From The Desk Of Clarence Bass
Fast-Twitch Muscle Fights Fat and Aging Metabolism
In his book Bending the Aging Curve, University of Miami Professor Joseph Signorile bemoans the decline in muscle and strength that begins at about 40 in the untrained person. He also rejoices in the fact that it doesn’t have to be that way. Two studies, one in 2008 and the other in 2013, bolster Signorile’s optimistic view.
Dr. Signorile explains that the lion’s share of the decline occurs in the fast-twitch muscle fibers, which predominate in sprinters, weight lifters, and other strength athletes. The slow-twitch, endurance fibers seen in marathon runners and other endurance athletes tend to stick around even in the untrained person. As shown by the bodies of athletes on either end of the strength-endurance spectrum, fiber type plays a major role in muscle size. Slow-twitch fibers are small, and fast-twitch fibers are large. Most people begin with a roughly equal balance of fast and slow fibers.
“As we age, the motor units [muscle and nerve] that we lose are mainly the fast-twitch variety,” Signorile writes. “The slow-twitch fibers show practically no change.”
We don’t need a graph to show the pattern of change in fast and slow twitch muscle fibers as we age. The curve of the slow-twitch fibers over time is no curve at all; it’s flat, showing essentially the same number of slow fibers at 60 and 90. On the other hand, the fast-fiber curve drops rapidly from 60 to 90. Translated to the activities of everyday life, this means the untrained person becomes slower and weaker with age. Independence suffers over time.
It’s a dismal picture, but all is not lost. Far from it. We can keep our fast-twitch fibers alive and well with high intensity exercise. Signorile is a big booster of resistance training and interval training.
Japanese and American researchers get under the hood and explore the impact of the fast fibers on body composition and metabolism. They show what happens when the fast fibers shrivel up and go away—and what happens when they are restored. It’s an inspiring story for those willing to help themselves.
The first study, led by Yasuhiro Izumiya, was published February 6, 2008, in Cell Metabolism.
It is well-established that slow, endurance fibers play an important role in regulating whole-body metabolism; for example, mice genetically altered to have more type 1 fibers can eat more without getting fat. That’s one reason why endurance athletes are generally quite lean. However, little research has been done on the role of the fast, strength fibers in the development of obesity and obesity-related diseases. Does muscle fight fat? Are sprinters lean because they’re muscular?
To find out Izumiya et al engineered mice to reversibly grow type IIb fast fibers. Activating a signaling protein in the mice induced fast-twitch muscle fiber growth; turning the protein off reversed the process. (Were it only so easy in humans.) This on-off process allowed the researchers to test the function of fast-twitch muscle mass. What happened is empowering.
It’s also complicated. It took 43 pages to explain it. Here’s the bottom line:
Feeding the mice a high-fat, high-sugar diet—with the muscle-switch off—made them fat. Turning the muscle-switch on—with no change in diet or physical activity—brought about an amazing transformation. It led to growth of type IIb muscle fibers and increased strength, while reducing body weight and fat mass. And there's more.
Izumiya et al also observed an improvement in whole-body metabolism linked to fat cell shrinkage, increased muscle glucose uptake, and increased fat uptake and oxidation (burning) in the heart and liver. These changes brought about a marked transformation in the control of energy balance. Calories in and calories out came into balance with no change in diet or physical activity.
A companion piece in the same issue of Cell Metabolism by Brooke C. Harrison and Leslie A. Leinwand, Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, summarized the findings:
“In summary, the work of Izumiya et al reveals the intricate interplay between diet, energy balance, and the function/morphology of diverse tissue systems such as skeletal muscle and liver. These findings indicate that interventions designed to increase skeletal muscle mass in at-risk human populations may prove to be critical weapons in the fight against obesity and obesity-related comorbidities including diabetes, heart disease, stroke, hypertension, and cancer.”
Think about that. It’s both scary and invigorating. Who knew that the loss of fast-twitch muscle fibers that begins in earnest at mid-life for most people is such a disaster? The second study reinforces and adds to the urgency of doing all you can to build and preserve your fast-twitch muscle fibers.
Many of the same researchers are involved in the second study, published online September 17, 2013, in Aging Cell; Kenneth Walsh, Molecular Cardiology Whitaker Cardiovascular Institute, Boston University School of Medicine, is the senior author in both studies.
While the first study focused on fat reduction, this study takes aim at age and obesity related disease. Aging is associated with the development of high blood sugar and accumulation of fat in tissues and organs such as the heart and liver. However, the connection between aging, muscle loss, and metabolic dysfunction is not well understood.
“The aging population and anticipated increase in the incidence of Type 2 diabetes underscore the critical need for better understanding how diabetes is influenced by age-associated changes in body composition,” lead author Yuichi Akasaki and colleagues wrote in introducing the study. “It is not known whether muscle loss and insulin resistance are independent…of the aging process, or if the loss of muscle mass is causally linked to the high incidence of insulin resistance and T2D in middle-aged persons,” they explained.
Here, the researchers used the same engineered mice to examine the consequences of fast-twitch muscle loss—or growth—in young and middle-aged animals fed standard low-fat chow diets.
