Maximizing Lutein from Spinach

Lutein is a potent antioxidant that offers a wide range of health benefits. It is best known for protecting the eyes and spinach along with other dark leafy vegetables contain the highest levels. Interestingly, a new study from Linkoping University, Sweden, has found that how you prepare fresh spinach and other dark green leafy vegetables can maximize lutein. Of course there are many other nutrients in natural foods that are also better preserved and absorbed using the same approach.

This study allowed the team to see what influence the level of lutein in the blood would have by increasing dietary intake of this antioxidant. The research group studied which method of spinach preparation allowed the greatest benefit of lutein maximization. Spinach was chosen as the vegetable of choice for the study because it contains comparatively high levels of lutein and is also consumed by many people.

Preparation methods that are typically used at home were used in the study. The researchers compared several temperatures and heating times along with cold preparations such as spinach in salads and in smoothies.

The research team used baby spinach from a supermarket in their study. The spinach samples which were prepared in cooked fashion were fried, steamed, and boiled for up to 90 minutes and the lutein content was measured at different times. The team also compared different heating times. Lutein like other nutrients degrades with heat.

The results shows that heating time was important when spinach is boiled. The longer the spinach is boiled the less lutein is retained. When spinach is fried at a high temperature, a large amount of lutein was degraded after just two minutes. And more lutein was lost when spinach was baked in the oven at a higher temperature than when it is cooked in a soup or stew.

The study did show that reheating spinach in the microwave actually compensated for some loss of lutein. More lutein was released from the spinach as the plant structure was further broken down by microwaving.

The best way to maximize lutein from spinach is to not heat it at all. Eating it raw in a salad or adding it to a smoothie gains the most benefits. And when spinach is chopped into small pieces and then a fat added such as a dairy product in a smoothie, more lutein is released and the fat actually increases the solubility of the lutein in the fluid.

Spinach is just one of the great sources of lutein. Other sources include kale, brussel sprouts, parsley, broccoli and peas along with orange juice, kiwi, red peppers, squash and grapes. As concluded in the above study, consuming any of the sources in their raw form gains the most benefits from lutein.

To view the original scientific study click here: Liberation of lutein from spinach: Effects of heating time, microwave-reheating and liquefaction.

A Houseplant that Cleans the Air

Pothos Ivy just got a remake and will now remove benzene and chloroform from the air around it! Researchers at the University of Washington genetically modified this common houseplant and the resulting plant can clean these two pollutants which are hazardous compounds that are too small to be trapped in HEPA air filters.

Benzene which is a component of gasoline can build up in homes when we store lawn mowers and cars in attached garages. Even burning candles produce this compound. Chloroform is present in small amounts in chlorinated water and can be released when we take showers or boil water. Both compounds have been found to be linked to cancer. They aren’t commonly talked about because previously nothing could be done about them in our homes.

The modified Pothos Ivy plants express a protein called 2E1 which will transform these compounds into molecules which the plants will then use to support their growth. The process took 2 years and while other lab plants might only take a few months to achieve the intended results, the team chose the pothos because it is a robust houseplant that grows very well under a variety of conditions.

The researchers used a protein called cytochrome P450 2E1 or 2E1 for short, which is present in all mammals including humans. This protein turns chloroform into carbon dioxide and chloride ions and turns benzene into a chemical called phenol. However, 2E1 is located in our livers and is actually turned on when we consume alcohol. It is not available to us to help us process any pollutants in the air.

The team decided to have this reaction occur outside the body in a plant which they call an example of the “green liver” concept. The p450 2E1 cytochorme was taken from rabbits. It was then introduced into the pothos ivy so that each cell would express the protein. Pothos ivy does not flower in temperate climates so the genetically modified plants would not be able to spread via pollen.

They then tested how well the modified plants could remove the two pollutants from air compared to how well normal pothos ivy would preform. Both types of plants were put in glass tubes and then either chloroform gas or benzene was added. Over the following 11 days the team tracked how the concentration of each pollutant changed in the tubes.

The concentration of chloroform gas did not change over time in the unmodified plants. But the concentration of chloroform dropped by 82 percent after three days in the modified plants. And by the sixth day was almost undetectable. The benzene concentration also decreased in the modified plants, however more slowly. By the eighth day though the benzene concentration dropped by almost 75 percent. Normal pothos ivy only broke down less than 10 percent in the first week.

