Neuroplasticity and Repetitive Practice: 2 secrets for Stroke Rehab Success

There are two essential ingredients that your rehabilitation regimen needs for success: neuroplasticity and repetitive practice.

These two things can make a MASSIVE difference in your recovery, so we’d like to share a quick lesson about it with you.

1. NEUROPLASTICITY IS THE BEST WAY TO GET RESULTS

Neuroplasticity is how your brain rewires itself and heals after stroke. When there is damage in the brain, neuroplasticity allows your brain to rewire new connections around the damage.

For example, if stroke damaged the motor cortex of your brain (which controls movement) then you may have impaired leg movement. In order to regain leg movement, you can engage neuroplasticity to rewire your brain.

Which begs the question, how can you engage neuroplasticity?

2. REPETITIVE PRACTICE IS THE FASTEST WAY TO ACTIVATE NEUROPLASTICITY AND GET BETTER Screen Shot 2018-01-03 at 11.53.33 AM

The answer is repetitive practice.

Repetitive practice involves practicing something over and over and over, which leads to stroke rehab success!

As they saying goes, “You are what you repeatedly do”.

Because the more you repeat something, the more ingrained it becomes in your brain.

And that’s why repetitive practice is sooo important for stroke recovery.

The more you repeat something over and over, the more you strengthen the new neural connections in your brain.

And the stronger those connections become, the stronger you become.

Repetitive practice is how you will get your life back after stroke and recover the fastest way possible.

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How to find the Motivation to Exercise

You have heard the expression “where there’s a will there’s a way.” This applies to exercise as it does to everything else. It is not easy to get out of bed early in the morning or head for the gym after a hard day’s work. If you are not in the best physical condition or are recovering from an illness or injury, it’s that much harder to put in the effort. So, how do you acquire the motivation to exercise?

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The following tips will help you drum up the motivation to start and maintain an exercise program:

  1. Think about the benefits of exercise – improved health, reduced stress, weight loss, better sleep, to name a few .
  2. Set realistic goals. If you have never exercised before, you want to start slowly, so your goal might be to exercise 3 days a week for 15 minutes, then increase the frequency and length as you become stronger.
  3. Find a buddy. Having someone who exercises regularly can encourage you, especially on days when your motivation is low.
  4. Do something you enjoy. Exercise does not have to be boring or strenuous. Dancing, walking, swimming, cycling are all enjoyable, effective forms of exercise. If you do it with a partner, it can be even more fun.
  5. Choose pleasant surroundings. A scenic park or countryside can provide sensual delights in addition to the benefits of exercise.
  6. Choose the right time. Some people work out best in the morning, others in the afternoon. Some like hot weather, others are invigorated by the cold. Know yourself and what suits you best.
  7. Choose the right clothing and footwear. You will not be motivated to exercise if you are not comfortable in what you are wearing. Dress to suit the weather and be careful to wear the right shoes.
  8. Listen to music. This can help you pass the time and make your workout more enjoyable.
  9. Vary your workout. As you become stronger, you may get tired of the same routine. You can incorporate other forms of exercise such as weights, swimming or Yoga.
  10. Keep a positive attitude. This will help you stay motivated.

Before beginning any form of exercise, consult a professional. If you need help getting started, you can see a physiotherapist who will set up a program that is just right for your age and physical condition.

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How to start a Walking Program

Whether you are an athlete in the prime of life, an elderly person or someone recuperating from an illness, walking is one form of exercise that nearly everyone can, and should, participate in. All you need is a comfortable pair of shoes and the will. In many physiotherapy programs, walking forms the basis of treatment. Walking as a form of exercise that costs you nothing and has many benefits which we will explore in this article.

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How to start a walking program:

Before you begin walking or any type of exercise, you should first consult a health care professional. The rate at which you begin walking will depend on your physical condition. If you have been ill or have followed a sedentary lifestyle for a long time, do not try to do a three-mile sprint during your lunch break. Take it slowly at first, wear comfortable clothing, sturdy shoes and don’t forget to breathe.

  • If you cannot breathe easily while you walk, it means you are going too fast.

