Marlon D. Satchell, MPH
Project Director
Jefferson School of Population Health
A recent Philadelphia Inquirer article highlighted the release of The Self-Sufficiency Standard for Pennsylvania 2010, written by Diana Pearce, PhD, director of the University of Washington Center for Women’s Welfare. This standard was prepared for PathWays PA, an organization that advocates for efforts to benefit low-wage workers throughout Pennsylvania. For the past 30 years, wages in the United States have stagnated, while income inequality has grown. The Self-Sufficiency Standard was developed in 1996 as a more comprehensive method of determining family economic stability and changes in the economic needs of families from year to year.
The Self-Sufficiency Standard presents sobering facts about the cost of meeting a family’s most basic needs, without relying on public or private assistance. The 2010-2011 Self-Sufficiency Standard of $60,000 for a family of four is in stark contrast to the unrealistic and outdated Federal Poverty Level estimate of $22,000.
In contrast to the Federal Poverty Level, which focuses on the cost of food and uses that to gauge all other expenses, the Self-Sufficiency Standard takes into consideration factors such as housing, child care, food, healthcare, transportation, taxes, geography, and family composition. Further compromising the Federal Poverty Level is that it only measures need for households in which there is only one wage-earner, thus negating the necessity of child care. The exclusion of families with two working adults also ignores the difficulties that such families have meeting their economic needs. It also excludes the essential but growing costs of housing, healthcare, and transportation.
Another important factor about the Self-Sufficiency Standard is that it calculates a standard for a number of different family compositions, and reflects the varying needs of families with and without more than one working parent, and families with children of different ages. The standard calculates the variations in economic needs and responsibilities at the state, county and local level as well. As an example, the standard for a family of four in Montgomery County is over $73,000, which is considerably higher than that for Philadelphia County. As a result, far more detailed information about the relative weight of household expenses across the country and across individual states can be used to more accurately assess the status of families living in those areas, and determine the range and scope of the services that they may need. Finally, the Self-Sufficiency Standard is updated every two years, allowing for policy-makers and other users to have current, up-to-date information on populations in need.
Ultimately, the Self-Sufficiency Standard is a far more comprehensive tool that can be used by employers, advocates, and legislators to assess wages, provide career counseling, and create programs that lead to self-sufficiency for working families. The enormous gap between the Self-Sufficiency Standard and the Federal Poverty Level serves as a clarion call that the existing standards by which the Federal Poverty Level is developed are profoundly out-of-date. The Federal Poverty Level conveys a lack of understanding of who needy families are, and the necessities they must pay for. The Self-Sufficiency Standard is therefore shown to be a far more comprehensive and realistic tool that reflects the changing times and the different hurdles that working families now face.
The full report, including information on methodology, data sources, the authors’ assumptions, and ways in which the data has been used can be found here.
Wednesday, June 30, 2010
Amodimethicone, Castor Oil for Sheen?
MORE READS:
AMODIMETHICONE + OTHER CONES
CLEANSING AGENTS FOR CONES
Healthy Hair Feature: Redecouverte
I've been natural since September 2006.
2) What mistakes have you made in your hair care journey?
I am not sure if it qualifies as a mistake but for the past two years I haven't made up my mind whether I wanted locs or just rock my loose hair. I love locs and think they're absolutely beautiful. I also love my loose hair, its thickness and versatility. So I've had a few past locking attempt that did not last more than 3 months. I end up missing my loose hair and take down the babies locs. My hair locks pretty fast and taking down my hair can be quite traumatic. In the long run, it affects my ends.
3) What is your current HEALTHY HAIR routine?
I don't really have a routine, I go with the flow. I usually wash my hair twice a week (Wednesdays and Sundays) and then do either a hot oil treatment or a deep conditioning. I use mostly natural products because they are more nourishing to my hair than commercial ones. Once in a while I'll do a rhassoul treatment.
Other than that, I don't really have a set routine.
4) Do you have a HEALTHY BODY routine? If so, what is it?
In regards to skincare, I use the oil cleansing method for my face. I exfoliate once or twice a week and do a facial mask as needed.
I mostly use shea butter for my body and I also love exfoliating once to twice a week.
In regards to diet, I still need to work on it. I have severe Polycystic Ovarian Syndrome and diabetes running in the family so last year I decided to change completely my diet and went vegan cold turkey. Eventually I decided to adopt a vegetarian diet with as little dairy products as I can (I still love lattes and ice cream) and include raw foods. My diet is still a work in progress and it has been hard to say goodbye to comfort meals such as chapatis, samosas, jollof rice etc..
