscle. In addition to this, research by Yoshida et al. (2012) has revealed a reduced activation in the quadriceps muscle group during a maximal isometric contraction. This reduction in activation of the muscle may be caused by a reduced ability for action potential to travel along the muscle sarcolemma, meaning the action potential will not reach certain areas of the muscle to stimulate calcium release and therefore muscle contraction.
Lean tissue (muscle) when viewed by a computed tomography (CT) scan in vivo can be divided into two distinct types; high density lean tissue where little fatty infiltration occurs and low density lean tissue where an elevated level of adipocytes can be found both between and within the muscle fibres which results in a decreased density when viewed on a CT scan (Addison et al. 2014). It has been stated that if the density of a muscle increases or if the area of low density muscle decreases post (exercise based) intervention, then the intervention has been successful in reducing both IMAT and IMCL.
Aside from the aforementioned physical changes to the muscle which are associated with IMAT, a number of metabolic changes take place within the muscle have been reported in individuals with IMAT. IMAT has been reported to reduce insulin sensitivity within the affected muscle (Goodpaster et al. 2000) although the exact mechanism for this interaction is unknown, it is assumed to be due to the proximity of the IMAT to the muscle (Beasley et al. 2009, Manini et al. 2007). There has also been a reduction in citrate synthase activity reported with increased IMAT levels (Jong-Yeon et al. 2000) which causes a reduction of Krebs cycle activity in the muscle. A third reported metabolic factor reported in conjunction with the aforementioned two aspects, is an increase in proinflammatory cytokines in high IMAT muscle (Beasley et al. 2009, Manini et al. 2007, Koster et al. 2011), the consequences of which are a reduction in muscular function (Schaap et al. 2006) and mobility ( Ferrucci et al. 2002)
There is increasing evidence that demonstrates IMAT’s role in reduced mobility in an aging population (Hilton et al. 2008, Marcus et al. 2012, Tuttle et al. 2011, Tuttle et al. 2012, Visser et al. 2005, Visser et al. 2002). Adults with significant IMAT levels have a decreased six minute walk distance (Marcus et al. 2012, Tuttle et al. 2012) potentially due to a reduced gait speed (Visser et al. 2002). There is also evidence in a reduced ability to perform ‘repeated chair stands’ (Visser et al. 2002) and stair descents (Marcus et al. 2012). With this in mind; IMAT is a strong indicator of future mobility impairment (Visser et al. 2005) but also of bone mineral density (Kim et al. 2012) which predicts an increase in hip fracture (Lang et al. 2010, Kim et al. 2012). This loss of mobility function associated with IMAT has been linked with the proinflammatory cytokines which are produced by the IMAT (Manini et al. 2007, Delmonico et al. 2009, Zoico et al 2010), which may be due to the fact that a number of authors have reported relationships between proinflammatory cytokines and reduced muscle and mobility function which are very similar to the relationships reported between IMAT and muscle and mobility function (Addison et al. 2014)
Reduction of IMAT
Exercise and a calorie restricted diet are often the first interventions most clinicians will prescribe in order for a patient with obesity and/or IMAT in order to achieve healthy weight loss and, in theory, reduction of IMAT accompanied by improved skeletal muscle function. Indeed a number of studies have reported a reduction in IMAT with intentional weight loss through calorie restriction or exercise (Ryan et al. 2012, Ryan et al. 2006, Goodpaster et al. 1999) and additionally, longitudinal twin studies have demonstrated that the inactive twin had significantly more IMAT than the active twin (Leskinen et al. 2009). Moreover, in SCI patients a high level of spasticity was found to protect against IMAT (Gorgey & Dudley 2008). The current consensus with regards to weight loss as a way of preventing or reversing IMAT is that IMAT is reduced following a nutritional or exercise based intervention (Prior et al. 2007, Durheim et al.2008, Ryan et al. 2000, Ryan et al. 2012, Christiansen et al. 2009, Marcus et al.2008, Murphy et al. 2009, Ryan et al. 2006, Taaffe et al.2009. Lee et al. 2005. Avila et al. 2010, Mazzali et al. 2006) and that exercise intervention has a significantly greater effect than nutritional intervention (Christiansen et al. 2009, Murphey et al. 2012, Mazzali et al. 2006). However, a recent study by Jacobs et al. (2014) showed no improvement in IMAT following a three month exercise intervention in elderly subjects. This difference in Jacob’s results compared to previous findings may be due to the population group examined, or perhaps the use of magnetic resonance imaging (MRI) to quantify IMAT levels as opposed to the CT scans used in many other studies.
