This blog post is about Atherosclerosis. According the National Institute for Health, Atherosclerosis effects about 1 in every 58 Americans, or about 4.6 million people in the United States. Obviously this disease is widespread and because coronary artery disease is associated with cardiovascular disease, it is important to know the ins and outs to stay protected, informed, and healthy! In this brief review of current medical literature, data, and peer-reviewed information I will attempt to outline the causative factors involved with atherosclerosis, tips to prevent developing it, and also debunk some myths. As a disclaimer, I am not a medical doctor or a research scientist, just a man with a passion to try to save the world, one carbohydrate at a time!
To begin with, the exact mechanism for developing atherosclerosis hasn’t officially been chiseled in stone. Researchers from many different camps, holding many different beliefs to be true are arguing, chastising, and muddying up research trying to prove their points as the one and only truth. The bickering won’t end because there is significant financial backing to all the camps, however if you listen closely you can hear the music. Just follow the money and you will find what preconceived notions these “un-biased” researchers are trying to prove. It makes sense, if General Mills is cutting you a 7-figure paycheck every year, you aren’t going to write a paper on how refined cereals are helping cause childhood obesity. Instead you’d pass the blame to the high-fat fast food industry or some other place that isn’t floating you the money. Anyway, the trick to get to the bottom of all the evidence is read as much as you can, compare studies, look at the author’s backgrounds, and make your best judgment in an educated way. This is what I’ve done and I’ve been reading this stuff for a couple years. This doesn’t make me an expert, but I like to think I started out as an unbiased naïve’ student and have taken in everything as a sponge. Without further ado…
According to the Medical Directory website, which is sponsored by the American Heart Association, National Heart, Lung, and Blood Institute, and the Texas Heart Institute atherosclerosis is essentially the hardening of the arteries, specifically the endothelium, intima, and other “layers” of the blood vessels. Plaques form in the arteries and are primarily made up of cholesterol, waste products of cells, calcium, fibrin, fat substances, etc. So there are two things at work here, the hardening of the arteries, and the development of the plaques. The hardening occurs because of aging, high blood pressure, and other diseases, most notably diabetes. It is important to note that diabetes is a very big risk factor for the development of atherogenesis. Diabetics, by definition, have a high level of insulin in the blood, also known as hyperinsulinemia. Basically the pancreas secretes insulin, but the cells in the body can’t absorb them because they are insulin resistant. Insulin is used to drive nutrients (especially glucose or sugar) into the cells. If the cells of the body can’t recognize or use insulin, the pancreas keeps pumping out more and more insulin to keep the blood sugar as close to normal as it can. Normal blood sugar is equal to about 1 teaspoon of sugar, and so you can imagine if someone is regularly eating starchy carbohydrates and is somewhat insulin resistant, or a full blow Type II diabetic, then they are going to need a lot of insulin to get all the sugar they’ve eaten to be absorbed into the cells. For the record, all carbohydrates are broken down into sugars at the end of the day, and a small potato is about five teaspoons, or five times what your normal blood sugar is. So the insulin resistant or diabetic person has all this insulin and sugar floating around in their blood because their cells aren’t responding to the normal insulin levels produced and we get what are called advanced glycation end products or AGE’s. These have also been referred to as free radicals, which cause oxidative stresses in tissues of the body, in this case the vascular system. The ways blood sugar and blood insulin make AGE’s is complex and beyond the scope of this brief blog, but for a more in depth look, pick up Protein Power by Dr. Michael and Mary Eades M.D. It’s a good read. Anyway, these free radicals react with the cells in the arteries by and cause damage. The damaged cells yield a product known as isoprostanes, which can be measured in the urine. Isoprostane levels in the urine or blood can determine how much free radical damage is occurring in the body, and people with diabetes or hyperinsulinemia (high levels of insulin in the blood) have higher isoprostane levels. A paper published in Journal of the American Medical Association called “Activation of Oxidative Stress by Acute Glucose Fluctuations Compared With Sustained Chronic Hyperglycemia in Patients With Type II Diabetes” reported this and went on to further say that the more fluctuation in blood sugar that someone had, the more oxidative stress and isoprostane production was going on. In lay terms, the more drastic the swings in blood sugar (as seen in diabetics, insulin resistant folks, and people following the food pyramid diet) a person had, the more oxidative stress we’d see. This lends itself to producing injury in the vascular tissue, among others, and leading to the beginning of atherosclerosis.
But wait there’s more….
The plaques we were talking about in the vessels don’t just arise from nowhere. Hypothetically, let’s say that a blood vessel is damaged, what happens? The inflammatory response is triggered, as it is every time something in the body gets damaged. Remember when you banged your knee against the table and it got red, hot, and swollen? That was the inflammatory response kicking in. You could feel it, because it was on the surface of your body. The same exact inflammatory response is taking place here, just inside the body where you can’t feel it. To coin a phrase from Dr. Barry Sears, this is called “silent inflammation”. Immune system molecules travel to the affected site to clean up debris, trigger the blood-clotting cascade (which contains fibrin, a molecule found within plaques), induce swelling for increased blood flow, among other functions. The damaged site is prone to absorbing very small, non-dense cholesterol particles (such as VLDL-very low density lipoproteins), and the fatty acids that make up every cell membrane (the outside of the cell) that were originally damaged end up in this matrix of junk and form a plaque. There are many other things that are going on here and continue to happen over time, especially with a lot of damage, but I seriously would write about another 10 pages on it and still not be done. Bottom line, the inflammatory response that is responsible for healing all damaged tissues in the body triggers plaques to be laid down in the vessels. The inflammatory response isn’t all-bad, though. We need it to repair tissue in the muscles and other injured tissues in the body. We just don’t want too much of it in our vessels.
Hypertension has also been touted as a big contributor to the development of hardened arteries and plaques. While high blood pressure can definitely be a sidekick to what is really going on, and cause the plaques to rip loose from the blood vessels, this should not be thought of as the root cause. P.J. Savage and M.F Saad wrote in the British Heart Journal that hyperinsulinemia is a major cause of increased smooth muscle in the vascular tissue (thicker blood vessels that can cause a more dramatic narrowing when stimulated), arterial wall lipid deposition (fatty acids and cholesterols deposited on the blood vessel), hypertension, and dyslipedemia (high levels of cholesterol or related molecules. Hyperinsulinemia can lead to high blood pressure because it increases Sympathetic Nervous System stimulation. This is your body’s “fight or flight” response. With respect to hypertension, sympathetic activation results in increased kidney sodium retention. You retain more sodium, and the water follows. This is especially true because elevated levels of insulin increase the number of aquaporins within the renal pelvis. These can be thought of as small floodgates that allow water to be reabsorbed into the body. Insulin opens them up. So hyperinsulinemia can cause high blood pressure and it can also cause dyslipedemia (high blood cholesterol levels) by increasing the amount of cholesterol your liver makes, which is specifically VLDL. Remember those guys? They are the ones that get deposited on the arterial walls. These aren’t my facts; they are the reviews and conclusions of many doctors who submit this stuff to peer-reviewed journals. So we can tell hyperinsulinemia is a bad mother.
But wait, there’s more….
In July of 1989 in the Archives of Internal Medicine Dr. Norman Kaplan wrote a ground breaking piece titled “The Deadly Quartet” and since it went into print, it has not been challenged, rebuked, or rebutted. Dr. Kaplan referred to this “quartet” as hypertriglyceridemia, hypertension, glucose intolerance, and central obesity. A similar paper has also been published by Dr. Gerald Reaven calling these four pathologies “Syndrome X”. At the center of the quartet was hyperinsulinemia. Dr. Kaplan reviewed many studies, and came to the conclusion that hyperinsulinemia was the root cause of high triglycerides, high blood pressure, glucose intolerance, and central obesity. Let me say that again, hyperinsulinemia is the root cause of all four of those problems! The big four are merely correlates of hyperinsulinemia. This means that not all of the big four may be present with hyperinsulinemia, but if any one or two are there, then there is a pretty good chance that hyperinsulinemia is also present. We also have to think that where there is smoke there is fire. If hyperinsulinemia is present, and we know if can cause one or all of the big four, then the chances of elevated levels of any of the big four are pretty good, even if they are not disease causing at that point.
But wait, there’s more….
Glucose intolerance is a pretty close relative of hyperinsulinemia. Not being able to tolerate glucose and having high levels of insulin go hand in hand. The Whitehall Study done by the University of London measured the glucose tolerance of a large group of both diabetic and non-diabetic adults. They classified them as diabetic, glucose intolerant, or healthy based on certain lab values and then followed these subjects for 33 years to see if they died from heart disease or lived a healthy life. The diabetic subjects were 3.7 times as likely to succumb to heart disease as the glucose intolerant or normal patients. That was expected, however. The borderline glucose intolerant and borderline healthy subjects (between 86 ng/dl and 95 ng/dl- the lab values used to designate this particular range) were only slightly better off, being only 3 times as likely to die from heart disease in 33 years. The optimal range ended up being 75ng/dl to 85ng/dl. This is considered normal to low by most labs, but these people had the lowest heart disease mortality among the subjects. Just to clarify how this test works, the subjects take a standard dose of glucose usually in the form of a sugary drink. Then at timed intervals there blood is drawn and blood sugar is measured. The more insulin resistant someone is, the higher their blood sugar will be after this test. So if a person is healthy, their blood sugar will be normal (lower) when the blood is drawn. So these subjects would have lower amounts of blood sugar floating around normally, lower insulin, and thus lower oxidative stress on the tissues, including the vascular system. Another interesting twist was that there were no differences statistically between the groups (diabetic, glucose intolerant, and normal) in their cholesterol levels (LDL and Total Cholesterol to HDL ratio). This means that having higher or lower cholesterol levels did not cause or prevent their mortality due to heart disease.