The team did use much higher pollutant concentrations that would typically be found in homes so they could detect changes. They anticipate that the levels of the two pollutants would drop similarly in homes and perhaps even faster over the same time frame.

If used in the home, the plants would need to be inside an enclosure with something to move the air past the leaves such as a fan. A plant sitting in a corner will have some effect on that particular room, but without airflow it would take a longer time for a molecule on another side of the room to reach the plant. And the transgenic plant also produces a green fluorescent protein that glows under UV light. This was added to make the plant more appealing and also to make it easy to spot!

The research team is now working on increasing the plants capabilities by adding a protein which can break down another hazardous molecule found in homes which is formaldehyde. This compound is present in some wood products such as laminate flooring and cabinets and in tobacco smoke.

All these hazardous compounds are very hard to get rid of. Without proteins to break down the molecules, high energy processes would have to be used. It makes more sense, is simpler and more sustainable to put the proteins all together in a common houseplant. And 2E1 is beneficial to the plant since they use chloride ions and carbon dioxide to make their food, and they use phenol to help make components of their cell walls.

The plant may soon be available in Canada where it does not grow outside. However it does grow in southern Florida so to get approval in the United States the research team has to show that the genetically modified pothos plant is no more likely to cause problems as a weed than regular pothos. Until it is available spider plants remove many pollutants so can be used in homes to help purify the air.

To view the original scientific study click here: Greatly Enhanced Removal of Volatile Organic Carcinogens by a Genetically Modified Houseplant, Pothos Ivy (Epipremnum aureum) Expressing the Mammalian Cytochrome P450 2e1 Gene. Environmental Science & Technology, 2018; DOI: 10.1021/acs.est.8b04811

Turning Stem Cells into Muscle Cells

In an effort to assist people with muscle disorders, researchers at The University of Texas Health Science Center at Houston have engineered a new line of stem cells to study how they may be converted into muscle.

Muscle disorders which affect over 50,000 people in the United States cause muscles to deteriorate and weaken. And in very severe cases, they can involve respiratory and cardiac muscles which can lead to death. Currently there are no cures for these types of disorders.

The team engineered a new human stem cell line just for skeletal muscle. By tagging the muscle genes which are known as PAX7 and MYF5 with two fluorescent proteins, they were able to ensure the purity of the muscle stem cells. They screened several bioactive compounds in order to improve formation of muscle from stem cells. They also used color tags to observe muscle stem cell activity.

In the lab which was at the Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases at UT, the researchers used CRISPR/Cas9, a gene editing method, to add the fluorescent color tags to the genes.

The stem cells which were generated from the patient’s stem cells were used to generate muscle. The team’s current research provided a step by step road map to make these stem cells into muscle stem cells.

Within a culture of human tissue, the stem cells that had been modified showed promising results. Additionally they showed promise in a mouse model of Duchenne muscular dystrophy. Compared to previous studies, the new strategy allowed more efficient and faster generation of muscle stem cells and with superior engraftment in the mice.

The team believes these muscle stem cells will be used by researchers initially to study the pathophysiology of muscular diseases and to create disease models that researchers are able to use to test promising treatments or to evaluate gene correction efficiency.

It is hoped that the cells can someday be used as a form of stem cell therapy. Our bodies our constantly replacing our skeletal muscle cells. However, muscle disorders make it difficult to replenish muscle because of the exhaustion and failure of muscle stem cells.

To view the original scientific study click here: A Myogenic Double-Reporter Human Pluripotent Stem Cell Line Allows Prospective Isolation of Skeletal Muscle Progenitors

Can Stem Cells End Back Pain?

Degeneration of the intervertebral disc is a very common problem which afflicts a large group of our population. Both neck and back pain are very often the result of progressive damage of the discs which separate our spinal vertebrae.

Healthy intervertebral discs work by absorbing stress which has occurred on the spine during movement. They then adjust our posture so we can move freely. If the discs wear out, pain develops in a variety of areas in a person’s neck and/or back.