Yes, first and foremost don't get caught up in hair typing. I grew up mainly in West Africa, mostly Ghana and Senegal and I've never heard about hair types until I came to the USA. I don't think it really matters whether you have 4 a, b, c, d because each head is unique. I still don't know what my hair type is and I am fine.
The second advice will be not to compare yourself to others and just be happy with your own progress. This is hard because we go to hair forums and stalk people's fotki to be inspired especially when we have little support outside of the online communities. But when I started finding myself resenting people who have big chopped and had more hair in 6 months than me in 4 years, I had to take a step back and remember that each person is different.
Last but not least, do what works for you and have fun. Sometimes we get caught up in hair challenges and we become stressed out if we don't see any progress.
Sunday, June 27, 2010
Fellows Day
Tomorrow is Fellow's Day for the Jefferson School of Population Health. It is an important and bittersweet day in our annual academic calendar. Tomorrow, we say good bye to three fellows, two of whom will go on to their industry assignments, and luckily, one will remain with us as a new faculty member. We have more than 35 graduates of our Outcomes Research Fellowship Program, one of the most successful such programs in the nation. This alumni group is now spread out across the globe in many different firms, and in senior leadership positions. We will also be welcoming a new cohort of fellows, with support from great companies like Ortho McNeil Janssen, Endo Pharmaceuticals, and Ethicon.Our 20 year experience in Outcomes Research is giving us a running head start as we plan to launch, pending TJU Board approval, our Masters Degree in Applied Health Economics, in September 2011. I am confident that this fifth new Masters Degree in our school will round out our total offerings and be very attractive in the marketplace. But, Fellows Day is bittersweet as we say good bye to talented young persons and they take their place as colleagues in the pharmaceutical and device industries. Hats off to our graduating team and welcome to the new team. Look for our new degree program soon. Finally, thanks again to all of the great companies who make our fellowship program so successful.If you would like to be a part of the team working to implement Comparative Effectiveness Studies and to participate in fixing our broken health care system, maybe one of these fellowships is for you!! We would be happy to share the details with you anytime. DAVID NASH
Exercise and blood glucose levels: Insulin and glucose responses to exercise
The notion that exercise reduces blood glucose levels is widespread. That notion is largely incorrect. Exercise appears to have a positive effect on insulin sensitivity in the long term, but also increases blood glucose levels in the short term. That is, exercise, while it is happening, leads to an increase in circulating blood glucose. In normoglycemic individuals, that increase is fairly small compared to the increase caused by consumption of carbohydrate-rich foods, particularly foods rich in refined carbohydrates and sugars.
The figure below, from the excellent book by Wilmore and colleagues (2007), shows the variation of blood insulin and glucose in response to an endurance exercise session. The exercise session’s intensity was at 65 to 70 percent of the individuals’ maximal capacity (i.e., their VO2 max). The session lasted 180 minutes, or 3 hours. The full reference to the book by Wilmore and colleagues is at the end of this post.
As you can see, blood insulin levels decreased markedly in response to the exercise bout, in an exponential decay fashion. Blood glucose increased quickly, from about 5.1 mmol/l (91.8 mg/dl) to 5.4 mmol/l (97.2 mg/dl), before dropping again. Note that blood glucose levels remained somewhat elevated throughout the exercise session. But, still, the elevation was fairly small in the participants, which were all normoglycemic. A couple of bagels would easily induce a rise to 160 mg/dl in about 45 minutes in those individuals, and a much larger “area under the curve” glucose response than exercise.
So what is going on here? Shouldn’t glucose levels go down, since muscle is using glucose for energy?
No, because the human body is much more “concerned” with keeping blood glucose levels high enough to support those cells that absolutely need glucose, such as brain and red blood cells. During exercise, the brain will derive part of its energy from ketones, but will still need glucose to function properly. In fact, that need is critical for survival, and may be seen as a bit of an evolutionary flaw. Hypoglycemia, if maintained for too long, will lead to seizures, coma, and death.
Muscle tissue will increase its uptake of free fatty acids and ketones during exercise, to spare glucose for the brain. And muscle tissue will also consume glucose, in part for glycogenesis; that is, for making muscle glycogen, which is being depleted by exercise. In this sense, we can say that muscle tissue is becoming somewhat insulin resistant, because it is using more free fatty acids and ketones for energy, and thus less glucose. Another way of looking at this, however, which is favored by Wilmore and colleagues (2007), is that muscle tissue is becoming more insulin sensitive, because it is still taking up glucose, even though insulin levels are dropping.