Moving right along, there has been a big push to lower fat intake, lower cholesterol intake, cholesterol levels, and to especially exile saturated fats to be “heart healthy”. A study published in The Journal of Clinical Nutrition entitled “Dietary Fats, Carbohydrates, and Progression of Coronary Atherosclerosis in Postmenopausal Women” followed 235 women with coronary artery narrowing as determined via angiography for 3 years. The women also reported their diets to the directors of the study. Those women with increase saturated fats in their diets had increase HDL cholesterol (good), lower total cholesterol (good), and lower total cholesterol to HDL ratio (very good). Their atheroslecrotic plaques did not grow and narrowing did not increase either. The researchers claimed these women now had a “better risk factor profile” than the other women. The other women ate more polyunsaturated fats and carbohydrates and had increased size of their plaques, and increased narrowing.
But wait, there’s more….
One of the biggest atherosclerosis studies ever done recently pulled a John Kerry and flip-flopped! The Framingham Heart study is one of the longest running heart, atherosclerosis, and cardiovascular disease studies that’s ever been done. In 1970, the director of the study wrote a brief review saying that people who had high blood cholesterol levels were at a high risk of atherosclerosis. He also said that because of the high cholesterol and fat content in the arterial plaques that high cholesterol levels in the diet and fat were one of the big causes of atherosclerosis. These are almost direct quotes, but as you can see he seems pretty sure of himself.
In 1992, the new director of the Framingham Study, Dr. William Castelli said in the Archives of Internal Medicine:
“In subsequent follow ups in metabolic ward-type studies higher saturated fat intake, higher cholesterol intake, and a higher calorie diet resulted in lower cholesterol levels”
Dr. Kannel wrote in the American Journal of Cardiology:
”It is not possible to select a critical lipid value that separates potential cardiovascular disease candidates from the rest of the population.”
In lay terms this means that it is impossible to set a value for total cholesterol or LDL cholesterol that separates those that are at risk for heart disease and those that aren’t. Dr Kannel went on to say that reducing fat in the diet gives us slightly lower LDL values, but drastically reduces HDL (the good stuff) values concurrently. In his opinion the best cholesterol related predictor of heart disease and atherosclerosis was the Total Cholesterol to HDL cholesterol ratio, even though he admitted this was a fairly weak correlate to heart disease in the grand scheme of things. His main point was that we want a relatively high HDL number, to get make our ratio better. Saturated fats anyone?
Uh oh.
So what can we do? There is so much information out there, and it seems as though every reporter, diet guru, or person hocking their get fit fast book is blubbering out the same mis-information. If we look at what relatively low carbohydrate diets have shown clinically we can get some answers.
To be fair, not every low carbohydrate diet it the Atkin’s diet. In fact, Atkin’s can be considered a ketogenic diet because it doesn’t allow much fruit or vegetables. But if we limit carbs to only fruit or vegetable sources, and increase fat accordingly, while eating enough protein, maybe even slightly more (not unlimited amounts), we are pretty close to a ketogenic diet and may even dip into ketosis depending on how much veggies and fruit are being eaten. Let’s see what happens.
A paper written for the Rejuvenation Research journal entitled ”Effect of Short Term Ketogenic Diet on Redox Status of Human Blood” the low carbohydrate diet increased total antioxidant status, uric acid levels, sulfhyldryl group content, and catalase and super oxide dimutase levels were unchanged. Antioxidants are good for us because they bind to free radicals and render them harmless. This lowers overall oxidative stress by reducing the amount of free radicals roaming about. So raising total antioxidant status in the blood is a good thing. Uric acid scavenges free radicals and prevents oxidative stress, so more of that is good news as well. Sulfhyldryl groups are also known as glutathione, which is an antioxidant made within the mitochondria (the engines within your cells). Increased glutathione is a good thing because it prevents the mitochondria from releasing free radicals when they make energy. It is also important that your body is making these things and you’re not just taking them from supplements, drinks, and pills containing antioxidants such as vitamin E and others. The problem is that these orally taken antioxidants never make it to the mitochondria, which is where we really need them. Also it is a good sign that catalase and super oxide dimutase levels remained unchanged when this diet was being eaten. These two substances are markers of oxidative stress, so if they had went up then we know the diet induced more oxidative stress and so the increased antioxidant activity would have all been a wash.
In conclusion, we just want to avoid inflammation, hyperinsulinemia, and eat a good diet that’s low in starch and sugar. The rest is up to you to get your learn on and find some answers to the questions that are plaguing you!
Thursday, November 12, 2009
Sunday, October 25, 2009
You Ain't Squat Unless You Squat
Earlier today after I finished working out I was rolling around on the foam roller and my Dad started talking about how he wished he could do some of the stuff I did workout-wise but he can't because of his knee. He had his entire (both medial and lateral sides) meniscus removed in his left knee about 20 odd years ago. Since orthopedics, physical therapy, and athletic training aren't what the are today, he has never had full pain-free function in this joint since. This has manifested itself into limited exercise ability, sometimes a painful gait (walking), and basically a pain in the ass all around. Enough background on my pops though, what would I, a responsible offspring do? Teach him to squat...duh....
Now perhaps you're of the opinion that people shouldn't squat, it's dangerous right? And well if they have a lower limb problem then squats are definitely out, right? My response to those comments are simply this: how exactly would you like me to get my butt on the toilet or get my butt off the couch? To keep this butt theme going, how would I upright myself from the floor/ground if flexion of the knee and hip weren't allowed? Now I must clarify, if someone has had a recent surgical intervention on a lower limb, then I wouldn't advocate mobilizing that joint just yet, or if someone has chondromalacia, or something like that. However if you're like 90% of the population you need to squat. So back to mi padre, a man with knee issues if I've ever seen one. How did I get him to squat pain free and thus embark on the road to better function and increased ability to perform exercise, daily activities, and plain move better? Read on...
The first step was to correct what in his mind was the correct squat stance. The CORRECT squat stance is with the heels almost shoulder width, possibly a touch wider, with the toes pointed out about 30*. Don't get the protractor out, this is an approximation. The reason why this is the correct squat is a multi-faceted answer, and also the reason why the commonly endorsed squat stances (narrow stance, toes straight, Plie', etc) are just bad coaching. I will go through them one by one. Narrow stance squats, with the feet being hip width apart force the athlete into a serious anterior pelvic tilt (hips rotated forwards) to maintain balance. This usually forces the pelvis to unlock and the lumbar spine to flex forward. This wouldn't be too big of a deal, unless you had some fairly heavy weights on your back compounding the issue. On top of that, it is extremely difficult to achieve proper depth without getting a soft tissue impingement in the hip. To clarify, proper depth in the squat is when the crease of the hip/thigh is below the top of the knee. If you can maintain a lordotic (neutral arch) lumbar spine while doing a narrow stance squat to these standards with a heavy load on your back AND don't feel the soft tissue around the top of your femur pressing against the joint capsule around the protruding hip bone (anterior supra illiac spine-ASIS) then my hats off to you, but you're still wrong. When engaging in a narrow stance squat you are forced to move your knees forward over your feet, maybe not all the way out over your toes, but damn close. This puts a lot of stress directly on the knee and specifically the patellar tendon. Magnify this by the weight you're squatting and this is a recipe for injured knees and/or chronic inflammation. If you still think narrow stance squats are the way to go, email me and we'll chat. On to the straight toed squats; if your toes are straight you don't allow for your hips to rotate effectively and engage during the bottom half of the squat. Also you are probably pushing your knees into a compromised position which can lead to a big angular force on the knee, which equals pain or injury. You will also probably have a hard time finding the proper depth, keeping your knees from caving in on the up portion, and maintaining a neutral spine throughout the movement. Next please. The plie' squat has gained momentum among the female crowd for inner thigh and glute development. While powerlifters often adopt a very wide stance, their toe angle is about half of what we see in the plie' squat. Furthermore, the plie' squat usually results in about half of the range of motion required to achieve proper squat depth. The lateral shear force on the knees is very high as well, and the lack of quadricep activation is startling. The most probable reason people don't get hurt doing this is because they are using very light (relative) weights to do this exercise, and have fairly healthy knees. Make a large person do plie' squats and you're in for some knee trouble, and weird looks from real athletes. So now that I've briefly gone over why the other squats are trash, let's go back to proper squatting form and why it's golden for people who say they have knee pain!
