The Unique Benefits Anaerobic Exercise Has on Fat Cells

Turns out that lifting can have positive effects on body fat at the cellular level. Muscles are also a main way for the body to store amino acids to fight infections.

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We all know that lifting weights can build up our muscles. But by changing the inner workings of cells, weight training may also shrink fat, according to an enlightening new study of the molecular underpinnings of resistance exercise. The study, which involved mice and people, found that after weight training, muscles create and release little bubbles of genetic material that can flow to fat cells, jump-starting processes there related to fat burning.

The results add to mounting scientific evidence that resistance exercise has unique benefits for fat loss. They also underscore how extensive and interconnected the internal effects of exercise can be.

Many of us pigeonhole resistance training as muscle building, and with good reason. Lifting weights — or working against our body weight as we bob through push-ups, squats or chair dips — will noticeably boost our muscles’ size and strength. But a growing number of studies suggest weight training also reshapes our metabolisms and waistlines. In recent experiments, weight workouts goosed energy expenditure and fat burning for at least 24 hours afterward in young womenoverweight men and athletes. Likewise, in a study I covered earlier this month, people who occasionally lifted weights were far less likely to become obese than those who never lifted.

But how weight training revamps body fat remains murky. Part of the effect occurs because muscle is metabolically active and burns calories, so adding muscle mass by lifting should increase energy expenditure and resting metabolic rates. After six months of heavy lifting, for example, muscles will burn more calories just because they are larger. But that doesn’t fully explain the effect, because adding muscle mass requires time and repetition, while some of the metabolic effects of weight training on fat stores seem to occur immediately after exercise.

Perhaps, then, something happens at a molecular level right after resistance workouts that targets fat cells, a hypothesis that a group of scientists at the University of Kentucky in Lexington, the University of Nebraska-Lincoln and other institutions recently decided to investigate. The researchers had been studying muscle health for years, but had grown increasingly interested in other tissues, especially fat. Maybe, they speculated, muscles and fat chatted together amiably after a workout.

In the past decade, the idea that cells and tissues communicate across the expanse of our bodies has become widely accepted, though the complexity of the interactions remains boggling. Sophisticated experiments show that muscles, for instance, release a cascade of hormones and other proteins after exercise that enter the bloodstream, course along to various organs and trigger biochemical reactions there, in a process known as cellular crosstalk.

Our tissues also may pump out tiny bubbles, known as vesicles, during crosstalk. Once considered microscopic trash bags, stuffed with cellular debris, vesicles now are known to contain active, healthy genetic material and other substances. Released into the bloodstream, they relay this biological matter from one tissue to another, like minuscule messages in bottles.

Intriguingly, some experiments indicate that aerobic exercise prompts muscles to release such vesicles, conveying a variety of messages. But few studies had looked into whether resistance exercise might also result in vesicle formation and inter-tissue chatter.

So, for the new study, which was published in May in The FASEB Journal, from the Federation of American Societies for Experimental Biology, the researchers decided to examine the cells of bodybuilding mice. They first experimentally incapacitated several of the leg muscles in healthy adult mice, leaving a single muscle to carry all the physical demands of movement. That muscle swiftly hypertrophied, or bulked up, providing an accelerated version of resistance training.

Before and after that process, the researchers drew blood, biopsied tissues, centrifuged fluids and microscopically searched for vesicles and other molecular changes in the tissues.

They noted plenty. Before their improvised weight training, the rodents’ leg muscles had teemed with a particular snippet of genetic material, known as miR-1, that modulates muscle growth. In normal, untrained muscles, miR-1, one of a group of tiny strands of genetic material known as microRNA, keeps a brake on muscle building.

After the rodents’ resistance exercise, which consisted of walking around, though, the animals’ leg muscles appeared depleted of miR-1. At the same time, the vesicles in their bloodstream now thronged with the stuff, as did nearby fat tissue. It seems, the scientists concluded, that the animals’ muscle cells somehow packed those bits of microRNA that retard hypertrophy into vesicles and posted them to neighboring fat cells, which then allowed the muscles immediately to grow.

But what was the miR-1 doing to the fat once it arrived, the scientist wondered? To find out, they marked vesicles from weight-trained mice with a fluorescent dye, injected them into untrained animals, and tracked the glowing bubbles’ paths. The vesicles homed in on fat, the scientists saw, then dissolved and deposited their miR-1 cargo there.

Soon after, some of the genes in the fat cells went into overdrive. These genes help direct the breakdown of fat into fatty acids, which other cells then can use as fuel, reducing fat stores. In effect, weight training was shrinking fat in mice by creating vesicles in muscles that, through genetic signals, told the fat it was time to break itself apart.

“The process was just remarkable,” said John J. McCarthy, a professor of physiology at the University of Kentucky, who was an author of the study with his then graduate student Ivan J. Vechetti Jr. and other colleagues.

