Failure is, like everything, a useful tool.

Those knowledgeable about bodybuilding will tell you failure is not necessary, nor is it sufficient. It is a useful tool.

For naturals, training to failure is a good way to burn yourself out most of the time. Most people don't use proper programming to begin with, and training to failure in a stupid way is a good way to over train.

That being said, if you control volume and frequency you can accept the increase in intensity from training to failure.

My advice: Don't use failure until you've hit a plateau without failure. Then, judicious use can take you over the top to a new level of fitness.

For a good program that allows you to go crazy with intensity, see Dante's Doggcrap training.

And the increase in HGH from training to failure is not really on the same scale as a pharmaceutical intervention. Also, it is transient and wouldn't explain a chronic elevation.

Short, sustained bursts of anaerobic activity (with weights and running or other cardio) will likely help boost endogenous GH levels, along with proper nutrition and rest (sleep).

As for "training to failure," one of the most interesting perspectives I've encountered is that of Frank Zane, three time Mr Olympia. When I got serious about weight training several years ago, I hired Frank to help me put together a program. This included working out for a couple of days at his home gym, near San Diego. At one point I mentioned "training to failure," to which he said, "Don't do that." I responded: "Don't train to failure?" He smiled and said, "Don't use the word failure when you're talking about a challenging workout. The subconscious mind is extremely powerful. Does the word failure have positive connotations in any other part of your life? Train for success, which includes training hard."

I asked him later whether his objection was chiefly linguistic. "Don't train all-out as often as you might think you should, or as often as some supposed expert says to," he said. "It's not necessary hit that marker all the time. But when you're rested and your goal is to go so hard that you can't get another repetition, don't call it failure."

For some reason recalling this brings to mind a favorite Rilke passage:

"Winning does not tempt that man. This is how he grows: by being defeated, decisively by constantly greater beings."

McGuff and Little's BBS protocol is that you should work out to failure once a week at most. As Little says over and over in his articles on the BBS website, "spend more days above baseline than below". No way can you do this by training to failure 5 days a week.

I repeat, once a week at most. They have no problem with stretching that out to 10 days or 2 weeks if your condition warrants it.

Many people reporting their workouts on the BBS blog actually split their routines so they only do 3 of the Big 5 exercises, once a week or even longer.

After 2 years on the BBS protocol, the Big 5 set done once a week became too much for me and I stopped making progress, felt burned out excessively, etc. Now I only do 2 of the exercises every 5-7 days or so, in the Max Pyramid protocol. Of course I'm not aiming for muscle hypertrophy, just slowly increasing strength and "metabolic headroom" as they call it.

I think you are on to something. I think my sprinting to failure workouts do this.

ALso with regards to the heart.

Stims are coffee, etc... Actually a very good idea to remove. And take the magnesium. Dont hold back on it. CQ10 is something to look into as well. For $350.00 you can buy a watch and hack your heart beat... or have the doc hook up a halter monitor. Get 7.5 hours sleep a night. And get tested for sleep apenea. Sounds strange but you might have it. Even being fit.

The only thing that helps me is removing chocolate. In particular dark chocolate.

EDIT (More resources):

Get forum username and password (same for all users) here:afibbers.org/toboards.htm Then use them to access the forum. and as the logon info for the protocol doc here:afibbers.org/resources/strategy.pdf29 amazing pages. A must read

ALSO SEE:

http://www.afibbers.com/atrial_fibrillation/prevention_general/F87g.htm

http://www.afibbers.org/arrhythmias.html

Adrenaline secretion in panic attacks MELBOURNE, AUSTRALIA. A connection between abnormalities in the sympathetic nervous system and panic attacks has long been suspected. As early as 1871 "irritable heart", a condition very similar to panic attacks, was attributed to hypersensitivity of the "cardiac nerve centers". Now a team of Australian researchers confirms that the secretion of epinephrine (adrenaline) does indeed increase dramatically during panic attacks (by an average 153 per cent) and may be accompanied by rapid heart beat and atrial fibrillation. The researchers performed a carefully controlled study of 13 patients with panic disorder and 14 healthy controls. They found no difference in sympathetic nervous activity among patients and controls when at rest. They did observe that epinephrine was released from the heart in panic disorder patients during rest. They speculate that this release is a result of the heart's uptake of large amounts of epinephrine during panic attacks. The researchers also found that the heart rate and systolic blood pressure increased significantly in both patients and controls when exposed to simulated mental stress (rapidly subtracting 1- digit numbers from a 3-digit number for 10 minutes). They conclude that there may be a selective increase in cardiac sympathetic activity during panic attacks and that release of epinephrine from the sympathetic nerves of the heart could trigger cardiac arrhythmias.

Dr. George Heninger, MD of Yale University School of Medicine concludes in an accompanying commentary that panic attacks originate in the brain and that the excessive epinephrine discharge is a secondary effect. He suggests that abnormalities in the body's GABA (gamma-aminobutyric acid) system could be the main trigger for panic attacks. Wilkinson, Dominic J.C., et al. Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. Archives of General Psychiatry, Vol. 55, June 1998, pp. 511- 20 Heninger, George R. Catecholamines and pathogenesis of panic disorder. Archives of General Psychiatry, Vol. 55, June 1998, pp. 522-23 (commentary)