So your feet are at or slightly wider than shoulder width apart, and your toes are pointed out at approximately 30*. You should try to push your hips down and back while attempting to rotate your thighs outward (don't move your feet). Also the weight of your body should be in your heels. You should be able to wiggle your toes at the top and bottom of the squat. While doing all of this, you should keep your chest up as high as possible and maintain a neutral (slightly arched) spine/back. You should feel a stretch in your inner thigh as you get below parallel, and the main coaching point is to keep your shins vertical. If you push your hips back and down far enough, your shins won't move forward at all. This accomplishes a few things. One, with a vertical shin, all the forces on the patellar tendon and knee are non-existent, your hip adductors are engaged, as well as your glutes, hamstrings, and hips. After you reach proper depth, you should drive your heels into the ground to create the force needed to stand up. This calls on your glutes, hamstrings, hips, and quadriceps to pull you back up to standing. So let's see, we used the maximum amount of muscle to do the movement (so we can use the most weight and get the biggest caloric bang for the buck), took all the forces off the knees (by keeping the shin vertical and keeping the tibia -lower leg , in a good position relative to the knee), and got to proper depth to recruit the posterior chain. Sounds like a good deal.
So after instructing my pops in all of this I started him out like I would any client with knee pain and an unfamiliarity with squats. Couch squats. Simply stand very close to the couch or ottoman and do the same squat as outlined above and sit all the way down like you were gonna watch TV. Then stand back up. The magic is in the movement. Once this movement is down we can move to free standing bodyweight squats, then to a weighted back squat. Squatting properly will achieve full leg development, especially the often undertrained and underdeveloped posterior chain (hamstring, glute, hip, lowerback), and will actively lengthen the muscles from the large range of motion. No longer will tight hamstrings, inactive glutes, and tight hips bother us anymore, all because we are now doing the most basic, yet important, movement ever created. Remember, you ain't squat unless you squat!
Now perhaps you're of the opinion that people shouldn't squat, it's dangerous right? And well if they have a lower limb problem then squats are definitely out, right? My response to those comments are simply this: how exactly would you like me to get my butt on the toilet or get my butt off the couch? To keep this butt theme going, how would I upright myself from the floor/ground if flexion of the knee and hip weren't allowed? Now I must clarify, if someone has had a recent surgical intervention on a lower limb, then I wouldn't advocate mobilizing that joint just yet, or if someone has chondromalacia, or something like that. However if you're like 90% of the population you need to squat. So back to mi padre, a man with knee issues if I've ever seen one. How did I get him to squat pain free and thus embark on the road to better function and increased ability to perform exercise, daily activities, and plain move better? Read on...
The first step was to correct what in his mind was the correct squat stance. The CORRECT squat stance is with the heels almost shoulder width, possibly a touch wider, with the toes pointed out about 30*. Don't get the protractor out, this is an approximation. The reason why this is the correct squat is a multi-faceted answer, and also the reason why the commonly endorsed squat stances (narrow stance, toes straight, Plie', etc) are just bad coaching. I will go through them one by one. Narrow stance squats, with the feet being hip width apart force the athlete into a serious anterior pelvic tilt (hips rotated forwards) to maintain balance. This usually forces the pelvis to unlock and the lumbar spine to flex forward. This wouldn't be too big of a deal, unless you had some fairly heavy weights on your back compounding the issue. On top of that, it is extremely difficult to achieve proper depth without getting a soft tissue impingement in the hip. To clarify, proper depth in the squat is when the crease of the hip/thigh is below the top of the knee. If you can maintain a lordotic (neutral arch) lumbar spine while doing a narrow stance squat to these standards with a heavy load on your back AND don't feel the soft tissue around the top of your femur pressing against the joint capsule around the protruding hip bone (anterior supra illiac spine-ASIS) then my hats off to you, but you're still wrong. When engaging in a narrow stance squat you are forced to move your knees forward over your feet, maybe not all the way out over your toes, but damn close. This puts a lot of stress directly on the knee and specifically the patellar tendon. Magnify this by the weight you're squatting and this is a recipe for injured knees and/or chronic inflammation. If you still think narrow stance squats are the way to go, email me and we'll chat. On to the straight toed squats; if your toes are straight you don't allow for your hips to rotate effectively and engage during the bottom half of the squat. Also you are probably pushing your knees into a compromised position which can lead to a big angular force on the knee, which equals pain or injury. You will also probably have a hard time finding the proper depth, keeping your knees from caving in on the up portion, and maintaining a neutral spine throughout the movement. Next please. The plie' squat has gained momentum among the female crowd for inner thigh and glute development. While powerlifters often adopt a very wide stance, their toe angle is about half of what we see in the plie' squat. Furthermore, the plie' squat usually results in about half of the range of motion required to achieve proper squat depth. The lateral shear force on the knees is very high as well, and the lack of quadricep activation is startling. The most probable reason people don't get hurt doing this is because they are using very light (relative) weights to do this exercise, and have fairly healthy knees. Make a large person do plie' squats and you're in for some knee trouble, and weird looks from real athletes. So now that I've briefly gone over why the other squats are trash, let's go back to proper squatting form and why it's golden for people who say they have knee pain!
So your feet are at or slightly wider than shoulder width apart, and your toes are pointed out at approximately 30*. You should try to push your hips down and back while attempting to rotate your thighs outward (don't move your feet). Also the weight of your body should be in your heels. You should be able to wiggle your toes at the top and bottom of the squat. While doing all of this, you should keep your chest up as high as possible and maintain a neutral (slightly arched) spine/back. You should feel a stretch in your inner thigh as you get below parallel, and the main coaching point is to keep your shins vertical. If you push your hips back and down far enough, your shins won't move forward at all. This accomplishes a few things. One, with a vertical shin, all the forces on the patellar tendon and knee are non-existent, your hip adductors are engaged, as well as your glutes, hamstrings, and hips. After you reach proper depth, you should drive your heels into the ground to create the force needed to stand up. This calls on your glutes, hamstrings, hips, and quadriceps to pull you back up to standing. So let's see, we used the maximum amount of muscle to do the movement (so we can use the most weight and get the biggest caloric bang for the buck), took all the forces off the knees (by keeping the shin vertical and keeping the tibia -lower leg , in a good position relative to the knee), and got to proper depth to recruit the posterior chain. Sounds like a good deal.
So after instructing my pops in all of this I started him out like I would any client with knee pain and an unfamiliarity with squats. Couch squats. Simply stand very close to the couch or ottoman and do the same squat as outlined above and sit all the way down like you were gonna watch TV. Then stand back up. The magic is in the movement. Once this movement is down we can move to free standing bodyweight squats, then to a weighted back squat. Squatting properly will achieve full leg development, especially the often undertrained and underdeveloped posterior chain (hamstring, glute, hip, lowerback), and will actively lengthen the muscles from the large range of motion. No longer will tight hamstrings, inactive glutes, and tight hips bother us anymore, all because we are now doing the most basic, yet important, movement ever created. Remember, you ain't squat unless you squat!
Friday, September 4, 2009
Intensity....The Great Debate!
Intensity is another word thrown around by fitness buffs throughout the industry but I think many lack a fundamental definition of this buzzword. Intensity, at it's most basic level is defined as Power. Power is defined by the amount of "work" done per unit "time". These are physics definitions, however everything in this world can be boiled down to physics, especially in our specific case- kinematic movements- or exercise. Let's continue down this path, what is work?
At its most simple level, work is the amount of force applied to an object (barbell, dumbell, heavy box, implement, etc) multiplied by the distance the object is moved. And to clarify, force is weight. To keep things simple, we will use the SI (metric) system here. A 100kg dumbell has a mass of 100 kilograms. It's weight is calculated by the mass multiplied by the local acceleration due to gravity which is about 9.81 meters/second/second. What that means is the Earth has a constant acceleration that is dependent on local altitude and other factors. Enough about that, let's continue on this examply. The 100kg dumbell requires a smidgen over 981 Newton-meters (Joules) of force (100kg x 9.81m/s/s) to move it off the ground. Why more than 981 Newton-meters (Joules)? Well if the dumbell weights 100kg and the acceleration due to gravity is 9.81 meters/second/second then the force the dumbell is exerting on the floor is 981 Newtons. So to lift it vertically, 981.1 Newton-meters (or Joules) would be needed to get it moving. Similarly, 1000 Newton-meters (Joules) could be exerted by the person lifting the dumbell off the floor and the only difference would be "how fast" the dumbell is lifted off the floor. This leads us back to power and intensity :-). By the way, Newtons is the term used in the SI system of measurement of work. In English terms, it is foot-lbs, which makes sense because when we think of weight, we think of pounds. And force is weight multiplied by distance, which in the English system of measurement is feet, so foot-pounds is akin to Newtons. Do not confuse torque for force. Although they are measured in the same way (ft-lbs) a torque is the "force" used to cause rotation, i.e. rotational work. Enough about that, onto power and intensity....
So if we know the work that is required to move the object, in this case a dumbell, then how do we figure out power. Well Power is work per unit time. So we can extrapolate this out to work/time, or Newton-meters (Joules)/second. By the way, 1 Joule is equal to 1 Newton-meter, and most scientists and physicists use Joules by convention. So how much power is is required to lift the 100 kg dumbell 2 meters vertically? Well since we know "work" is equal to force multiplied by distance, and force is mass times acceleration let's get some known quantities figured out here. A 100kg dumbell at 9.81meters/second/second local gravity that is on the ground exerts a force of 981 Newtons on the floor and if the person doing the exercise is lifting it 2 meters vertically, the distance is 2 meters. This gives us the work total, so in this case work, which is equal to force times distance is 981 Newtons x 2 meters= 1962 Newton-meters (or 1962 Joules). So the work is 1962 Joules, and the lifter is doing this "work" all in 1 second. This fits nicely into our power equation. Power is work per unit time, or Work/time. In this case we have 1962 Newton-meters/ 1 second, which in Power is 1962 watts. So 1 Newton-meter per 1 second = 1 watt.