Currently treatments for this disc degeneration have included replacing the damaged discs with new artificial ones or spinal fusion surgery. These approaches unfortunately have limited benefits because they cannot replace the full function of the discs they replace.

Now a research team at the University of Pennsylvania’s Perelman School of Medicine, School of Veterinary Medicine and the School of Engineering and Applied Science are aiming to solve this problem. They are working on developing bioengineered intervertebral discs which are harvested and made out of a person’s own stem cells. Because stem cells are undifferentiated cells which have the ability to transform into specialized cells, they are the focus of a variety of medical research studies.

For the past 15 years the team at the University of Pennsylvania has been working on these new disc models beginning with lab studies, then progressing to studies on small animals, and now recently studies on large animals.

Previously the team tested the new discs which they call disc like angle ply structures (DAPS) for 5 weeks in rat tails. In the next study, the research team further developed the engineered discs. The new model called endplate modified DAPS (eDAPS)were tested in the rats once again for up to 20 weeks. The new structure allowed the disc to retain its shape better and was more easily integrated in the surrounding tissue.

Several tests were run which included MRI scans and a variety of in depth tissue and mechanical analysis. The team discovered that in the rat model the eDAPS effectively restored the original disc function and structure.

With this success, the team was motivated to study eDAPS in goats. They proceeded to implant the device within the cervical spines of some of the goats. Goats were chosen for the study because the cervical spine discs of these animals have similar dimensions of those in humans. Goats also have semi upright stature which allowed the team to bring this study one step closer to conducting human trials.

The teams tests on goats proved to be successful. The eDAPS integrated quite well with the surrounding tissue. Additionally, the mechanic function of the discs either matched or surpassed that of the original cervical discs of the goats.

The next step will involve conducting more extensive trials on goats which will help the scientists to better understand how well eDAPS works. The team then plans to test eDAPS in human models of intervertebral disc degeneration which hopefully gets them one step closer to conducting clinical trials.

Implanting a device made of a person’s own cells is highly desirable. Using a true tissue engineered motion preserving replacement device in arthroplasty is something that has not been done yet in orthopedics. It would certainly be a large shift in treating spinal diseases and how surgeons approach motion sparing reconstruction of joints.

To view the original scientific study click here: watch-these-tissue-engineered-spinal-disks-mimic-real-thing

Breathe through the Nose to Improve Memory

Researchers at the Karolinska Institute in Sweden have discovered that when we breathe through our nose rather than our mouth we are able to consolidate memories better. How breathing affects the brain has become a popular field of study in recent years and with new methodologies, more studies have been enabled.

The recent study in Sweden shows that people remember better when they breathe through their nose while the memory is being consolidated which is the process that happens between learning something and then memory retrieval. This is the first study that demonstrated this. The reason this phenomenon had not been studied earlier is that the common laboratory animals such as mice and rats do not breathe naturally through their mouths.

Memories go through 3 stages in their development. Encoding occurs first, then consolidation and finally retrieval. By breathing through the nose rather than the mouth during consolidation this enhances recognition memory. Nasal respiration is very important during the critical period where memories are activated and then strengthened. And it also suggests that the neural mechanisms which are responsible may emerge through nasal respiration.

For the study the team had the 24 Swedish participants learn twelve different smells occurring on two different occasions. Six fragrances were familiar such as strawberry and six were unfamiliar smells like pungent alcoholic scent 1 butanol.

The participants were then instructed to either breathe through their mouths or noses for one hour. When the hour was up, the participants were presented with the old set of smells along with the new set of twelve smells which also were six familiar smells and six unfamiliar smells. They were then asked if each one was from the learning session or new.

The findings indicated that when the participants breathed through their noses between the learning time and then the recognition, they remembered the smells much better. Those who breathed through their nose were twice as successful at recognizing whether the smells were old or new.

Previous research has indicated that receptors in the olfactory bulb detect not just smells but also variations in the airflow. Different parts of the brain will be activated in different phases of exhalation and inhalation. How the synchronization of brain activity and breathing happens and how that affects the brain and, subsequently our behavior, is unknown.

Growing evidence from human and animal studies indicates that respiration plays an important role in the neural and behavioral mechanisms associated with encoding and recognition. Nasal but not mouth respiration entrains neural oscillations that enhance the encoding and recognition processes and also the consolidation stage.

