building strength in the benchpress

 


      The greater the amount of type 2b fibers, the greater the weight bench pressed. Ergo how does one train type2b muscles?

The normal functioning of the prostate is influenced by hormonal secretions from the hypothalamus, pituitary gland, and testes. Luteinizing hormone releasing hormone (LHRH) (also known as gonadotropin releasing hormone) secreted by the hypothalamus stimulates the secretion of luteinizing hormone (LH) and follicle stimulating hormone from the anterior pituitary. LH stimulates the secretion of testosterone by the testes. Testosterone is metabolized in the prostate to dihydrotestosterone (DHT), which binds to androgen receptors, and which in turn bind to DNA sequences influencing gene expression, leading to the synthesis of proteins such as PSA, and triggering cell proliferation. The production of adrenocorticotropic hormone (ACTH) from the pituitary is also increased, resulting in secretion of inactive androgen precursors from the adrenal gland, which may also activate androgen receptors in the prostate gland.¹⁴

nicotine and cardiovascular effects/exercise

    "...Three randomized controlled trials have examined the efficacy and safety of NRT in patients with cardiovascular disease (Working Group, 1994; Tzivoni et al., 1998; Joseph et al., 1996). Although each study examined different endpoints, none showed significant differences in the rates of death, myocardial infarction, frequency of angina, arrhythmia, or withdrawal from therapy due to adverse events, comparing NRT to placebo. In one trial, smoking concurrently while using transdermal nicotine was not associated with an increase in adverse events (Joseph et al., 1996). Two of the trials showed a statistically significant increase in cessation rates with active treatment (Working Group, 1994; and Tzivoni et al., 1998); however one failed to demonstrate the efficacy of transdermal nicotine to accomplish long-term abstinence from smoking (Joseph et al., 1996).

A meta-analysis of adverse events, recorded in the course of 35 trials to evaluate the efficacy of nicotine patches, also failed to document a difference in the rate of acute myocardial infarction between active (n=5501) and placebo (n=3752) treatment groups (Greenland et al., 1998). A more recent meta-analysis (Mills et al., 2010) included 120 studies (92 randomised clinical trials and 28 observational studies) for a total of 177,390 individuals, and found no increased risk for myocardial infarction or death from NRT (for a review on adverse effects and tolerability see also Hays & Ebbert, 2010). The majority of these studies, however, specifically excluded patients with cardiac disease at baseline. A secondary analysis of subjects in the Lung Health Study, a randomized, controlled trial for the prevention of chronic obstructive pulmonary disease, demonstrated that cardiovascular deaths were associated with continuing smoking, but not among those who used nicotine gum for five years. The use or dose of nicotine gum, or concurrent smoking and gum use, was not associated with increased cardiovascular morbidity or mortality (Murray et al., 1996). A case control study of acute myocardial infarction, stroke and death in the UK found no evidence of increased risk in the 56 days after starting NRT for smoking cessation (Hubbard et al., 2005)."

Effect of transdermal nicotine administration on exercise endurance in men

Nicotine is widely reported to increase alertness, improve co-ordination and enhance cognitive performance; however, to our knowledge there have been no attempts to replicate these findings in relation to exercise endurance. The purpose of this study was to determine the effects nicotine might have on cycling endurance, perception of exertion and a range of physiological variables. With local ethics committee approval and having obtained informed consent, 12 healthy, non-smoking men (22 ± 3 years; maximal O₂ uptake, 56 ± 6 ml kg⁻¹min⁻¹, mean ± S.D.) cycled to exhaustion at 18°C and 65% of their peak aerobic power, wearing either a 7 mg transdermal nicotine patch (NIC) or a colour-matched placebo (PLA) in a randomized cross-over design; water was available ad libitum. Subjects were exercising at approximately 75% of their maximal O₂uptake with no differences in cadence between trials. Ten out of 12 subjects cycled for longer with NIC administration, and this resulted in a significant 17 ± 7% improvement in performance (P < 0.05). No differences were observed for perceived exertion, heart rate or ventilation. There were no differences in concentrations of plasma glucose, lactate or circulating fatty acids. In the absence of any effect on peripheral markers, we conclude that nicotine prolongs endurance by a central mechanism. Possible modes of action are suggested
-Mundel T, Jones DA: Effect of transdermal nicotine administration on exercise endurance in men. Exp Physiol2006, 91:705–713

