From Dr Paul Batman PhD
Continuing our greta series of articles on all things fitness. The gift of information. Not picked up 1-21, take a look on our website. Remember to share these articles on your own websites and social media as a gift from Dr Paul Batman.
22. How can I monitor physical activity for weight loss?
Successful fitness programming requires a dose response prescription. The most widely used method for monitoring intensity has always been heart rate.
Heart Rate Method
One method is to initially calculate our maximum heart rate by subtracting our age from 220 beats per minute, which is regarded as the generic maximum heart rate for everyone.
If we were 30 years old our maximum heart rate would be: 220-30 = 190 beats per minute. This is now our maximum heart rate. As you can see our maximum heart rate decreases as you get older.
The dose of intensity required to train our oxygen transport system is 60-85% of our maximum heart rate. Within this range the intensity is great enough to stress our heart, lungs, muscles, nervous system which will ultimately lead to an improvement in our ability to perform endurance type movements.
Again if we were 30 years old your exercise dose would be 220-30=190 beat per minute.
Lowest intensity level is 60% of 190 = 144 beats per minute Highest intensity level is 85% of 190 = 162 beats per minute
Our exercise dose prescription would now be 144-162 beats per minute.
Next time we go for a walk or run or bicycle we need to get our heart up to 144 beats per minute and maintain it between 144 and 162 beats per minute usually for 15–35 minutes.
This method of monitoring intensity is great for fitness improvements, but has limitations in weight loss and active living programs.
MET or Metabolic Equivalent
A much more reliable method is using METS or metabolic equivalents. Everything we do in our lives requires oxygen.
If we are sitting whilst reading this post our heart pumps blood, our lungs breathe air in and out, our blood pumps around our body all to help us to send enough oxygen to the systems that need to be primed to help us sit and read. In other words we are incurring an oxygen cost just to sit and read.
We call this the VO2 or oxygen cost.
If we were to get up from our computer and mow the lawn our oxygen costs would increase. It would increase to help us now pay a higher oxygen toll to activate our muscles and produce more energy to mow the lawn.
Now mowing the lawn is much more strenuous than sitting and reading this book and so costs more energy.
While we are mowing the lawn our body produces heat and we feel hot and sweaty. This is a normal reaction to help us cool down. We know that the amount of heat we produced was directly proportional to the amount of energy required to mow the lawn.
It doesn’t matter if we are thin or obese everyone pays a similar oxygen cost of 3.5 millilitres of oxygen per kilogram of body weight per minute to keep our vital organs working at rest (1 MET).
We paid this cost when we were sitting and reading this book. However, when we got up and started to mow the lawn our muscles and other organs wanted us to pay a higher oxygen cost because we were now doing something that was much more intense.
The oxygen cost of 3.5 millilitres of oxygen per kilogram per minute is called 1 MET.
One MET is a metabolic equivalent for our body to be at rest and it’s the same for nearly everyone.
While we were mowing the lawn the intensity of the effort increased, so did our oxygen costs or MET value.
Mowing the lawn is equivalent of 4 METS. This means that we expended 4 times the amount of energy that we required when we were sitting down reading.
As mowing the lawn costs 4 METS we can say that the amount of oxygen required to finish mowing the lawn was 4 x 3.5 millilitre of oxygen per kilogram per minute or 14 millilitres of oxygen per kilogram per minute.
From this we can also calculate the Kcal expended by using the following formula :
4 METS X 3.5 ml of Oxygen X Body Weight divided by 200
If we weighed 70 kilograms then the formula would look like this: 4 METS X 3.5 X 70kg divided by 200 = 4.9 Kcal per minute
If mowing the lawn took we 30 minutes then we would have expended 147Kcal (4.9 X 30).
Everyone has a different level of aerobic endurance. Some people are very fit and can run, swim or bike intensely for ages, while others who are not so fit can only perform these activities at much lower intensity for less time.
The maximum amount of oxygen we can consume at our maximal exercise capacity is our VO2max.
Some people will have a VO2max of 10 METS while others will only be able to pay 5 METS. When we become aerobically fitter we increase our VO2max, which means we can produce more energy and can go faster for longer.
There are MET tables available that assist us in calculating intensity and duration of active living programs more accurately than using heart rate or other similar methods for monitoring intensity for weight loss. It’s a great method for monitoring workload.