Who may benefit from walking:

Walking benefits everyone. If you are in the peak of health, walking can help maintain your condition, but if you are recovering from illness or injury, walking is a safe and effective means of regaining stamina and conditioning weak muscles.

Walking is highly recommended for:

  • Cardiac rehabilitation: walking is a major part of therapy for persons recovering from a cardiac condition.
  • Stroke rehabilitation: helps correct gait abnormality and increase strength.
  • Sports injury: repairs damaged tissue, strengthens muscle and promotes healing.
  • Arthritis: relieves pain and improves joint flexibility.
  • Diabetics: helps the body metabolise sugar, thereby decreasing glucose levels in the blood.
  • Obesity: increases metabolism, reduces fat, tones and strengthens muscles.
  • Osteoporosis: the weight-bearing mechanism of walking helps increase bone mass.

Walking is a whole body exercise which benefits not just your leg muscles, but your upper body, heart and lung muscles as well. It tones and conditions the body, helping you lose weight, feel better and look better. Walking increases endorphins (the feel-good hormones), and if you walk outdoors you receive the added benefit of Vitamin D which strengthens bones. If you are thinking of beginning a walking program and don’t know where or how to start, give us a call. We will give you all the help you need.

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Can Science make us immortal?

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If you’re alive in 20 years, you may be able to live forever.

In 1786, average life expectancy was just 24 years. A hundred years later (1886) it doubled to 48. Right now a newborn can expect to live an average of 76 years. With recent discoveries in biology, many scientists predict that life expectancy will continue to triple-digits. In fact, if they are correct, humans shouldn’t have to die at all in the future. Screen Shot 2017-11-19 at 11.02.10 AM

“Over half the baby boomers here in America are going to see their hundredth birthday and beyond in excellent health. We’re looking at life spans for the baby boomers and the generation after the baby boomers of 120 to 150 years of age.” — Dr. Ronald Klatz of the American Academy of Anti-Aging.

Today’s quest for the fountain of youth is taking scientists inside the genetic structure of cells and paying less attention to the role of stress and diet on life spans. Would-be immortals flock to anti-aging clinics and shell out as much as $20,000 a year for treatments that include hormone therapy, DNA analysis, even anti-aging cosmetic surgery. These experimental therapies offer no guarantees of immortality — just the promise of prolonging life.

“Anti-aging medicine is not about stretching out the last years of life. It’s about stretching out the middle years of life… and actually compressing those last years few years of life so that diseases of aging happen very, very late in the life cycle, just before death, or don’t happen at all.” — Dr. Klatz.

Why do we age and die?

The cause of what we call “aging” is now being understood. This new understanding may soon move anti-aging cosmetics and surgery to the ranks of snake oil and Siberian yogurt as life-extension fads — but not yet. There are a few obstacles that need to be addressed.

Just when you thought that holographic TV and outer space travel were on the future horizon of modern technology, immortality has silently been revealing itself to scientists like Doctor John Langmore [right] of the University of Michigan’s Department of Biology.

Dr. Langmore and his group looked inside human cells, at the very essence of human life: the DNA molecule. Specifically, Dr. Langmore looked at the tips of the DNA molecule — a previously overlooked part of the double-helix molecule — that contain a kind of chain of repeating pairs of enzymes.

 

 

 

 

Called telomeres, these molecular chains have often been   compared to the blank leaders on film and recording tape. Indeed, telomeres seem to perform a similar function. During the replication process the spiral DNA molecule must split in half and reassemble a copy of itself. Protecting the vital DNA molecule from being copied out of synch, telomeres provide a kind of buffer zone where mis-alignments (which are inevitable) will not result in any of the important DNA code being lost.

Perhaps the best analogy I have heard is to compare the telomeres to the white margin surrounding an important type written document. In this analogy, the printed text is the vital DNA code while the white space is the “blank” telomeres. Imagine that this paper is repeatedly slapped on a copy machine, a copy is made, and then that copy is used to make another copy. Each time the paper is subject to errors of alignment and these errors accumulate. After enough copying, it is probable that the white space will diminish and some of the actual text will not be copied. That’s what happens inside our cells and it is the reason we get old and die.