Let's put power into a more identifiable term, horsepower. 1962 watts (the power it takes to move a 100kg dumbell 2 meters vertically in 1 second) is equal to about 2.6 horsepower! This should make you respect your 300 horsepower sports car a little more. Now let's get back to the exercise relevance of all this. You can measure your output by figuring out how much power (work/time) you've exerted during a workout. All you need to know is how much weight you've moved, how far you've moved it, and how long it took you to do it. Thus, you can see real gains in your capacity to do work by figuring out your power output. Power is synonymous with Intensity. That is the more power you exert, the more intense the workout was. Let's do an example for clarification.
Say your workout is 100 pullups as fast as you can. To measure your weight, simply stand on a scale and get your weight in kilograms. If you can only get pounds, divide the weight by 2.2 and you will be pretty darn close. So let's say you are 60kg (remember that is a mass, not a weight). So the force you are applying to the pullup bar is 60kg x gravity's acceleration. So 60 x 9.81 (acceleration due to gravity) is about 589 Newtons for every pullup. To figure out the distance you have to exert that "force" over, you need to measure the distance your center of gravity travels during a pullup. Interestingly enough, this is fairly simple. Your center of gravity (CoG) is located somewhere between your bellybutton and your groin. However, even if you seriously miss the mark on measuring this, as long as you use the same point for reference you won't have a very large error in your data. Ironically, most compound movements' (pullup, pushup, squat, overhead press, etc) distances are the length of a particular limb. For instance, in a pullup the distance your CoG moves is approximately the length of your arm, since when you go from the bottom of a pullup (full extension) to the top (head above the bar) you brought your shoulders to your hands, in effect, your entire arm (from shoulder to hand) is the distance you travel in 1 rep of a pullup. So we have the force you're exerting (589 newtons) and a distance (the average arm is .8 meters long for men). This gives us the opportunity to find the work for 1 rep of exercise. 1 pullup for a person who is 60kg (589 Newtons) and has a .8 meter arm requires 471.2 Newton-meters of "work" to complete. Now since the person is doing 100 reps, he needs to expend 47120 Newton-meters to complete the task (471.2 Newton-meters x 100 reps). Let's say it took 4 minutes to complete this task. So that's 4 minutes x 60 seconds= 240 seconds. This plugs into our power formula, which is work/time. So 47120N-m/240s~ 196 watts. This is approximately 0.2 horsepower!
Let's say the same athlete does the workout at a later date and did it in 3 minutes even. He still weighs the same and has the same arm length (hopefully). So now we still have the same work being done- 471.2 N-m per rep x 100 reps= 47120 N-m total but divided by 180 seconds, instead of 240 seconds like the first go around. This gives us an output of approximately 262 Watts, or 0.4 horsepower! That's double the power and intensity by shaving a minute off his time! This is real improvement, and the intensity was very high for this athlete! So let's put it all together.
High intensity exercise has vast benefits for the human body, such as increased muscle growth, increased fat loss, increased bone density, increased cardiorespritory fitness, increased muscular capacity (endurance), increased strength, among many others. In order to increase the intensity of a workout, you must either increase the force output (weight lifted) or decrease the time in which the force was applied (time to complete the task). You can imagine a situation where a person is squatting 225 lbs 50 times. Let's say it takes him 10 minutes to do this (slow-btw haha). If the person wants to increase the intensity then he should want to do the same workout at a later date in less than 10 minutes, or increase the weight to 250lbs and not increase his time to such an extent that his power output suffers, more on that delicate balance in the next post. What we can surmise from all this physics and numbers is that if we do lower our time for a given set of tasks, then we got stronger, have a higher capacity for work, and probably all the other good things that we get from high intensity exercise, and we ARE improving. However if there is no improvement, or we get slower then we know our program isn't working to help us be better in any single measurable facet of fitness.
So, hopefully after reading that you get the sense that measuring your intensity is worth the time and can yield better results in the long term. Now get those calculators out and get to work!
At its most simple level, work is the amount of force applied to an object (barbell, dumbell, heavy box, implement, etc) multiplied by the distance the object is moved. And to clarify, force is weight. To keep things simple, we will use the SI (metric) system here. A 100kg dumbell has a mass of 100 kilograms. It's weight is calculated by the mass multiplied by the local acceleration due to gravity which is about 9.81 meters/second/second. What that means is the Earth has a constant acceleration that is dependent on local altitude and other factors. Enough about that, let's continue on this examply. The 100kg dumbell requires a smidgen over 981 Newton-meters (Joules) of force (100kg x 9.81m/s/s) to move it off the ground. Why more than 981 Newton-meters (Joules)? Well if the dumbell weights 100kg and the acceleration due to gravity is 9.81 meters/second/second then the force the dumbell is exerting on the floor is 981 Newtons. So to lift it vertically, 981.1 Newton-meters (or Joules) would be needed to get it moving. Similarly, 1000 Newton-meters (Joules) could be exerted by the person lifting the dumbell off the floor and the only difference would be "how fast" the dumbell is lifted off the floor. This leads us back to power and intensity :-). By the way, Newtons is the term used in the SI system of measurement of work. In English terms, it is foot-lbs, which makes sense because when we think of weight, we think of pounds. And force is weight multiplied by distance, which in the English system of measurement is feet, so foot-pounds is akin to Newtons. Do not confuse torque for force. Although they are measured in the same way (ft-lbs) a torque is the "force" used to cause rotation, i.e. rotational work. Enough about that, onto power and intensity....
So if we know the work that is required to move the object, in this case a dumbell, then how do we figure out power. Well Power is work per unit time. So we can extrapolate this out to work/time, or Newton-meters (Joules)/second. By the way, 1 Joule is equal to 1 Newton-meter, and most scientists and physicists use Joules by convention. So how much power is is required to lift the 100 kg dumbell 2 meters vertically? Well since we know "work" is equal to force multiplied by distance, and force is mass times acceleration let's get some known quantities figured out here. A 100kg dumbell at 9.81meters/second/second local gravity that is on the ground exerts a force of 981 Newtons on the floor and if the person doing the exercise is lifting it 2 meters vertically, the distance is 2 meters. This gives us the work total, so in this case work, which is equal to force times distance is 981 Newtons x 2 meters= 1962 Newton-meters (or 1962 Joules). So the work is 1962 Joules, and the lifter is doing this "work" all in 1 second. This fits nicely into our power equation. Power is work per unit time, or Work/time. In this case we have 1962 Newton-meters/ 1 second, which in Power is 1962 watts. So 1 Newton-meter per 1 second = 1 watt.
Let's put power into a more identifiable term, horsepower. 1962 watts (the power it takes to move a 100kg dumbell 2 meters vertically in 1 second) is equal to about 2.6 horsepower! This should make you respect your 300 horsepower sports car a little more. Now let's get back to the exercise relevance of all this. You can measure your output by figuring out how much power (work/time) you've exerted during a workout. All you need to know is how much weight you've moved, how far you've moved it, and how long it took you to do it. Thus, you can see real gains in your capacity to do work by figuring out your power output. Power is synonymous with Intensity. That is the more power you exert, the more intense the workout was. Let's do an example for clarification.
Say your workout is 100 pullups as fast as you can. To measure your weight, simply stand on a scale and get your weight in kilograms. If you can only get pounds, divide the weight by 2.2 and you will be pretty darn close. So let's say you are 60kg (remember that is a mass, not a weight). So the force you are applying to the pullup bar is 60kg x gravity's acceleration. So 60 x 9.81 (acceleration due to gravity) is about 589 Newtons for every pullup. To figure out the distance you have to exert that "force" over, you need to measure the distance your center of gravity travels during a pullup. Interestingly enough, this is fairly simple. Your center of gravity (CoG) is located somewhere between your bellybutton and your groin. However, even if you seriously miss the mark on measuring this, as long as you use the same point for reference you won't have a very large error in your data. Ironically, most compound movements' (pullup, pushup, squat, overhead press, etc) distances are the length of a particular limb. For instance, in a pullup the distance your CoG moves is approximately the length of your arm, since when you go from the bottom of a pullup (full extension) to the top (head above the bar) you brought your shoulders to your hands, in effect, your entire arm (from shoulder to hand) is the distance you travel in 1 rep of a pullup. So we have the force you're exerting (589 newtons) and a distance (the average arm is .8 meters long for men). This gives us the opportunity to find the work for 1 rep of exercise. 1 pullup for a person who is 60kg (589 Newtons) and has a .8 meter arm requires 471.2 Newton-meters of "work" to complete. Now since the person is doing 100 reps, he needs to expend 47120 Newton-meters to complete the task (471.2 Newton-meters x 100 reps). Let's say it took 4 minutes to complete this task. So that's 4 minutes x 60 seconds= 240 seconds. This plugs into our power formula, which is work/time. So 47120N-m/240s~ 196 watts. This is approximately 0.2 horsepower!
