In our last lecture, we presented three models for visualization of the concept of energy
consumed and energy expended as strongly linked together. Each model requires estimating the amount
of energy consumed and the amount of energy expended [I recommend the easy way, by allowing
software such as DietAnalysis+ to do the estimating for you]. After entering the data into the
model of your choice, you can assess the probable weight dynamics (increasing, stable, decreasing)
for the patient, based on the linkage of intake and output.
We spent the rest of the lecture examining strategies for managing the energy consumed side of the ledger (I & O chart). The strong recommendation was to avoid fad diets and organized weight loss programs, and instead control energy consumed by controlling portion sizes for energy supplying food, while maintaining variety in the diet to assure that no nutrients would become deficient.
We shall now examine various strategies for managing the energy expenditure side of the ledger
(I & O chart). We can classify [being scientists, “we can” is usually translated into
“we should,” and in plain English means, “we intend to”] Human energy
expenditures into the following 5 groups:
1. basal metabolism (BMR),
2. nonexercise activity, including Activities of Daily Living (ADLs),
3. thermic effect of food (thermogenesis),
4. [intentional] physical activity, and
5. Savings (or contributions to the adipose)
Basal metabolism (BMR) is the amount of energy you use while “doing nothing;” BMR tends to remain fairly constant over long periods of time (except after large changes in intentional activity levels). Non-exercise activity includes ADLs, and do not count as exercise. The thermic effects of food are the Calories consumed in chewing, swallowing, digesting food to nutrients, (sometimes) absorbing nutrients, and voiding undigested remains of food. The more I work with estimating Calorie requirements of sedentary people, the more convinced I am that thermogenesis (thermic effects of food) should be included in BMR and/or ADLS. It is only when the Humans go on their hunting and gathering expeditions that they spend energy beyond BMR, but these hunting and gathering activities are ADLs, and don't count as exercise [no matter how many steps your pedometer says you took hunting and gathering at your local friendly supermarket]. Exercise is any physical activity you didn't have to do, but chose to do anyway. Exercise is the only energy expenditure that you can control as part of a weight management program. After accounting for all the above energy expenditures, any [and all] surplus is deposited in your savings account at the First National Bank of Adipose. It is no easier to get money out of this account than it is to cash out your pension [if you have one; and pensions are harder to cash out than are retirement plans into which you contribute (IRA, 403-b, or 401-k)].
While preparing for in-class lectures over several semesters, I developed a model to describe the
mechanisms Humans evolved to process energy, especially when the energy consumed is either excessive
or deficient. Such mechanisms were, at one time in our evolutionary history, critical to our survival
as the food supply alternated between plentiful (during the growing season) and very scarce (during
winters). The ability to store excess energy, and later retrieve it, became increasingly important to
us [and other omnivores (creatures capable of eating just about anything that doesn't eat them first)
like Bears] as the Ice Age became more severe year after year. Clearly, we had some survival
mechanisms to get through the Pleistocene Ice age, because the last time I checked there still seemed
to be at least a few living specimens of Humans on this planet. What we did not have during the Ice
Age was a calendar to tell us when the growing season was about to end, so it came as a big surprise
every year. The concept of predictable seasons has been with us for only a few to several millennia.
Humans, as a new species (Homo sapiens), would have needed a purely physiological mechanism to store excess energy, as the opportunity arises, and later retrieve it, as the need arises. You already know [from A & P] that the liver
1. intercepts excess glucose from the hepatic portal vessel;
2. converts the glucose to glycogen, using insulin [from the pancreas];
3. stores the glycogen in the liver;
4. when serum glucose drops too low, converts glycogen to glucose, using glucagon [from the pancreas]; and
5. dumps glucose back into the hepatic vein.
This well known process is able to manage serum glucose over periods of minutes to hours. Adding a few refinements to this process may provide management of energy storage over periods of months to years, and unfortunately for currently living Americans, even decades. The following is my hypothesis for how the physiology of long term energy storage works to allow long term Energy Storage, and Energy Retrieval.