As any cell gets older, it is under attack by oxides and free-radicals in the body and environment. We survive as living beings because our cells have the ability to duplicate and replace themselves before being killed by these natural causes. Each time our cells divide, the DNA molecule makes a new copy of itself.

DNA is a complex molecule that resembles a spiral ladder. When it divides, it splits along the “rungs” then each half of this “ladder” rebuilds the missing half — viola! — two DNA molecules. Now the cell can divide. The old cell dies and the new cell continues on.

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But the procedure is very complex and not perfect. Usually a small portion of the DNA molecule is lost, misaligned and not copied. Since errors are more frequent on the ends of the DNA molecule, this area, the telomere, does not contain any important DNA information and the effect is insignificant.

Telomeres — programmed to die!

Scientists observe that the length of telomere chains becomes shorter as we grow older. Eventually the telomeres become so short that cell replication produces lethal errors or missing pieces in the DNA sequence, ending the cell’s ability to replace itself. This point, when the cell has lost vital DNA code and cannot reproduce, is called the Hayflick limit. It’s the measure of how many times a cell can copy itself before it dies.

Some cells in our body have a very high hayflick limit. Cells that line the inside of your mouth and intestines, for example, are constantly being worn away and replaced. Indeed these cells appear to have the ability to regrow telomeres even in aged bodies. Scientists were curious why some cells shut down telomere growth with age, and some do not.

Dr. Langmore used physical, biochemical, and genetic techniques to study the structure and function of telomeres. His group developed a cell-free system to reconstitute functional model telomeres using synthetic DNA, and studied the mechanism by which telomeres normally stabilize chromosomes and how shortening of the telomeres could cause instability.

The protein factors responsible for stabilizing the ends of chromosomes are being identified, cloned, and studied. Electron microscopy is used to directly visualize the structure of the model telomeres. Dr. Langmore’s group used new enzymatic assays to determine the structure of telomere DNA in normal and abnormal cells grown in vivo and in vitro, in order to address specific hypotheses about the role of telomeres in aging and cancer. It’s exciting research, for sure, and there have been some promising discoveries.

Scientists have discovered an important enzyme that can turn the telomere production on the DNA molecule “on” and “off.” It’s called telomerase. Not surprisingly, it seems that as we get older, the amount of telomerase in our cells decreases.

The Cancer Problem

You might be wondering why biologists don’t simply find a way to keep our body’s telomeres long. This would prevent replication errors and humans could live indefinitely. The big problem is cancer.

Usually, if a cell makes an error in copying itself, the error will prevent the cell from duplicating itself in the future. So the mistake is limited. But with cancer, cells with errors somehow “turn on” the production of telomerase and make the mutant cell immortal. Now, aberrant cells can reproduce unchecked and outlive normal cells. This is the process that creates tumors.

Since we all have mutant, pre-cancerous cells in our bodies, nature has decided to shut off the telomerase as we age, thus preventing these mutant cells from growing telomeres. It’s a kind of programmed death — a trade off to reduce our lifespan in order to save us from being riddled with tumors. Nevertheless, some pre-cancerous cells manage to re-activate their telomeres and this has caused the research to focus more on blocking telomere production rather than trying to extend it.

[Right: A 3-d rendering of the telomerase enzyme.] The molecular structure shows an interesting “groove” (show in green) where the enzyme attaches to the end of the DNA molecule.

Ant-cancer researchers believe that by introducing a molecule to block this groove, the telomerase would become unable to attach itself to the DNA and thereby limit the length of telomere production. While this work holds hope for stopping tumor cells from reproducing forever, it does little to extend healthy cells from being rejuvinated. However, if the molecular “blocker” could specifically target only cancerous cells, without blocking telomerase activity in healthy cells, it could be a step towards human life extension if and when a pharmaceutical can be developed that activates telomerase in the human body. [4]

Interview with Dr. LangmoreViewzone asked Dr. Langmore to give us his thoughts on the role of telomerase, and the possibilities of using it to repair and lengthen telomeres in human cells. His comments follow:

Telomeres are special, essential DNA sequences at both ends of each chromosome. Each time chromosomes replicate a small amount of the DNA at both ends is lost, by an uncertain mechanism. Because human telomeres shorten at a much faster rate than many lower organisms, we speculate that this telomere shortening probably has a beneficial effect for humans, namely mortality. The telomere hypothesis of aging postulates that as the telomeres naturally shorten during the lifetime of an individual, a signal or set of signals is given to the cells to cause the cells to cease growing (senesce). At birth, human telomeres are about 10,000 base pairs long, but by 100 years of age this has been reduced to about 5,000 base pairs.