IMAT appears to operate in a positive feedback loop, which is to say that dysfunction in the muscle leads to inactivity (or vice-versa) which then leads to increased levels of IMAT and further increasing insulin resistance and muscle dysfunction (Addison et al. 2014). This is supported by the notion that the changes in muscle performance and metabolism from IMAT may limit the degree to which the muscle responds to training stimulus (Marcus et al. 2013) and also the fact that SCs become adipocytes which limit the number of SCs dedicated to repairing muscle damage caused by training.
Editor’s Note:  So you may be thinking, “What’s the takeaway here?”  This is basically a cautionary tale against inactivity.  Everyone knows that sitting on your tail all the time is bad for you – this is one specific way that inactivity can negatively affect your strength and health, and being active (not just “working out,” but living a generally active life) can benefit them.  It should also be noted that not all intramuscular fat is bad.  With training (specifically aerobic training), intramuscular adipose stores increase to provide the muscles with a supply of stored energy for activity (similar to muscle glycogen).  However, this process is substantially different from the one outlined above for a few different reasons.
1) There’s not the same shift in stem cells toward adipocytes, compromising recovery.  The bulk of IMAT stores resulting from training are in the form of lipid droplets within the muscle fibers themselves, not fat cells around the muscle fibers.
2) Accumulation of intramuscular adipose tissue resulting from training doesn’t decrease insulin sensitivity.
3) The accumulation of IMAT as a result of training is accompanied by increased number and size of mitochondria, increased levels of aerobic enzymes, and increases in the proteins necessary for the handling and transport of the lipids from the lipid droplets to the mitochondria.
References:
Addison, O., Marcus, R.L., LaStayo, P.C., Ryan, A.S. (2014) ‘Intermuscular Fat: A Review of the Consequences and Causes’ International Journal of Endocrinology Article ID: 309570
Asakura, A., Konmaki, M. & Rudnicki, M. (2001) ‘Muscle satellite cells are multipotential stem cells that exhibit myogenic, osteogenic and adipogenic differentiation’ Differentiation 68 pp:245-253
Avila, J.J, Gutierres, J.A., Sheehy, M.E., Lofgren, I.E. & Delmonico, J. (2010) ‘Effect of moderate intensityresistance training during weight loss on body composition and physical performance in overweight older adults’ European Journal of Applied Physiology 109(3) pp:517-525
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Beasley, L.E., Koster, A., Newman, A.B., Javaid, M.K., Ferrucci, L., Kritchevsky, S.B., Kuller, L.H., Pahor, M., Schaap, L.A., Visser, M., Rubin, S.M., Goodpaster, B.H. & Harris, T.B. (2009) ‘Inflammation and race and gender differences in computerized tomography measured adipose depots’ Obesity 17(5) pp:1062-1069
Christiansen, T., Paulsen, S.K., Bruun, J.M., (2009) ‘Comparable reduction of the visceral adipose tissue depot after a diet induced weight loss with or without aerobic exercise in obese subjects: a 12 week randomized intervention study’ European Journal of Endocrinology 160(5) pp:759-767
Collins, C.A, Olsen, I., Zammit, P.S., Heslop, L., Petrie, A., Partridge, T.A. & Morgan, J.E. (2005) ‘Stem cell function, selfrenewal, and behavioural heterogeneity of cells from the adult muscle satellite cell niche’ Cell122 pp:289-301
De Coppi, P., Milan, G., Scarda, A., Boldrin, L., Centobene, C., Piccoli, M., Pozzobon, M., Pilon, C., Pagano, C., Gamba, P.& Vettor, R. (2006) ‘Rosiglitazone modifies the adipogenic potential of human muscle satellite cells’ Diabetologia 49 pp:1962-1973
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