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  F*CKING CRAMPS!!!!!

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Author Topic:   F*CKING CRAMPS!!!!!
Fonz

Pro Bodybuilder

Posts: 586
From:Mt. Olympus
Registered: Jun 2000

posted February 21, 2001 05:30 AM

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Ok, at the end of my first week
using 1000mg Deca combined with
200mg mifegyne every 2 days..
and I'm getting rhe worst cramps
I've ever had. I mean, I can
barely sit down. Can this be
related to the Deca dosage or
the RU-486 dosage.(RU-486 bocks
cortisol akin to Cytadren as was
already discussed). The funny
thing is I have no joint pain, just
these god-awful cramps and sometimes
muscle twitches...
Any theories?anyone?

Godspeed


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The_Iron_Game

Olympian

Posts: 1930
From:
Registered: Oct 2000

posted February 21, 2001 05:40 AM

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Yes RU 486 can lead to cramps in higher doses, however there are, at the moment, no studies I know of that have shown the potential sides/damage caused by using such high amounts of it. After all it is a 'womens' pill and I have not heard of studies carried out on men using it in relation to progesterone related gyno. You should never attempt to kill or prevent cortisol production. Cortisol is not only what everyone would consider a bad hormone (catabolic) but is essential for healthy function. By using it at such high doses you can only find out 'first hand' what sides it can cause and what the lack of cortisol will do. As for the cramps, try drinking plenty of water and then more in addition too pottasium chloride supplementation and a good multi vitamin/mineral tablet 2 to 3 times a day.


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Fonz

Pro Bodybuilder

Posts: 586
From:Mt. Olympus
Registered: Jun 2000

posted February 21, 2001 05:44 AM

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Thanks Iron Game, I think
I'm going to lower the dose
to 200mg every 3 days...
see how that goes.

Godspeed


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The_Iron_Game

Olympian

Posts: 1930
From:
Registered: Oct 2000

posted February 21, 2001 05:55 AM

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"When the body is exposed to stress, whether it be physical or psychological, the hypothalamus in the brain releases a hormone called corticotropin-releasing hormone or CRH. This hormone travels a short distance to the pituitary gland, stimulating it to release adrenocorticotrophic hormone (ACTH). ACTH then travels by circulation to the two adrenal glands situated atop each kidney, stimulating them to release glucocorticoids like cortisol. There are several glucocorticoids - the primary ones being cortisol, corticosterone and cortisone. Their actions are very similar, so to simplify things, we will use the term cortisol when describing the workings of glucocorticoids.
Going back to where the body is initially exposed to stress, in this case at the beginning of a workout, the above described hormonal cascade is all executed for the key purpose of liberating stored energy and getting it out into circulation where it can be delivered to the working muscles. This process of cortisol release is one component, albeit a slow one, of the "fight or flight" response the body makes in preparation for action.
Cortisol's role in assisting in the supply of energy to the working muscles is multifaceted. It assists in the supply of the three main energy substrates: glucose, fatty acids and amino acids. Once released by the adrenal glands, cortisol acts systemically (throughout the whole body) via blood circulation. A primary destination is the liver, where in conjunction with glucagon and the catecholamine epinephrine and norepinephrine, it stimulates glycogen breakdown (glycogenolysis) for glucose release. This liberation of glucose from storage maintains an even concentration of blood glucose, ensuring adequate energy supplies to the muscles. Because of its role in glucose metabolism, cortisol is given its distinction as a glucocorticoid.
Another destination for cortisol is adipose tissue, where it stimulates the release of free fatty acids into circulation. Although fat generally contributes less than carbohydrate to muscles' energy needs during exercise, mobilization and oxidation of fatty acids are critical to performance in long endurance exercise bouts. It has also been observed that the higher the concentration of fatty acids in blood, the greater their use by muscle.Along with growth hormone, epinephrine and norepinephrine, cortisol activates an enzyme called lypase which breaks down triglycerides, the storage form of fat, into free fatty acids and glycerol. For fat to be used as energy, it must be in a free fatty acid state. The newly created glycerol is either transformed into glucose (gluconeogenesis) in the liver or later reesterified into triglycerides for fat storage.
Cortisol also travels to muscle tissues where it stimulates the release of amino acids for energy use. These amino acids will either be directly oxidized by the working muscles or travel to the liver and be converted to glucose, another gluconeogenic process. It is this role of protein catabolism that gives cortisol its bad reputation, and may explain, in part, why endurance athletes, with their extended bouts of exercise, generally don't have the musculature that a strength or speed athlete may have. It is this reason, as well, that some coaches and athletes believe that taking steps to minimize the daily stresses of life may help in the recovery process - it's difficult to recover when excessive cortisol levels are chewing up your muscle.
It is interesting to note, once exercise commences, serum cortisol levels don't begin to increase in concentration until about 15 minutes into the activity. This delay may explain why serum fatty acids decline so rapidly in the first minutes of exercise, no matter what the pace is, and why the body is so reliant on glucose for energy during the early stages of activity.
However, at or around the 15 minute period of exercise, serum cortisol will rise and peak in just 10 to 15 minutes. After that, surprisingly, cortisol concentrations decline and reach resting levels at about the 90 to 100 minute period of exercise. Cortisol may even continue to decline below resting levels as exercise continues, indicating that other mechanisms may take over cortisol's energy-supplying role of freeing fatty acids, amino acids and glucose from their perspective storage sites. In all likelihood, it is the catecholamines, epinephrine and norepinephrine that play increasing roles the longer an activity lasts.
Unlike anabolic steroid hormones, like testosterone, cortisol is a catabolic (tissue break-down) steroid hormone. It is this catabolic action that gives cortisol its "bad boy" reputation. Many athletes, particularly the physique athletes, go to great lengths to limit cortisol�s 'tissue-breakdown" effects, including taking anabolic steroids. However, it is also very clear that cortisol plays a very important role in the endurance athlete's physiology. Without it, supplies of energy to the working muscles may not meet demands, causing decreased performance. This may explain why some endurance athletes, particularly some of the pro cyclists, abuse corticosteroids - celestone (betamethasone), for example - during racing events. Along with the possible pain-reducing effects, corticosteroid use may enhance the liberation of energy stores, providing more energy to the working muscles".

1. Brooks and Fahey, Neural-Endocrine Control of Metabolism. In: Exercise Physiology Ch.9, Macmillan Publishing Co. 1985.
2. Moran and Schrimgeour. Integration of Fuel Metabolism in Mammals. In: Biochemistry (2nd ed.) Ch.23, Prentice Hall. 1994.
3. Wilmore and Costill, Hormonal Regulation of Exercise. In: Physiology of Sport and Exercise Ch.6, Human Kinetics. 1994.


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