“Now Hack Wilson and Babe and some of the others did a
lot of lifting, all right, but it was done a glass of beer at a time.”
- Coach Bibb Falk
It’s no secret that college aged kids enjoy consuming alcohol. We’ve all seen “Animal House” and “Old School”. Whether we’ve “been there” or not we know it goes on. So why does it matter? Who cares if these kids are binging on the weekends if their grades stay up and they stay out of trouble?
Well it definitely matters if they are athletes! An athlete is day by day trying to get better and improve. And as a strength and conditioning coach it is our job to facilitate this through proper programming and education. And if the athlete is sabotaging this how can we do our job?!?
A little while ago Eric Cressey had a post on the web page Testosterone Nation titled “What I learned in 2008”. One of the things Cressey mentions is alcohol and it’s effects on skeletal muscle. While we would all like to assume that alcohol consumption is bad, what does the research say?
There are many problems associated with chronic alcoholism and alcohol abuse including degeneration of skeletal muscle and loss of contractility (Chung and Lang 2008). While these are problems that definitely effect how an athlete performs, we hope the majority of collegiate athletes don’t have problems with sever long term alcohol abuse.
The problems that the weekend binger has are a little different. While you don’t see protein degeneration to the extent that you do with chronic alcohol abuse protein synthesis is disrupted.
In 2009 Lang et al found that, “acute alcohol (EtOH) intoxication decreases muscle protein synthesis via inhibition of mTOR-dependent translation initiation. (Lang et al. 2009)”. Mammalian target of rapamycin (mTOR) is a regulatory protein that regulates cell growth and repair. When mTOR is inhibited cell growth is halted, including myocite repair which is important for athletes.
Acute alcohol consumption and intoxication also has some detrimental effect on sleep and sleep patterns. Deep sleep coincides with the release of growth hormone in children and young adults. Many of the body's cells also show increased production and reduced breakdown of proteins during deep sleep. Since proteins are the building blocks needed for cell growth and for repair of damage from factors like stress and ultraviolet rays, deep sleep is important.
Additionally, alcohol increases non-REM sleep and reduces REM sleep during the first portion of the night. We know that the majority of cell repair and protein synthesis takes place during non-REM sleep. Non-REM sleep promotes physical healing and growth. Seventy percent of growth hormone secretion occurs during this type of sleep. Growth hormone stimulates protein anabolism for cell repair and influences the metabolism of proteins, fats, and carbohydrates. In a sleep-deprived patient, the loss of NREM sleep causes immunosuppression, slows tissue repair, lowers pain tolerance, triggers profound fatigue, and increases susceptibility to infection (Lower et al 2003).
So who cares?! I can still get my non-REM sleep even after I consume alcohol. And since non-REM sleep is where cell repair takes place I can still get blasted and repair soft tissue no problem. Right?!
Here is the catch, alcohol is metabolized rapidly and blood concentrations are negligible by the middle of the night even for individuals who have had only a couple drinks prior to bedtime, often resulting in withdrawal symptoms thereafter. These may include shallow sleep and multiple awakenings, REM rebound associated with nightmares or vivid dreams, sweating, and general activation (Yules1967, madsen 1980). Therefore, although alcohol may be effective in sleep induction, it impairs sleep during the second half of the night and can lead to a reduction in overall sleep time.
Acute alcohol consumption also has an effect on growth factors, particularly those that are anabolic in nature. Alcohol has been seen to decrease the secretion of HGH by as much as 70 percent! Also, when alcohol is in your body, the production of a substance in your liver is triggered that is directly toxic to testosterone, a hormone essential to the development and recovery of your muscles.
So what’s the PSA here? What do I tell my athletes? How do I keep tham away from this stuff? Unfortunately I don’t have all the answers, and to be honest a beer every now and then tastes pretty darn good! But it is certainly not beneficial to growing young athletes who are trying to reach their “genetic potential”. So the take home message: Moderate drinking for of age adults is probably okay, but for athletes in intense training programs there are no upsides.
-SM
Sunday, February 8, 2009
Wednesday, February 4, 2009
From Stay Puffed to Hercules all at the same time?
Yesterday I was watching The Biggest Loser at a friends house. There was a moment when one contestant being weighed gave the excuse that she was turning fat into muscle which is why she isn’t losing as much weight as the other contestants. The trainers freaked out and said that it was untrue and she was just making excuses.