They began by comparing body composition and metabolic function in young (3 month old) and middle-aged (12 month old) mice. The older mice displayed reductions in overall lean muscle mass, along with metabolic irregularities including high blood sugar and fatty liver.
They then flipped the muscle switch—reversing the loss of lean muscle mass observed upon aging. Good things happened. The increase in muscle mass led to reductions in fat mass, including reduced fat in the liver, and corrected age-associated impairments in blood sugar control.
“These results indicate that the loss of lean muscle mass is a significant contributor to the development of age-related metabolic dysfunction and that interventions that preserve or restore fast/glycolytic [sugar burning] muscle may delay the onset of metabolic disease,” they concluded.
“Based upon this rodent study, it is tempting to speculate that the surge in newly diagnosed cases of Type 2 diabetes seen in midlife (Centers for Disease Control and Prevention, 2011) may be in large part attributable to the loss in glycolytic [sugar burning] muscle mass that occurs within this time frame,” they wrote.
“Work with this model system supports the concept that exercise regimens, such as resistance training…may be particularly efficacious in promoting metabolic health in the aging population,” they added.
In short, muscle fights diabetes and other age and obesity-related diseases.
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Farsighted exercise scientists and others have long maintained that muscle drives the aging process. BIOMARKERS: The 10 Determinants of Aging You Can Control (Simon & Schuster, 1991) was far and away the most detailed and visionary tome written for a mass audience.
Biomarkers authors Evans and Rosenberg called muscle mass and strength the lead dominoes of aging. The Tufts University professors wrote that the first biomarker, muscle mass, is responsible for the vitality of our whole physiological apparatus. Muscle mass and strength, the second signpost, are the primary biomarkers. When they start to topple, the other indicia of aging soon follow. On the other hand, when muscle mass and strength are maintained, the other markers of aging are likewise maintained. That is where strength training comes to our aid. Aerobic exercise and diet are important, but strength training, Evans and Rosenberg declared decades ago, is pivotal if you want to stay young longer.
To paraphrase Satchel Paige, the ageless baseball pitcher, biomarkers are those things that tell how old you would be “if you didn’t know how old you was.” In Biomarkers, Evans and Rosenberg isolated the following signposts of vitality that can be altered for the better by changes in lifestyle: 1) Muscle Mass, 2) Strength, 3) Basal Metabolic Rate, 4) Body Fat Percentage, 5) Aerobic Capacity, 6) Blood-sugar Tolerance, 7) Cholesterol/HDL Ratio, 8) Blood Pressure, 9) Bone density, 10) Ability to regulate Internal Temperature.
Significantly, all 10 biomarkers can be revived or improved through strength training.
To help people understand how strength training affects the biomarkers, Evans and Rosenberg coined the term “sarcopenia” to describe an ailment that affects many old people and deprives them of their independence. “Sarco” refers to flesh, “penia” means a reduction in amount. So sarcopenia describes an overall weakening of the body caused by a change in body composition in favor of fat and at the expense of muscle. Sedentary people usually begin losing muscle and gaining fat in earnest at about 40; the decline becomes more rapid with each passing decade.
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Professor Edward Coyle, Human Performance Lab, University of Texas at Austin, was perhaps the first to explain the effectiveness of sprint interval training in terms of muscle fiber type.
It seems logical, Coyle wrote in The Journal of Applied Physiology, that “aerobic endurance performance is only enhanced by aerobic endurance training, but it has been proven wrong in the realm of athletics as well as muscle biochemistry.” Referencing a research paper about the evolutionary underpinning of modern chronic diseases, Coyle suggested that sprint interval training might be an efficient way to keep our sedentary population from crossing “a biological threshold, beyond which chronic health conditions develop.”
Going for the jugular, Coyle said that both sprint interval training and prolonged sub-maximal aerobic exercise increase mitochondrial potential, but reminded us that the muscle fibers affected are different. The specific fibers affected probably explains why very brief sprint training has proven to be as effective [or more effective] for improving endurance as much longer and less intense aerobic training, Coyle related. “All-out sprint training especially stresses recruitment and adaptation of fast twitch muscle fibers that are remarkably and equally responsive as slow twitch muscle fibers in their ability to increase mitochondrial enzyme activity,” Coyle explained. “In fact, the low-intensity aerobic exercise that is typically prescribed for endurance training or health is not very effective at increasing aerobic activity in [fast twitch] muscle fibers, which comprise approximately one-half of the fibers within the muscles of most people,” he continued. “Thus low-intensity aerobic training is not a very effective or efficient method for maximizing aerobic adaptation in skeletal muscle because it generally does not recruit [fast twitch] fibers.”
In other words, sprint interval training increases the endurance capacity in all muscle fibers, fast and slow, while long slow training leaves half of the fibers unused and untrained. Makes perfect sense, doesn’t it? It’s like pulling the wagon with one horse, when two would get you a lot farther down the road.
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For mice and man: Go hard and go home--in both strength and endurance training. Staying active between workouts is also important.
Warning: It you are not accustomed to exercise or
have health issues, see your doctor before attempting high-intensity training.
It’s always wise to begin a new exercise regimen slowly and increase effort
gradually as strength and stamina improve.
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