Gary Taubes in his excellent book “Why We Get Fat” offers an interesting analysis of why women and men deposit fat in different areas.
Throughout our lifetime, fat is constantly being released from our fat cells to be used as a fuel. In the event that it is not used it then comes back to the fat cell where it is stored again to be used at another time. Once in the fat cell the fatty acid is combined with glycerol and two other fatty acids and forms a triglyceride.
When a meal is consumed that contains both carbohydrates and fats there is an initial release of insulin from the pancreas to control this increase in blood sugar.
As more carbohydrate is eaten there is concomitant increase in insulin release to control the flow of blood sugar.
The insulin opens the door of the cells for the blood glucose to be taken in and stored as glycogen. It is stored in the muscle and the liver as glycogen. If too much glucose is sent to the liver to be stored a glycogen it will be converted to fat and stored in the fat cells.
As the blood glucose levels start to decrease insulin levels also decrease and more fat is released from the fat cells for energy at rest.
In the intervening periods between meals more fat will be released and used as fuel.
The fat cell is used as a reservoir. The fat is stored as triglycerides in the fat cells and liver until there is a need to release them again usually in the absence of insulin.
Fat is the preferred source of fuel during rest.
Because of its size, it is difficult for the triglycerides to move through the cell membrane into the blood. It needs to be broken down into fatty acids to move through the membrane into the blood. The reverse occurs when it comes back to be stored, the fatty acids diffuse back into the fat cell and then bind to glycerol and fatty acids to form triglycerides.
The hormone that dominates this action is insulin. While it opens doors of cells to control blood sugar it also aids in the storage of fatty acids in the fat cell and regulates protein ensuring that there is enough for muscle rebuilding.
To regulate these processes insulin acts on the LPL and HSL enzymes.
Lipoprotein lipase (LPL) is an enzyme responsible for drawing fat out of the blood and into either fat cells or muscle cells. The LPL enzyme is found on both the fat and muscle cells.
On the muscle cell it forces fat to enter the cell to be used for fuel at a later stage. On the fat cell the LPL draws the fatty acids into the fat cell increasing its size.
The other enzyme that insulin affects is the HSL (hormone sensitive lipase). This enzyme breaks down the triglycerides in the fat cell so they can escape back into the blood stream. When insulin levels increase, the HSL is prevented from breaking up the triglycerides in the fat cell stopping it from entering the blood stream. This in turn traps the fat in the fat cell and increases its size.
The greater the activity of the HSL the more fat can escape the fat cell and be used for fuel and vice versa and the less stored in the fat cell.
The increased insulin levels also stimulate the movement of glucose into the fat cell building more triglycerides and further increasing the size of the fat cell. If the fat cells are unable to store any further triglycerides insulin assists in building new fat cells!! This ensures there is always room to store both fat and glucose.
In males the LPL activity is higher in the fat cells of the belly. As more fat is deposited into the blood, insulin directs more fat to be stored by the LPL drawing the fat from the blood into the abdominal fat.
As men get older and their testosterone levels begin to decrease LPL activity increases. This is one reason why men put more weight on around their stomach region.
Increased testosterone means less activity of the LPL enzyme, which stops it from drawing fat from the blood into the abdominal fat cells.
In women the reverse is true. Women carry more active LPL enzymes in the fat cells at the top of their hips and bottom and have low LPL activity in the fat cells of the abdominal region. This causes an increase in fat deposits on the hips and thighs in comparison to the abdominal region.
After menopause, the LPL activity of the fat cells of the abdominal region catches up with the men due to the lower levels of estrogen.
From this information it appears that the main regulator of fat metabolism is insulin. The more insulin we release the more LPL activity on the fat cell that forces the fat in the blood to be diverted into the fat cells. At the same time the increased insulin also suppresses the activity of HSL forcing more fat to remain in the fat cell.
In summary, it is very likely that insulin forces fat into the fat cell and decreases the amount that can be burned for fuel.
So if we are trying to lose fat weight we need to get fat out of the fat cell and burn it initially by lowering our insulin levels.
A simple way to achieve this is could be to reduce our carbohydrate intake and replace it with good fat and moderate amounts of protein.
I was on plane a few months ago when a large obese man sat next to me. We exchanged pleasantries and over the course of the flight had a great conversation on many different topics. I was in the middle aisle of the aircraft with seats on either side.