Smells are first processed by the olfactory bulb in mammals. This starts inside the nose and runs along the bottom of the brain. This has a direct connection to two areas of the brain that are strongly involved in memory…the hippocampus. Hippocampal rhythms are involved in the transfer of information between sensory and memory networks. With humans, bypassing nasal airflow by breathing through the mouth abolishes the rhythms and affects encoding as well as the recognition processes which reduces memory performance.

The concept that breathing affects our behavior is not new. The evidence has been around for thousands of years in areas such as meditation. However, no one has been able to scientifically prove what actually does go on in the brain. Researchers have tools now that can help reveal new clinical knowledge.

The next step for the team is to measure what really happens in the brain while breathing and how it is linked to memory. Previously it was not practical to measure this, however now the team has developed a new method of measuring activity in the brain and olfactory bulb that is non-invasive.

To view the original scientific study click here: Respiration modulates olfactory memory consolidation in humans.

Western Diet and Blood Pressure

Researchers at John Hopkins Bloomberg School of Public Health have conducted a study on two tribes that shed new light on the role the Western diet plays on blood pressure. The study involved a South American tribe which lives in near total isolation and has no Western dietary influences and a nearby tribe which is more exposed to Western dietary influences.

Researchers took blood pressure measurements from 72 Yanomami tribe members aged one to 60 and found no trends that pointed to lower or higher readings as the participants aged. Blood pressure measurements were also taken from 83 members of the neighboring tribe where there were Western dietary influences. They found a very clear trend pointing to higher blood pressure readings with advancing age.

The Yanomami tribe are hunter gatherers and also gardeners in a very remote rain forest region in Northern Brazil and Southern Venezuela. Their diet is low in salt and fat and high in fiber and fruits. Previous studies beginning in the 1980s have shown that obesity and atherosclerosis are virtually unknown among this tribe. They have extraordinarily low average blood pressure which does not appear to increase with age.

This study has shown that the age stability of blood pressure among this tribe begins in early childhood. It is the first study to compare this tribe to the nearby Yekwana tribe which has experienced an exposure to Western influenced lifestyles and diet.

In the United States and most other countries, blood pressure increases with age beginning early in life. The studies results support the thought that the tendency in Westernized societies for blood pressure to increase with age is not part of the natural aging process but might be the result of the cumulative effect of the Western lifestyle and diet.

The team found the blood pressures of the Yanomami tribe to be averaged at 95 systolic over 63 diastolic. In the United States the average systolic is 122 and 71 diastolic. The data shows that blood pressure within the Yanomami population remains very close to the same low levels from one to at least through the age of 60.

In contrast, the Yekwana who have been exposed to Western lifestyle and diet which includes processed foods was statistically indicating clear trends towards increasing blood pressure levels with advancing age. The Yekwana tribe members showed levels averaging 5.8 mm Hg higher by the age of 10 and 15.9 mm Hg higher by the age of 50.

With this age related increase in blood pressure which begins in early childhood, an opportunity exists for lifestyle and diet interventions to prevent later increases in blood pressure readings.

In the United States, systolic blood pressure increases by about 1.5 mm Hg. and 1.9 mm Hg per year among girls and boys respectively and 0.6 mm Hg per year among adults.

The research team involved is this study plans to follow up with a study of gut bacteria among the two tribes to determine if gut microbiome accounts for the tribe’s differences in blood pressure with aging.

To view the original scientific study click here: Association of Age With Blood Pressure Across the Lifespan in Isolated Yanomami and Yekwana Villages

Why it Takes So Long to Wake Up in the Morning

A study conducted by Raphael Vallat, Ph.D. at The University of California, Berkeley, has shown why people have a hard time waking up in the morning. Sleep Inertia or brain fog is real and makes it difficult for some people to drag themselves out of bed in the morning.

Early risers might deny it but as evidenced by the study, brain fog can take quite a while to dissipate and prior to the current study, researchers weren’t sure why it existed. Dr. Vallat asserts that even though the body is awake and moving in the morning, the brain can be asleep in some capacity following the wake up time.