The liver is known to intercept excess glucose from the hepatic portal vessel for temporary storage
either as glucose [very limited] or as glycogen (“animal starch”) in the liver. The
synthesis of glycogen from glucose involves insulin. Glycogen can be stored in the liver (and muscle
tissue) for days, providing a good intermediate term storage of energy. The retrieval of energy
as glycogen requires that the glycogen be digested back to glucose which involves another pancreatic
secretion, glucagon. The insulin - glucagon mediated intermediate term energy storage system is
considerably more complicated than this simple explanation, but the simplified version will suffice
for the purposes of a Nutrition course. However, the liver and muscle tissues have a limited capacity
to store glycogen, although it is greater than the capacity for glucose storage. And storage over a
period of days is insufficient to get us through an early or late Pleistocene winter without grocery
stores [like the winters of 1978-79, 1983-84, and 2008-09; actually the winters of 16th
and 17th Centuries were much worse, and the period is known as the “Little Ice
Age;” the cooling began as early as A.D. 1250 and warming didn't begin until A.D. 1850 and has
continued to today (dates from www.windows.ucar.edu/tour/link=/earth/climate/little_ice_age.html)
[although global cooling may have resumed as early as A.D. 1990 - 1995]; 1850 is also the approximate
date of the Industrial Revolution, and the start of the presumed “Human-caused” global
warming which ignores the 40+ year long hot, dry period ending 1300 A.D. at the end of a global
warming event which began around A.D. 600, not to mention the more severe global warming event of
220 million year B.P. (before present), when our species wasn't even here].
When the capacity of the liver to store glycogen is exceeded, a longer term storage option is needed to store the surplus energy. The mechanism for this is the conversion of glycogen to fatty acids, then to fat which can be stored in the liver. If the liver were to continue to add fat storage in itself, the resulting condition is called cirrosis which can become fatal. The liver can avoid cirrosis by converting excess fat back to fatty acids for transport via the blood stream to alternate fat storage tissues, or adipose tissue. Adipose storage of energy as fat occurs initially in sex-specific locations, but can spread into the abdomenal and thoracic cavities [where it becomes a serious medical issue]. Fat can be stored in adipose tissues indefinitely… months to a life-time (where the lifetime can be shortened by the presence of too much stored fat).
When serum glucose (at the hepatic portal vessel) drops, the liver returns some of the stored
glucose to the hepatic vein, which reduces the amount of stored glucose. A secondary source of
glucose for return to the circulating serum is from the glycogen storage. This requires digestion of
glycogen to glucose, with glucagon to activate the appropriate enzymes. This glycogen to glucose
digestion can also provide glucose to replace the stored glucose. This, in turn reduces the amount
of stored glycogen. The glycogen can be replaced by converting fat from the liver to fatty acids,
then back to glycogen (also stimulated by glucagon). Typically, liver stored fat is replaced only
from dietary fatty acids and surplus serum glucose.
When the liver cannot replace the stored glycogen from fat stored in the liver, the liver will initiate mobilization of adipose fat. The adipose tissue will then digest fats back to fatty acids and return the fatty acids to the blood stream for transport. The liver can then take the fatty acids from the serum and use them to synthesize more glycogen. Clearly, this hypothesis requires that the liver somehow communicates to the adipose tissue, to initiate fat deposition in the adipose tissue, and to initiate mobilization of adipose-stored fat to meet current energy needs. In 2007, it was reported in Science, the journal of the American Association for the Advancement of Science (AAAS, pronounced triple-A, S), that researchers have discovered that the liver does exactly this by communicating to the brain stem via the vagus nerve the message to start fat deposition, or the message to start mobilizing fat. This message has two effects: the message is relayed via the sympathetic nerve system directly to the adipose, and the hypothalamus stimulates the production of appropriate hormonal signals (to the adipose) either to store more, or to mobilize the existing stores of, fat. In summary, it is relatively easy to get more fat stored -simply consume too many Calories in your diet; but far less easy to get the fat mobilized to be used as an energy source -the liver will try all other options before tapping into the only long term energy storage system it has. The liver has obviously seen the Weather Channel show, It Could Happen Tomorrow, and wants to maintain the long term energy storage in case the Pleistocene returns tomorrow.