Niacin effective in the treatment of atrial fibrillation VICTORIA, CANADA. Dr. Abram Hoffer, a world-renowned psychiatrist in Victoria, reports on the successful treatment of six patients with atrial fibrillation. One 76 year old physician who suffered from atrial fibrillation was completely cured after starting a vitamin supplementation program which included megadoses of niacin and folic acid. Other patients report complete disappearance of their irregular heart beat symptoms after supplementing with high doses of niacin, folic acid, and vitamin B-12. Dr. Hoffer believes that one of the main causes of atrial fibrillation is excessive stress. High levels of stress release large amounts of adrenalin which in turn is oxidized to adrenochrome. Adrenochrome is known to cause fibrillation and other cardiac dysfunctions. Adrenochrome is a natural free radical and is primarily produced in the heart tissue, but circulates in the blood throughout the body. It can cross the blood-brain barrier and excessive amounts of it are believed to be a main cause of schizophrenia. Antioxidants protect against the formation of excessive amounts of adrenochrome and schizophrenics have been successfully treated with large amounts of niacin and ascorbic acid. Penicillamine has also been successfully used in the treatment of schizophrenia. Dr. Hoffer points out that adrenochrome is not all bad. He believes that the leucocytes use adrenochrome to destroy abnormal cells like cancer cells and that we therefore need a certain amount of adrenochrome in order to control cancer. The fact that schizophrenics rarely develop cancer supports this hypothesis. Dr. Hoffer concludes that we need a certain amount of stress in order to produce enough adrenochrome to enable our leucocytes to kill bacteria and tumor cells. However, we also need an adequate supply of natural antioxidants such as vitamins C and E and beta-carotene in order to neutralize an excess of adrenochrome after its work is done. (51 references) Hoffer, A. Schizophrenia: an evolutionary defence against severe stress. Journal of Orthomolecular Medicine, Vol. 9, No. 4, Fourth Quarter, 1994, pp. 205-21

Magnesium helps control afib Canadian researchers have done a meta-analysis of studies dealing with the benefits of intravenous administration of magnesium in the acute treatment of atrial fibrillation. They found that effective rate control (reduction in heart rate to below 100 bpm) and/or conversion to normal sinus rhythm was achieved in 84% of patients given magnesium as compared to 53% given a placebo. Seven trials used calcium channel blockers or placebo as controls. In these trials 69% of patients in the magnesium group experienced relief as compared to 53% in the control group. The researchers conclude that intravenous magnesium is an effective and safe strategy for the acute treatment of afib. PACE, Vol. 29, April 2006, Suppl 1, Abstract #36, p. S19 (European Cardiac Arrhythmia Society, 2nd Annual Congress)

Fish oil prevents atrial fibrillation KUOPIO, FINLAND. The three most important components of fish oil are eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and docosapentaenoic acid (DPA). Extensive research has established that EPA and DHA play a vital role in the prevention of Alzheimer’s disease, atherosclerosis, heart attack, angina, stroke, congestive heart failure, depression and cancer. Clinical trials have also shown that fish oil supplementation is effective in the treatment of many disorders including high blood pressure, rheumatoid arthritis, diabetes, ulcerative colitis and Raynaud’s disease.

Now Finnish researchers report that high serum levels of EPA, DHA and DPA are associated with a significantly reduced risk of developing atrial fibrillation (AF). Their study included 2174 men enrolled in the Kuopio Ischemic Heart Disease Risk Factor Study begun in 1984-1989. The men were 42, 48, 54 or 60 years of age at the baseline examination. During 17.7 years of follow-up, 11% of the participants were found to have AF upon admission to hospital (for arrhythmia or other reasons). This corresponds to an incidence rate of 0.6% a year. NOTE: Considering that the study only included men admitted to hospital, it is clear that the population-wide incidence would be significantly higher than 0.6% a year.

At baseline, the mean percentages of EPA, DPA and DHA in serum fatty acids were 1.67%, 0.55% and 2.46% respectively. After adjustment for age and other possible confounders the researchers observed that men in the highest quartile of EPA+DPA+DHA concentration (5.3 – 15.6%) had a 35% reduced risk of developing AF when compared to men in the lowest quartile (1.7 – 3.6%). The absolute risk in the lowest quartile group was 13.4% vs 8.7% in the highest quartile group. Further analysis revealed that DHA accounted for the entire risk reduction and that EPA and DPA levels were not associated with risk of developing AF.

Considering only lone afibbers (no heart disease prior to diagnosis of AF) strengthened the association between serum fatty acid concentration of DHA and AF risk. Men in the lowest quartile had a risk of 10.9%, while those in the highest quartile had a risk of only 5.6% – a relative risk reduction of 49%.

The mean serum fatty acid concentration of alpha-linolenic acid (found in flaxseed and other vegetable oils) was 0.74% and was not related to the risk of developing AF. A hair analysis revealed no correlation between methylmercury level (methylmercury is an increasingly common contaminant of fish) and risk of AF, nor did a high methylmercury level attenuate the beneficial effects of DHA. There was also no evidence that age, hypertension, systolic blood pressure or a history of ischemic heart disease modified the association between DHA level and AF risk. Virtanen, JK, et al. Serum long-chain n-3 polyunsaturated fatty acids and risk of hospital diagnosis of atrial fibrillation in men. Circulation, Vol. 120, December 8, 2009, pp. 2315-21

I stopped training to failure on a regular basis awhile back. Not because of hormones but because I felt like I was "overtraining", burning myself out, what have you. I still will push myself to failure occasionally, but my routine these days is more of a Smolov/Smolov Jr type routine where the reps are set and the weight based off a % of my 1RM.

I think timing of lifting needs to be yoked to time of day its most beneficial. Most body builders and weight lifters seem clueless about timing of work outs