When a person wakes up from sleeping, the brain doesn’t immediately switch from that sleeping state to a fully awakened state. Instead it goes through a transition period called sleep inertia which can last even up to 30 minutes after awakening. During this particular period, the brain will progressively switch from sleep to a normal wakefulness and our mental & cognitive performance does also.
To test this transitional period and prove how real it is, the team had 34 participants take 45 minute naps during which time they entered two periods of a deep sleep which are known as N2 and N3. The participants did not however enter REM (Rapid Eye Movement) sleep which is the deepest type of sleep. Upon awakening, Dr. Vallat tested the participants alertness using two subtraction tests which was one five minutes after awakening and one 25 minutes after awakening.

Similar to anyone who has experienced brain fog, the participants tended to make more mistakes after awakening, and their brain scans revealed why this happened. When a person is awake, the brain switches between two different modes which occur in two separate circuits. One is the task active mode such as when we are being productive or reading, and the second one is non focused task negative mode which is mind wandering. When we are awake we oscillate between the two modes and when the task active mode is functioning, there will usually be a decrease in activity with the task negative circuit.

What causes the sleep inertia to be different is the brain struggling to switch fluidly between the two circuits. It seems the brain is not really able to switch between these two different modes during sleep inertia resulting in lower performance with a mental calculation task.

The research team’s results indicate that during the period of sleep inertia the brain will slowly regain its ability to switch between the two modes divided by functional segregation. They believe it will take about 30 minutes to ultimately achieve this.

Unfortunately, they know there isn’t much a person can do to speed up their wake up process. Even a caffeine boost is not a true solution. There were some results that indicated caffeine increased the functional segregation between the two modes (task active and task negative networks) resulting in an enhancement of the brain’s ability to switch between the two modes. But it seems it does not actually work rapidly enough to cut through sleep inertia.

Caffeine takes about 30 to 60 minutes to reach peak level. Sleep inertia dissipates in about 30 minutes which is before the caffeine would even begin to work on the body. Instead of trying to caffeinate through slow brain functioning, Dr. Vallat suggests the only real fix for sleep inertia is time. Waiting a few minutes before making important decisions or hitting the road running is the best tonic especially if waking up from a very deep slumber.

How Important is Genetics for Longevity?

A new study that analyzed more than 400 million people has revealed that genetics has a smaller impact on how long a person will live than scientists had previously thought. Researchers from Calico Life Sciences in collaboration with Ancestry (an online genealogy company), have established that inherited life span is much below what was previously estimated as earlier beliefs did not take into account people’s tendency to select partners who had similar traits to their own.

The goal of the study was to assess the heritability of lifespan…whether a person’s parents who lived long lives could predict whether that person lived a long life. Heritability measures to what extent specific genes can explain differences in a person’s traits. In the case of this study, life span. This is different than non genetic differences such as sociocultural factors, lifestyle and accidents. Previous human life span heritability estimates ranged from about 15 to 30 percent.

The researchers looked at a carefully chosen set of family trees and relevant information from over 400 million people who were surveyed by Ancestry. They began with 54 million subscribers to Ancestry which represented six billion ancestors. They then removed entries that were redundant and people who were still living thereby stitching all remaining pedigrees together.

Ancestry then stripped away any identifiable information from pedigrees leaving just the birth year, death year, birth place and familial connections that are part of the family tree structure. Most of the people were based in the U.S. and of European descent and connected to another by either spouse/spouse or parent/child relationship. The researchers then examined the similarity of life span between relatives so they could estimate heritability from each family tree.

They combined statistical and mathematical modeling to analyze data of relatives who were born during the 19th and early 20th centuries. They observed that first cousins and siblings showed same heritability estimates that were observed in previous studies. They also noted the life spans of spouses were likely to be correlated and were actually more similar than in siblings of opposite gender.

The correlation between spouses could be attributed to a variety of non genetic factors such as living in the same household or shared environment. The results then really started to surprise the researchers when they compared different types of first cousins in laws and siblings in law though there was no blood relatives and typically did not share households.

The researchers were able to focus in on correlations for other even more remote relationships which included uncles in laws and aunts, first cousins that are once removed in law and also a variety of configurations of co siblings in law. The findings which indicated that a person’s siblings, spouse siblings or their spouses siblings spouse had similar life spans, made it obvious that something besides a person’s genes was in place.