testosterone and diet

Testosterone diffuses from the testes into the bloodstream for transport to target tissues. Approximately 1% to 2% of all testosterone circulates in the blood as free T, while the other 98% to 99% is protein-bound. Most protein-bound T is strongly associated with SHBG (60%), while the other 38% fraction is bound to albumin. Only the albumin-bound and fT forms are available for binding at target tissues, and are thus called bioavailable T (bioT).1Advancing age is accompanied with changes in testosterone binding due to an increase in SHBG.2

References:

Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting.Int J Clin Pract. 2010;64:682-696. PMID: 20518947.

Kaufman J-M, T'Sojen G, Verleulen A. Androgens in male senescence. In: Nieschlag E, Behre HM, eds. Testosterone: Action, Deficiency, Substitution. Cambridge, UK: Cambridge University Press; 2012: Chapter 16.

Testosterone and cortisol in relationship to dietary nutrients and resistance exercise (

Volek et al., 1997)

Effects of replacing meat with soyabean in the diet on sex hormone concentrations in healthy adult males(Habito et al., 2000)

 Body composition and hormonal responses to a carbohydrate-restricted diet (Volek et al., 2000)

Intensive insulin therapy increases sex hormone binding globulin in newly diagnosed type 2 diabetic patients (Tong et al., 2013)

Lower serum testosterone is independently associated with insulin resistance in non-diabetic older men: the Health In Men study (get it? H.I.M.) (Yeap et al., 2009)

Food energy

The energy value per gram of various food components includes:

• fat – 37 kJ (9 Cal) – not all fatty acids may provide the same amount of energy
• alcohol – 29 kJ (7 Cal)
• carbohydrates – 16 kJ (4 Cal) – not all carbohydrates may provide the same amount of energy
• protein – 17 kJ (4 Cal)
• dietary fibre – 13 kJ (3 Cal) – if fermented by bacteria in the large intestine
• water – 0 kJ (0 Cal).
• SINCE 1 KILOWATT HOUR => ENERGY USED BY 10 X100WATT BULBS TURNED ON FOR 1 HOUR=3600 KILOJOULES= 3600/37~97 GRAMS OF FAT 

ketogenics song

REGULATION OF KETOGENESIS
(Sung to the tune of “Clementine”)

In starvation, diabetes, sugar levels under strain
You need fuel to keep going saving glucose for your brain
Ketone bodies, Ketone bodies, both acetoacetate
And its partner on reduction, 3-hydroxybutyrate.

Glucagon’s up, with low glucose, insulin is down in phase
Fatty acids mobilised by hormone-sensitive lipase
Ketone bodies, Ketone bodies, all start thus from white fat cell
Where through lack of glycerol-P, TG making’s down as well.

Fatty acyl, CoA level, makes kinase phosphorylate
Acetyl-CoA carboxy-lase to its inactive state
Ketone bodies, Ketone bodies, because glucagon they say
Also blocks carboxylation, lowers Malonyl-CoA.

Malonyl-CoAs a blocker of the key CPT-1
Blocking’s off so now the shuttle into mito’s is begun
Now we’ve ß oxidation, now we’ve acetyl-CoA
But what’s to stop it’s oxidation via good old TCA?

In starvation, glucose making, stimulating PEP CK
Uses oxaloacetic, also lost another way
Ketone bodies, what is odd is that the oxidation state
Also favours the reduction of OA to make malate.