One of our friends asked if that was true, if you can’t gain muscle while losing fat? Or rather can you “turn fat into muscle”?
Unfortunately this is impossible. To burn fat you need to be in a negative caloric state. In other words you need to be ingesting fewer calories than you are expending. Through this process your body utilizes fat as an energy source by breaking tri-glycerides (fat) into it’s four basic components, glycerol and fatty acids. This reaction is called Lipolysis.
Glycerol follows the glycolytic pathway (glycolysis). During this process it is converted into pyruvic acid. For entry into the Krebs Cycle, the pyruvic acid must be converted to acetyl CoA. Acetyl CoA then enters the krebs cycle and forms ATP. Fatty acids are converted into Acetyl CoA via a process called beta-oxidation. During this process the fatty acid chains are broken apart, forming two acetic acid molecules. They then become acetyl CoA which can enter the krebs cycle and become ATP.
Here’s the kicker, in order for you to build muscle you need to be ingesting extra calories. Your body cannot make something out of nothing. Skeletal muscle has cells surrounding each muscle fiber called satellite cells. Satellite cells function to facilitate growth, maintenance and repair of damaged skeletal muscle tissue. Usually these cells are inactive, but they become excited when the muscle fiber receives any form of damage, such as from resistance training. Especially in an overloaded state. This satellite cell activation period lasts up to 48 hours after the trauma. There are a number of other reactions that occur during this trauma period. The immune system causes a sequence of events in response to the injury of the skeletal muscle. Macrophages move to the injury site and secrete cytokines, growth factors and other substances. This is called phagocytosis. Cytokines stimulate the arrival of lymphocytes, neutrophils, monocytes, and other healer cells to the injury site to repair the injured tissue. Growth factors stimulate the division and differentiation of a particular type of cell. With skeletal muscle hypertrophy, growth factors involved are: insulin-like growth factor (IGF), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF). Hormones such as testosterone help to increase protein synthesis which leads to hypertrophy. This whole process requires a significant amount of energy to take place. Without the appropriate energy there can be no growth in the muscles.
So the trainers were absolutely right. No muscle gained in a negative caloric environment. Which is why when an athlete asks how to gain muscle mass you tell them "EAT EAT EAT EAT…"
Now this doesn’t mean eat anything, stick to high protein diets with adequate carbohydrates, dairy proteins and vegetables. Also no alcohol but more on that later…
-SM
One of our friends asked if that was true, if you can’t gain muscle while losing fat? Or rather can you “turn fat into muscle”?
Unfortunately this is impossible. To burn fat you need to be in a negative caloric state. In other words you need to be ingesting fewer calories than you are expending. Through this process your body utilizes fat as an energy source by breaking tri-glycerides (fat) into it’s four basic components, glycerol and fatty acids. This reaction is called Lipolysis.
Glycerol follows the glycolytic pathway (glycolysis). During this process it is converted into pyruvic acid. For entry into the Krebs Cycle, the pyruvic acid must be converted to acetyl CoA. Acetyl CoA then enters the krebs cycle and forms ATP. Fatty acids are converted into Acetyl CoA via a process called beta-oxidation. During this process the fatty acid chains are broken apart, forming two acetic acid molecules. They then become acetyl CoA which can enter the krebs cycle and become ATP.
Here’s the kicker, in order for you to build muscle you need to be ingesting extra calories. Your body cannot make something out of nothing. Skeletal muscle has cells surrounding each muscle fiber called satellite cells. Satellite cells function to facilitate growth, maintenance and repair of damaged skeletal muscle tissue. Usually these cells are inactive, but they become excited when the muscle fiber receives any form of damage, such as from resistance training. Especially in an overloaded state. This satellite cell activation period lasts up to 48 hours after the trauma. There are a number of other reactions that occur during this trauma period. The immune system causes a sequence of events in response to the injury of the skeletal muscle. Macrophages move to the injury site and secrete cytokines, growth factors and other substances. This is called phagocytosis. Cytokines stimulate the arrival of lymphocytes, neutrophils, monocytes, and other healer cells to the injury site to repair the injured tissue. Growth factors stimulate the division and differentiation of a particular type of cell. With skeletal muscle hypertrophy, growth factors involved are: insulin-like growth factor (IGF), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF). Hormones such as testosterone help to increase protein synthesis which leads to hypertrophy. This whole process requires a significant amount of energy to take place. Without the appropriate energy there can be no growth in the muscles.