Let's say the same athlete does the workout at a later date and did it in 3 minutes even. He still weighs the same and has the same arm length (hopefully). So now we still have the same work being done- 471.2 N-m per rep x 100 reps= 47120 N-m total but divided by 180 seconds, instead of 240 seconds like the first go around. This gives us an output of approximately 262 Watts, or 0.4 horsepower! That's double the power and intensity by shaving a minute off his time! This is real improvement, and the intensity was very high for this athlete! So let's put it all together.
High intensity exercise has vast benefits for the human body, such as increased muscle growth, increased fat loss, increased bone density, increased cardiorespritory fitness, increased muscular capacity (endurance), increased strength, among many others. In order to increase the intensity of a workout, you must either increase the force output (weight lifted) or decrease the time in which the force was applied (time to complete the task). You can imagine a situation where a person is squatting 225 lbs 50 times. Let's say it takes him 10 minutes to do this (slow-btw haha). If the person wants to increase the intensity then he should want to do the same workout at a later date in less than 10 minutes, or increase the weight to 250lbs and not increase his time to such an extent that his power output suffers, more on that delicate balance in the next post. What we can surmise from all this physics and numbers is that if we do lower our time for a given set of tasks, then we got stronger, have a higher capacity for work, and probably all the other good things that we get from high intensity exercise, and we ARE improving. However if there is no improvement, or we get slower then we know our program isn't working to help us be better in any single measurable facet of fitness.
So, hopefully after reading that you get the sense that measuring your intensity is worth the time and can yield better results in the long term. Now get those calculators out and get to work!
Tuesday, August 11, 2009
Functional Movements?
A commone buzzword in today's fitness industry is functional fitness, or to do functional movements. While giving specific exercises an ambigous name is good for selling memberships and personal training, it is not doing anything for your average gym goer. So let's first define functional fitness and functional movements. Functional fitness (and by association functional movements) is the ability to do real-world tasks or work at a high capacity. An example would be the ability to lift a heavy box from the floor and place it on an overhead shelf, or picking up a large rock off of a fallen compadre while hiking. At any rate, we can pare this down to being ready for any of life's challenges that may be presented to us at any time. A functional movement is an exercise that lends itself relatively well to any essential skill or task that someone could possibly face. Again, these skills or task can be simplified into squatting, jumping, running, upper-body pressing (overhead, horizontally, and from all positions), punching, pulling and things like that. At any point in time, all movements in life arise from any or all of these basic movements. The reason why this is important is that we want to improve our ability to cope with daily stresses as well as perform at a high level at a sport or during an unexpected challenge (like a fire, flood, etc). So in a nutshell, functional training would carryover quite well to improving a persons ability to do any and all tasks well. There is another benefit of functional training, and that is it is better for you from a standpoint on weightloss, aesthetics, and longevity. Bear with me, this is going to get good.
Most functional movements involve many body parts or muscle groups. This means there is an increase in muscle mass (cross sectional area) being used in a movement and therefore there is an increased demand for energy when compared to isolating a single muscle group. This leads to an increased use of oxygen, calories, metabolites, and coordinating mechanisms within the brain. The outcome of a gym session chocked full of functional movements at a high intensity (heavy weight or high reps done in a short time period) will be an increase in calories expended, increase stimulus for increased cardiorespritory capacity, increased proprioceptive (balance and coordination) awareness, and increased hormonal response to exercise (insulin sensitivity, increased growth hormone, etc). Let's take for instance a squat compared to a leg press. The squat requires the legs to function at a high level, the core for stability, the hips for extension, and the arms for balance. The leg press only requires the legs to move the weight stack, and also doesn't require any balance so the core can rest, and the hips aren't allowed to move through a full range of motion and so their involvement suffers. Also this doesn't take into account placing a relatively heavy load on the back of a client and having them squat. This involved the spinal extensors of the back and hip flexors to an even greater degree during both the concentric and eccentric phases of exercise. So with all these advantages of this functional movement, why would anyone use the leg press? Because it's hard and can be very taxing if done correctly. Let's go to another example...
People do bicep curls like crazy in front of the mirror everyday to exhaustion. What purpose does this serve? I'm not really sure, but these guy's and girl's arm never seem to get anymore muscular, that's for sure. I would propose that these curlin' fools try to do 10 pullups in a row with full range of motion. I gauruntee that the effect will be more profound as far as growth, aesthetic value, and body compostion are concerned. This is because the range of motion is greater in a pullup, the muscles overcome a greater load, and you can't take the load off of the bicep at any point during the movement, it is there during the eccentric and concentric portion of the movement like it or not.
The whole point of this is to get people away from isolation movements like bicep curls, tricep extensions, leg extensions, dumbell flyes, front raises, lateral raises, and crunches. I would like to see a shift to pullups, dips, squats, overhead press, rows, lunges, deadlifts, and things like this. Of course these are difficult movements but someone can teach you if you have the desire to learn. The juice is definitely worth the squeeze so get to your local trainer or coach ASAP and get after it.
Most functional movements involve many body parts or muscle groups. This means there is an increase in muscle mass (cross sectional area) being used in a movement and therefore there is an increased demand for energy when compared to isolating a single muscle group. This leads to an increased use of oxygen, calories, metabolites, and coordinating mechanisms within the brain. The outcome of a gym session chocked full of functional movements at a high intensity (heavy weight or high reps done in a short time period) will be an increase in calories expended, increase stimulus for increased cardiorespritory capacity, increased proprioceptive (balance and coordination) awareness, and increased hormonal response to exercise (insulin sensitivity, increased growth hormone, etc). Let's take for instance a squat compared to a leg press. The squat requires the legs to function at a high level, the core for stability, the hips for extension, and the arms for balance. The leg press only requires the legs to move the weight stack, and also doesn't require any balance so the core can rest, and the hips aren't allowed to move through a full range of motion and so their involvement suffers. Also this doesn't take into account placing a relatively heavy load on the back of a client and having them squat. This involved the spinal extensors of the back and hip flexors to an even greater degree during both the concentric and eccentric phases of exercise. So with all these advantages of this functional movement, why would anyone use the leg press? Because it's hard and can be very taxing if done correctly. Let's go to another example...
People do bicep curls like crazy in front of the mirror everyday to exhaustion. What purpose does this serve? I'm not really sure, but these guy's and girl's arm never seem to get anymore muscular, that's for sure. I would propose that these curlin' fools try to do 10 pullups in a row with full range of motion. I gauruntee that the effect will be more profound as far as growth, aesthetic value, and body compostion are concerned. This is because the range of motion is greater in a pullup, the muscles overcome a greater load, and you can't take the load off of the bicep at any point during the movement, it is there during the eccentric and concentric portion of the movement like it or not.
The whole point of this is to get people away from isolation movements like bicep curls, tricep extensions, leg extensions, dumbell flyes, front raises, lateral raises, and crunches. I would like to see a shift to pullups, dips, squats, overhead press, rows, lunges, deadlifts, and things like this. Of course these are difficult movements but someone can teach you if you have the desire to learn. The juice is definitely worth the squeeze so get to your local trainer or coach ASAP and get after it.
Wednesday, July 1, 2009
Fat and Exercise
So I know it's been a long time since I've updated this, and I apologize for that but I've been crazy busy. At any rate, hopefully this is thought provoking to some and I can get some feedback, read on :-).
Most people I know that exercise regularly do so to for a number of reasons: to lose body fat, recompose their body, stay in shape, increase strength or some combination of all of the above. I am going to focus on the lose weight crowd today.
The dogma is that if we exercise more and watch our eating we will lose weight, specifically fat, and improve out body composition. In fact, the ACSM recommends exercise of 150 minutes a week will improve body composition over the long haul in combination with a healthy diet. However, what most anectodal evidence and clinical trials of implementing exercise in previously untrained peoeple along with giving nutritional guidelines result in marginal to little body fat loss. On the flip side, people who are educated on nutrition and eat properly, tend to lose body fat independent of exercise or not. That is, they lose weight and body fat regardless if they exercise or not. The amount of weight lost is about the same, the body fat difers (in favor of the exercisers typically), but the important part of the equation is the ability to keep this up for life and it seems as though the exercisers have an edge here. So where does exercise fit into this whole deal? Well let's get back to that in a moment, while first addressing another quandry.
What is obesity? Or in less dramatic terms, what is the definition of carrying extra unwanted fat tissue around? The powers at large will say that having extra fat or being obese is the result of not eating right (eating too much) or exercising too little. So a decrease in eating (amount) and increasing activity should work to rid the nation of this obesity epidemic. As it turns out, even though we (as a nation) are trying to become modestly more active and advised to eat more and more healthy, we are becoming more fat. Is this just a case of us being lazy and gluttons? I truly do not believe that people will continually eat themselves into submission, nor decrease activity on purpose to a level that makes them gain weight. What if it's all a byproduct of this two pronged attack on obesity (the advice to eat less and exercise more)? And moreover, what if obesity and less dramatic cases (such as having a few lbs to lose) are merely the accumulation of fat in fat stores? If we take that simple definition, then we would want to decrease the amount of fat in fat stores to lose the pounds. What regulates this and is exercise involved in that anyway?
