Lack of Exercise, Not Aging, Causes Weakness and Loss of Muscle in Older People

Aging does not cause you to lose muscles. Loss of muscle is caused by lack of exercise. You can preserve both muscle size and strength by continuing to exercise a long as you live. Compare the MRIs of the legs of 40- and 70-year-old triathletes, and a 70-year-old non-exerciser:

The dark areas are muscle, the light areas are fat. Which legs would you rather have?

Forty competitive athletes, aged 40-81, who trained four to five times a week, had the same size muscles, the same absence of fat around their muscles, and close to the same strength as much younger athletes (The Physician and Sportsmedicine, September 2011). Many of the diseases and debilitating conditions associated with aging are caused by lack of exercise. "Exercise decreases body fat and obesity, increases muscle strength, improves balance, gait, and mobility, decreases likelihood of falling, improves psychological health, reduces arthritis pain, and heart attacks, osteoporosis, cancer, and diabetes."

After age 40, the average person loses more than eight percent of muscle size per decade. This loss increases to 15 percent per decade after age 75 years. Older people who lose muscles are four times more likely be disabled, have difficulty walking, and need walkers and other mechanical devices to help them walk (Am J Epidemiol, 1998; 147(8):755-763).

Exercise Makes You Smarter

People who exercise regularly are far less likely to suffer dementia and had less than half the risk of death during the 17-year study period, compared to those who do not exercise (Medicine & Science in Sports & Exercise, February, 2012).

Researchers followed 45,000 men and 15,000 women, ages 20 to 88 years, in the United States for an average of 17 years. Six times as many people in the low fitness group suffered from dementia, compared to those who exercised regularly. While deaths in the United States associated with heart disease, breast cancer and stroke have declined in recent years, deaths related to dementia and Alzheimer's disease rose 46 percent between 2002 and 2006.

Another exciting study, from Japan, shows that many of the benefits that exercise provides to muscles are also provided to your brain (The Journal of Physiology, February, 2012;590(Pt 3):607-16).

THE STUDY: Adult male rats exercised to exhaustion at moderate intensity on a treadmill. Glycogen, sugar stored in muscles, was depleted by 82-90 percent. One day later, the rats' muscles could store 43-46 percent more than they could originally, In a like manner, brain glycogen levels decreased by 50-64 percent with exhaustive exercise, and were able to store 29-63 percent more on the next day. The greater the depletion of sugar in muscles and brain, the greater the ability to store more sugar after the rats were fed. The brain filled with sugar before the muscles did and after four weeks of training, the rats' brains could store significantly more glycogen.

EXPLANATION: Sugar is the most efficient source of energy for your muscles during intense exercise. Sugar is the most efficient source of energy for your brain ALL the time. When you exercise regularly, you increase the ability of your muscles to store sugar so you can move faster and longer. This study suggests that exercise also increases the energy supply to your brain, which will help you to think and reason better.

Rheumatoid Arthritis Patients Benefit from Cortisone Injections

Cortisone-type injections into joints control painful rheumatoid arthritis by blocking protein changes that damage joints (Arthritis Research & Therapy, published online Feb. 2012).

REACTIONS THAT CAUSE RHEUMATOID ARTHRITIS: Rheumatoid arthritis (RA) is characterized by the production of PAD enzymes that convert an amino acid, arginine, into citrullinated proteins. Then the victim's immunity makes highly specific anti- citrullinated protein antibodies that attack the synovium and cause it to swell, thicken, and hurt.

WHY CORTISONE INJECTIONS WORK: Injecting cortisone-type drugs into the joints blocks the production of the PAD enzymes that produce citrullinated proteins, and this decreases the thickness of the synovium, and the resultant pain.

THE STUDY: The authors biopsied the swollen knees of patients with rheumatoid arthritis and normal controls. One group was given methotrexate, a common RA treatment used for more than 40 years. The other group was given cortisone-type injections (40 mg triamcinolone hexacetonide) into the knee joint.

Antibodies to citrullinated proteins were found in 86 percent of biopsy samples from the RA patients and in none of the healthy tissue samples. After eight weeks, those receiving the cortisone- type injections had far less swelling of their synovia, far less evidence of inflammation under the microscope, and lower levels of cutrullinated proteins and PAD enzymes. Methotrexate had no effect on citrullinated proteins, PAD enzymes or inflammation in the synovium, although these patients did feel better.

CONCLUSION: This study explains why cortisone-type injections are such an effective treatment for rheumatoid arthritis. However, the effects of the injections do not last and a few months later, the patient may need another injection that may increase risk for diabetes, osteoporosis, and other side effects.

Fasting Slows You Down

Fasting for just a few hours slows an athlete down and the longer he fasts, the slower he moves. A recent study from Denmark shows that after 72 hours of fasting, a person's muscles accumulate far more fat and glycogen (stored sugar) than after 10 hours of fasting (American Journal of Physiology, Endocrinology and Metabolism, January 2012). This slows a competitive athlete down because it keeps muscles from responding to insulin and using more sugar for energy.

Insulin drives sugar into muscles most effectively when muscles are low on sugar and fat. Filling muscles with sugar or fat blocks insulin and reduces the amount of sugar that can enter muscle cells. Remember that when you exercise for more than an hour, you need to keep on taking sugar. The more intensely you exercise, the greater percentage of sugar your muscles use for energy. Emptying your muscles of sugar causes sugar to enter muscles even faster.