OA’s low now, citrate synthase, thus loses activity
So the flux into the cycle cuts off (temporarily)
Ketone bodies, Ketone bodies situation thus is this
Acetyl-CoA’s now pouring into Ketogenesis.

It’s a tricky little pathway, it’s got HMG-CoA
In effect it’s condensation in a head-to-tailish way
Ketone bodies, Ketone bodies, note the ratio of the pair
Is controlled by NAD to NADH everywhere.

Don’t despise them, they’re good fuels for your muscles, brain and heart
When you’re bodies overloaded though, that’s when your troubles start
Ketone bodies, ketone bodies, make acetone, lose CO2
You can breath those out, but watch out - acidosis does for you!


The biochemists songbook 2nd edition 1995

EXCESS SUGAR STOPS SHBG PRODUCTION

Too Much Sugar Turns Off Gene That Controls Effects Of Sex Steroids
SHBG IS BELIEVED TO BE A TRANSPORTER OF STEROIDS IN THE BLOOD, IT IS NOT VERY ACTIVE. TESTOSTERONE IS EITHER FREE (1 TO 2 %) , LOOSELY BOUND TO ALBUMIN-THIS IS AVAILABLE TESTOSTERONE THAT IS USABLE IE BIOAVAILABLE- (~59%) AND THE REST IN BOUND TO SHBG W/C IS UNUSABLE-NON BIOAVAILABLE. ScienceDaily (Nov. 21, 2007) — Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, shows a new study in mice and human cell cultures that’s published this month in the Journal of Clinical Investigation. This discovery reinforces public health advice to eat complex carbohydrates and avoid sugar. Table sugar is made of glucose and fructose, while fructose is also commonly used in sweetened beverages, syrups, and low-fat food products. Estimates suggest North Americans consume 33 kg of refined sugar and an additional 20 kg of high fructose corn syrup per person per year.

Glucose and fructose are metabolized in the liver. When there’s too much sugar in the diet, the liver converts it to lipid. Using a mouse model and human liver cell cultures, the scientists discovered that the increased production of lipid shut down a gene called SHBG (sex hormone binding globulin), reducing the amount of SHBG protein in the blood. SHBG protein plays a key role in controlling the amount of testosterone and estrogen that’s available throughout the body. If there’s less SHBG protein, then more testosterone and estrogen will be released throughout the body, which is associated with an increased risk of acne, infertility, polycystic ovaries, and uterine cancer in overweight women. Abnormal amounts of SHBG also disturb the delicate balance between estrogen and testosterone, which is associated with the development of cardiovascular disease, especially in women.

“We discovered that low levels of SHBG in a person’s blood means the liver’s metabolic state is out of whack – because of inappropriate diet or something that’s inherently wrong with the liver – long before there are any disease symptoms,” says Dr. Geoffrey Hammond, the study’s principal investigator, scientific director of the Child & Family Research Institute in Vancouver, Canada, and professor in the Department of Obstetrics & Gynecology at the University of British Columbia.

“With this new understanding, we can now use SHBG as a biomarker for monitoring liver function well before symptoms arise,” says Dr Hammond, who is a Tier 1 Canada Research Chair in Reproductive Health. “We can also use it for determining the effectiveness of dietary interventions and drugs aimed at improving the liver’s metabolic state.”

Physicians have traditionally measured SHBG in the blood to determine a patient’s amount of free testosterone, which is key information for diagnosing hormonal disorders. In addition, SHBG levels are used to indicate an individual’s risk for developing type 2 diabetes and cardiovascular disease.

The discovery dispels the earlier assumption that too much insulin reduces SHBG, a view which arose from the observation that overweight, pre-diabetic individuals have high levels of insulin and low levels of SHBG. This new study proves that insulin is not to blame and that it’s actually the liver’s metabolism of sugar that counts.

This research was supported by a grant from the Canadian Institutes of Health Research, the Michael Smith Foundation for Health Research, and the BC Children’s Hospital Foundation.