Telomerase is actually an enzyme (a catalytic protein) that is able to arrest or reverse this shortening process. Normally, telomerase is only used to increase the length of telomeres during the formation of sperm and perhaps eggs, thus ensuring that our offspring inherit long “young” telomeres to propagate the species.

ViewZone: How is mortality in non-germ line cells a beneficial effect?Dr. Langmore: The telomere hypothesis of cancer is that the function of telomere shortening is to cause cells that have lost normal control over growth to senesce (i.e. stop growing) before being able to replicate enough times to become a tumor, thus decreasing the frequency of cancer.

Immortal cells like cancer have an unfair advantage over normal human cells which are designed to senesce. But nature seems to have planned this human telomere shortening perhaps to prolong life by hindering the otherwise unchecked growth of non-immortal or benign tumors. Malignant, or immortal tumors can simply outlive the rest of the organism.

Malignant cancer cells are being studied because they appear to have altered the shortening of telomeres by turning “on” the telomerase. Thus it appears that some cancers and aging are both connected with the biology of telomeres.

It is possible that increasing telomerase activity in normal cells might stop the biological clock of aging, yet the side effect of this intervention might be an increase in the rate of cancer. Further understanding and refinement in the telomere hypothesis might lead to a way to slow the aging process and prevent or arrest cancer.

However telomeres function, they are an integral part in the very complex process of cell growth, involving many other factors as well. Telomerase might be the Achilles Heal of aging and cancer, but as our understanding of factors that interact with telomerase, factors that are responsible for telomere shortening in the first place, and non-telomerase mechanisms for increasing the length of telomeres, we might find that one of these factors is more easily manipulated to slow aging or prevent cancer. Also there are additional factors that affect aging and cancer, which might prove in the end to be more important than telomeres and telomerase.

ViewZone: Are telomeres unique to individual DNA? If so, does this preclude any universal treatment for aging?

Dr. Langmore: Different individuals have telomeres with exactly the same DNA sequence but of different lengths. It is too early to say whether there is any relationship between telomere length in an individual and his or her life expectancy, or whether a treatment that would artificially lengthen telomeres would arrest (or reverse) the aging process. One problem is that even in one individual the telomeres of different chromosomes have very different lengths. Therefore an individual might have on average long telomeres; but, he might have one chromosome with a very short telomere that could affect cell growth.

ViewZone: In the work of Shay and Wright (see below), increased telomere length was positively associated with telomerase. How significant is this?

Dr. Langmore: Shay, Wright and all their many collaborators stimulated telomerase activity in normal cells. This was expected to 1) Increase the length of telomeres and 2) Prolong the lifetime of the cells in tissue culture. The treatment did both, in perfect agreement with the telomere hypothesis of aging.

ViewZone: How much was cell lifetime prolonged due to this treatment that reactivated telomerase?

Dr. Langmore: The increased proliferation of the cells was perhaps equivalent to hundreds of years of human life.

Dr. Langmore received his Ph.D. degree from the University of Chicago in 1975. He has held postdoctoral fellowships at the Laboratory of Molecular Biology in Cambridge and at the University of Basel.

 

[Above:] One of the more surprising developments in telomere structure was the discovery by collaborative efforts from Jack Griffith’s and Titia de Lange’s groups that mammalian telomeres looped back on themselves to form large lariat-like structures, called t-loops (Griffith et al., 1999).

This structure may help to conceal the end of the molecule from DNA damage surveillance mechanisms and guard against recognition of the chromosome terminus as a double-strand break.

More links to cancer

In the March 15 issue of the European Molecular Biology Organization (EMBO) Journal, Dr. Jerry Shay and Dr. Woodring Wright, both professors of cell biology and neuroscience at UT Southwestern Medical Center at Dallas, report manipulating the length of telomeres to alter the life span of human cells. Shay and Wright are the first to report this important finding. They received an Allied-Signal Award for Research on Aging to explore this line of research last year.