LACK OF SUGAR LIMITS SPEED: The time it takes to get oxygen into muscles is the limiting factor for how fast an athlete can move in competition. If he can get more oxygen into muscles, he will move faster. Muscles use fat, sugar and (to a lesser degree) protein for energy. Since sugar requires the least oxygen, an athlete moves faster when his muscles burn a greater percentage of sugar. If he fasts, he gets almost all of the energy to drive his muscles from his own body fat. Using fat for energy requires more oxygen, so he has to slow down.

MUSCLES CAN STILL FILL WITH SUGAR DURING FASTING: How can muscles start to fill up with sugar after three days of fasting? With fasting, the body breaks down its own protein for energy. Protein is made up of chains of building blocks called amino acids. Some of the amino acids are called branched-chain amino acids. The liver can convert these amino acids into sugars (called gluconeogenesis) which then travel in the bloodstream to be stored in muscles as glycogen.

HOW TO EAT TO COMPETE: If you are competing in sporting events that require speed, you should eat a meal that contains carbohydrates closer than three hours before the start of your event. If the event lasts more than an hour, take some source of sugar during your event, such as sugared drinks, fruit, candy, grain bars or dried fruit paste (fruit leather).

Cancer Cells Need More Sugar

Cancer cells are different from normal cells. Every normal cell in your body has programmed into its genetic material, a process called APOPTOSIS, that lets it live and multiply only so long and then it dies. For example, skin cells live 28 days and die; cells lining your mouth live 24-48 hours and die; and red blood cells live up to 120 days. Cancer cells lose their ability to die. They try to live forever and they kill by going from one type of tissue to invade another type of tissue and destroy it. For example, breast cancer cells can eventually spread to your brain or lungs. They replace and destroy these tissues, and you die because your brain or lungs are not able to work properly.

Cancer cells grow and multiply so rapidly that they need huge amounts of the sugar, glucose, to supply them with the energy necessary for growth. Let me explain why cancer cells need so much sugar.

HOW CELLS GET ENERGY: All cells get their energy from two major processes:
• glycolysis, and
• the Krebs Cycle.
Normal cells primarily use the Krebs Cycle for energy since it is more efficient and provides more energy. However, cancer cells do not use the Krebs Cycle well, and therefore must depend on glycolysis. Because they use this inefficient pathway for energy, cancer cells that have forgotten to die have an incredible increase in need for energy from the sugar, glucose. Since insulin drives sugar into cells, insulin and ILGF-1 (insulin-like growth factor-1) feed cancer cells glucose, encouraging them to grow and multiply.

CANCER CELLS USE GLYCOLYSIS: In the early 1920s, Otto Warburg demonstrated that cancer cells can live without oxygen by getting their energy from glycolysis. Since glycolysis uses the single sugar, glucose, for energy, cancer cells use tremendous amounts of glucose to grow. Since cancer cells depend on glucose for energy, anything that interferes with the body's normal use of glucose supplies more sugar to the growing cancer cells, which will increase growth of an existing cancer and risk for new cancers. This is one of the reasons why diabetes and excess weight increase risk for cancer (see the third report below).

MITOCHONDRIA: In every cell are from a few to hundreds of small areas called mitochondria. They provide energy for cells through the Krebs Cycle, which is far more efficient than glycolysis, the process that supplies energy inside cells but outside the mitochondria. All cells need functioning mitochondria, where the Krebs Cycle occurs, to have apoptosis. Cancer cells have defective mitochondria which forces them to use glycolysis for energy. Since cancer cells have defective mitochondria, and do not use the Krebs cycle effectively, they do not have apoptosis, so they live indefinitely and kill by invading and destroying normal cells.

A CURE FOR CANCER? Researchers today are trying to cure cancer by blocking glycolysis. This could force mitochondria to become active again and use the Krebs Cycle for energy so that the cells can stop being cancerous and regain apoptosis, their programmable cell death. The chemical dichloroacetic acid (DCA), which increases the chemical reactions of the Krebs cycle in mitochondria, has been shown to kill cancer cells in laboratory tests and in animals. Anything that activates or restores mitochondria can restart apoptosis and cause cancer cells to kill themselves. At the University of Alberta, Dr. Evangelos Michelakis is doing research on DCA. Another activator of mitochondria, 3-BrOP, is being studied at The University of Texas M. D. Anderson Cancer Center. 2-deoxyglucose (2-DG) is being used at Emory University School of Medicine, and lactate dehydrogenase A is being researched at Johns Hopkins University.

DIANA'S FATHER WORKED WITH KREBS: In the 1930's, my wife Diana's father, Donald Purdie, was a professor at Cambridge University in England and spent his career working with Nobel Prize winner, Hans Krebs (1900-1981) whose research group worked out most of the chemical reactions that supply energy for cells. Her father published with Hans Krebs.

In the early 1940s, the Germans bombed England daily. Donald Purdie accepted the professorship and chair of the Department of Chemistry at Raffles College in Singapore, to get away from the war in Europe. Diana was born in Singapore in January 1942. Two weeks later, the Japanese invaded Singapore and her father was taken prisoner. The Japanese killed this great academic, starving him to death while he was forced to do manual labor to build the Burma-Thai railroad.

Diana and her mother and brother escaped on a boat that arrived in Bombay six weeks later. They then came to the United States and her mother didn't learn of Donald's death until three years later.