Initially I noticed that as this large man began looking for his seat how many people looked around and were obviously hoping that he would not sit near them. There was a certain disdain on their faces almost intimating that they didn’t want to be bothered by a fat man who obviously was this way because of his uncontrollable eating.
On my return journey I sat in a similar seat and was placed near another large man, only this time he was very well built with his physique indicating that he spent many hours in the gym to cultivate such a body. The people surrounding him looked in awe of his body with envied glances.
It is interesting that two very large men could receive such different responses from others on the flight. The fat man was looked on with ridicule while the muscular guy was looked on with undeniable envy.
People often think that obesity is caused almost entirely by overeating and lack of self control when it is becoming more obvious that obesity is a much more complex problem.
What was entirely thought as an imbalance between Kcal eaten and Kcals expended it is now seen as an endocrine system problem just as diabetes and metabolic syndrome.
An area of research that supports this notion is the impact that the hormone estrogen has on fat mass in post-menopausal women or those who have had a hysterectomy.
Women once past the menopause or who have reduced functioning of their ovaries often have difficulty in controlling body weight while their body shape starts changing as well.
By removing the ovaries of animals, researchers have found that they puts weight on. Conversely when they are given additional estrogen they lose weight.
This same process appears to happen in women.
Estrogen removal forces the fat cell to draw more fat from the blood, increasing its volume. More fat Kcals are now being stashed away in the fat cell for storage forcing the woman to now eat more. If this doesn’t occur the woman will expend less energy and become more sedentary.
What causes this to happen?
A very important enzyme (used to speed up reactions) called LPL has the job of pulling fat from the blood and taking it into any cell that releases LPL. Significantly, LPL is found on the muscle and the fat cell.
Low levels of estrogen causes the LPL to increase forcing more fat from the blood into the fat cell and weight is eventually increased.
Under certain conditions when there is less LPL on the fat cells they accumulated less fat.
When the increased fat is stored and not used we have an increased urge to eat in order to provide the energy necessary to provide fuel for the systems that control our body.
This becomes cyclic, as we can’t be satisfied even though more fat is being drawn from the blood and stored in the fat cell. We have to eat even more, which forces even more in the fat cell and we can become obese.
Remember this process was not a function of lack of will power or gluttony but more the under or over regulation of the endocrine or hormonal system.
So next time you are forced to sit next too or near an obese person have some consideration for what they are facing. Its not that they too weak to refuse that extra Kcal. It could be that they are victims of how their fat cells are being regulated that could lead to an eating disorder.
It is not surprising to find that the vast majority of diets that address Kcal restriction only result in minimal weight loss that will only last for a maximum of months before the weight reappears.
These diets attack the symptoms and not the root physiological cause.
It’s about controlling the hormones in the body that are responsible for storing fat.
“Too much sitting is not the same as too little exercise. It is still possible to meet the current exercise guidelines to be active and still sit for too long..”
An “active couch potato” is a person who sits for up to 9-10 hours of the waking day and yet still goes to the gym and performs moderate to vigorous exercise for at least one hour per day.
This is very controversial, as studies using very sensitive equipment have now supported the idea of sedentary behaviour in active people.
In a study reported by Genevieve Healy, subjects accumulated over 30 minutes of moderate to vigorous activity in the gym, while still spending 71% of their waking time in sedentary activities such as sitting.
This indicates that people can be very active yet be highly sedentary and still suffer from its consequences!!
Some landmark information now reveals that those fit people who exercise for over 150 minutes of vigorous exercise still spend over 60% of their free time in sedentary activities.
Based on the new information available we could be regarded as physically active and fulfilling the national general exercise recommendations while spending as little as 3% of our waking time performing moderate to vigorous exercise in an exercise environment.
The remaining time has been reported in sedentary activity (58%) and light intensity activity (39%).
The most important point to realise is that if we are vigilant in going to the gym for an hour every day that this still will not stop or solve the problems of a sedentary lifestyle!! It is not just about doing intense fitness activities for one hour per day, it is about changing our lifestyle to move throughout the day as much as possible at a low to moderate intensity.
If we performed 60-70% of our waking hours in low to moderate intensity activity areas such as domestic, occupational, transportation etc. and 20-30% in sedentary activity without any vigorous exercise activity we can still be regarded as active producing significant reductions in risk factors.