If people did not share genetic backgrounds and also did not share households, then the question became what best accounts for the life span similarity between individuals that had these types of relationships. The team went back to the data set and proceeded to perform analyses that would detect assortative mating which means the factors which are important to longevity tend to be very similar between mates. People tend to choose partners that have traits similar to their own and in this case how long they live.

Because people marry obviously before one is deceased, then assortative mating must be based on other characteristics. The mate choice could be sociocultural or genetic or both. In regards to non-genetic characteristics, wealthy people tend to marry other wealthy people for example. Or related to genetics, tall people might prefer to marry another tall person and height is somehow correlated to how long a person will live which would also inflate estimates of heritability life span.

The new analysis found that by correcting for the effects of assortative mating, life span heritability is likely no more than seven percent and perhaps even lower. The findings in this study certainly point to how low heritability of lifespan is. There are many things to learn about the biology of aging from human genes, however the recent findings temper expectations about what types of things can be learned and how easy it will be.

To view the original scientific study click here: Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating

Nuts Help Control Weight Gain

Two separate studies have shown that consuming nuts on a daily basis may provide benefits to controlling weight gain, achieving overall metabolic health, and other cardiovascular benefits. Both studies delved into the influence eating nuts has on feeling full and improving insulin and glucose responses. These are things that can influence body weight.

The first study was conducted at the Nutrition Department at the Harvard T. H. Chan School of Public Health in Boston and involved 3 different groups of adults: 25,394 healthy men through Healthy Professionals Follow-up Study, 53,541 women through Nurses’ Health Study and another 47,255 women in Nurses Health Study II. Each of the participants in each group filled out food frequency questionnaires each year for 4 years.

The study team discovered that by replacing foods with less nutritional value with a one once serving of nuts on a daily basis resulted in a lower risk of obesity and weight gain over the 4 year length of the studies. They also found that substituting just one serving a day of nuts instead of one serving of a red meat, processed meat, desserts, potato chips or french fries, resulted in less weight gain. One serving of nuts is one ounce of whole nuts or two tablespoons of a nut butter. The study team believes their findings can be applied to the general population even though most of the participants were part of a health profession and mostly white.

Many people look at nuts as foods that are high in calories and fat and so do not consider them as a healthy snack item. However, the study shows that they actually are associated with less weight gain issues. When people reach adulthood they will begin gaining weight about one pound per year. Over 20 years that is quite a bit of weight gain. Substituting nuts for less nutritionally healthy foods can help prevent this gradual weight gain and also reduce risks of cardiovascular diseases related to weight gain and obesity.

The second study involved Brazil Nuts and was conducted at San Diego State University in 2017 with a grant provided by the American Heart Association. This study involved 22 healthy adults with two men and 20 women all age 20 or older and with a mean body mass index of 22.3. The participants ate either 20 grains of Brazil nuts which is about five nuts or 36 grams of pretzels in addition to their normal diet. The pretzels and Brazil nuts both had about the same number of calories and sodium content. They did this in two trials with 48 hours between each trial.

The team found that both the pretzels and Brazil nuts created reduced hunger feelings and a sense of fullness, however the Brazil nuts created a much fuller feeling of satiety. At forty minutes after the snacks were consumed, the team found the pretzels created a significant increase in insulin and blood glucose levels while the Brazil nuts did not. Brazil nuts actually stabilized both the insulin and blood glucose levels after they were consumed which could be beneficial for preventing weight gain.

Brazil Nuts are very rich in Selenium which is a mineral that might be associated with the insulin and blood glucose improvements noted in the study. Nuts are packed with fiber, protein, unsaturated fatty acids and a variety of beneficial chemicals. Consuming nuts can help reduce appetite and promote fullness which means people tend to eat less throughout the day. In addition to Brazil nuts, almonds, walnuts, pecans, macadamias and pistachios are other good choices!

Exercise Improves Elimination of Toxic Proteins from Muscles

A new study conducted by researchers at the University of Sao Paulo in Brazil in partnership with colleagues in the U.S. and Norway and published in Scientific Reports, has shown that lack of muscle stimulus results in a buildup of inadequately processed proteins in muscle cells which in turn leads to muscle wasting and weakness. This typical muscle dysfunction is a condition commonly effecting the elderly, individuals who sit for long periods of time without any exercise and bedridden patients.