Since a temporary decline in Calorie intake actually triggers fat deposition, and since the liver is programmed to manage energy resources by maintaining an energy reserve in long term storage, ‘dieting’ is unlikely to be efficacious in reduction of body weight for the over-weight population. This leaves the other side of the I & O chart, the energy expended. In fact, the body can be “tricked” into mobilizing body fat as an energy source by increasing energy expended, by increasing what Roizen & Oz call “intentional activity.”
Exercise is, at its simplest, any activity that you didn't have to do,
but did anyway. The best advice from MD's knowledgable in weight management for wellness is to hide
the bathroom scale, and use a tape measure to monitor shape, specifically: chest, waist and hips.
Most, and perhaps all, over weight patients will need to reduce calorie intake by using portion
control to limit calorie intake, while using a variety of foods to assure broad nutrient intake
guidelines are met. Unfortunately, the most critical change in the over-weight patient's behavior
will be to increase energy output by increased exercise. It remains important for the patient to
recognize that slow weight loss is healthier than rapid weight loss, and that most rapid weight loss
results in eventually regaining at least as much weight as was lost [often more weight is regained
than was initially lost].
It seems counter-intuitive that if you need to lose weight, you should stop watching your weight. However, the typical bathroom scale does not do a very good job of estimating weight for several reasons. The instrument is not very precise, where “precise” is the statistical term for “repeatability,” or if you step on and off the scale five times, you may get five different weights. Based on data collected by my students [one example was quoted in the previous lecture (“Weight Management 1”). This example is typical of the tens of data sets analyzed], weight fluctuates by about a half pound daily when weight is [statistically] stable, in part due to hydration status [remember about 90 lbs of a 148 lb Human is water], so it is difficult to interpret whether or not any detected change is real. But, most importantly, total body weight is a lousy predictor of weight-related wellness issues; the critical weight is the weight of internal [as opposed to sub-cutaneous] fat, which normal bathroom scales can not measure. The newer scales which also estimate body fat percent do a better job of estimating internal fat [and are only slightly more expensive than good spring-type scales], but at very low precision and with very high sensitivity to hydration. Daily measured fluctuations in body fat percent [again on a patient with statistically stable body fat percentage] are about 5% of the 20-day sliding average body fat percent. Finally, it has been reported [correctly] that patients on properly designed weight loss programs often lose up to two dress sizes while gaining up to 15 lbs. This occurs because muscle mass is more dense (lbs per cubic inches of body) than is adipose; so the smaller dress size reported involved a loss of adipose (cubic inches) and a gain of muscle (net gain in pounds). The patients in the study were frustrated by their failure to lose pounds, until it was pointed out to them that their dress size had gone down.
The key element of the weight loss program above that produced a gain in weight and a reduction in size is that it was a “properly designed” weight management program, combining reduced portion sizes of high energy density foods and increased exercise. For now, exercise comes in only two categories: aerobic and anaerobic [in our next lecture, we will look at fitness training and sports, where we will need a more detailed listing of types of exercise].
Aerobic means “with oxygen,” or any exercise where the heart can supply oxygen at least as fast as the muscles are consuming it;
Anaerobic means “without oxygen,” or any exercise in which the muscles are demanding oxygen faster than the heart can supply it.
Hopefully you have anticipated that this implies that exercise may put some stress on the heart, so you have an uneasy feeling that you ought not to be telling patients to do too much exercise. If you were thinking that, then you were absolutely correct [I prefer to think that you were in fact thinking exactly that]. Prior to introducing exercise to a patient, you must know how much exercise they can realistically tolerate without triggering the heart attack for which excess weight is one of their several risk factors. I would recommend first collecting a self-reporting history of recent exercise intensity and frequency. A Nursing assessment based on their self-reported history will determine whether or not you should chart the need for a stress test (or other assessment) to determine the intensity of exercise the patient can tolerate. Heart attacks may drive weight loss, but are not the best treatment option for over-weight patients.