We have now become an “active non-exerciser”. While this profile is quite common its impact and benefits have received little attention.
In combination with the current formal exercise recommendations people who accumulate movement during their day within small time frames of multiple muscle contractions make significant impacts on energy expenditures.
Non Exercise Activity Thermogenesis (NEAT) or NEPA is used to describe the energy expenditure that accompanies physical activities other than voluntary movements in an exercise program and includes activities of daily living, fidgeting, spontaneous muscle contractions, maintaining posture, standing etc.
NEAT/NEPA could be any low-moderate intensity movements that are not structured into a formal exercise program.
To demonstrate the importance of NEAT, if we “walked and worked” for half of the working day and weighed 70Kg we would expand an additional 100 Kcal per hour, which could over a working day translate into 400 Kcal per day, a weekly energy deficit of 2,000 Kcal, a monthly deficit of 8,000 Kcal and weight loss over 12 months of over 13 kilograms!!
Without any other activity-based intervention it is possible to lose in excess of 12 kilograms of body weight per year with very little change in normal behaviour. If additional movement was employed during leisure time, home time and travelling to and from work greater significant changes to body weight could be made without additional financial cost and time.
The Australian Longitudinal Study on Women’s Health, which has been gathering information since 1996 reveal that:
Younger women who sat for more than 8 hours a day weighed 3.40kg more than those who sat less than 3 hours a day. Each additional hour of sitting was associated with 227grams weight gain.
Middle age women who sat for more than 8 hours per day weighed 5.92kgs more than those who sat for less than 3 hours a day. Each additional hour of sitting was associated with 747 grams weight gain.
Older women who sat for over 8 hours a day weighed 5.64kgs more than those who sat for less than 3 hours a day
What can we do!!
Our societies interaction with its current environment promotes labour saving sedentary behaviour and the convenience of eating in combination are powerful forces.
The first step in gaining improved health is to create opportunities to move in our already existing environment to the point where output can at least match energy intake.
Opportunities have to be created in our home, with transport variations, in our workplace and during our leisure time for additional movement to be performed at a comfortable variable intensity in multiple bouts that can be maintained at a moderate level of intensity.
We need to treat “moving as an opportunity rather than an inconvenience”.
We have to become more active at a low to moderate intensity for at least 9- 10 hours of a 16 hours waking day.
We need to create an environment for constant postural change from sitting to standing to walking to sitting.
Breaks in sitting time can have beneficial effects on our metabolic health
In another study by Healey (2008) those subjects who interrupted their sitting time by transitioning to standing or walking short distances were regarded as “breakers” demonstrated a reversal of many of the side effects of sedentary behaviour.
The other subjects who remained in a sitting position were regarded a “prolongers” continued to show detrimental effects of sedentary behaviour.
Become a breaker, not a prolonger!
These results were independent of performing moderate to vigorous exercise.
Remember that standing and walking for one minute in 30 minutes can result in an additional 3 Kcal of energy expended. Taken over a full 5 days week or 8 hours per day, if we stood and walked for one minute every hour we would effectively expend an additional 120 Kcal per week compared to our work colleagues who sit for the same period.
If we chose to stand and move at a self-selected pace for two minutes per hour per day per week it would result in 296 Kcal expended per week.
A significant 660 Kcal would be expended if we stood and moved for 5 minutes per hour per day per week.
Based on this information if we stand and walk at work/home for 5 minutes per hour for 8 hours, 5 days per week for at least 50 weeks we could expend an additional 33,000 Kcal or 5 kilograms keeping all other aspects of life constant and so on………
In your weight loss journey would you choose to be an “Active Couch Potato” or an “Active Non Exerciser”?
All successful weight loss journeys need a physical activity component not just for the weight change but also for its significant health benefits.
To understand why there has been such a significant increase in obesity over the last 35 years Dr Carl Lavie in his excellent book the “Obesity Paradox” searches through government records to unearth same amazing findings.
Since 1865 males have grown about 1.5 BMI points heavier, which translates into an increase of 5 kilograms in weight for a man of average modern height today. In comparison, between 1980–2000 the average male BMI increased by 2.3 BMI points, which translates into an additional 8 kilograms. In other words in the 20 years between 1980-2000 the BMI of men rose 7 times faster than the previous 115 years.