Mice are not people, though. So, as a final facet of the study, the scientists gathered blood and tissue from healthy men and women who had performed a single, fatiguing lower-body weight workout and confirmed that, as in mice, miR-1 levels in the volunteers’ muscles dropped after their lifting, while the quantity of miR-1-containing vesicles in their bloodstreams soared.

Of course, the study mostly involved mice and was not designed to tell us how often or intensely we should lift to maximize vesicle output and fat burn. But, even so, the results serve as a bracing reminder that “muscle mass is vitally important for metabolic health,” Dr. McCarthy said, and that we start building that mass and getting our tissues talking every time we hoist a weight.

New “Obesity Fighting” Drug That Claims to Cut Body Weight by Up to 20 Percent

People have been looking for weight loss in a pill for ages. The issue is whether this drug will have any major side effects on certain people, and if it does, whether those side effects are worth the benefits of weight loss. The natural way to lose weight is to simply burn more calories than you consume, thus entering what’s known as a caloric deficit. The importance of “calories in, calories out,” is not emphasized enough in our systems of education, and it is a massive detriment to the population that that’s the case. In the trial, one of the people began gaining weight after the administration of the drug stopped, and that shows how losing weight remains an issue to address outside of medically-supervised drug usage. Additionally, I have to question how much of the weight loss was from the drug when the participants of the trial were also supposedly eating less and doing more exercise.

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The drug – semaglutide – hijacks the body’s appetite regulating system in the brain, leading to reduced hunger and calorie intake.

Rachel Batterham, professor of obesity, diabetes and endocrinology who leads the Centre for Obesity Research at UCL and the UCLH Centre for Weight Management, said: “The findings of this study represent a major breakthrough for improving the health of people with obesity.

“Three quarters (75%) of people who received semaglutide 2.4mg lost more than 10% of their body weight and more than one-third lost more than 20%.

The professor, who is one of the principal authors on the paper, added: “No other drug has come close to producing this level of weight loss – this really is a game-changer.

“For the first time, people can achieve through drugs what was only possible through weight-loss surgery.”

The drug will soon be submitted for regulatory approval as a treatment for obesity to the National Institute of Clinical Excellence (NICE), the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA).

As well as the drug, participants received individual face-to-face or phone counselling sessions from registered dietitians every four weeks to help them adhere to the reduced-calorie diet and increased physical activity.

They also received incentives such as kettle bells or food scales to mark progress and milestones.

A placebo group observed an average weight loss of 2.6kg (0.4 stone) with a reduction in BMI of minus 0.92.

Semaglutide is clinically approved to be used for patients with type 2 diabetes, but they are prescribed a lower dose.

Obesity May Dull the Sense of Taste

The study here found that obese mice had about 25 percent fewer taste buds than mice of a healthy weight. As some similar effect is likely found in humans, this research should provide an increased motivation (that is, enjoyment of food) for reducing the obesity epidemic, which I have written about at more length before.

Previous studies have indicated that weight gain can reduce one’s sensitivity to the taste of food, and that this effect can be reversed when the weight is lost again, but it’s been unclear as to how this phenomenon arises. Now a study publishing March 20 in the open-access journal PLOS Biology by Andrew Kaufman, Robin Dando, and colleagues at Cornell University shows that inflammation, driven by obesity, actually reduces the number of taste buds on the tongues of mice.

A taste bud comprises of approximately 50 to 100 cells of three major types, each with different roles in sensing the five primary tastes (salt, sweet, bitter, sour, and umami). Taste bud cells turn over quickly, with an average lifespan of just 10 days. To explore changes in taste buds in obesity, the authors fed mice either a normal diet made up of 14% fat, or an obesogenic diet containing 58% fat. Perhaps unsurprisingly, after 8 weeks, the mice fed the obesogenic diet weigh about one-third more than those receiving normal chow. But strikingly, the obese mice had about 25% fewer taste buds than the lean mice, with no change in the average size or the distribution of the three cell types within individual buds.

Unfinished Coverage of the Obesity Epidemic

The statistics on the epidemic of too many people being obese and overweight are disturbing. There are reports finding that — within a decade — the number of people who will be overweight or obese will be about a third of Earth’s total human population. That makes it a significant issue of public health costs, but it’s unsurprising that the corporate mass media hasn’t given this (or a number of other problems) much coverage. The latest idiocy appearing out of today’s Oval Office is too often granted precedence instead.

As is the case frequently enough, the United States provides an extreme example of this world trend of rising obesity rates. A recent study by the Centers for Disease Control and Prevention found that the American obesity epidemic is at a record high, with almost 40 percent of adults being considered obese. Over two thirds of Americans were also found to be overweight or obese, and of those, about a fifth of American adolescents fit in the obese range.