Truth be told, the discussion in the paragraph above is mostly academic, because muscle tissue can take up glucose without insulin. Insulin is a hormone that allows the pancreas, its secreting organ, to communicate with two main organs – the liver and body fat. (Yes, body fat can be seen as an “organ”, since it has a number of endocrine functions.) Insulin signals to the liver that it is time to take up blood glucose and either make glycogen (to be stored in the liver) or fat with it (secreting that fat in VLDL particles). Insulin signals to body fat that it is time to take up blood glucose and fat (e.g., packaged in chylomicrons) and make more body fat with it. Low insulin levels, during exercise, will do the opposite, leading to low glucose uptake by the liver and an increase in body fat catabolism.
Resistance exercise (e.g., weight training) induces much higher glucose levels than endurance exercise; and this happens even when one has fasted for 20 hours before the exercise session. The reason is that resistance exercise leads to the conversion of muscle glycogen into energy, releasing lactate in the process. Lactate is in turn used by muscle tissues as a source of energy, helping spare glycogen. It is also used by the liver for production of glucose through gluconeogenesis, which significantly elevates blood glucose levels. That hepatic glucose is then used by muscle tissues to replenish their depleted glycogen stores. This is known as the Cori cycle.
Exercise seems to lead, in the long term, to insulin sensitivity; but through a fairly complex and longitudinal process that involves the interaction of many hormones. One of the mechanisms may be an overall reduction in insulin levels, leading to increased insulin sensitivity as a compensatory adaptation. In the short term, particularly while it is being conducted, exercise nearly always increases blood glucose levels. Even in the first few months after the beginning of an exercise program, blood glucose levels may increase. If a person who was on a low carbohydrate diet started a 3-month exercise program, it is quite possible that the person’s average blood glucose would go up a bit. If low carbohydrate dieting began together with the exercise program, then average blood glucose might drop significantly, because of the acute effect of this type of dieting on average blood glucose.
Still exercise is health-promoting. The combination of the long- and short-term effects of exercise appears to lead to an overall slowing down of the progression of insulin resistance with age. This is a good thing.
Reference:
Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.
The figure below, from the excellent book by Wilmore and colleagues (2007), shows the variation of blood insulin and glucose in response to an endurance exercise session. The exercise session’s intensity was at 65 to 70 percent of the individuals’ maximal capacity (i.e., their VO2 max). The session lasted 180 minutes, or 3 hours. The full reference to the book by Wilmore and colleagues is at the end of this post.
As you can see, blood insulin levels decreased markedly in response to the exercise bout, in an exponential decay fashion. Blood glucose increased quickly, from about 5.1 mmol/l (91.8 mg/dl) to 5.4 mmol/l (97.2 mg/dl), before dropping again. Note that blood glucose levels remained somewhat elevated throughout the exercise session. But, still, the elevation was fairly small in the participants, which were all normoglycemic. A couple of bagels would easily induce a rise to 160 mg/dl in about 45 minutes in those individuals, and a much larger “area under the curve” glucose response than exercise.
So what is going on here? Shouldn’t glucose levels go down, since muscle is using glucose for energy?
No, because the human body is much more “concerned” with keeping blood glucose levels high enough to support those cells that absolutely need glucose, such as brain and red blood cells. During exercise, the brain will derive part of its energy from ketones, but will still need glucose to function properly. In fact, that need is critical for survival, and may be seen as a bit of an evolutionary flaw. Hypoglycemia, if maintained for too long, will lead to seizures, coma, and death.
Muscle tissue will increase its uptake of free fatty acids and ketones during exercise, to spare glucose for the brain. And muscle tissue will also consume glucose, in part for glycogenesis; that is, for making muscle glycogen, which is being depleted by exercise. In this sense, we can say that muscle tissue is becoming somewhat insulin resistant, because it is using more free fatty acids and ketones for energy, and thus less glucose. Another way of looking at this, however, which is favored by Wilmore and colleagues (2007), is that muscle tissue is becoming more insulin sensitive, because it is still taking up glucose, even though insulin levels are dropping.
