Follow our series of articles from Dr Paul Batman Phd on all things fitness. Use these articles as part of your blogs with your own clients to engage them in your site and content. 

Article 6: Let your brain do the walking..

As our population ages and people live longer there is always the fear that age related dementia or Alzheimer’s disease could rob us of quality of life in our remaining years.

I look at my old mum who at 92 years old was as sharp as a tack. I marvelled at her ability to recall events with clarity that happened in her childhood some 80 years ago. She was one of the lucky ones to have escaped the ravages of dementia but sadly time took its toll on her once robust body.

With the increased awareness of dementia and Alzheimer’s disease we often think that it is a disease that can only affect us in the latter stages of our life. We are told that it is important to keep our brain active by reading more, doing more Sudoku puzzles, cross words or even mental gymnastics with luminosity.

But now things are changing….

For what seems like forever we have known that adopting a physically active lifestyle could potentially help us live longer and/or improve the quality of our life.

For years in exercise programs we have directed our dose of exercise to making the cardiovascular system healthier to combat heart disease.

The heart has been a focal point in many cardio exercise programs

New information is emerging that suggests that the heart is instrumental in brain function to an extent that we have never realised.

Could it be that the heart and its systems are responsible for the destruction of our memory, intellect and personality?

Professor Jonathan Stone reports that there are five possible contributors to age related dementia that have not been previously identified. These include the heart, brain, aorta, small vessels supplying the brain and the last is….. time.

Heart and brain

The heart is a very trainable organ that responds extensively to physical activity. Physical activity also forms a significant part of the cardiac rehabilitation process in those that have suffered and recovered from a heart attack.

The heart is an impressive organ. It beats 60 to 70 times per minute with an approximate volume of 50-60 millilitres of blood per beat. In the space of 60 seconds it pumps about 5-6 litres to transport blood containing oxygen around the body while at the same time transports carbon dioxide to the lungs for removal.

In a rested state the heart will pump 35 million beats per year, which could end being 2-3 billion beats in our lifetime.

During intense exercise the heart can pump 150-200 beats per minute with a volume of blood up to 200 millilitres per beat. This translates approximately into a cardiac output of 30-40 litres of blood per minute.

Truly an impressive pump given that we only have a blood volume of between 5-7 litres.

For the brain to function optimally the heart must pump oxygen and nutrients to the smallest blood vessels that surround and feed it.

Because of its critical function the heart is now being regarded as a potentially significant player in age related Dementia and Alzheimer’s disease.

As the heart begins to age its ability to transport the nutrients and oxygen starts to decline by reducing the blood flow through the many small vessels to the brain.

The major artery that exits the heart is the Aorta. This vessel is very elastic, which helps it to contract and relax to pump the blood in a continuous fashion. It directs blood to the head and upper limbs.

With ageing the Aorta becomes brittle and hardened preventing it from stretching and pumping the blood through the exit vessels to the brain. In the young heart the aorta stretches up to 15% of its diameter to soften the pulse to the brain ensuring a continuous flow of the blood is uninterrupted.

By losing its flexibility there is a build up of pressure in the arteries as the heart contracts.

The increased pressure caused by the inflexibility of the body’s largest artery increases the pressure in the small vessels that supply blood and nutrients to the brain. The increased pressure begins to damage the brain’s small vessels by tearing the inside layer forming clots and small aneurysms.

Regrettably this can lead to bleeding into the brain. This initially starts with small vessels and over time leads to the involvement of many larger blood vessels, which can eventually lead to intermittent stoppages of blood flow. Initially this might occur as a loss of consciousness or memory. Eventually as the number of episodes increase over time it can finally lead to dementia.

The initial silent bleeding in the brain can start at a very young age.

It is not inconceivable for our children to have already been affected by the insidious continual damage caused by the small bleeds in the brain that occurs over time.

The new risk factors of dementia are now those that are associated with stroke and cardiovascular disease.

How can we prevent it or at least delay it?