During aerobic exercise, the heart is able to keep up with the increased oxygen demand by the
muscles. This should mean that the heart can also supply most of the increased glucose demand as
well. Although the muscles will consume some of their store of gylcogen, the heart will supply
sufficient glycogen from the liver to replace that used in the muscles. As a result, although
energy expended increases, the result will be to reduce the rate at which fat is deposited into
the adipose, but it may do little to reduce the total adipose storage of fats. On the other hand,
one of the muscles being exercised is the heart, so cardiovascular health will be improved [the time
frame for the beneficial cardiovascular health is weeks]. If the aerobic exercise continues, at least
two days a week for a few months or more, resting metabolic rate may accelerate slightly. After
about three months of regular aerobic exercise, the muscle cells appear to develop more mitachondria
[up to double the number in the sedentary muscles], and it is probably the number of mitachondria
that establishes the resting metabolic rate. “Dance aerobics” sometimes produces
“weight loss” by mis-representing the weight loss. Some dance aerobics classes for weight
loss put the scales on the gym floor rather than in the locker room. The clients change into their
suitably fashionable Danskins in the locker room, then go out to the gym floor to weigh in.
After the session, they weigh out on their way to the locker room; showing a weight loss of 4 to 7
pounds (2 - 3 kilos). However, the particpants are thirsy and drink a coupla pounds of water, then
change back into street clothes. On the way out of the building, they pass by the vending machines
where they buy diet cola (they are still thirsty), and, of course, Snickers really satisfies,
so they buy a candy bar too. By the time they get back home they may have gained back a pound more
than they “lost.” The mis-representation is that the “weight loss” was 100%
water, lost as sweat. The participants did not notice that they were sweating because the air
conditioner was running as a dehumidifier, so sweat immediately evaporated. Four to seven pounds
of water lost as sweat is not unlikely, because athletes can lose up to 22 lbs (10 kilos) of water as
sweat in a single athletic event.
For the over-weight, sedentary patient, aerobic exercise for two weeks to two months is an excellent way to get them started, because of the beneficial effects on cardiovascular (and respiratory) health. It does, however, take a minimum of two weeks to see any appreciable cardiovascular & respiratory benefits. For the sedentary population, it may take several two week periods of cardiovascular workouts to raise cardiovascular-respiratory health enough to be able to tolerate the more strenuous exercise needed for weight management. Your patients can be advised that the simplest test of whether or not they are still in aerobic exercise is that they will be able to speak in full sentences without catching their breath. For most of the over-weight population, two months of strictly aerobic exercise is necessary to raise their cardiovascular health to minimal levels needed to begin the weight management exercise they need. Walking with a friend (or spouse) with whom they can chat while exercising is an excellent way to build their cardiovascular health. Since most Americans normally walk at about 2 to 3 miles per hour, it is unlikely that they will over-stress themselves in a 10 to 30 minute walk, while chatting (unless their stress test says otherwise!). You should warn them that they can walk only half-way to ‘tired’ before turning around to return home. Their first exercise walk should not exceed 5 to 10 minutes out, so they can make the 7 to 12 minute return trip safely. [And you can be certain that the return trip will be at a slower pace!] They will probably sleep better after even the first short walk (unless they have sleep apnea). The other advantage of limiting them to 5 minutes out (and 7 minutes back) is that they are more likely to be compliant with what they think will be a 10 minute walk than if you ask for a longer walk [don't tell them that it will take longer to return, but do tell them it's OK to gradually increase the time (distance) they go, as they get accustomed to the exercise]. Ideally, you should aim for two or three days a week for their walk, with a 10 to 20 minute duration.
