Alcohol and bodybuilding
Ethanol , also known as "alcohol" is probably the most commonly used drug worldwide . Of its effects on heart disease apart once , would say only a few , it would be good. But , because of its legality, ubiquity , and the mere fact that makes it such a fun, and do not worry about most of the consumption of a few beers or even a few six packs . This includes many a bodybuilder .
Nevertheless, it is far from being a harmless vice , even for non-alcoholics . It affects numerous neurotransmitters , metabolic processes , and hormones - and many of these effects extend well beyond the period of intoxication beyond . They have far-reaching consequences , not only for the health in general, but , as you will see, even for the physique.
We will deal first with the basic science of ethanol, then we go to its effects on building body mass. We will not deal with the effects that occur with chronic consumption, addiction and withdrawal, as these are not relevant for those who I would describe as the predominant readers of this text . It is needless to say that such a lifestyle is totally inappropriate when it comes to getting the best from their own body .
Ethanol , in addition to being a drug , a nutrient. Unlike other nutrients, such as carbohydrates , fat and protein , the body ethanol but not save - it is also the only toxic nutrient. These two properties lead to some important consequences - namely, to be metabolized , and this process takes precedence over all other nutrients.
It is metabolized in either of two possible ways depending on the blood concentration. The first , via alcohol dehydrogenase ( ADH) to aldehyde . At high concentrations , however, increasingly that path is taken , which is called the microsomal ethanol oxidizing system ( MEOS ) . Both result in the conversion to acetate , then acetyl -CoA - where it enters either the tricarboxylic acid cycle and is oxidized to CO2 and water , or it is stored as fat.
With oral administration of alcohol is bioavailable , but oral clearance rate and absorption in the post-prandial state (ie with other food) from , this is due to ADH activity in the stomach. The more food in the stomach , the longer the ethanol stays there and is metabolized before it reaches the bloodstream. The type of food effect this, with protein and fat have a greater effect . Fat, due to slower transport in the small intestine , by binding directly to the protein molecule of ethanol .
The type of drink can also influence the level of achieved blood alcohol concentration - particularly in the fed state. So after a meal less concentrated drink will be ( such as beer ) absorbed faster than a more concentrated ( as a shot ) - in rats, this led to an 80 % increase in peak blood alcohol level and higher by 95 % overall absorption . On an empty stomach, the opposite , the extent of the difference could be detected , although not as large failed.
It is also interesting to note that when large amounts are ingested, absorbed through the systemic distribution, can go and thus may occur exceptionally high concentrations in arterial blood - and therefore in the brain. That is the reason why a six beers directly cut down consecutively more than eight over a period of two hours.
Despite popular opinion to the women ethanol no slower than men - in fact the opposite is true. The error in the account differences in total body water (or in the dry body mass ) must be included between men and women has been paid much attention for much of the confusion. But if you look at the total body water, women metabolize ethanol to 33 % faster than men because they have a proportionally larger liver.
Due to restrictions the ADH follows the metabolism of a constant rate ( about one drink per hour is equivalent ) , in contrast to the half-lives that have the most drugs in the body.
It could be shown that DHT the breakdown of ethanol decreased by an increase of ADH , thus increasing a good testosterone cycle susceptibility to intoxication.
Aldhyd is , as mentioned above, a product of the metabolism of ethanol . In the literature, its presence has generally caused negative attitudes , as is the basis of treatment for alcoholics with disulfiram . It is responsible for the redness, which can be observed in drinkers usually Asians - this may be reduced by antihistamines . However, a few studies have shown ethanol reinforcing effects.
Aldehyde has also been associated with the hepatotoxic effects of ethanol . The amino acid taurine increases the metabolism of aldehyde by the activation of hepatic enzyme aldehyde dehydrogenase , thus lowering levels - though this was the eqivalent of 45 grams for a person of about 90 kg , so who knows whether supplementation with reasonable doses would be effective .
For oral , intravenous or intraperitoneal administration of ethanol causes effects in the CNS , the nature of two things. Lower concentrations (10 to 25 mmol according to 3-8 drinks ) call mainly produce euphoric effects , while higher doses result in dejection.
Some time was believed ethanol effects through nonspecific way by acting as a solvent or alternate WOULD with fatty membranes. Until the recent past, it still taught that ethanol it worked by coating the cells rather than with specific receptors to interact , as is the case with all other drugs. This approach was believed lately increasingly unpopular for reasons that I will not discuss here , and now is considered to exert its effects by binding to proteins at specific receptors. There is a widespread view that no specific ethanol receptor exists , although a prominent researcher puts the theory suggests that the evidence suggests that we should think about such a receptor .