Physical activity and weight loss have been documented as two of the most successful interventions for improving cardiovascular health. An active lifestyle and an improvement in physical fitness could improve our chances of delaying the onset of dementia and Alzheimer’s disease.

We also need to recognise the importance of encouraging physical activity in our children at an early age to improve their neuro-protection i.e. protect their brain from potentially age related dementia that can occur later in their life.

So while we think that age related dementia and Alzheimer’s disease is an old person’s disease there is now a growing awareness that it might have its roots in childhood and in a sedentary lifestyle.

Another reason to keep on moving..

Article 7: Overweight and anxiety, what can we do?

Some overweight and or obese people can develop a poor self-image, leading to an increase in anxiety levels particularly when confronted with social or formal occasions.

These people can have a heightened anxiety level when meeting new people for fear of being judged because of their obesity. These increased anxiety levels can take a serious toll on their quality of life.

Anxiety

 

Anxiety can lead to depression, hypersensitivity, tension and generally thinking the worst of situations. Medical practitioners will often prescribe medications to help reduce their anxiety.

A study conducted in 2004 reported that being physically active produces physical responses within the body that reduces stress and anxiety levels irrespective of its intensity.

Generally in weight loss programs physical activity is used as an intervention to expend more Kcal and increase energy expenditure and ultimately to lose weight.

However, there are many more positive benefits that physical activity can cause that far out weight the increased energy expenditure. In fact, most weight loss occurs through the combinations of food being eaten rather than the exercise that accompanies it.

Physical activity has always been recommended as an effective treatment for depression and anxiety but how it reacts within our body has received little attention.

How does physical activity make us less anxious?

For a start physical activity reduces the resting tension in the muscles that interrupt the anxiety feedback loop to the brain.

As we begin to move, our body begins to break down free fatty acids for fuel and releases them into the bloodstream. The free fatty acids compete with tryptophan (one of the eight essential amino acids) increasing the free fatty acids in the blood stream. This forces the tryptophan to push through the blood-brain barrier where it begins to build more serotonin. The increased serotonin level calms us down and makes us feel more secure.

Another neurotransmitter in the brain that affects anxiety is GABA. When GABA is released through physical activity it inhibits anxiety as it interrupts the obsessive feedback loop within the brain allowing us to calm down. Anti anxiety prescriptions often target an increase in the release of GABA.

When we undertake physical activity the heart starts to pump harder and faster to supply more blood to the muscles responsible for the movement. The

heart muscle cells can also produce a peptide molecule that slows down the hyper aroused state.

So the bottom line is that aerobic exercise can play a major role in reducing stress in our body. It is not just about exercising intensely to lose weight or to produce a cathartic effect.

A study of high school students reported that those who were involved in physical activity on most days of the week reduced their anxiety levels more significantly than those who were sedentary.

Increased physical activity levels in the home, garden, active transport, active leisure time can make a major contribution to reducing our stress levels and our anxiety levels, clearly establishing a connection between how much we move and how anxious we feel.

So if you feel anxious get out there and stand more, walk your minimum 10,000 steps per day or increase your free-living daily experiences and feel the difference…

Article 8: Let me introduce you to the fat cell

There is a great deal of information written and communicated about obesity and its effects on our health. What is not so clear is information on the site where this complex disease initiates some of its problems.

What is an adipocyte?

 

The adipocyte or fat cell is the main type of cell in adipose tissue and is recognised as a critical player in obesity related cardiovascular disease.

An adipocyte is more than just storage for fat or adipose tissue, it is an intelligent cell that constantly monitors and changes the other molecules that are part of its structure.

The adipocyte is a tiny cell that is packed with triglycerides (stored fat) and occupies most of the cell. The cytoplasm, nucleus, mitochondria, endoplasmic reticulum and Golgi apparatus are pushed towards the edges of the cell.