“By lengthening the telomere, we were able to extend the life of the cell hybrids,” Wright explained. “This study is strong evidence that telomere length is the clock that counts cell divisions.”

“The expression of the enzyme telomerase maintains stable telomere length. Telomerase is not detected in normal cells and telomeres shorten and then the cells stop dividing and enter a phase called cellular senescence.”

Shay and Wright have shown in earlier studies that telomeres maintain their length in almost all human cancer cell lines. This correlated with inappropriate expression of telomerase and as a consequence allowed the cell to become “immortal.” Cell immortality is a critical and perhaps rate-limiting step for almost all cancers to progress. Previous work by the UT Southwestern investigators showed that in a special group of advanced pediatric cancers the lack of telomerase activity correlated with critically shortened telomeres and cancer remission.

Naturally, the exploration of this enzyme is now the focus of much investigation, but for now the research is aimed at understanding how to turn telomeres “off” to limit the spread of “immortal” cancer cells.

Abnormally high levels of telomerase have been found in cancerous breast cells and have been evident in many kinds of tumors.[1]

Consequently, an idea gaining momentum is that the ability to measure and perhaps alter telomere length and/or telomerase activity may give physicians new diagnostic and treatment tools for managing the care of patients with cancer.

Shay and Wright tried to alter already-immortal cells by attempting to inhibit telomerase activity and cause telomeres to shorten. “Unexpectedly, we found the opposite result. Rather than inhibiting telomerase, our treatment caused the immortal cells to develop longer telomeres,” Shay explained. “Although we were surprised with the result, we now know there is a causal relationship between telomere length and the proliferate capacity of cells.

“Essentially, we combined the tumor cells containing experimentally elongated telomeres with normal cells and extended the life span of those cell hybrids compared to similar hybrids using cells without experimentally elongated telomeres.”

Shay and Wright said the mechanism that causes telomeres to lengthen is still unclear. However, Shay said, “Our observations increase confidence in the hypothesis that immortal cells and reactivated telomerase are essential components of human tumors. Ultimately, we may be able to regulate tumor cells by inhibiting telomerase activity.”

The potential implications for research on human aging also are significant. “It is still speculative, but understanding the role of telomere shortening in cell aging may give us the information we need to increase the life span of an organism,” Wright said. (News Releases from UT Southwestern)

 

 

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Some data from the WHO for the elderly

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Adaptation in the kitchen for Elderly and Handicaps

By reflecting about the logic that cooking is an habit, and that this habit can be hard for elderlies and handicaps, the German Designer Dirk Biotto developed a completely adapted kitchen that attends to the needs of those populations. Check it out!

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Entitled ChopChop, the modern kitchen has adjustable legs for different heights, as well as the distribution of the utensils. Therefore, either a handicap in the well chair or an elderly with limitations in their movements can access all the utensils, manipulate objects and use the sink.

In the sink, an extensible hose allows to use water from different distances.

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There is also a clamp close to the faucet that facilitates to open glass jars, cans and bottles. By developing the clamp, the German Designer thought about handicaps amputees, who cannot use both limbs to perform tasks in the daily basis.

For those ones who face difficulties in holding the food and also cutting them, there is an apparatus that keep fruits and vegetables stable to be cut, as well as a grinder for cheese and other foods held with screws on the table, facilitating the manipulation of objects with only one hand.

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The German project of the accessible kitchen is still a prototype, but we look forward to seeing it for sale!

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My favorite things (about aging) by Julie Andrews

‘My Favorite Things’ about Aging By Julie Andrews Geffen Playhouse's Annual "Backstage At The Geffen" Gala - Arrivals

This is yet another perspective on age and aging!

To commemorate her 69th birthday on October 1, actress/vocalist Julie Andrews made a special appearance at Manhattan’s Radio City Music Hall for the benefit of the AARP. One of the musical numbers she performed was “My Favorite Things” from the legendary movie “Sound Of Music.”