The exact mechanisms behind its subjective effects are still not fully understood, and the numerous , conflicting studies is further complicated by the fact that ethanol preferably affects certain subtypes of different receptors . An exhaustive presentation is best kept in a five hundred page book , but I have analyzed the research results and selected for the present what I would describe as the best overall view of the effects on the various systems .
Values of the concentration of the central neurotransmitter dopamine are , have been consistently shown increased by ethanol, and it is considered to be the primary mediator of the reinforcing effects of all drugs of abuse . It is also generally involved in behavioral reinforcement . Of particular importance is the mesolimbic dopamine system, which of neurons in the ventral Tagamental Area (VTA ) and the nucleus accumbens (NAC ) is regulated .
Alcohol preferring rats have lower basal mesolimbic dopaminergic activation and innervation as non- preferring rats - contribute as well as altered activity of serotonin, GABA and opioids , all of which are modulators of mesolimbic dopamine system and the sub-function of this area. Acute administration of ethanol increases the extracellular dopamine levels in the NAC as a result of increased firing of dopamine neurons in the VTA , and thus brings the mesolimbic activity beyond the ordinary . Therefore, ethanol intake is more of self-medication and brings a behavioral activation (analogous to human euphoria ) and decreased anxiety in alcohol preferring rats , while non- preferring rats tend only to calm .
Ethanol could increase the concentration of endogenous opioid beta-endorphin in the brain studies , and it is likely that the opioid system much of its effects on dopamine levels , are mediated through GABA mediated inhibition of the activation of dopamine neurons is turned off.
It has been found that alcoholics have lower basal levels of endogenous opioids than non -alcoholics, and when ethanol is consumed , these levels increase to a level that is not reached by non- alcoholics. Antagonists of opioid receptors appear to inhibit the reinforcing effects of ethanol in animals and the euporisierenden effect in humans. One of these, naloxone , appears as a very promising drug in the fight against ethanol addiction.
Anyway, if I may just take a position , I would like to emphasize that opioids are endorphins in the brain , so operate that alcoholics self-medication to make yourself happy; a drug that someone keeps them from drinking , because it makes the beatific Drinking ineffective at seems to me to be a piss poor attempt. But of course they would never allow a long-acting morphine, because , God forbid, someone might want more happiness than mankind deems it necessary and thus might abuse.
The NMDA receptor is one of the three forms of glutamate receptors - the neurotransmitter that excites the body before anyone else. He is n- Methyl-d -aspartate , named after its synthetic , high-affinity ligands. Ethanol blocks this receptor . The probable mechanism is about preventing the removal of a magnesium glutamate , calcium influx into the cell is blocked . This reduces the excitability of the cell, which , together with increased inhibition by GABA , the calming effects of ethanol , particularly at high doses.
This blockage leads to up-regulation of glutamate receptors , which leads to hyperexcitability of the cell when ethanol is no longer present - this is one of the mechanisms that are responsible for damage to the nervous system by ethanol withdrawal. It has also been postulated that the end of each phase represents a mini- drink withdrawal together with the previously mentioned effects . Since magnesium is a natural antagonist of this receptor , it seems likely no bad idea , 400 to 800 mg and to take after a night of drinking . Zinc and the amino acid taurine may also be antagonists.
The NMDA receptor complex is also associated with memory loss or blackouts by ethanol - this is due to its effects on the long-term potentiation (LTP) . We will come to that later .
Another very important system is the gamma -amino- butyric acid (GABA ) - the preferred inhibitor of the body. Ethanol potentiates the effects of GABA to its receptor . It probably has a biphasic effect on the behavior , with low doses of GABA interneurons inhibit dopamine receptors in the VTA and thus dopamine -induced stimulation and euphoria cause , while higher doses cause extensive inhibition of CNS activity and overshadow the stimulating effects . This is probably one of the main mechanisms through which its sedative-hypnotic and anxiolytic actions .
Ethanol also has significant effects on serotonin (5- HT ), although it is not as well characterized as those mentioned previously . Ethanol has a biphasic effect on serotonin, first increases concentration and then lowering them .
5 -HT antagonists, such as serotonin reuptake inhibitors , were found in drug tests as a substitute for ethanol. 5-HT activity is likely responsible for the nausea which occurs at excessive consumption . It is probably part of the explanation for the increased dopamine release as antagonists ethanol- induced dopamine release seem to block .