All the adipocyte cell components are bounded by a cell membrane (covering) that permits the movement of molecules into and out of the cell, surveys the environment for danger, protects itself and has builder and scavenger molecules to maintain its order.

There are over 30 billion adipocytes in our body, which we carry as approximately 15kg of weight. It was originally designed as a small package of stored energy.

To give some idea of the size of an adipocyte, it weights about 0.5 of a micron compared to a teaspoon that can hold 6 million microns!!

Amazingly one gram of fat releases 9 Kcal of energy. This translates into approximately 135,000 Kcal of stored energy in our adipocytes, which would allow us to go without food for about 45-60 days.

As more food is taken in and not expended as energy the adipocyte increases in size (hypertrophy) and number (hyperplasia) to store more triglycerides.

As the energy imbalance increases it is accompanied by abnormalities in the adipocycte, particularly in two of its factories, the endoplasmic reticulum (ER) and mitochondria.

Where is the fat stored?

The ER is responsible for storing the fat, building proteins and sensing and regulating cholesterol. The proteins that are built in the ER must be folded correctly and then packaged in the Golgi Apparatus (GA) where they are stored for future use.

Normally as the amount of food we eat is increased, the endoplasmic reticulum (ER) in turn increases its ability to build proteins for the cell and surrounding structures and everything remains in balance.

What happens when we overeat?

However, an oversupply of food causes the adipocyte to increase in size and the Endoplasmic Reticulum (ER) becomes overwhelmed and begins to produce damaged proteins making them unable to fulfil their cell building and repairing role.

At the same time the ER’s ability to store fat and its cholesterol sensing ability is also adversely affected. The damaged proteins and excess nutrients build up in the cytosol (inside of cell) interfering with other functions of the cell.

To overcome this situation the adipocyte slows down the building of proteins and increases the clearance of the damaged proteins. If the ER and the cell cannot restore order the damage proteins die causing the ER additional stress.

At this point the ER releases free fatty acids and inflammatory molecules into the system to cope with their problem.

Once this occurs the result is an increase in fat and glucose concentrations throughout other cells in body as well as serious cellular insulin resistance, which can lead to hyperglycaemia (high blood sugar) and long-term diabetes. The insulin resistance extends to both liver and muscle cells.

What happens to the mitochondria?

In addition to the stress of the ER, hypertrophy of the adipocyte also creates oxidative stress in the mitochondria. Oxygen attempts to burn the fat in the mitochondria. The Mitochondria is the part of the fat cell that produces the energy and is regarded as the powerhouse of the cell.

When the excessive amounts of fat cannot be burned by oxygen in the mitochondria it causes a release of the immune cells that produce an inflammatory response. The inflammatory response causes the over production of free radicals and oxidative stress in the cell.

As the increase in free fatty acids build up the mitochondria has difficulty in processing the excess.

As the mitochondria become overworked and unable to process the excess fatty acids it produces an increase in reaction oxygen species (ROS) or free radicals that will ultimately impair mitochondrial function, which in turn creates more free radicals.

With obesity comes a depletion of antioxidant resources needed to neutralise the over production of free radicals. The production and release of key anti oxidant enzymes is severely depleted in obese people.

The increased oxidative stress causes damage to the adipocyte membrane, covers the membrane with a plastic coating and hinders the action of the mitochondria.

The uncontrolled oxidative stress changes the lining of the blood vessels and is the major contributor of cardiovascular disease and metabolic syndrome.

Next time you are offered that upsized meal remember where is might finally end up and the problems that overeating can lead too.

Article 9: I have never met a “Free Radical” that I REALLY liked!!

You are probably sitting at work completing your day’s tasks totally unaware of the complex metabolic interactions that are taking place in your cells, just to give you the energy to complete your dailyresponsibilities.

We all know that oxygen is critical to our existence… but did you know that in excess oxygen could be very toxic and actually harm you?

As part of maintaining equilibrium in the metabolic activity of your cells, oxygen is transported to the mitochondria of the cell where it is used to burn either carbohydrates and fats for fuel for the remake of ATP.

