Readers of previous CME books have commented upon my dislike for aerobics as a means of oxidizing (burning) fat stores. Normally I simply defend my views with " boring and ineffectual". Why?
The place where fat is burned or oxidized is the cellular mitochondria. There are two primary types of mitochondria; S-mitochondria that is found in the connective tissue of muscle (sarcolemma), and M-mitochondria found in the muscle fibers themselves (myofibrilla).
Standard aerobic training mostly favors beta-oxidation (fat burning) in S-mitochondria, where as near-anaerobic-threshold- training favors beta-oxidation in M-mitochondria. Near-anaerobic-threshold-training is defined as the point in which muscle fatigue is induced by the build-up of muscle by-products such as lactic acid (feel the burn baby!) caused by increased exercise intensity. About 10 % of total muscle mitochondria exists as S-mitochondria, and about 90 % exists as M-mitochondria.
This in itself should prove near- anaerobic-threshold-training is 9 times (900%) more effective as a means of causing beta-oxidation (fat burning) when compared to standard aerobic training. The mitochondria ratio/stimulation factor is cool, but there is more.
When near-anaerobic-threshold-training is utilized, a build-up of citrate and lactate in muscle tissue results. Both of these by-products inhibit glycogenolysis, which is the break-down of muscle glycogen and glucose. When glycogenolysis is inhibited, an elevation in plasma GH levels is realized thus forcing the muscles to rely more on fat (from beta-oxidation)as an energy source.
These fats for energy come from circulatory free-fatty acids and stores of muscle triglycerides. How? (Be patient) When we exercise intensely, insulin secretion is suppressed by a group of chemicals from the adrenal gland called catecholamines. You probably know them as either epinephrine and norepinephrine, or adrenaline and noradrenaline. These catecholamines in turn trigger the release of free fatty acids (from bodyfat stores) into the circulatory system by stimulation of hormone-sensitive-lipase-enzyme found in lipocytes (fat cells).
The greater the mitochondria stimulation (or number of mitochondria stimulated), the greater the amount of fatty acids /triglycerides burned as fuel. Since about 90% of mitochondria exist as M-mitochondria, (stimulated by near-anaerobic-threshold-training) and the level of intensity increases, the level of catecholamines released ...duh, you do the math.
Additionally realize that by structuring near-anaerobic-threshold-training into interval aerobic/anaerobic training, your body becomes much more efficient at breaking down all the nasty fatigue produced metabolic by-products.
Why interval aerobic/anaerobic training? Who can handle 20-30 minutes of consecutive near-anaerobic-threshold-training?
So how did we structure this into a realistic training protocol for Frank and the rest of the beasts? (Sex is still best!!)
• Find a high intensity aerobic activity you enjoy, or hate less then others.
• Find your maximum heart rate (220 minus your age) and subtract 10%. Example: 220-30=190- 10%=171 heart rate.
• Do 2-3 minutes of near-anaerobic-threshold-activity at a heart rate of maximum minus 10%.
• Lower the intensity to 50-60 % of maximum heart rate until you feel sufficient recovery.
• Repeat for a total of 20-30 minutes 2-3 times per week.
Interval aerobic/anaerobic training burns 100-120 % more fat in 30 minutes than traditional aerobic training burns in one hour. And Frank's lean muscle mass was preserved or increased depending upon diet/calorie structure and co-administered chemical muscle enhancement.
"IMPORTANT: Never attempt this or any other training technique without a doctor's approval (Weasel Statement)
When I first agreed to write about the strategies and protocols that had been employed to induce chemical muscle enhancements, the political and media dictated morals were of issue. To say the least, any dogma that can subjugate the AMA is persuasive. And to be blunt, such tactics as those integrated into law to punish medical professionals for remaining true to their oath, are insane.
The obvious conclusion being that anabolic / androgenic steroids (AAS) such as testosterone are deadly and evil. Evidently all things that produce, convert to, or increase, testosterone levels within ones body must also be satanic to some extent. Why else would such practices as male bashing (they produce testosterone) be legal? (Watch any day-time-whine-and-talk-show)
For the above reason I strongly suggest readers should review the following reference sites and sources so I can get on with this book. My morals rest in truth. (Lots more at the end of course)
1. Does testosterone cause "roid rage"? No, just an improved mood, self- confidence and feeling of well being. Oh, and heightened libido similar to an average 1 4 year old boy with a Playboy Magazine.