Ethanol administration eventually results in decreased 5 - HT levels, and thus activity , this is due to increased peripheral metabolism of its precursor , L- tryptophan. Low concentrations of 5 -HT to be associated with increased aggression and it is also quite likely that subsequent drinking episodes ( and their accompanying increase of 5 -HT) medication, to be followed by a fall in levels and repeat the cycle. It seems possible that reduced levels of 5 -HT could contribute to the discomfort of hangover the next day , so 50 mg of 5- HTP upon waking might not be a bad idea .
The cholinergic system is still a target for the actions of ethanol. It has been found that with acetylcholine acts as a co- agonist at the nicotinic acetylcholine receptors , as well as to potentiate the effect of nicotine at this receptor , both of which eventually results in an increase of the mesolimbic dopamine. This interaction quite nicely for the fact that 90 % of alcoholics are nicotine dependent .
There are likely some interaction of ethanol with the endocannabinoid system. They are very similar in their effects in that both produce euphoria and stimulation at low and CNS depression at high doses. Cross - tolerance between the effects of THC and ethanol was observed in rats and down-regulation of the CB1 subtype of cannabinoid receptors has been reported in rats chronically exposed to ethanol.
N- Arichidonyl - ethanolamide ( AnNH ) is a naturally occurring derivative of the long chain fatty acid , arachidonic acid, binds to the CB1 receptor and simulate the effects of THC. Ethanol increases the formation of AnNH from arachidonic acid .
The administration of a CB1 antagonist was able to limit ethanol consumption , which suggests that it is involved in the enhancement of ethanol.
Ethanol intake increases central and peripheral levels of epinephrine and norepinephrine, which contribute to the stimulatory effects of ethanol, particularly in the ascending part of the curve of blood alcohol . Brain concentrations of norepinephrine tripled . These increases occur mainly as a result of increased release and decreased clearance, rather than increased synthesis . A consequence is depletion of E and NE memory - in the adrenal glands to 8% and 20 % after four days. This fall likely contributes to the CNS depression associated with prolonged drinking .
There is a real and significant relationship between ethanol and aggression , which could be of particular importance especially for bodybuilders who supplement with exogenous androgens or do other things that already can promote aggressive behavior .
The mechanisms are many. As an anxiolytic , it can reduce the fear of punishment and consequences that result from their own behavior , as a stimulant , it can increase the sensation-seeking and as an analgesic , it may reduce the perception of the consequences of painful , provocative stimuli.
Another interesting possibility is the property of ethanol to interfere with the executive cognitive functions ( ECF) . ECF includes higher order mental abilities such as abstract reasoning , attention, planning, self-observation and reflection and the ability to adapt future behavior by reactions of the environment - ECF is the ability above to consciously use for self-regulation of the target behavior.
ECF are controlled by the prefrontal cortex, and patients with lesions in this area have a reduced regulation of social behavior. ( To suppress as the ability aggression in favor of a monetary reward ) Lower scores on tests of ECF processes have been obtained both in patients and in humans intoxicated with ethanol . It should also be mentioned that essentially the ECF be influenced with increasing blood alcohol concentrations .
The neurotransmitter serotonin has been implicated in this ethanol induced aggression . Sinking serotonin concentrations could be correlated with aggressive behavior . Acute ethanol consumption reduces the availability of the 5- HT precursor L- tryptophan to the brain. So if you are prone to aggressive , it would at least be good to take before drinking 25 to 50 mg of 5 -HTP .
Alcohol is neurotoxic and this toxicity is supported by several factors. Fatty acid ethyl esters are a toxic by-product of fatty acids and ethanol, can increase the mitochondrial uncoupling and disconnection of lipids of cell membranes, - the formation of these esters may by three to six times can be prevented by L- carnitine and acetyl L-carnitine at a dose of 50 mg / kg.
There is evidence that ethanol induces oxidative damage - it increases free radicals and Fettperoxyde and Proteincarbonyl , indirect cause of oxidative damage - thus the use of antioxidants is recommended. As already mentioned NMDA excitotoxicity modulated a different mechanism .
Hepatotoxicity will not be treated here , since there are no major concerns for non-alcoholics , and alcoholics are not the target audience of this article. Nonetheless, I will say that one time accompanying Tylenol and ethanol use, probably not, as claimed , leads to permanent liver damage.
The NMDA receptor complex is involved in memory loss by ethanol . This follows from its long-term potentiation ( LTP) in the hippocampus . LTP is a conservative increase in synaptic activity that follows a short, intense stimulation of presynaptic inputs - basically it is a physiological change , are shaped by the memories.