So the trainers were absolutely right. No muscle gained in a negative caloric environment. Which is why when an athlete asks how to gain muscle mass you tell them "EAT EAT EAT EAT…"
Now this doesn’t mean eat anything, stick to high protein diets with adequate carbohydrates, dairy proteins and vegetables. Also no alcohol but more on that later…
-SM
To Stretch or not to stretch
Stretching has become fairly controversal in the past few years. We know not to static stretch prior to any anaerobic power activity. But why stretch at all. there are many Studies that discuss performance enhancing characteristics of increased flexibility. There also studies that claim stretching will help reduce injuries. But for the studies that claim the increased performance and decreased injuries are due to strtetching there are just as many that show either no impact or the opposite.
The reasoning behind increased performance levels behind stretching and flexibility is this: a decrease in muscle stiffness by altering the passive visco-elastic properties of the skeletal muscle through stretching will decrease muscle stiffness, thus less energy is required to move the limb and therefore the speed of contraction will increase. However Stretching guru Dr. Ian Shrier in a recent literature review discussed that the decreased stiffness may decrease storage of recoil energy, which would lead to greater energy requirements. So anaerobic athletes may be actually impairing their true athletic potential by increasing flexibility.
As for injury prevention there is no good scientific evidence showing a cuase and effect relationship between increased flexibility and a significant reduction in injuries. A famous study by Hartig and Henderson in 1999 tried to test this idea on military basic trainees. One company was taken through a hamstring stretching routine while another company was left alone. They were pre and post tested for hamstring flexibility. Bothe were monitored for lower extremity overuse injuries throughout the six week basic training program. The results showed that both the control and the intervention group gained flexibility in the hamstring. The control group gained three degrees of hamstring flexibility. While the intervention group increased their mean by seven degrees. With the difference of initial flexibility there was a gap of four degrees already. With the authors logic doesn’t this already pre-dispose that control group to overuse injuries as opposed to the intervention group? Also trying to compare a group of basic trainees going through bootcamp to athletic training and conditioning is a pretty far reach.
In my opinion stretching does not seem to add up. While full ROM throughout a joint for an athlete is important, I believe this can be maintaines through dynamic warm-up and full ROM strength training. ROM is a very dependent upon the requirements of each individuals sport. A sprinter and a marathoner have very different ROM requirements as do Football players vs. Baseball Players.
Unobstructed movement is what all athletes should strive for. Just as with anything, the SAID principle applies. If you can perform your athletic movements unhindered and painfree, why try and become more flexible at the expense of power?
The reasoning behind increased performance levels behind stretching and flexibility is this: a decrease in muscle stiffness by altering the passive visco-elastic properties of the skeletal muscle through stretching will decrease muscle stiffness, thus less energy is required to move the limb and therefore the speed of contraction will increase. However Stretching guru Dr. Ian Shrier in a recent literature review discussed that the decreased stiffness may decrease storage of recoil energy, which would lead to greater energy requirements. So anaerobic athletes may be actually impairing their true athletic potential by increasing flexibility.
As for injury prevention there is no good scientific evidence showing a cuase and effect relationship between increased flexibility and a significant reduction in injuries. A famous study by Hartig and Henderson in 1999 tried to test this idea on military basic trainees. One company was taken through a hamstring stretching routine while another company was left alone. They were pre and post tested for hamstring flexibility. Bothe were monitored for lower extremity overuse injuries throughout the six week basic training program. The results showed that both the control and the intervention group gained flexibility in the hamstring. The control group gained three degrees of hamstring flexibility. While the intervention group increased their mean by seven degrees. With the difference of initial flexibility there was a gap of four degrees already. With the authors logic doesn’t this already pre-dispose that control group to overuse injuries as opposed to the intervention group? Also trying to compare a group of basic trainees going through bootcamp to athletic training and conditioning is a pretty far reach.
In my opinion stretching does not seem to add up. While full ROM throughout a joint for an athlete is important, I believe this can be maintaines through dynamic warm-up and full ROM strength training. ROM is a very dependent upon the requirements of each individuals sport. A sprinter and a marathoner have very different ROM requirements as do Football players vs. Baseball Players.
Unobstructed movement is what all athletes should strive for. Just as with anything, the SAID principle applies. If you can perform your athletic movements unhindered and painfree, why try and become more flexible at the expense of power?
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