Does this mean that there has also been a dramatic increase in the number of Kcal to match this increase in BMI?
From the US Department of Agriculture records it appears that between 1970- 2003 there has been an increase in calorie consumption by a massive 523 calories per day (1970: 2,234 Kcal to 2003: 2,757 Kcal).
If we were to investigate the break up of these Kcal we find that 292 came from fats, oils, sugars and sweeteners while more grains (refined) made up the additional 188 Kcal).
Between 1977 and 1995 the eating of fast foods increased by 300%. By 1997 obesity rates began to soar from 13% in 1962 to 19% in 1997.
By 2008 obesity rates increased to 38% nationwide. At this time the WHO reported that worldwide there were 1.5 billion people 20 years and older that were overweight, and of those more than 200 million men and 300 million women were obese.
In 2010 the medical costs associated with obesity in the United States rose to
$160 billion per year. The average cost per male as a result of obesity was
$2,646 per year and for a female was $4,879 per year. If we continue at the same rate by 2030 almost 50% of United States citizens will be obese while an alarming 86% will be overweight.
Since 1945 there has been an abundance of easy to get food and a surge in labour saving devices that have robbed us of the much-needed movement of our grandparents era.
The question is “what is the most powerful factor in obesity epidemic…. Too much food or too little movement.”
Eminent epidemiologists suggest that both these factors have contributed to this epidemic. However, they also suggest that while we know and understand that we are increasingly eating high-energy dense empty caloric foods as equally important is the decrease in our energy expenditure or physical inactivity.
Dr Tim Church, Dr Steven Blair and Dr Ed Archer have reported dramatic decreases in energy expenditure over the past 50 years in occupational activities and household duties. So dramatic have these decreases been that they could almost explain the increase in obesity levels even without considering the increase in caloric intake.
This is heady stuff!!
We know that what we eat is critical to weight loss and that high intensity energy exercise does not always produce the weight loss that we might want.
So does physical activity have a significant role in weight loss?
Physical activity can have a dramatic effect on the prevention of cardiovascular disease, diabetes, metabolic syndrome and cancer etc. even in the absence of weight loss.
Given that if we increase our daily physical activity levels at low to moderate levels of intensity over time we can also see long term dramatic increases in the amount of Kcal we expend.
Sadly many people want rapid weight loss, which we know is very hard to sustain and maintain.
We need to recognise that being more physically active throughout the day in all our daily endeavours is a major component in any long-term weight loss program.
I firmly believe that low to moderate physical activities of daily living (NEPA) is the cornerstone for all long-term weight loss and health improvements. It just needs to be built back into our lifestyle.
Our bodies require frequent and unexpected physical activity to sustain life.
In the event that weight loss does not occur for whatever reason it is also important to recognise the importance of improvements in physical fitness can have on our overall health profile.
Some suggest that the loss of physical fitness can be a much stronger predictor of mortality than weight loss.
In a 2011 study citing information from the famous Aerobics Centre Longitudinal study (commenced in 1970) and using data from its 100,000 participants, researchers reported that a small improvement in physical fitness over a 6 years period (no weight loss) was associated with a 15% reduction in the chance of dying from cardiovascular complications.
We need took at our own lifestyle and select times during the day where we are sitting or inactive and see if we can substitute it with some form of additional physical activity.
We can’t underestimate the importance of lifestyle physical activity in the weight loss journey.
As a child I was always impressed with strongman performances. I would miss school and go to carnivals and be captivated by the amazing feats of strength of the strongmen in sideshow alley. These men were often half naked, dressed in loincloths and treated as oddities by those who went to see them. They performed an array of rare and crazy strength activities.
Many of the famous strongmen of the 19th century initially came from hard working backgrounds.
Strongmen like Louis Uni known by his stage name “Apollon” reportedly lifted 175 kg then held it in one hand above his head while balancing on one leg and then threw it up in the air and caught it with his elbows!
Another noted strongman of the same era was Thomas Topham who stood
1.76 meters and weighed less than 90 kg. He was well known for lifting large weights greater than 175 kg above his head, bending and unbending steel rods 75 mm in diameter and broke ropes of 1,000 kg capacity. Pretty impressive stuff or so it seems.
So who was the strongest……. our ancestors or us?