For the induction of an activation of NMDA is needed , but not maintenance of LTP , and as mentioned , ethanol leads to blockage of the transmission of NMDA receptors. In fact it could be shown that ethanol inhibits LTP already at concentrations of 10 mM (or two to three drinks ) .
This effect mainly depends on the dose (and also of the individual differences ) and is composed as a continuum , with lower concentrations producing less waste and concentrations between 50 and 100 mmol ( 20 drinks ) so-called " black-outs " .
Contrary to popular opinion , the accumulation of blackouts is not a harbinger of a slow onset of alcoholism. Blackouts and short-term memory deficits could be related ; So if you want to test if your drunk friend is experiencing a blackout on the next day , he asks about the content of a conversation five minutes before - he does not remember , this is a clear sign .
GABA , dopamine and serotonin are likely to bring with ethanolinduziertem memory loss related to, although the data are currently still sparse. When serotonin , this is probably related to the decrease in tryptophan availability , so it is 25 to 50 mg HTP to recommend again.
ALCOHOL AND BODYBUILDING
Now that we have left the basic science behind us , we can look at the ways in which ethanol affects our efforts with regard to fat loss and muscle growth - they are numerous , and they are not good .
First : unlike most drugs , alcohol is a nutrient , and a dense it. Ethanol containing 7.1 kcal per gram , almost twice as much as carbohydrates and protein. And , unlike the other nutrients, it seems to cause no significant satiety. In other words, it does not replace any calories but adds to lie to them.
Considering the fact that a drink ( a beer, a glass of wine, liquor) contains about 12 grams of ethanol , this can end badly . I think it would not be unusual for a person of 90 kg to tilt 20 drinks in a good Friday night - that would be around 1600 kcal just from the alcohol. This should consider beer 'm fat and hard liquor does not , put the death blow (although the carbohydrates provide additional 500-100 calories in beer, depending on whether it is light or not). That's as much as the total daily ration of calories for someone who wants to lose body fat - and I think I need not mention only that we then often by three clock at night nor in any fast food stall or an all-you - can-eat go buffet and cram a few more thousand into us .
There is some speculation in the literature that alcohol calories do not count , so we should look at this one closely. This idea comes mainly from the fact that studies have shown that drinkers lower body mass indexes ( BMIs ) than would foreshadow their calorie consumption. In men and women are identical and even lower BMIs show despite a higher caloric intake by several hundred calories compared with nondrinkers .
Most of these studies have not considered the actual body composition, thus weight differences with different dry body mass could be explained - and this would not be the only surprise , you can see on some of the effects of ethanol on anabolic hormones , which we will cover later . In addition, in most cases both food intake and body dimensions in self- directed by the subjects were sent by mail to the researchers , the reported daily caloric intake was only 60 to 70 % of the average intake of a person.
Was, however, a more interesting study of Addolorato et al. carried out , which not only considers the BMI , but also the body composition (via DEXA ) of 34 alcoholics and 43 control subjects - all of them male. The group of alcoholics had less body fat , but the same dry body mass. A possible explanation would be that the alcoholic group increased concentrations of extracellular water had , as it was known to be found in liver cirrhosis and recently also in alcoholics without liver disease. It should also be noted that these were chronic alcoholics metabolic abnormalities had that do not concern us .
Other studies have shown weight loss with isocaloric substitution of ethanol for carbohydrates as well as a lower than expected weight gain in addition of ethanol to a maintenance diet . Nevertheless, this could be due to some extent to differences in the storage of glycogen (as opposed to carbohydrates ethanol is not stored as glycogen) and muscle ( due to hormonal issues - more on that below ) .
Now that we have seen a few empirical studies, we should come to the more basic physiology. Ethanol is well received and processed, so this can be ruled out. At a high concentration, the aforementioned MEOS can come into play - this results in oxidation of ethanol without concomitant production of ATP . Also, as already mentioned, Ethanol-induced catecholamine increase thermogenesis . A further possibility is the uncoupling of mitochondrial oxidative phosphorylation , . Also, there are data that suggest that an interaction between ethanol and leptin takes place, although the consequences of it must be explained in more detail by the research.
On the other hand, is the view that ethanol would almost magically produce fat gain , excessive. De novo lipogenesis from ethanol accounts for only about 3% ( less than 5% ) of total calories - the radical is oxidized. It directly suppressed fat burning , unlike carbohydrates, where insulin plays a major role - however , ethanol does not have the accompanying anabolic effect of insulin. The ethanol (as acetate ) rather takes precedence over the burning of fat and carbohydrates , so it's always basically comes down to a total utilization of calories.