When we exercise, we create a hormonal status withint the body that signals various pathways that we need to feed. This was referred to as "working up an appetite". Remember that? That phrase has seemed to disappear. To show this, a few studies I have came across indicate that people who were in an exercise group (who previously weren't) tended to eat more food than those who didn't exercse. In fact, the people tended to eat only as much more food as they needed to to make up for any extra activity. In lay terms, if someone burned a total of 2,300 calories throughout the day (by way of previous nutritional intake's effect on hormones, activity, cellular metabolism, environment, etc) then they would only willingly eat 2,300 or so calories a day. If this person wanted to lose weight, the establishment would say cut your calories down to 1800 or so and maintain the same or more activity level. Here's the rub, subconciously, that person will be less active overall or be active at a lower intensity to make up for the difference. Weight loss over the long term (6 months plus) will be small because the body is trying to maintain its set point. The set point got lower by changing the intake level of the person, and if the person ever varies from this calorie restricted diet, then the person will gain more weight, regardless of activity (since the hormonal status is already at a temporary set point and will only reset itself once the intake and output changes results in a change in size-better or worse).
Now there is noone out there who can tell you their exact intake down to 100 calories per day (accurately), nor is there a person who knows their exact output withing 100 calories of energy a day either. Think about it, was that 1 cup of brocolli, or 1.1 cups. Was it 6 ounces of chicken, or was their some marinade on the scale as well. Easily, throughout the course of a day that could result in well over a 100 calorie discrepancy. Also, did you take 15 steps to the door, or was it 14, and was it faster or slower than usual. And further, did your heart rate go up 7 beats a minute, or 6 during that walk? Again, this could cause a miscalculation over a day. So with all this uncertainty on input and output and because the dogma is that if the difference between calories in and calories out equals weight loss why do we almost always stay around the same weight (within 5 lbs) regardless of our diligence? How do we decrease the fat accumulation so we can decrease the fat stores with all this variance? It all boils down to hormones and maybe exercise :-).
Many hormones in our body (specifically testosterone, estrogen, growth hormone, insulin, glucagon, cortisol, etc) are involved in regulating fat metabolism (storage and breakdown). Insulin is the chief regulator of fat accumulation (lipogenesis) and in it's relative absence we see fat break down and be released into the blood stream as free fatty acids to be burnt as fuel (lipogenolysis and fatty acid oxidation). The sex steroids (testosterone and estrogen), growth hormone, and glucagon are all involved as well. Glucagon levels are elevated (relatively) when insulin is lower (again, relatively-not absolutely lower in overall values, that means that the overall value of insulin might be higher-3 units/milliliter of blood versus 1 unit/ milliliter of blood for glucagon). Testosterone works to increase protein synthesis (muscle rebuilding, cell turnover, and increased metabolism) only when insulin levels aren't elevated and growth hormone kicks off the whole cocktail only when insulin is low as well. These hormones work in unison while insulin is off on holiday to break down fat stores to be burnt as fuel and excreted in the urine/breath as ketone bodies. It makes sense that if we can consistently achieve a net flow of fat out of the fat stores, then we will lose body fat. So if we consistently have low or lower (relatively) insulin levels we will lose body fat because all of our other hormones are signalling the fat stores to unleash the beast (fatty acids) to be used as fuel. What's even more interesting is that without a decent amount of insulin (relative to the individual) we will not store fat either. That's right, without insulin to signal the accumulation of free fatty acids from the blood stream to be transported into the fat stores for storage as triglycerides we won't store fat. Higher than baseline levels of insulin are needed to store fat (specifically to activate an enzyme that transports free fatty acids from the blood to the fat stores and turns them into triglycerides). Think of triglycerides as statues in the body, they are hard to move around and even harder to break down and use for other useful purposes. Insulin wants to keep the existing statues where they are (inside the "house"-fat stores) and build new statues as well. The other hormones want to break down the statues into rocks to use for other purposes, as well as keep the rocks that aren't yet statues from being made into statues and keep them floating around for other uses. So if we could do one thing to help jumpstart the net movement of fat out of stores and into the bloodstream for use we would try to drop our insulin levels. How do we do this and dear God will someone tell me how exercise is involved in all of this?
Okay so a brief rundown of how insulin is increased in the body. When you eat, you produce a little insulin from your pancreas to help in absorbtion of the nutrients. The tricky part is how much and for how long does this insulin keep flowing. Meals consisiting of mostly starch (carbs) or sugars (carbs) will spike insulin sky high and keep it there a long time (depending on the size of the meal and your pancreas' status at the time). A meal rich in green veggies, fats, and protein will do just about nil for your insulin release, that is it will be small unless there is a sugary topping (like BBQ sauce) involved or a bread roll. I could go on for hours, but here's the gist, carbs- especially starch, sugar, and the like spike insulin sky high and for a prolonged period of time, and proteins, fats, and fiber don't do much. So without spiking our insulin throughout the day, we could keep it low and keep the body fat melting off. Good stuff. Now what about exercise, and the whole point of this post? Here goes...
So rememeber that the net flow of fat out of the stores results in free fatty acids being available for burning. Muscle cells use these, as do brain and nerve cells (preferentially), as well as other cells within the body. Now if these free fatty acids don't have a place to go to be burnt, they have the opportunity to be re-transported to the fat stores and rebuilt as statues (triglycerides). Here is why I wrote this whole thing. Do people exercise because they want to lose fat or do they exercise because they have all of these free fatty acids floating around that need to be used/expelled? Sounds kinda funny at first but check this; what if the presence of a bunch of free fatty acids in the bloodstream prompted various pathways to become active to increase activity at some level? This makes sense because typically the most fit folks have very low insulin in the blood and thus would have a bunch of free fatty acids at any given time, encouraging them to be more active and exercise (even if it's not necessarily formal exercise that's in a gym). Kind of an interesting theory, although I'm sure I'm not the first to come up with it. So what comes first, the fat or the exercise?
Most people I know that exercise regularly do so to for a number of reasons: to lose body fat, recompose their body, stay in shape, increase strength or some combination of all of the above. I am going to focus on the lose weight crowd today.
The dogma is that if we exercise more and watch our eating we will lose weight, specifically fat, and improve out body composition. In fact, the ACSM recommends exercise of 150 minutes a week will improve body composition over the long haul in combination with a healthy diet. However, what most anectodal evidence and clinical trials of implementing exercise in previously untrained peoeple along with giving nutritional guidelines result in marginal to little body fat loss. On the flip side, people who are educated on nutrition and eat properly, tend to lose body fat independent of exercise or not. That is, they lose weight and body fat regardless if they exercise or not. The amount of weight lost is about the same, the body fat difers (in favor of the exercisers typically), but the important part of the equation is the ability to keep this up for life and it seems as though the exercisers have an edge here. So where does exercise fit into this whole deal? Well let's get back to that in a moment, while first addressing another quandry.
What is obesity? Or in less dramatic terms, what is the definition of carrying extra unwanted fat tissue around? The powers at large will say that having extra fat or being obese is the result of not eating right (eating too much) or exercising too little. So a decrease in eating (amount) and increasing activity should work to rid the nation of this obesity epidemic. As it turns out, even though we (as a nation) are trying to become modestly more active and advised to eat more and more healthy, we are becoming more fat. Is this just a case of us being lazy and gluttons? I truly do not believe that people will continually eat themselves into submission, nor decrease activity on purpose to a level that makes them gain weight. What if it's all a byproduct of this two pronged attack on obesity (the advice to eat less and exercise more)? And moreover, what if obesity and less dramatic cases (such as having a few lbs to lose) are merely the accumulation of fat in fat stores? If we take that simple definition, then we would want to decrease the amount of fat in fat stores to lose the pounds. What regulates this and is exercise involved in that anyway?
When we exercise, we create a hormonal status withint the body that signals various pathways that we need to feed. This was referred to as "working up an appetite". Remember that? That phrase has seemed to disappear. To show this, a few studies I have came across indicate that people who were in an exercise group (who previously weren't) tended to eat more food than those who didn't exercse. In fact, the people tended to eat only as much more food as they needed to to make up for any extra activity. In lay terms, if someone burned a total of 2,300 calories throughout the day (by way of previous nutritional intake's effect on hormones, activity, cellular metabolism, environment, etc) then they would only willingly eat 2,300 or so calories a day. If this person wanted to lose weight, the establishment would say cut your calories down to 1800 or so and maintain the same or more activity level. Here's the rub, subconciously, that person will be less active overall or be active at a lower intensity to make up for the difference. Weight loss over the long term (6 months plus) will be small because the body is trying to maintain its set point. The set point got lower by changing the intake level of the person, and if the person ever varies from this calorie restricted diet, then the person will gain more weight, regardless of activity (since the hormonal status is already at a temporary set point and will only reset itself once the intake and output changes results in a change in size-better or worse).
Now there is noone out there who can tell you their exact intake down to 100 calories per day (accurately), nor is there a person who knows their exact output withing 100 calories of energy a day either. Think about it, was that 1 cup of brocolli, or 1.1 cups. Was it 6 ounces of chicken, or was their some marinade on the scale as well. Easily, throughout the course of a day that could result in well over a 100 calorie discrepancy. Also, did you take 15 steps to the door, or was it 14, and was it faster or slower than usual. And further, did your heart rate go up 7 beats a minute, or 6 during that walk? Again, this could cause a miscalculation over a day. So with all this uncertainty on input and output and because the dogma is that if the difference between calories in and calories out equals weight loss why do we almost always stay around the same weight (within 5 lbs) regardless of our diligence? How do we decrease the fat accumulation so we can decrease the fat stores with all this variance? It all boils down to hormones and maybe exercise :-).