Truth be told, the discussion in the paragraph above is mostly academic, because muscle tissue can take up glucose without insulin. Insulin is a hormone that allows the pancreas, its secreting organ, to communicate with two main organs – the liver and body fat. (Yes, body fat can be seen as an “organ”, since it has a number of endocrine functions.) Insulin signals to the liver that it is time to take up blood glucose and either make glycogen (to be stored in the liver) or fat with it (secreting that fat in VLDL particles). Insulin signals to body fat that it is time to take up blood glucose and fat (e.g., packaged in chylomicrons) and make more body fat with it. Low insulin levels, during exercise, will do the opposite, leading to low glucose uptake by the liver and an increase in body fat catabolism.
Resistance exercise (e.g., weight training) induces much higher glucose levels than endurance exercise; and this happens even when one has fasted for 20 hours before the exercise session. The reason is that resistance exercise leads to the conversion of muscle glycogen into energy, releasing lactate in the process. Lactate is in turn used by muscle tissues as a source of energy, helping spare glycogen. It is also used by the liver for production of glucose through gluconeogenesis, which significantly elevates blood glucose levels. That hepatic glucose is then used by muscle tissues to replenish their depleted glycogen stores. This is known as the Cori cycle.
Exercise seems to lead, in the long term, to insulin sensitivity; but through a fairly complex and longitudinal process that involves the interaction of many hormones. One of the mechanisms may be an overall reduction in insulin levels, leading to increased insulin sensitivity as a compensatory adaptation. In the short term, particularly while it is being conducted, exercise nearly always increases blood glucose levels. Even in the first few months after the beginning of an exercise program, blood glucose levels may increase. If a person who was on a low carbohydrate diet started a 3-month exercise program, it is quite possible that the person’s average blood glucose would go up a bit. If low carbohydrate dieting began together with the exercise program, then average blood glucose might drop significantly, because of the acute effect of this type of dieting on average blood glucose.
Still exercise is health-promoting. The combination of the long- and short-term effects of exercise appears to lead to an overall slowing down of the progression of insulin resistance with age. This is a good thing.
Reference:
Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.
Thursday, June 24, 2010
Sugar, Acne, and Skin Care Recap!
*************
In case you missed previous skin care topics on this blog, here is a recap:
1. Black Skin and Sunscreen
2. Hyperpigmentation in Black Skin
3. Building a Skin Care Regimen
4. Hey Med School ... Skin Care, Please?
5. Household Makeup Removers
6. Natural Skin Care ... On a Budget
and more!
Wednesday, June 23, 2010
Compensatory adaptation as a unifying concept: Understanding how we respond to diet and lifestyle changes
Trying to understand each body response to each diet and lifestyle change, individually, is certainly a losing battle. It is a bit like the various attempts to classify organisms that occurred prior to solid knowledge about common descent. Darwin’s theory of evolution is a theory of common descent that makes classification of organisms a much easier and logical task.
Compensatory adaptation (CA) is a broad theoretical framework that hopefully can help us better understand responses to diet and lifestyle changes. CA is a very broad idea, and it has applications at many levels. I have discussed CA in the context of human behavior in general (Kock, 2002), and human behavior toward communication technologies (Kock, 2001; 2005; 2007). Full references and links are at the end of this post.
CA is all about time-dependent adaptation in response to stimuli facing an organism. The stimuli may be in the form of obstacles. From a general human behavior perspective, CA seems to be at the source of many success stories. A few are discussed in the Kock (2002) book; the cases of Helen Keller and Stephen Hawking are among them.
People who have to face serious obstacles sometimes develop remarkable adaptations that make them rather unique individuals. Hawking developed remarkable mental visualization abilities, which seem to be related to some of his most important cosmological discoveries. Keller could recognize an approaching person based on floor vibrations, even though she was blind and deaf. Both achieved remarkable professional success, perhaps not as much in spite but because of their disabilities.
From a diet and lifestyle perspective, CA allows us to make one key prediction. The prediction is that compensatory body responses to diet and lifestyle changes will occur, and they will be aimed at maximizing reproductive success, but with a twist – it’s reproductive success in our evolutionary past! We are stuck with those adaptations, even though we live in modern environments that differ in many respects from the environments where our ancestors lived.
Note that what CA generally tries to maximize is reproductive success, not survival success. From an evolutionary perspective, if an organism generates 30 offspring in a lifetime of 2 years, that organism is more successful in terms of spreading its genes than another that generates 5 offspring in a lifetime of 200 years. This is true as long as the offspring survive to reproductive maturity, which is why extended survival is selected for in some species.
We live longer than chimpanzees in part because our ancestors were “good fathers and mothers”, taking care of their children, who were vulnerable. If our ancestors were not as caring or their children not as vulnerable, maybe this blog would have posts on how to control blood glucose levels to live beyond the ripe old age of 50!
