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View Full Version : Testosterone Reduces the proliferation of fat cells.



dreww
05-30-2011, 08:26 PM
Bioavailable testosterone refers to testosterone that either circulates freely in the bloodstream or is loosely bound (held) by the nonspecific protein-carrier, albumin. Testosterone in these two states (free or albumin-bound) can easily pass into target tissue, such as skeletal muscle, and interact with intra-cytoplasmic receptors and co-regulators to affect changes (the albumin-bound testosterone “breaks free” first). In the muscle, this means free and albumin-bound testosterone are primarily responsible for the androgen-related muscle hypertrophy. The contrasting state is testosterone bound to the more specific protein-carrier called “sex hormone-binding globulin” (SHBG). SHBG-bound testosterone is considered to be “unavailable” to cause changes in androgen-sensitive tissue, such as muscle. This is not entirely correct, as it is believed that SHBG-bound testosterone, as well as albumin-bound testosterone, may interact with androgen receptors in cell membranes. The quick responses of these membrane-bound receptors are called nongenomic, as they do not travel to the nucleus of the cell (where the DNA lies). Instead, the nongenomic receptor responses take place at or near the membrane, changing the activity of enzyme pathways that trigger anabolic cell functions.


In the Nutrition Reviews article, the observation was that people who lose weight by following a hypocaloric diet experienced an increase in SHBG while total androgen concentration did not change. It was noted that the type of diet followed (low-fat, low-carb, etc.) did not affect the effect of weight loss on androgen status. This implies that people who are actively losing weight experience a reduction in free and bioavailable testosterone. This is consistent with previous studies that show a decrease in SHBG in men in association with weight gain. This finding is not a real surprise if one considers the everyday experience of dieters or more specifically, those of athletes/bodybuilders who are cutting weight to meet a weight-class restriction or to get “ripped” for competition. Dropping calories below maintenance is subjectively associated with a marked lowering of 1-rep max and loss of lean body mass. Many athletes combat this by depending more heavily upon ergogenic aids (e.g., supplements, stimulants, anabolic drugs). For the drug-free athlete, there are a few strategies that can ameliorate the weight-loss induced decrease in bioavailable testosterone. Focusing on hypertrophy-oriented lifting (higher volume, shorter rest) induces a greater spike in testosterone (and cortisol) than powerlifting schemes. The protocol followed in one study showing this using salivary testosterone (and cortisol) was 10 sets of 10 reps with 2-minute breaks between sets. Also, while the media focuses on the “bacon and eggs” component of Atkins-like diets, including a significant amount of carbohydrates, poly- and mono-unsaturated fats will help maintain total testosterone. Zinc, magnesium and other micronutrients may also aid in maintaining androgen status, particularly for those who follow diets with narrowly defined food choices.


The interesting tangent to the relationship between weight loss and androgen status is defining the relationship. Is hypocaloric weight loss the cause of reduced bioavailable testosterone, or does an abnormal ratio of bioavailable to SHBG-bound testosterone support the growth of fat mass? During weight loss, adipocytes release stored fats from triglyceride vacuoles. These vacuoles are like oil droplets in water. Unfortunately, these vacuoles may have held not only stored fat, but also fat-soluble environmental pollutants. Endocrine disruptors are chemicals present in the air or water, commonly released from industrial sources. The chemical bisphenol A that is present in certain plastics is one example that has been in the news recently. Bisphenol A exposure is postulated to increase the risk of numerous cognitive, reproductive and metabolic problems, in part, through its agonistic actions at the estrogen receptor (ER-alpha). Estradiol, the natural estrogen produced as a metabolite of testosterone, increases SHBG production.


Elevations in bioavailable testosterone could be a protective adaptation to early weight gain, as testosterone reduces the proliferation of fat cells from stem cell reserves and activates the breakdown and release of stored fat. If fat gain goes unchecked though, the fat cells are capable of inactivating testosterone and converting it into estradiol to promote the further storage of fat and growth of new fat cells. The binding of bioavailable testosterone to the sequestered (hidden away) SHBG-bound testosterone may be a physiologic adaptation to encourage the return to a normal weight and release further stored fat to provide energy during a period of relative starvation. Increasing the SHBG-bound component of testosterone during weight loss may allow for fat cell proliferation and prevent the development of hypertrophic adipocytes (fat cells) which are associated with many of the metabolic problems of obesity.


These simple observations and thoughts do not begin to touch upon the complexity of these findings, as the actions of other tissues and hormones that are affected by the relative energy stores (fat) have not been addressed. Adipokines, leptin, ghrelin, insulin sensitivity, etc., all combine to harmonize in the hormonal orchestra of human metabolism. When one section is out of tune, it is inevitable that the symphony is ruined regardless how much louder the rest of the orchestra plays.
Obesity is an imbalance between a person and his environment. In some cases, it is an inevitable consequence of a genetic error in coding. In most cases, it is the consequence of the body being forced to accommodate illogical or unnatural conditions. In response to obesity and attempts to return to normal weight, changes occur, including changes in the endocrine system. Androgens, including testosterone, are potent anabolic hormones that dictate the function of many tissues and are regulated in response to physiologic conditions. When food supply is low, bioavailable testosterone is decreased to reduce the demands for protein and other nutrients during food shortages. For the athlete, the consequence may be a loss of strength or lean mass. It is possible that testosterone concentrations, particularly bioavailable testosterone, may be maintained by paying close attention to including specific nutrients (e.g. poly- and mono-unsaturated fats, zinc, magnesium, etc.), but awareness of lessened anabolic support is necessary for the athlete so he/she may tailor their efforts and expectations appropriately.

Boomer
05-30-2011, 11:19 PM
anyone have a quick break down of what all means? to hard for me to read right now.

Presser
05-31-2011, 05:47 PM
fuck if i can make heads or tails from this as well brutha lol

mcgaret
05-31-2011, 08:45 PM
fuck if i can make heads or tails from this as well brutha lol

I am also looking for someone else to read it and let me know what it says.
LOL

big in vegas
06-01-2011, 08:29 PM
I am also looking for someone else to read it and let me know what it says.
LOL

I need cliff notes

warlord
06-02-2011, 05:26 PM
So they are saying SHBG helps fat loss but I thought high levels of SHBG effects our gains during a cycle not just fat gains also lean mass gains. It;s kind of confusing

Presser
06-08-2013, 09:44 AM
copied 2 articles

MonkeyWrench
06-08-2013, 03:02 PM
I felt like I was trapped in a maze, I have no idea where that article was going.

Presser
06-10-2013, 08:24 AM
I felt like I was trapped in a maze, I have no idea where that article was going.

lol, yep