To answer this question we need to go back and look at the strength of our Neanderthal cousins.
Peter McAllister, in his brilliant book “ Manthropology” decided to measure the strength between our Neanderthal counsin and the 2004 world arm wrestling champion Alexei Voevoda.
In the red corner he selected a 153cm/80 kg Neanderthal female as the challenger with surprising results.
McAllister reported that the Neanderthal female would have had bigger biceps than the average modern man, her cross sectional area of her biceps being 16% larger than modern man and she possessed a shorter forearm, which altogether translated into a lower mechanical disadvantage, important for arm wrestling.
The last advantage that our Neanderthal female cousin possessed was a biceps attachment that wound around her forearm giving her increased strength in rotating the wrist. This advantage was added too by an increased muscle mass of other forearm muscles and increased forearm bone strength.
With these mechanical advantages our Neanderthal female was almost unbeatable in two arm wrestling techniques, the hook and the top roll. This was not taking into account the potential differences in muscle fibre types where our ancient cousin had muscle fibres that were bigger and much stronger
Alexei never stood a chance and would have been soundly beaten! Sadly the Neanderthals became extinct possibly due to climate change.
The new question is now “why are we now being outperformed by our evolutionary ancestors?”
The answer lies in the increased muscle mass of our ancestors relative to their limb length, which translates into an overall increased strength four times greater than us!
The muscle mass that we have lost could have been due to freeing up some space for an increase in our brain size. Apparently the increase in our brain size bought with it a need to feed the greedy brain at the expense of other muscle development.
In theory our more recent ancestors traded the muscle mass and strength for greater fine motor control that allowed us to make tools and throw objects, necessary for hunting and gathering.
In the past 20 years there has been an explosion of fossil evidence that has allowed anthropologists to compare us to our ancestors. This evidence suggests that over the past million years or so we have lost approximately 40% of our bone mass and muscle strength, most of it in the past 1,000 years.
This would indicate that over this time there has been a steady decline in the loads placed on our muscles and bones mainly due to moving and lifting less resulting in us no longer being as strong and powerful as our ancestors!!.
What can we do to claw back some of this strength that we have lost?
For a start we could go the to the gym more often and lift some weights on a regular basis. But as only a small proportion of people attend the gym we could start by doing more manual things around the home, on our way to work, at work or during our leisure time.
I think the main thing is to find time to stand more, walk more, squat more, lunge more, step up more, push more, pull more and lift more.
If we were to increase these movements, who knows, maybe we could bring back sideshow alley and get a job demonstrating some of those great feats of strength!
We know that obesity is associated with chronic mild inflammation throughout the body caused by the hypertrophy of the adipocyte (fat cell) resulting in an increase in oxidative stress.
The increased oxidative stress causes harmful effects to all cells of the body and can eventually lead to chronic disease and or death. We know that oxidative stress is produced by free radicals and can lead to diseases such as cancer, ageing and ultimately death.
Oxidative stress occurs as cells use oxygen to produce energy for normal functioning. As cells age they become less effective in clearing these free radicals, leading to cell damage.
Some recent findings indicate that some marathon runners are now presenting with an increased risk for coronary artery disease. One theory for this surprising fact is the high carbohydrate consumption of these athletes, which could induce oxidative stress creating an inflamed response within tissues leading to blood vessel damage.
In animal models the restriction of calories by 30-60% results in a slow functional decline of ageing. Caloric restriction appears to prevent many age related disorders such as the decline in the immune system to fight infection.
The caloric restriction (CR) is usually in the form of reduced carbohydrates.
In WW 2 food shortages in some European countries was commonplace, and were associated with a sharp decline in CHD mortality, a reduction that lasted until the end of the war and the food shortagesended.
We know that Okinawans consume 30% fewer calories than the average Japanese and have a 30% lower incidence of CHD and cancer mortality. They are amongst the healthiest people the world.
A review of over 30 studies has concluded that weight loss is an integral component in reducing the inflammation within the cells of the body by reducing oxidative stress. The most effective way to reduce oxidative stress is through dietary and low to moderate intensity physical activity interventions.
The studies reviewed also reported that caloric restriction in the form of carbohydrate reduction lowers oxidative stress and has the potential to reduce the occurrence of metabolic syndrome even in the absence of any weight loss. Caloric restriction (CR) is often reported as a decrease of 20-40% of our daily caloric consumption.