However, the lyrics of the song were deliberately changed for the entertainment of her “blue hair” audience. Here are the lyrics she recited:

Maalox and nose drops and needles for knitting,
Walkers and handrails and new dental fittings,
Bundles of magazines tied up in string,
These are a few of my favorite things..

Cadillacs and cataracts and hearing aids and glasses,
Polident and Fixodent and false teeth in glasses,
Pacemakers, golf carts and porches with swings,
These are a few of my favorite things.

When the pipes leak,
When the bones creak,
When the knees go bad
I simply remember my favorite things,
And then I don’t feel so bad.

Hot tea and crumpets, and corn pads for bunions,
No spicy hot food or food cooked with onions,
Bathrobes and heat pads and hot meals they bring,
These are a few of my favorite things.

Back pains, confused brains, and no fear of sinnin’,
Thin bones and fractures and hair that is thinnin’,
And we won’t mention our short shrunken frames,
When we remember our favorite things.

When the joints ache,
when the hips break,
When the eyes grow dim,
Then I remember the great life I’ve had,
And then I don’t feel so bad.

Ms. Andrews received a standing ovation from the crowd that lasted over four minutes and with an encore.

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Infographic for Brain Exercises

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Let`s understand better about our Circadian Rhythm

ritmo circadiano

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You must try these exercises to get rid of your Double Chin

As we age, we all lose firmness of our facial muscles. Due to this reason, even skinny people can have double chin.

The exercises bellow should be performed daily, and it may help you to strength facial muscles and get rid of the double chin.

Check it out!

1. Warming up the muscles

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Just like before any other workout, you’ll want to warm up your facial muscles.

For this purpose, move your lower jaw forward and backward and then side to side. All movements should be performed slowly and smoothly without sudden jerks. Repeat the exercise 8-10 times.

2. The Scoop

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Open your mouth, and roll your bottom lip over your lower teeth. Imagine that you need to scoop water with your lower jaw. Move your head down in a scooping motion, and close your mouth while lifting your head.

While performing this exercise make sure that the corners of your lips are completely relaxed. Repeat 5-7 times.

3. Touch your nose

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A double chin is also associated with weakness of the hyoid muscles. That is why they also need to be strengthened.

Stick out your tongue as far as possible, and try to reach your nose with the tip of your tongue. Keep your lips relaxed. Repeat 5 times.

4. The perfect oval face

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If you want to return the shape of your face to a younger look and pull your cheeks up, do the following exercise: turn your head to the left, and pull your lower jaw forward, straining the muscles of your neck. You should feel the muscles on the left of your neck stretching. Then turn your head to the right and do the same movement. Repeat 5 times on each side.

5. “Kiss the giraffe”

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Imagine you need to kiss a giraffe (or someone who is very tall).

Lift your face up, and look at the ceiling. Slightly bring your lower jaw forward, and pucker your lips as if you are going to kiss someone. If you are performing the exercise correctly, you should feel a strong tension in your neck. Hold the position for 5 to 8 seconds and release. Repeat 5 times.

6. Resistance

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For this exercise, you need to make two fists and place them directly under your chin. Then begin to move your lower jaw slightly down on your fists, and strain your muscles while overcoming the resistance. The pressing force should gradually increase. When you reach maximum resistance, hold for 3 seconds. Then relax, and repeat the exercise 5-7 times.

7. Smile

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Clench your teeth with your mouth closed, and try to stretch the corners of your lips as wide as possible. Now push your tongue against your hard palate, gradually increasing the pressing force.

If you feel a strong tension in your chin muscles, then you have performed the exercise correctly. Hold this feeling of tension for 5 seconds, and then relax for 3 seconds. Repeat 5-8 times.

8. Puffy cheeks

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Inhale deeply with your mouth, and fill it with air. Close your mouth, and puff up your cheeks. Now press your palms on your cheeks so that you feel tension in your muscles. Hold for 3-5 seconds, then release the air and relax. Repeat the exercise 5-6 times.

9. Bellow, you can watch a video that demonstrates the exercises above

 

Source: ladyformula, brightside.me
Illustrator Daniil Shubin, Photographer Roman Zakharchenko, Model Olga Zakharchenko for BrightSide.me
Based on materials from fitnesshealthzone, huffingtonpost

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