The CA prediction related to responses aimed at maximizing reproductive success is a straightforward enough prediction. The difficult part is to understand how CA works in specific contexts (e.g., Paleolithic dieting, low carbohydrate dieting, calorie restriction), and what we can do to take advantage (or work around) CA mechanisms. For that we need a good understanding of evolution, some common sense, and also good empirical research.
One thing we can say with some degree of certainty is that CA leads to short-term and long-term responses, and that those are likely to be different from one another. The reason is that a particular diet and lifestyle change affected the reproductive success of our Paleolithic ancestors in different ways, depending on whether it was a short-term or long-term change. The same is true for CA responses at different stages of one’s life, such as adolescence and middle age; they are also different.
This is the main reason why many diets that work very well in the beginning (e.g., first months) frequently cease to work as well after a while (e.g., a year).
Also, CA leads to psychological responses, which is one of the key reasons why most diets fail. Without a change in mindset, more often than not one tends to return to old habits. Hunger is not only a physiological response; it is also a psychological response, and the psychological part can be a lot stronger than the physiological one.
It is because of CA that a one-month moderately severe calorie restriction period (e.g., 30% below basal metabolic rate) will lead to significant body fat loss, as the body produces hormonal responses to several stimuli (e.g., glycogen depletion) in a compensatory way, but still “assuming” that liberal amounts of food will soon be available. Do that for one year and the body will respond differently, “assuming” that food scarcity is no longer short-term and thus that it requires different, and possibly more drastic, responses.
Among other things, prolonged severe calorie restriction will lead to a significant decrease in metabolism, loss of libido, loss of morale, and physical as well as mental fatigue. It will make the body hold on to its fat reserves a lot more greedily, and induce a number of psychological responses to force us to devour anything in sight. In several people it will induce psychosis. The results of prolonged starvation experiments, such as the Biosphere 2 experiments, are very instructive in this respect.
It is because of CA that resistance exercise leads to muscle gain. Muscle gain is actually a body’s response to reasonable levels of anaerobic exercise. The exercise itself leads to muscle damage, and short-term muscle loss. The gain comes after the exercise, in the following hours and days (and with proper nutrition), as the body tries to repair the muscle damage. Here the body “assumes” that the level of exertion that caused it will continue in the near future.
If you increase the effort (by increasing resistance or repetitions, within a certain range) at each workout session, the body will be constantly adapting, up to a limit. If there is no increase, adaptation will stop; it will even regress if exercise stops altogether. Do too much resistance training (e.g., multiple workout sessions everyday), and the body will react differently. Among other things, it will create deterrents in the form of pain (through inflammation), physical and mental fatigue, and even psychological aversion to resistance exercise.
CA processes have a powerful effect on one’s body, and even on one’s mind!
References:
Kock, N. (2001). Compensatory Adaptation to a Lean Medium: An Action Research Investigation of Electronic Communication in Process Improvement Groups. IEEE Transactions on Professional Communication, 44(4), 267-285.
Kock, N. (2002). Compensatory Adaptation: Understanding How Obstacles Can Lead to Success. Infinity Publishing, Haverford, PA. (Additional link.)
Kock, N. (2005). Compensatory adaptation to media obstacles: An experimental study of process redesign dyads. Information Resources Management Journal, 18(2), 41-67.
Kock, N. (2007). Media Naturalness and Compensatory Encoding: The Burden of Electronic Media Obstacles is on Senders. Decision Support Systems, 44(1), 175-187.
Compensatory adaptation (CA) is a broad theoretical framework that hopefully can help us better understand responses to diet and lifestyle changes. CA is a very broad idea, and it has applications at many levels. I have discussed CA in the context of human behavior in general (Kock, 2002), and human behavior toward communication technologies (Kock, 2001; 2005; 2007). Full references and links are at the end of this post.
CA is all about time-dependent adaptation in response to stimuli facing an organism. The stimuli may be in the form of obstacles. From a general human behavior perspective, CA seems to be at the source of many success stories. A few are discussed in the Kock (2002) book; the cases of Helen Keller and Stephen Hawking are among them.
People who have to face serious obstacles sometimes develop remarkable adaptations that make them rather unique individuals. Hawking developed remarkable mental visualization abilities, which seem to be related to some of his most important cosmological discoveries. Keller could recognize an approaching person based on floor vibrations, even though she was blind and deaf. Both achieved remarkable professional success, perhaps not as much in spite but because of their disabilities.