The mitochondria act like furnaces and are the site where oxygen burns fuel for energy.

At rest, while oxygen burns the fuel, it produces by products called free radicals or reaction oxygen species (ROS). These are unpaired electrons that have the potential to cause serious damage to the membranes of all cells.

The cell membrane

During normal breathing the free radicals or ROS react with the fat (bi-lipid) composition of the cells membrane or boundaries causing a reaction called lipid peroxidation. The cell membrane is the boundary of the cell that regulates the movement of molecules into and out of the cell and prevents any leakage. It consists of protein and lipids (fat) that maintain it structure and function critical for healthy living.

At rest, the number of rebel oxygen molecules and the production of free radicals is neutralised by a group of enzymes that maintain equilibrium and stop the free radicals from causing any damage to the cell membrane, creating a nice balance between the good and bad. The good guys that are responsible for this balance are the anti oxidant defence system, the cell’s enzymes and numerous antioxidants such as vitamin A, E, C glutathione, ubiquinone, and flavonoids.

If uncontrolled lipid peroxidation occurs from the inability of the cell’s defence system to neutralize the excess production of free radicals, the membrane of the cell will be seriously compromised. If it continues over a long period of time irreversible damage can occur to the cell membrane.

Sometime during the day we are going to head down to the gym ready and excited about our upcoming exercise bout, the muscle contractions that we are about to recruit will cause an increase in the amount of oxygen sent to the mitochondria to produce energy, allowing us to complete our training session. If the exercise is within our capabilities the free radical production from the mitochondria will be neutralized by the immune and antioxidant defence system.

However, if we participate in an exercise bout where the intensity is beyond our normal capacity, there is the potential for the additional oxygen consumed to produce an excess of free radicals, which cannot be neutralized and damage to our cell’s membrane could result.

We called this oxidative stress. Oxidative stress has been mentioned in studies as a possible contributor to cancer, heart disease and metabolic disorders.

In low to moderate levels of exercise intensity the production of free radicals and ROS are adequately neutralized by the body’s defence system.

If we exercise at intensities in excess of 10 to 15 times our resting level, the production of free radicals is difficult to control, potentially leading to oxidative stress and damage to our cells.

Oxidative stress highlights some of the potential dangers in prescribing exercise when the intensity is far too great for our current level of fitness.

It brings into question the “duty of care” we have for obese people who are subjected to levels of intensity that can far outweigh their capabilities. Obese clients are already in an inflamed state and heightened oxidative stress.

This is of particular concern with some of the newer exercise regimes that promote high intensity exercise as a means of weight loss and health gains without any exercise progression.

This is a great example of “giving with one hand and taking away with the other”.

Alternatively, if we are prescribed exercise where each training session builds upon the benefits of the previous session, we can build a tolerance to oxidative stress. We will receive an overcompensation effect by progressively increasing our tolerance to intense exercise.

It is difficult to change some people’s perception of how hard they should be trained. They have been influenced into thinking that the only benefits from exercise can occur if they are trained very hard or pushed in the session to train hard. Some trainers forget the specificity principle, which states that the responses from exercise occur according to the duration, frequency and intensity of the session.

The take home message is to progressively expose ourselves to moderate to high intensity exercise over a period of time so that we can enjoy all its significant benefits and reduce the potential for oxidative stress.

If we choose high intensity exercise from the very start before building a tolerance to it, we are potentially putting ourselves in harms way and at risk of cell damage throughout all the systems of our body.

Article 10: I have never met an enzyme I didn’t like!

When I was a school kid, I would sit in science classes and look out the window and concentrate on anything but the topic being taught. It was all too hard, too boring and too useless….. until now!!.

Then I discovered enzymes… It’s All About Speed

Enzymes are like the sprinters of the cell!!

Enzymes are proteins that control the speed of chemical reactions in our body. They make the small components of the cell work faster and are critical to our health and wellbeing.