Once you have successfully improved the patient's cardiovascular health, you can shift them to phase
two of their weight management program. We want the patient to add some anaerobic exercise to their
routine. Anaerobic exercise begins when the muscles oxygen demand exceeds the ability of the heart to
supply oxygen. The patient can determine that they have reached anaerobic exercise because they will
no longer be able to chat with their friend; they will not be able to speak an entire sentence
without pausing to catch their breath. Physiologically, exercise becomes anaerobic when the muscles
shift to anaerobic respiration, or lactic acid fermentation. Since the heart can not deliver oxygen
as fast as the muscles use it, it is safe to assume that the heart cannot supply glucose as fast as
the muscles can burn it either. The muscle must now rely heavily on stored (in the muscle tissue)
glycogen as an energy source. At about 20 minutes of glycogen-fueled cellular respiration, you
trigger mobilization of adipose fat to replace the depletion of glycogen storage in the muscle;
importantly, the liver is not involved in this utilization of fat reserves. The actual conversion of
fat to fatty acids to glycogen typically [but not always] will not begin until the exercise session
ends [some evidence suggests that some athletes use fat mobilization as a energy source during the
exercise session], but will then continue for up to two hours. Once fat mobilization has been
triggered [about 20 minutes of anaerobic exercise] adding more exercise has no additional effect.
Forty minutes does not get you four hours of fat mobilization, but only two hours. Twenty minutes of
anaerobic exercise followed by a minimum two hour break, then repeating twenty more minutes of
anaerobic exercise may trigger another two hours of fat mobilization. The old rule [from the last
decade of the 20th Century] that the patient must exercise for 30 minutes to an hour has
been replaced by the new 21st Century idea that 20 minutes in the morning, and 20 minutes
in the evening is more effective [faster fat loss] and less stressful [lower risk of heart attack].
The evening session will also promote sounder sleep, while the evening session followed by sleep and
another morning session will increase hunger, increasing the likelihood that patient will eat
breakfast [another counter-intuitive observation of Humans and weight is that persons who skip
breakfast gain weight more easily than persons who eat breakfast]. Only active adolescents can safely
go from resting to anaerobic exercise, the rest of us will require stretching and warm-up (or
aerobic exercise of the same muscles as will be used for the anaerobic exercise) at least 5 minutes
before beginning the 20 minute anaerobic exercise, followed by another 5 minutes of cool-down
(aerobic exercise of the same muscles) to avoid cramping. As for phase one, we want to encourage
patients to get the twice daily dose of anaerobic exercise at least two days a week. It would be
much better at 3 to 5 days a week, but not over 7 days a week [but if you tell the patient this, they
will probably drop out of the program before they drive past the McDonald's drive-thru on their
way home from talking to you]. Compliant patients [two 20 minute anaerobic exercise session a day, 2
days per week] are very likely to lose 2 inches off their waistline and to gain 5 pounds over six
months to a year into the program. They will also exhibit an increased life expectancy [age at death
for 50% of a same aged population of individuals following the same exercise regime] and
statistically significant decline in probability of developing non-Alzheimer's, age-related
dementia. When living beyond say 98 years without dementia becomes unacceptable, all you have to do
is cease exercising, eat junk food, drink diet cola, and watch TV [which according to an ad on TV
for TV back in January of 2009, shrinks your brain to a small lump of jelly-like substance] and you
too can become demented and die.
This was not a professional driver on a closed course; you can try this at home. However, should you try this at home, you will experience a cascade of physiological effects. At first, the anaerobic cellular respiration (lactic acid fermentation) will produce the mildly toxic lactic acid as a by-product. The purpose of the cool-down period is to maintain the elevated pulse rate long enough to supply Oxygen to support synthesis of pyruvate from the lactic acid [reverse fermentation], then aerobic respiration of the pyruvate to CO2 and H2O, but the increased blood flow will transport some of the lactic acid out of the muscle tissue. It was probably the lactic acid in the capillary beds of the adipose that triggered fat mobilization in the first place [as soon as the serum concentration of lactic acid reached the necessary threshold at about 20 minutes of exercise]. When the hypothalamus detects serum lactic acid [at a higher concentration than the threshold for fat mobilization], it triggers anabolic steroid production in the pituitary gland, and the anabolic steroid drives growth of muscle tissue by stimulating muscle stem cell division. Each new muscle cell produced will have more than one mitachondrion (and remember, exercise, even aerobic exercise, stimulated the production of mitachondria in existing muscle cells). The increase in mitachondria causes an increase in resting metabolic rate. Idle muscle tissues requires up to 75 kilocalories per pound per day, compared to the huge 3 kilocalories per pound per day for adipose tissue.