From a diet and lifestyle perspective, CA allows us to make one key prediction. The prediction is that compensatory body responses to diet and lifestyle changes will occur, and they will be aimed at maximizing reproductive success, but with a twist – it’s reproductive success in our evolutionary past! We are stuck with those adaptations, even though we live in modern environments that differ in many respects from the environments where our ancestors lived.
Note that what CA generally tries to maximize is reproductive success, not survival success. From an evolutionary perspective, if an organism generates 30 offspring in a lifetime of 2 years, that organism is more successful in terms of spreading its genes than another that generates 5 offspring in a lifetime of 200 years. This is true as long as the offspring survive to reproductive maturity, which is why extended survival is selected for in some species.
We live longer than chimpanzees in part because our ancestors were “good fathers and mothers”, taking care of their children, who were vulnerable. If our ancestors were not as caring or their children not as vulnerable, maybe this blog would have posts on how to control blood glucose levels to live beyond the ripe old age of 50!
The CA prediction related to responses aimed at maximizing reproductive success is a straightforward enough prediction. The difficult part is to understand how CA works in specific contexts (e.g., Paleolithic dieting, low carbohydrate dieting, calorie restriction), and what we can do to take advantage (or work around) CA mechanisms. For that we need a good understanding of evolution, some common sense, and also good empirical research.
One thing we can say with some degree of certainty is that CA leads to short-term and long-term responses, and that those are likely to be different from one another. The reason is that a particular diet and lifestyle change affected the reproductive success of our Paleolithic ancestors in different ways, depending on whether it was a short-term or long-term change. The same is true for CA responses at different stages of one’s life, such as adolescence and middle age; they are also different.
This is the main reason why many diets that work very well in the beginning (e.g., first months) frequently cease to work as well after a while (e.g., a year).
Also, CA leads to psychological responses, which is one of the key reasons why most diets fail. Without a change in mindset, more often than not one tends to return to old habits. Hunger is not only a physiological response; it is also a psychological response, and the psychological part can be a lot stronger than the physiological one.
It is because of CA that a one-month moderately severe calorie restriction period (e.g., 30% below basal metabolic rate) will lead to significant body fat loss, as the body produces hormonal responses to several stimuli (e.g., glycogen depletion) in a compensatory way, but still “assuming” that liberal amounts of food will soon be available. Do that for one year and the body will respond differently, “assuming” that food scarcity is no longer short-term and thus that it requires different, and possibly more drastic, responses.
Among other things, prolonged severe calorie restriction will lead to a significant decrease in metabolism, loss of libido, loss of morale, and physical as well as mental fatigue. It will make the body hold on to its fat reserves a lot more greedily, and induce a number of psychological responses to force us to devour anything in sight. In several people it will induce psychosis. The results of prolonged starvation experiments, such as the Biosphere 2 experiments, are very instructive in this respect.
It is because of CA that resistance exercise leads to muscle gain. Muscle gain is actually a body’s response to reasonable levels of anaerobic exercise. The exercise itself leads to muscle damage, and short-term muscle loss. The gain comes after the exercise, in the following hours and days (and with proper nutrition), as the body tries to repair the muscle damage. Here the body “assumes” that the level of exertion that caused it will continue in the near future.
If you increase the effort (by increasing resistance or repetitions, within a certain range) at each workout session, the body will be constantly adapting, up to a limit. If there is no increase, adaptation will stop; it will even regress if exercise stops altogether. Do too much resistance training (e.g., multiple workout sessions everyday), and the body will react differently. Among other things, it will create deterrents in the form of pain (through inflammation), physical and mental fatigue, and even psychological aversion to resistance exercise.
CA processes have a powerful effect on one’s body, and even on one’s mind!
References:
Kock, N. (2001). Compensatory Adaptation to a Lean Medium: An Action Research Investigation of Electronic Communication in Process Improvement Groups. IEEE Transactions on Professional Communication, 44(4), 267-285.
Kock, N. (2002). Compensatory Adaptation: Understanding How Obstacles Can Lead to Success. Infinity Publishing, Haverford, PA. (Additional link.)
Kock, N. (2005). Compensatory adaptation to media obstacles: An experimental study of process redesign dyads. Information Resources Management Journal, 18(2), 41-67.
Kock, N. (2007). Media Naturalness and Compensatory Encoding: The Burden of Electronic Media Obstacles is on Senders. Decision Support Systems, 44(1), 175-187.
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