Many hormones in our body (specifically testosterone, estrogen, growth hormone, insulin, glucagon, cortisol, etc) are involved in regulating fat metabolism (storage and breakdown). Insulin is the chief regulator of fat accumulation (lipogenesis) and in it's relative absence we see fat break down and be released into the blood stream as free fatty acids to be burnt as fuel (lipogenolysis and fatty acid oxidation). The sex steroids (testosterone and estrogen), growth hormone, and glucagon are all involved as well. Glucagon levels are elevated (relatively) when insulin is lower (again, relatively-not absolutely lower in overall values, that means that the overall value of insulin might be higher-3 units/milliliter of blood versus 1 unit/ milliliter of blood for glucagon). Testosterone works to increase protein synthesis (muscle rebuilding, cell turnover, and increased metabolism) only when insulin levels aren't elevated and growth hormone kicks off the whole cocktail only when insulin is low as well. These hormones work in unison while insulin is off on holiday to break down fat stores to be burnt as fuel and excreted in the urine/breath as ketone bodies. It makes sense that if we can consistently achieve a net flow of fat out of the fat stores, then we will lose body fat. So if we consistently have low or lower (relatively) insulin levels we will lose body fat because all of our other hormones are signalling the fat stores to unleash the beast (fatty acids) to be used as fuel. What's even more interesting is that without a decent amount of insulin (relative to the individual) we will not store fat either. That's right, without insulin to signal the accumulation of free fatty acids from the blood stream to be transported into the fat stores for storage as triglycerides we won't store fat. Higher than baseline levels of insulin are needed to store fat (specifically to activate an enzyme that transports free fatty acids from the blood to the fat stores and turns them into triglycerides). Think of triglycerides as statues in the body, they are hard to move around and even harder to break down and use for other useful purposes. Insulin wants to keep the existing statues where they are (inside the "house"-fat stores) and build new statues as well. The other hormones want to break down the statues into rocks to use for other purposes, as well as keep the rocks that aren't yet statues from being made into statues and keep them floating around for other uses. So if we could do one thing to help jumpstart the net movement of fat out of stores and into the bloodstream for use we would try to drop our insulin levels. How do we do this and dear God will someone tell me how exercise is involved in all of this?
Okay so a brief rundown of how insulin is increased in the body. When you eat, you produce a little insulin from your pancreas to help in absorbtion of the nutrients. The tricky part is how much and for how long does this insulin keep flowing. Meals consisiting of mostly starch (carbs) or sugars (carbs) will spike insulin sky high and keep it there a long time (depending on the size of the meal and your pancreas' status at the time). A meal rich in green veggies, fats, and protein will do just about nil for your insulin release, that is it will be small unless there is a sugary topping (like BBQ sauce) involved or a bread roll. I could go on for hours, but here's the gist, carbs- especially starch, sugar, and the like spike insulin sky high and for a prolonged period of time, and proteins, fats, and fiber don't do much. So without spiking our insulin throughout the day, we could keep it low and keep the body fat melting off. Good stuff. Now what about exercise, and the whole point of this post? Here goes...
So rememeber that the net flow of fat out of the stores results in free fatty acids being available for burning. Muscle cells use these, as do brain and nerve cells (preferentially), as well as other cells within the body. Now if these free fatty acids don't have a place to go to be burnt, they have the opportunity to be re-transported to the fat stores and rebuilt as statues (triglycerides). Here is why I wrote this whole thing. Do people exercise because they want to lose fat or do they exercise because they have all of these free fatty acids floating around that need to be used/expelled? Sounds kinda funny at first but check this; what if the presence of a bunch of free fatty acids in the bloodstream prompted various pathways to become active to increase activity at some level? This makes sense because typically the most fit folks have very low insulin in the blood and thus would have a bunch of free fatty acids at any given time, encouraging them to be more active and exercise (even if it's not necessarily formal exercise that's in a gym). Kind of an interesting theory, although I'm sure I'm not the first to come up with it. So what comes first, the fat or the exercise?
Saturday, May 23, 2009
Cholesterol and Fat
I had a conversation with a friend last night about milk and how I like organic whole milk in comparison to skim milk. She was stunned that as a trainer I advocate the higher fat version of milk. However, I stick to my guns because the whole milk is more natural, has less added sugar and less refinement. Besides the milk fat and protein (casein and whey) is good for you. The discussion took a turn when she said what about clogging your arteries? Well let's look at the role of fat intake, cholesterol, and "clogging" our arteries. Here goes....
Let's begin with cholesterol. There is an overall fear of it in America and westernized countries, that we need to control our cholesterol levels, and the dogma seems to be that lower is better. I have to disagree, but let's save that for later. First, what is cholesterol? Cholesterol is a solid alcohol (not that kind) chemical that is soapy to the touch. Only a small percentage (around 7%) is circulated in the blood, the other 90-something percent is stored in every cell of the body as one of the constituents of the cells membranes (the things that regulate the flux of nutrients and hormones in and out of the cell, basically the liner of the cell). Also, cholesterol is used to make hormones, literally the building blocks. These hormones are involved in blood pressure, sex hormones (testosterone and estradiol), etc. If there is a lack of cholesterol you could test pathologically low for sex steroids (not good if you like a normal sex life, sex characteristics, and normal moods). Furthermore, cholesterol is involved in brain and peripheral nervous system development among other things. At any rate, the bottom line is we need cholesterol to do a bunch of things, and lowering it to extreme levels would not be advantageous to chasing health. What about cholesterol and it's respect to food intake? Well it's a lot smaller than we think. Read on....
Only a fraction of the cholesterol in our body comes from dietary intake (~15-20%), and the rest is produced by the body (mainly the liver, but also the intestines and skin). What's more, if you decrease your cholesterol and cholesterol stimulating foodstuffs intake, your body will just rev up the cholesterol production to meet its needs, and if you eat more cholesterol/cholesterol producing foodstuffs your body will ramp down the production. In people with very high cholesterol levels (over 220-250ng/dL or similar) simply eating less cholesterol will not warrant a significant change. What we need to address is the internal mechanism of cholesterol production. The actual main issue with cholesterol levels, is that too high levels in the blood can cause some issues (we'll get to that later), and the body can't regulate the blood levels. Cells constantly need cholesterol for repair and regeneration, but don't always just take it from the blood, sometimes they just make their own. Also, cells don't know how much cholesterol is floating around outside that specific cell, they just know what they have. So if they need to get some cholesterol for various processes, they'll just make it, completely oblivous to any aberration in blood cholesterol levels.
So we have this cholesterol floating around, and it's usually in one of 3 forms. VLDL, LDL, and HDL. At this point, most people know that LDL is the bad cholesterol, and they carry around mostly all cholesterol molecules to body tissues. It can do one of 3 things, be removed from circulation via the liver, absorbed by tissues needing cholesterol, or be deposited in the arteries. So how do we lower LDL blood levels so none is laid down in the arteries? Well to remove as much LDL as possible we need to get them in contact with as many LDL receptors (in the liver and other tissues) as possible. Cells that need more cholesterol send receptors (LDL receptors) to the cell surface to aquire the LDLs. Then they pull them inside and remove them from the blood. So, simply enough, we just need to increase the LDL receptors in tissues to get rid of LDL in the blood. However there is another side of the equation, if we can't significantly increase LDL receptors in each cell, we need to limit the production of cholesterol inside the cell, so that at least we give ourselves a shot at scavenging LDL particles with our few LDL receptors. At the same time we start sending our LDL receptors to the cell surface, we crank up the machinery to produce cholesterol within the cell. How does this happen?
When we have our LDL receptors out trying to get LDL from the blood, we are simultaneously acruing the raw materials to make cholesterol within the cell to meet the demand. There is one enzyme that is crucial to this in-cell synthesis, and it's HMG-CoA. Most cholesterol lowering drugs (statins) reduce this enzymes activity, and thus lower cholesterol production. However, we can do this naturally, without the need for expensive drugs, side effects, and do a lot better job anyway. It should be noted, that if we slow down in-cell production of cholesterol, then we will concurrently make more LDL receptors in make up for the lag in cholesterol production. Good right?
There are certain hormones that increase HMG-CoA activity, and certain hormones that reduce or blunt its activity (what we want). Insulin, stimulates HMG-CoA activity, and glucagon blunts it. Also of importance, insulin trumps glucagon in all cases, so an increase in insulin for whatever reason means glucagon is relegated to the red headed step child. So if we can keep insulin levels low (which they are normally without ingestion of refined sugars, grains, and high starch intake) we will make a plethora of LDL receptors that will scavenge all that nasty LDL out of the blood and keep our arteries safe.