**Rabijewslo,.M., et al (1998) Pol Arch Med Wew N100 (3):21 2-21 **Almeida, O.P. (1 999) Arg Neuropsiquiatr. 57 (3a): 701-6 ** Tricker, R., et al (1 996) J. Clin. Endocrinol Metab. 81 (10): 3754-8
2. Does testosterone increase the risk of heart disease? Difficult question, but several studies show that testosterone actually reduces heart disease risks and complications. "Shapiro, J. et al. (1 999) Amer. J. Ther. 6(3): 1 67-74
**Zmuda, J.M., et al. (1 997) 1 30(1 -2): 1 99-202 (Atherosclerosis) **Zmuda, J.M., et al. (1 997) AM. J. Epidemiol. 1 46 (8): 609-61 7 **Salke, R.C., et al (1 985) Med Sci. Sports Exer. 1 7 (6):701 -4
3. Actually, testosterone has been shown to have a positive effect upon high-density-lipo-protein /(HDL) cholesterol levels.
**Zhao, S; L; X;and and Wang, Z., (1 998) Hunan I Ko Ta Hseah Pao. 23(3): 299 **Barrett-Connor, E. I. (1995) Diabete. Metab. 21 (3) : 156-61
4. Testosterone has been shown to significantly improve chronic angina as well as myocardio ischemia from exercise.
**English, K.M.et al. (2000) Circulation. 1 02(1 6):1 906-1 1
5. Speaking of heart risk factors, doesn't testosterone and AAS raise low density-lipo-protein (the bad cholesterol-LDL) and Lipoprotein (a)? Actually the opposite is still the truth. Testosterone has been shown to lower LDL and Lipoprotein (a) **Zmunda, J.M. et al. (1 996) AM. J. Cardiol 77 (1 4): 1 244-7 **Rabijewski, M., et al. (1998) Pol. Arch. Med. Weun. 100 (3): 212-21 **Uyanik, B.S., et al. (1997)Jpn. Heart J. 38 (1): 73-82 **Zgliczynski, S., et al. (1996) Atherosclerosis. 121 (l):35-43.
6. Testosterone reduces to DHT (dihydrotestosterone) so testosterone will increase the risk of prostate cancer, right? It should be of interest to hear that DHT has been patented as a treatment for BPH (Benign Prostate Hyperplasia). However several studies have shown that estrogen elevation and subsequent interaction with factors of DHT activity cause the negative effects in prostate size and PSA levels. (Prostate-Specific-antigen) (Is estrogen evil?) "Kenny, A.M., et al. (2000) Endocr. Res. 26 (z): 1 53-68 "Cooper, C.S., et al. (1 998) J. Urol 1 59 (2): 441 -3
An interesting note concerning prostate cancer is that 2 out of 3 individuals with PSA levels high enough to indicate cancer of the prostate, test negative in pathology. Scary huh? Oh, this is after prostate removal surgery. That could be a pain in the ass!
Additionally, a study by J. Ghosh et al (1998) Proc. Nati. Acad. Sci. USA 27: 1382-7 showed another interesting aspect of prostate cancer. It seems that inhibition of the enzyme archidonate-5-lipooxygenase (5-LO) triggers massive apoptosis (suicide) in human prostate cancer cells. 5-LO is an enzyme that acts upon a fatty acid called arachidonic acid that is found in all animal fats and induces proliferation of prostate cancer cells. It is also a substrate for some types of prostaglandin production.
There seems to exist an over simplification concerning the mechanisms by which AAS trigger muscular hypertrophy or growth, common to most literature on the subject. In most cases, it should be assumed that the authors of these simplifications did so as a means of generalizations for a purpose referred to as "dumbing it down".
As a whole, it is believed that most readers are idiots waiting to be told what to think and do, rather than educated through truth and "necessary" information. Some authors lack personal experience or take research as conclusive rather than realizing that calling a cat a dog won't make it bark. Please realize that many writers are just boring or scared to say "fuck you" when they mean it. Some are great, and their simplifications are for the generalization purpose.
BUT the statement "AAS induce growth solely due to molecule mergence with an androgenic receptor-site and subsequent message transcription" is totally unacceptable. If we were to leave it at that, my books would have the value of toilet paper. So "fuck them", and lets discuss the primary and secondary mechanisms and factors relating to maximizing AAS potential. (This info applies to natural hormone profiles also.)
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