Test results from rats with induced sciatic nerve injury which stopped receiving stimuli, showed the protein buildup was caused by impairment of autophagy which is the cellular machinery responsible for identifying then removing damaged toxins and proteins. The analysis of the tests on the rats subjected to a regime of aerobic exercise training which were previous to injury enabled the researchers to demonstrate that physical exercise can keep the autophagic system primed and then facilitate its activity as necessary. This is similar to muscle dysfunction due to the lack of stimulus.

Daily exercise will sensitize the autophagic system which facilitates the elimination of organelles (any of a variety of organized or specialized structures within a living cell) and proteins that are not functional in the muscles. It is important that removal of these dysfunctional components occur. When they accumulate they will become toxic and contribute to muscle cell impairment and death.

A good example of what muscle autophagy is, is by comparing muscles working in a similar manner as a refrigerator which runs on electricity. If the signal ceases due to someone pulling the plug on the frig or in the case of muscles blocks the neurons that innervate the muscles, it won’t take too long for food in a frig to spoil and proteins in muscles to spoil at different rates according to their composition. At this point an early warning mechanism in cells activates the autophagic system which will identify, isolate and then incinerate the defective material which prevents propagation of the damage. If the muscles do not receive the right electric signals for long periods of time, the early warning mechanism will stop working properly and cell collapse will occur. Without autophagy, a cascade effect will occur which leads to cell death.

In the current study, rats were submitted to sciatic nerve ligation surgery which created an effect equal to that of sciatic nerve compression in humans. The pain this injury can cause prevents people from using the leg affected by the injury which will lead to weakened muscles and eventually atrophy of those muscles.

Previous to surgery, the rats were divided into two groups. One group remained sedentary while the other group was given exercise training which consisted of running at 60% maximum aerobic capacity for one hour a day, five days per week. After four weeks of exercise training, surgery was performed. The muscular dysfunction induced by sciatic nerve injury was discovered to be less aggressive in the group which had aerobic exercise than the group of rats that were sedentary. Biochemical and functional parameters in the affected muscles were also evaluated. The aerobic training increased autophagic flux and therefore reduced dysfunctional protein levels in the muscles of the rats. Occurring at the same time was improvement in the muscle tissue’s contractility properties. Exercise is a transient stress which will leave memory in the organism and in this case via the autophagic system. When the organism is subjected to a variety of stress, it is better prepared to respond and combat the effects.

The team performed two other experiments which were designed to more thoroughly investigate the link between autophagy and exercise. One experiment involved mice in which the autophagy related gene ATG7 was silenced in the skeletal system. ATG7 encodes a particular protein responsible for synthesizing a vesicle called the autophagosome which forms around dysfunctional organelles and then transports them to the lysosome where they are broken down and then digested. This particular experiment validated the importance of autophagy in muscle biology. ATG7 will knockout mice that had not been subjected to sciatic nerve litigation although displayed muscular dysfunction.

In the second experiment, muscles from rats with sciatic nerve injury and control rats without injury were treated with chloroquine, a drug which inhibits autophagy by raising the lysosomal pH or alkalinity and therefore prevents the degradation of defective proteins. These tests showed less muscle strength in the control group of rats treated with the drug than in the untreated group. Chloroquine had no effect at all on the muscles of the rats with the sciatic nerve injury showing that the inhibition of autophagy is critical to muscular dysfunction caused by lack of stimulus.

Rather than aiming to find a treatment for people who are unable to exercise adequately, the goal of the studies was to use an experimental model for future research to help understand the cellular processes involved in muscle dysfunction. This will help facilitate the development of interventions capable of minimizing or even reversing an increasingly serious problem with muscle weakness and atrophy caused by lack of movement. By identifying a molecule that will selectively keep the autophagic system alert similar to what happens during physical exercise, treatments may be developed which can be given to people with this type of muscle disorder which includes people who are bedridden for extended periods of time, patients with degenerative muscular diseases and the elderly.

To view the original scientific study click here: Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy.

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