Now this is only one part of the story, what about HDL? The good cholesterol, HDL is responsible for collecting the extra cholesterol from tissues (including atery linings) and converts this extra to LDL. So you see, it's important to still be able to get rid of the LDL when HDL is normal or high. In fact, we would like to see a shift of more HDL than LDL so that the net activity is removing extra cholesterol from tissues rather than depositing it in arteries or having it circulate looking at places to deposit it.
Now, what about all this low-fat recommendation we hear and preach (and what I was talking about in the introduction)? Remember, if we lower fat, we concommitantly lower protein intake (since protein is generally associated with fat-think animal meats, milk, etc) and since you have to give to get, low fat equals high carbohydrate. Some may argue, but you have to eat something, and a diet low in fat, is high in carbohydrates, and moderate or low in protein as well. It's just a balanced equation here, let's not get too misty eyed over this.
Most studies show that a high carb, low fat diet lower LDL (which is good right?) but also lower HDL, by an even greater percentage (uh oh!). This is bad news. How are we supposed to clean up the extra cholesterol laying around with even less HDL, and our LDL is still doing its job, floating around depositing it on arteries and such (now with even more lag time until its cleaned up by the lower HDL levels)?? What about a low carb, high fat diet (and higher protein, naturally)? We see an overall lowering of total cholesterol (although slightly less than a low fat diet), but a greater reduction in LDL cholesterol percentage-wise, and an INCREASE in HDL! So while low fat diets offer a lowering of LDL and HDL, we get the best of both worlds with low carb diets which offer a lowering of LDL and an increase in HDL. This is ultimately what will help people stave off the effects of high cholesterol (atherogenic plaques, circulatory obstructions, etc).
So the gist of it is this, high fat, high cholesterol diets won't in and of themselves make you have clogged arteries. If your carbs are restricted (say under 120g a day), and you don't have a metabolic disorder involving insulin, then your cholesterol levels will improve, and you won't have to worry about HDL, VLDL, LDL, or any other DL thing-a-ma-jig the rest of your life. So tip your glasses to whole milk....mmm mmmm good.
Let's begin with cholesterol. There is an overall fear of it in America and westernized countries, that we need to control our cholesterol levels, and the dogma seems to be that lower is better. I have to disagree, but let's save that for later. First, what is cholesterol? Cholesterol is a solid alcohol (not that kind) chemical that is soapy to the touch. Only a small percentage (around 7%) is circulated in the blood, the other 90-something percent is stored in every cell of the body as one of the constituents of the cells membranes (the things that regulate the flux of nutrients and hormones in and out of the cell, basically the liner of the cell). Also, cholesterol is used to make hormones, literally the building blocks. These hormones are involved in blood pressure, sex hormones (testosterone and estradiol), etc. If there is a lack of cholesterol you could test pathologically low for sex steroids (not good if you like a normal sex life, sex characteristics, and normal moods). Furthermore, cholesterol is involved in brain and peripheral nervous system development among other things. At any rate, the bottom line is we need cholesterol to do a bunch of things, and lowering it to extreme levels would not be advantageous to chasing health. What about cholesterol and it's respect to food intake? Well it's a lot smaller than we think. Read on....
Only a fraction of the cholesterol in our body comes from dietary intake (~15-20%), and the rest is produced by the body (mainly the liver, but also the intestines and skin). What's more, if you decrease your cholesterol and cholesterol stimulating foodstuffs intake, your body will just rev up the cholesterol production to meet its needs, and if you eat more cholesterol/cholesterol producing foodstuffs your body will ramp down the production. In people with very high cholesterol levels (over 220-250ng/dL or similar) simply eating less cholesterol will not warrant a significant change. What we need to address is the internal mechanism of cholesterol production. The actual main issue with cholesterol levels, is that too high levels in the blood can cause some issues (we'll get to that later), and the body can't regulate the blood levels. Cells constantly need cholesterol for repair and regeneration, but don't always just take it from the blood, sometimes they just make their own. Also, cells don't know how much cholesterol is floating around outside that specific cell, they just know what they have. So if they need to get some cholesterol for various processes, they'll just make it, completely oblivous to any aberration in blood cholesterol levels.
So we have this cholesterol floating around, and it's usually in one of 3 forms. VLDL, LDL, and HDL. At this point, most people know that LDL is the bad cholesterol, and they carry around mostly all cholesterol molecules to body tissues. It can do one of 3 things, be removed from circulation via the liver, absorbed by tissues needing cholesterol, or be deposited in the arteries. So how do we lower LDL blood levels so none is laid down in the arteries? Well to remove as much LDL as possible we need to get them in contact with as many LDL receptors (in the liver and other tissues) as possible. Cells that need more cholesterol send receptors (LDL receptors) to the cell surface to aquire the LDLs. Then they pull them inside and remove them from the blood. So, simply enough, we just need to increase the LDL receptors in tissues to get rid of LDL in the blood. However there is another side of the equation, if we can't significantly increase LDL receptors in each cell, we need to limit the production of cholesterol inside the cell, so that at least we give ourselves a shot at scavenging LDL particles with our few LDL receptors. At the same time we start sending our LDL receptors to the cell surface, we crank up the machinery to produce cholesterol within the cell. How does this happen?
When we have our LDL receptors out trying to get LDL from the blood, we are simultaneously acruing the raw materials to make cholesterol within the cell to meet the demand. There is one enzyme that is crucial to this in-cell synthesis, and it's HMG-CoA. Most cholesterol lowering drugs (statins) reduce this enzymes activity, and thus lower cholesterol production. However, we can do this naturally, without the need for expensive drugs, side effects, and do a lot better job anyway. It should be noted, that if we slow down in-cell production of cholesterol, then we will concurrently make more LDL receptors in make up for the lag in cholesterol production. Good right?
There are certain hormones that increase HMG-CoA activity, and certain hormones that reduce or blunt its activity (what we want). Insulin, stimulates HMG-CoA activity, and glucagon blunts it. Also of importance, insulin trumps glucagon in all cases, so an increase in insulin for whatever reason means glucagon is relegated to the red headed step child. So if we can keep insulin levels low (which they are normally without ingestion of refined sugars, grains, and high starch intake) we will make a plethora of LDL receptors that will scavenge all that nasty LDL out of the blood and keep our arteries safe.
Now this is only one part of the story, what about HDL? The good cholesterol, HDL is responsible for collecting the extra cholesterol from tissues (including atery linings) and converts this extra to LDL. So you see, it's important to still be able to get rid of the LDL when HDL is normal or high. In fact, we would like to see a shift of more HDL than LDL so that the net activity is removing extra cholesterol from tissues rather than depositing it in arteries or having it circulate looking at places to deposit it.
Now, what about all this low-fat recommendation we hear and preach (and what I was talking about in the introduction)? Remember, if we lower fat, we concommitantly lower protein intake (since protein is generally associated with fat-think animal meats, milk, etc) and since you have to give to get, low fat equals high carbohydrate. Some may argue, but you have to eat something, and a diet low in fat, is high in carbohydrates, and moderate or low in protein as well. It's just a balanced equation here, let's not get too misty eyed over this.
Most studies show that a high carb, low fat diet lower LDL (which is good right?) but also lower HDL, by an even greater percentage (uh oh!). This is bad news. How are we supposed to clean up the extra cholesterol laying around with even less HDL, and our LDL is still doing its job, floating around depositing it on arteries and such (now with even more lag time until its cleaned up by the lower HDL levels)?? What about a low carb, high fat diet (and higher protein, naturally)? We see an overall lowering of total cholesterol (although slightly less than a low fat diet), but a greater reduction in LDL cholesterol percentage-wise, and an INCREASE in HDL! So while low fat diets offer a lowering of LDL and HDL, we get the best of both worlds with low carb diets which offer a lowering of LDL and an increase in HDL. This is ultimately what will help people stave off the effects of high cholesterol (atherogenic plaques, circulatory obstructions, etc).
So the gist of it is this, high fat, high cholesterol diets won't in and of themselves make you have clogged arteries. If your carbs are restricted (say under 120g a day), and you don't have a metabolic disorder involving insulin, then your cholesterol levels will improve, and you won't have to worry about HDL, VLDL, LDL, or any other DL thing-a-ma-jig the rest of your life. So tip your glasses to whole milk....mmm mmmm good.
Thursday, May 14, 2009
Pledge of Health
Alright, I'm extending this offer out to everyone and trying to rally the troops to see what kind of impact I/we can have. Take the pledge of health to start out this summer, and I promise the results will be phenomonal. Inspired by one of my clients (Jana), here it is:
I promise to abstain from dining out or eating anything with sugar for the next 30 days.
Now the sugar thing may be confusing, but in general, I mean processed foods (skim milk, low fat dairy, breads, pasta, chips, sweets, etc), not fruit. Fruit is good in moderation, and hell even green leafy vegetables have some sugar (as well as nuts, nut oils, seeds, seed oils, etc). But that's besides the point. So come on, give yourself 30 days of solid eating and see what happens!!!
I promise to abstain from dining out or eating anything with sugar for the next 30 days.
Now the sugar thing may be confusing, but in general, I mean processed foods (skim milk, low fat dairy, breads, pasta, chips, sweets, etc), not fruit. Fruit is good in moderation, and hell even green leafy vegetables have some sugar (as well as nuts, nut oils, seeds, seed oils, etc). But that's besides the point. So come on, give yourself 30 days of solid eating and see what happens!!!
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