Enzymes cut and paste products such as nutrients. They speed up all vitally important processes in our body. The enzymes in our stomach, for example, ensure that food is cut into tiny particles that can be converted into energy in our body.

Wherever one substance needs to be transformed into another, nature uses enzymes to speed up the process.

Some enzymes break down large molecules into smaller ones. Others, like the enzymes that make DNA, use small molecules to build up large complex ones. Enzymes also help cells to communicate with each other, keeping cell growth and life and death under control.

My Favourite Enzyme

One important enzyme that is a key to our good health is called Lipoprotein Lipase or LPL. This is a special enzyme that attaches to the inner surface in the walls of our blood vessels and is responsible for changing and clearing fat molecules from the blood and sending them to the fat cells and the muscle.

LPL clears the blood of unhealthy fatty deposits and improves blood flow and keeps the inner lining of your blood vessel’s healthy. Once it converts and clears the LDL there is greater concentration of High Density Lipoproteins (HDL), which is the good cholesterol that contributes to good health.

HDL is a friendly scavenger who cruises the bloodstream removing any harmful or bad cholesterol. High HDL levels reduce the risk for heart disease. On the other hand if HDL levels are low there is an increased risk of heart disease.

LPL is most widely distributed in our fat cells, heart, and skeletal muscle tissue, as well as in lactating mammary glands (breast).

What slows the LPL enzyme down?

Inactivity can have a major effect on lipoprotein lipase (LPL) activity. The less we move, the lower the levels of this important enzyme.

Muscular inactivity reduces LPL activity resulting in more fatty deposits in our blood and a reduction in HDL activity contributing to an increased risk for diabetes and heart disease.

The consequence of low levels of LPL also includes: blunted fat uptake, an increase in hypertension, increased diabetes and metabolic problems in ageing and coronary heart disease.

So it is a pretty important enzyme!

In studies using rats there was a reduction in LPL activity when they were stopped from performing physical activity. In the same studies when the rats were allowed to move again the decline in LPL activity reversed back to normal levels within several hours. In these studies the reduction in LPL levels in the muscle fibres occurred within the first 18-24 hours of inactivity.

Its pretty scary but the decrease in LPL activity begins to appear within 4 hours of inactivity!! This means that within only a few hours of not moving or being sedentary fatty deposits are starting to build up in our blood vessels.

The decrease in LPL activity during inactivity is more pronounced in local weight bearing skeletal muscles such as the legs but was not evident in continuously contracting muscles such as the diaphragm (below the lungs) and heart muscle. In other words the more we move the less the chance of reducing the activity of LPL.

The reduction in LPL activity has also been seen in subjects during bed rest studies where increases in fatty deposits and decreases in HDL were also observed within short periods of time.

Most studies have focussed on slow twitch muscle fibres, specifically the muscles of the leg recruited for postural support. LPL is found in significant quantities in slow twitch muscle fibres compared to faster muscle fibres.

Can high intensity exercise fix it?

It appears that high intensity training produces very little change in LPL activity in the slow twitch fibres but does have some effect on LPL activity of the faster fibres that are not necessarily used to support our body or adjustments.

It was also reported that rats that were exposed to vigorous activity demonstrated similar levels of LPL activity to the restrained rats, implying that local lower intensity longer duration muscle activity was a more significant stimulus for activating LPL activity.

Can low to moderate intensity exercise fix it?

Apparently the most effective method to increase LPL enzyme activity is low to moderate intensity movements for long periods as well regularly interrupting sedentary activities with small movements breaks. So in addition to going to the gym just stand and move more at a lower intensity for longer periods during your day.

What we need to do..

We should start by staying on our feet as much as possible, walking to work or the shops, doing more gardening, walking the dog, washing the car, put out the garbage, standing up while washing the dishes, hanging out the clothes, and generally being more active and reducing the time we spend in sedentary activities.

Always look for a reason to use our muscles and just move more!!