The addition of antioxidant foods might also result in a reduction of free radicals and oxidative stress, which further reduces inflammation throughout the body contributing to a healthier profile.
CR can reportedly reduce the risk of disease such as autoimmune disease, atherosclerosis cardiomyopathies, diabetes, renal disease, cancer, respiratory diseases and neurodegenerative diseases.
CR can also lead to major changes in the endocrine system and the metabolic adaptations.
Metabolic syndrome is a disorder of energy utilisation and storage, diagnosed by a combination of three out of five of the following medical conditions: abdominal (central) obesity, elevated blood pressure, elevated fasting plasma glucose, high serum triglycerides, and low high-density cholesterol (HDL) levels.
Metabolic syndrome increases the risk of developing cardiovascular disease particularly heart failure and diabetes. Some studies have reported the prevalence of diabetes of up to 35% of the adult population.
Carbohydrate restriction (CR) has been used successfully for weight loss, but in addition can improve glycaemia control, reduce insulin levels, reduce blood triglycerides and increase HDL levels all of which help to control metabolic syndrome.
There are some people who have great difficulty in losing weight and who generally give up without some success. If initially they were encouraged to take the focus off weight loss and concentrate on becoming healthier and fitter by reducing their consumption of carbohydrates they could potentially reduce their risk profile significantly.
Carbohydrate restriction is obese people can have many other advantages without weight loss such as a decrease in blood pressure and an increase in insulin sensitivity in the body tissues.
Clients with a high BMI and high blood triglyceride levels also appear to benefit from a reduction in carbohydrates. Alternatively a diet high in carbohydrates can potentially raise glucose levels, insulin release and triglycerides and lowers HDL (the good cholesterol).
Carbohydrate restriction has the potential to improve lipid profiles and to decrease the risk of cardiovascular disease and diabetes in obese people.
These improvements could be amplified if accompanied by an increase in low to moderate intensity physical activity.
The results obtained by calories restriction mainly through the restriction of carbohydrates could be the first line of treatment against the onset of metabolic syndrome symptoms.
The main reason reported for these favourable changes with carbohydrate restriction are the low insulin levels creating an increase in the use of lipids rather than storage. It also reduces energy expenditure with the consequence of a reduction in the production of free radical or oxidative stress.
So, next time you are at a restaurant think twice about the entrée before the main meal and the desert after….you might have just had enough.
During the Christmas period we always have the choice to either over indulge or control our holiday urges.
Typically the first sign of overindulgence we notice is an increase in our belly fat!
In the New Year we will look in the mirror and see these handles appearing on the sides of our trunk or we will have to let out the belt that extra notch.
We know that the fat on our body is divided into storage fat and essential fat.
Essential fat is needed for normal healthy functioning and is found in small amounts in your bone marrow, organs, and nervous system and in muscle.
Male essential fat comprises approximately 3% of a male’s body weight, while in females it is about 12% of body weight and is further stored in the breasts, pelvis, hips and thighs.
Storage fat is something entirely different. This is accumulated under our skin, in our muscles and at other sites within our body. Storage fat also surrounds our internal organs affording some protection.
When storage fat surrounds our liver, kidneys, heart and intestines there is usually an increased health risk. We call this an increase in abdominal adiposity.
These abdominal adipocytes can cause an increase in the release of fatty acids, inflammatory compounds and other hormones that can lead to adverse changes in blood fats, glucose and blood pressure.
The increased toxicity of abdominal fat (visceral fat) causes a general increase in oxidative stress, which in turn causes an increase in inflammation of all tissues in the body.
The increased oxidative stress is responsible for an increase in blood pressure, increased blood sugar levels and increased in risk profile for all forms of metabolic disease.
The visceral fat cells release a significant amount of their metabolic products into the blood via the arteries that supply the liver after having passed through the spleen and gastrointestinal tract.
The increased free fatty acids and triglycerides that are now in the blood make their way to the liver. The liver, pancreas, muscles and heart do not have the ability to store the increased free fatty acids that are now in the circulation
As a consequence the free fatty acids begin to pile up in these organs causing an increase in blood sugar levels, increased release of insulin, increased blood cholesterol and a general increase in inflammation throughout the body.
The visceral adipocytes responsible for this cascade also become inflamed causing a disruption tin the functioning of its endoplasmic reticulum and mitochondria within the cell.