If you the calorie content of ethanol has not yet convinced that it is not the best thing for the body structure , this will hopefully do its effects on muscle growth. Ethanol, this has been shown time and again , resulting in a sustainable and significant decrease of testosterone and growth hormone - and it increased cortisol levels in many studies . The effects of these hormones are hopefully known and need not be explained in detail. Ethanol directly inhibits protein synthesis.
Growth hormone (GH)
The devastating effects of ethanol in humans and animals are well known : declining levels of GH , GH mRNA and GH- distributing mRNA levels . In adolescent and adult rats caused an equivalent of 4-6 drinks a massive waste of GH concentrations to 4-7 % after 1.5 h After 24 h , the levels were still at 66-86 %. In adult rats caused 3g/kg a complete suppression of GH secretion , 2g/kg generated strong but not total suppression . Inhibition of hepatic IGF-1 synthesis and 1/IGFBP-1-Rate a mark for the bioavailability of IGF-1 have also been adversely affected by ethanol.
Ethanol increased both directly and indirectly, ie ( by an increase of ACTH) , cortisol production. In addition, the consumption of ethanol resulted in combination with physical exercise to 61% more cortisol than for alcohol alone . 1.75 g / kg increased the concentrations of 152% after 4 hours and still significant after 24 hours. Some researchers have concluded that the increase in the cortisol level is likely due to stress reactions by nausea than to a direct effect of ethanol . Subjects who vomited , had compared four times higher concentrations.
Leptin is indicated by the metabolism of glucose into the fat cells - most likely on the path of the hexosamine biosynthesis. The metabolism of ethanol to acetate, followed by oxidation does not contribute directly to the Hexosaminfluss , thus are likely to be many empty calories in this consideration . Nevertheless, there are some interesting studies that combine leptin and ethanol.
Serum concentrations of leptin were found to be increased in active alcoholics , compared with control groups and former alcoholics , suggesting that alcohol increases leptin levels . By ethanol prolactin is increased, which can in turn increase leptin. Subsequent studies could bring increases of leptin with desire and consumption of ethanol in combination and suggest that leptin probably the ethanol consumption controls than vice versa. The only study that has examined the effects of ethanol consumption on leptin , found a decrease of leptin , but this could be explained by the above-mentioned differences between the metabolism of glucose and ethanol. There really is no other data.
Finally, we come to the most important part . Acute administration of alcohol could significantly reduce the production of testosterone in humans and animals in many studies . We will first look at the mechanisms , then to current studies.
Ethanol exerts its effects hypogonadal through various direct and indirect mechanisms . The primary runs through direct suppression of functions of Leydig cells ( increase selenium could ethanol induced Testosteronünterdrückung ) both through a direct toxic effect (including a reduction of LH- receptors ) as well as on the activity of free radicals by the reduction of 3- beta HSD (the enzyme that converts androstenedione to DHEA ) and 17 - Beta -HSD (converts androstenedione to testosterone) , and by reduction of the NADPH producing enzymes. NADPH is a cofactor that is used in many steps of steroidogenesis and ethanol administration resulted in a decrease in the enzymes that are necessary for the production of NADPH.
Ethanol reduces the LH- distributing hormone on the hypothalamus by decreasing LH secretion at the pituitary as well as it inhibits LH mRNA in vitro. This could be done through endogenous opiates, which are increased by ethanol, and increase their antagonists block ethanol and LH to the testicles .
Nitric oxide (NO) is also involved in this suppression ( reminds you if you the next time a Viagra or Tribulusprodukt swallows ) . While NO LH production is stimulated in the pituitary its overall effect on testosterone because of its negative effects on the gonadal level. Substances which increase NO levels, inhibit the secretion of testosterone and possibly also of steroidogenic enzymes. L-NAME , L -NA or concomitantly with ethanol 7Ni completely prevented the decrease of testosterone was observed at 3g/kg . The mechanism probably involves a direct gonadal effects.
Another interesting possibility is a natural mechanism that connects the brain and gonadal and beta- adrenergic receptor involved . Direct injection of adrenergic antagonist in the hypothalamus decreased testosterone production in the testis , without affecting the LH level . Ethanol increases catecholamines in the CNS. And injections of both phentolamine (alpha -adrenergic antagonist) as well as propranolol ( beta antoganist ) covered in part, the suppressive effect of ethanol on the hCG -stimulated testosterone production