The costs associated with the American obesity problem have been estimated at $190 billion annually, or an amount that’s about 1 percent of GDP and nearly twice the annual budget of the Department of Education. This amount may of course rise even higher if obesity rates continue expanding.

While the costs are difficult to quantify, as it’s difficult to truly attach monetary costs to the overall well-being of livelihoods, there’s ample evidence to conclude that a lot of people being too overweight is a serious problem. It’s therefore time to more actively discuss solutions.

For starters, all products containing sugar could be required to have a daily recommended limit of 50 grams of sugar labeled on the package. That’s about the amount of sugar the World Health Organization recommends people limit themselves to daily. The sugar industry has of course tried to prevent these sorts of labels, as they represent a threat to their profits — even as the lack of them continues to take its toll on public health.

Beyond sugar being “empty calories,” there is bitter proof that an excess consumption of sugar has inherently negative effects. An overabundance of sugar consumption accelerates the decay of teeth, often causes undesirable weight gain, raises risks for a lot of diseases, and presents problems from potential cognitive damage to a higher chance of developing various consequential health conditions. A study recently released even discovered a correlation between sugar intake and worsened outcomes from cancer. The study’s lead researcher said that “Our research reveals how the hyperactive sugar consumption of cancerous cells leads to a vicious cycle of continued stimulation of cancer development and growth.”

The important point about sugar being raised, it’s also worth noting that the direct cause of weight gain is typically the continual intake of more calories than is burned off. A pound of fat is about 3500 calories, so the excess consumption of those is obviously contributing to more pounds. What a lot of people do not realize though is that a pound of muscle burns a higher amount of calories than a pound of fat does, even at rest. Aerobic exercise (such as running) is regularly seen as a way of losing weight, but anaerobic exercise (such as doing pushups) is primarily what will create the muscles that could prevent a lot of weight gain to begin with.

Obesity Can Cause Scarring of Fat Tissue That Makes Weight Loss More Difficult

This research is insight into the common adage that weight is easier to gain than it is to lose. Further examination into the Lysyl oxidase molecule that’s associated with the scarring is found at the link and in the actual study.

The fat of obese people becomes distressed, scarred and inflamed, which can make weight loss more difficult, research at the University of Exeter has found.

An analysis of the health of adipose (fat) tissue in overweight people found that their fat can cease to cope as it increases in size and becomes suffocated by its own expansion.

Dr Katarina Kos, Senior Lecturer at the University of Exeter’s Medical School, examined samples of fat and tissue from patients, including those with weight problems who have undergone bariatric surgery.

Fat in obese people can suffocate and struggle for oxygen supply, due in part to the increase in the fat cells’ size. As cells get bigger they become distressed and struggle for oxygen which triggers inflammation in the fat tissue. The inflammation spills over from fat tissue into the blood stream and is eventually measurable in the circulation by a blood test.

Stressed and unhealthy fat tissue is also less able to accommodate more unused dietary energy. With fat tissue not being able to do its most vital job, which is storing excess calories, the excess energy can be increasingly diverted from fat tissue to vital organs, including the liver, muscle and heart. This can lead to obesity-related health complications such as fatty liver disease and cardiovascular disease.

Dr Kos found that fat tissue which is fibrous is also stiffer and more rigid. Previous studies of people who have had weight loss surgery showed that increased levels of scarring can make it harder to lose weight.

“Scarring of fat tissue may make weight loss more difficult,” Dr Kos said. “But this does not mean that scarring makes weight loss impossible. Adding some regular activity to a somewhat reduced energy intake for a longer period makes weight loss possible and helps the fat tissue not to become further overworked. We know that doing this improves our blood sugar and is key in the management of diabetes.”

Dr Kos, who leads the adipose tissue biology group at the University of Exeter, said where obese people carry their fat can have an impact on their health.

Scarring of fat tissue can change a person’s body shape. They can develop an ‘apple’ body shape with a large tummy and more fat within the deeper layers of the tummy and around the organs. However, they can retain thin arms and legs, as there is little fat just below the skin. Although such people can appear relatively slim, fat can be deposited in their abdomen and in their internal organs, including their liver, pancreas, muscle and the heart. Fat can also be stored around and in the arteries causing arteriosclerosis, a stiffening of arteries predisposing people to high blood pressure, heart disease and strokes. Scarring of fat tissue has also been linked to diabetes.

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Dr Kos added: “Further research is needed to determine how to avoid our fat tissue becoming unhealthy and how protect it from inflammation and scarring. There is evidence that once fat tissue becomes scarred, despite weight loss, it may not recover fully. We need to look after our fat tissue which can cease to cope if it is overworked when being forced to absorb more and more calories. As a clinician, I would advise exercise or at least a ‘walk’ after a meal which can make a great difference to our metabolic health.”