The most significant problem caused by this reaction is insulin resistance within body tissues. This is one of the reasons why an increase in abdominal adiposity can be so damaging as it further contributes to Type 2 diabetes and cardiovascular disease.
The essential fat that surrounds a female’s thigh and hips can have an opposite effect to abdominal fat deposition.
The adipocytes found around these regions can control their cells content preventing them from spilling over into the circulatory system and eventually to the other organs.
The control of the cell’s content effectively protects the liver and other organs
This is why it is sometimes very difficult to move fat from these areas in weight loss programs.
Strangely enough there are some researchers who are now reporting how this lower extremity body fat is important in potentially reducing cardiovascular risk.
A corollary to this is the suggestion that liposuction typically used on these areas could in the long term increase a persons’ risk of heart disease.
A study conducted in 2005 that examined over 3,000 subjects all in their seventies, found that those with fatter thighs had a reduced risk of cardiovascular risk factors when compared to those with thinner thighs.
This has got to good news for those of us who not matter what just cannot trim those thighs down!
30: Could it be your brain that’s stopping you from exercising?
One of the most interesting areas of sedentary behaviour research is brain activity and movement. Dr Catherine Kotz has been investigating the activity of a neurochemical called Orexin and its effect on sedentary behaviour.
Orexin causes us to wake up. It could be a key element in getting people to move more. In some animal studies it has been found that without Orexin they are always falling asleep.
In one of her landmark studies Dr Kotz injected Orexin in half of her rodents while the other half received just a water injection. The results showed that those rats injected with Orexin moved considerably more than those injected with the water. This confirmed Dr Kotz theory that there are specific neurochemicals that can control our activity patterns.
To investigate this further Dr Colleen Novak studied the brain networks and chemicals that are responsible for sitting in a chair or moving about.
Dr Novak’s study involved mating multi generational obese rates with obese rates and lean rats with lean rats.
Dr Novak discovered that the obese rats did not have the ability to initiate movement.
Irrespective of the types and amount of neurochemicals, these animals did not have the wiring in the brain to respond to the injected chemicals and so remained sedentary.
Alternatively when the brain of the lean rats was injected their movement was almost uncontrollable. The lean rats were bred to move while the obese rats were bred to sit.
The question was “What makes the lean rats active and the obese rats sedentary?
To answer this question Dr Novak compared rats that had been bred for marathon running and rats that had been bred for sedentary sitting.
She discovered that the muscles of marathon running rats were different to the muscles of the sedentary rats. There was a direct relationship between the muscles of the marathon rats and the signalling to the brain to keep moving.
The sedentary sitters did not respond the same way. Their muscles were trained to be sedentary and as such the signal to move was stopped.
Obese clients tend to be less sensitive and unresponsive to moving signals from either the muscles or the brain. Their muscles are trained to sit as the marathon rats were trained to run
Whereas clients who are movers are sensitive to moving neurochemicals and have a strong feedback loop from the muscles to the brain which encourages movement.
It could be that the movers’ brains are hard wired to move.
While we are the product of our DNA, the environment that we exist in still influences us. DNA provides the structure of our being but if the structure is either enhanced or destroyed then there are consequences.
More recently we have been told to keep our brain active throughout our lifetime to maintain its optimal function. The term used for the changes in the brain is neuroplasticity, which allows the brain to change with its environment.
As with other organs of the body if we do not stimulate our brain it will eventually turn off and become as dormant as the lifestyle it leads.
If we choose to sit all day and watch television then our brain will adapt to the specific type of environment.
Those people leading sedentary lives have a brain that will form a sedentary structure due to its interaction with their environment. A sedentary brain will ultimately lead to a sedentary lifestyle and vice versa.
Just as a muscle adapts to movement so will the brain.
Obese clients are faced with a double-edged sword. They have a brain that is not responsive to the neurochemicals for movement and have muscles that are trained to sit and that do not send feedback signals back to the brain to get them moving.
As the need to move is taken from us, our brains will form to create a more sedentary lifestyle.
As a Collaroy to this, as the sitters become the majority, the environment further evolves to meet their sedentary lifestyle requirements by introducing more labour saving devices, more cars and less walking, more office sitting rather than standing, more screen based entertainment during leisure time etc.