The simplest anaerobic exercise is a brisk walk. Remember, the average American walks at about 2 to 3 miles per hour (and we suggested walking as the cardiovascular exercise above). Now we want the patient to step up the pace, with a target of 4 miles per hour (15 minutes to walk one mile, about 1,250 steps on your pedometer after a ten minute walk). Jogging would be acceptable, but most people associate jogging with “serious” fitness exercise [the kind done by fitness freaks]. There are numerous books available explaining “how to jog,” or walk. Unfortunately, all of these books are wrong; they recommend jogging (or walking) patterns which will damage the knees. The popular books on jogging and walking all suggest that you should land on your heel and roll up to the ball of the foot, then push off with your toes. This ignores the anatomic design of the Human leg. Most opposing pairs of muscles, such as the quadriceps - hamstring of the thigh (origin on pelvis, insertion on distal femur) and the biceps - triceps of the upper arm (origin proximal humerus, insertion proximal radius & ulna), are similar in size. The big exception is the tibialis anterior (dorsiflex) and gastrocnemius (plantar flex) pair. Why is the gastrocnemius so large compared to the tibialis anterior? If you stand and hop straight up, then land on the balls of your feet, as soon as the balls of the feet contact the ground, the gastrocnemius will reflexively contract and absorb most of the blow. If you hop again, but this time land on your heels, the blow will be transmitted bone to bone to the weak link in the leg, the knee [and will also be transmitted bone to bone to the hip, pelvis, spine, and eventually the cranium will bounce on top of the spine, joustling the brain inside the cranium; remember: “foot bone connected to the ankle bone, ankle bone connected to the shin bone, shin bone connected to the knee bone, knee bone connected to the leg bone…”]. Rather than following the advice of the authors of books teaching you to walk/run incorrectly, you need to practice walking correctly. As the leg swings forward, you should do a plantar flex (of the ankle; a &$8220point” in gymnastics) so the ball of the foot and toes contact the ground first (using the gastrocnemius as a shock absorber), then lower the heel [optional] down to the ground. Now lift the heel, roll up to the toes and flex the toes to push off for the next step. This awkward-looking method of walking is instinctive in Humans; just watch an infant learning to walk - they walk on the balls of their feet until their parents sneak up behind them, place their hands on the toddler's shoulders, and push the toddler down to get heel contact. The toddlers finally re-learn to walk incorrectly. A side effect of walking correctly [digitigrade] rather than the customary flat-footed walk [plantigrade] is that balance is improved sufficiently that ankle strains and sprains are less likely even in shoes without ankle support. The theraputic effect is a 15% increase in metabolic cost of walking digitigrade compared to plantigrade (from the abstract of a paper presented at the 2009 annual meeting of the Society for Integrative and Comparative Biology: Wednesday, Jan. 7 Plantigrade foot posture increases locomotor economy in walking but not in running humans. CUNNINGHAM, C; SCHILLING, N; ANDERS, C; CARRIER, D*; Univ. of Utah, Salt Lake City; Friedrich-Schiller-Univ. Jena; Univ. Hospital Jena; Univ. of Utah, Salt Lake City)
As you may have anticipated, the behavior modification we are looking for in the patients is not the usual weight loss diet version (restrict calorie intake), but on the calorie expended side of the ledger or I & O chart. We want the patient to alter their long term behavior to include intentional physical activity. We will examine the options for exercise as a means of improving wellness in the next lecture (“Fitness & Sports”), under the sub-heading “Fitness” [mostly to keep this lecture within a reasonable file size so it downloads quickly, even on a dial-up service].
TABLE OF CONTENTS
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revised: 25 Mar 2009