Tuesday, December 7, 2010

The 5 Factors of Fat Loss Training

We’re using resistance training as the cornerstone of our fat loss programming. Our goal is to work every muscle group hard, frequently, and with intensity that creates a massive “metabolic disturbance” or ”afterburn,” leaving the metabolism elevated for several hours post workout. Here are a few studies to support this:

Schuenke MD, Mikat RP, McBride JM. Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management.
European Journal of Applied Physiology. March 2002, Vol 86 (5): 411-7. Epub 2002 Jan 29.

This study used a circuit training protocol of 12 sets in 31 minutes. EPOC was elevated significantly for 38 hours post workout, which is a pretty significant timeframe for metabolism to be elevated. If you trained from 9 to 10 a.m. on Monday morning, you’re still burning more calories (without training) at midnight on Tuesday! Can we compound this with additional training within that 38 hours? No research has been done, but I have enough case studies to believe that you can.

Another study: Kramer, Volek et al. Influence of exercise training on physiological and performance changes with weight loss in men. Medicine & Science in Sports & Exercise, 1999, Vol. 31, No. 9: 1320-1329

Overweight subjects were assigned to three groups: Diet-only, diet plus aerobics, diet plus aerobics plus weights. The diet group lost 14.6 pounds of fat in 12 weeks. The aerobic group lost only one more pound (15.6 pounds) than the diet group (training was three times a week starting at 30 minutes and progressing to 50 minutes over the 12 weeks). Now, the weight training group lost 21.1 pounds of fat (44% and 35% more than diet- and aerobics-only groups respectively). The addition of aerobic training didn’t result in any real worldsignificant fat loss over dieting alone. Thirtysix sessions of up to 50 minutes is a lot of work for one additional pound of fat loss. However, the addition of resistance training greatly accelerated fat loss results.

One more: Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R. Effects of resistance vs. aerobic training combined with an 800-calorie liquid diet on lean body mass and resting metabolic rate. Journal of the American College of Nutrition, April 1999, 18 (2): 115-21.

The aerobic group performed four hours of aerobics per week. The resistance training group performed 2-4 sets of 8-15 reps, 10 exercises, three times per week. VO2 max increased equally in both groups. Both groups lost weight.

1) High Intensity Resistance Training

The resistance training group lost significantly more fat and didn’t lose any lean body mass, even at only 800 calories per day. The reason the calories were so low was to really take any dietary variables completely out of the equation and compare the effects of the exercise regime on LBM and metabolism. The resistance training group actually increased metabolism compared to the aerobic group, which decreased metabolism. It seems that aerobic training is a more significant stress to the body than a starvation diet.

In my experience, full body training in a superset, tri-set, or circuit format (with non-competing exercises) in a rep range that generates lactic acid (and pushes the lactic acid threshold or LAT) seems to create the biggest metabolic demand. It makes sense; training legs, back, and chest will burn more calories and elevate metabolism more than an isolated approach training one of them. The rep range that seems to work best is the 8-12 hypertrophy range, although going higher will work just as well with a less-trained population.

2. High Intensity Anaerobic Interval Training

The second key “ingredient” in fat loss programming is high intensity interval training (HIIT). I think most readers are well aware of the benefits of interval work. It burns more calories than steady state and elevates metabolism significantly more than other forms of cardio. The only downside is that it flat-out sucks to do! Interval training works. Too bad it isn’t more fun to perform!

The landmark study in interval training was from Tremblay: Tremblay A, Simoneau JA, Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism, July 1994, 43 (7): 814-8

This study pitted 20 weeks of endurance training against 15 weeks of interval training:

• Energy cost of endurance training = 28,661 calories.
• Energy cost of interval training = 13,614 calories (less than half)

The interval training group showed a nine times greater loss in subcutaneous fat than the endurance group (when corrected for energy cost). Read that again. Calorie for calorie, the interval training group lost nine times more fat overall. Why? Maybe it’s EPOC, an up-regulation of fat burning enzyme activity, or straight up G-Flux. I don’t care. I’m a real world guy. If the interval training group had lost the same amount of fat as the endurance group, we’d get the same results in less time. That means interval training is a better tool in your fat loss arsenal.

3. High Intensity Aerobic Interval Training

The next tool we’ll pull out is essentially a lower intensity interval method where we use aerobic intervals. Here’s the study we’ll be referring to: Talanian, Galloway et al. Two weeks of High-Intensity Aerobic Interval Training increases the capacity for fat oxidation during exercise in women. Journal of Applied Physiology, April 2007, 102 (4):1439-47. Epub 2006 Dec 14.

This study looked at high-intensity aerobic interval training and its influence on fat oxidation. In summary, seven sessions of HIIT over two weeks induced marked increases in whole body and skeletal muscle capacity for fatty acid oxidation during exercise in moderately active women. In layman’s terms, the interval work appeared to “up-regulate” fat burning enzymes. This means we can burn more fat in other activities as a result of this inclusion. In other words, we get a bit more bang for our buck.

A quick disclaimer, though: My colleague Alan Aragon once said, “Caring about how much fat is burned during exercise is equivalent to worrying about how much muscle is built during exercise.” In other words, substrate utilization during exercise isn’t really an important variable in the big picture of fat loss. Total calories burned overall is.

4. Steady State High Intensity Aerobic Training

Tool number four is just hard cardio work. This time we’re burning calories. We aren’t working hard enough to increase EPOC significantly or to do anything beyond the session itself. But calories do count. Burning another 300 or so calories per day will add up.

5. Steady State Low Intensity Aerobic Training

This is just random activity, such as going for a walk in the park. It won’t burn a lot of calories or increase muscle or EPOC. There isn’t very much research showing that low intensity aerobic training actually results in very much additional fat loss, but you’re gonna have to really work to convince me that moving more is going to hurt you when you’re in fat attack mode.

Just a reminder... I will be designating 15 or so hours a week at a local personal training center running boot camps, group training, and personal training. I love it and it will be great for clients of Total Health & Fitness. Email me if you are interested. mike.butler@thfonline.com

Telomerase reverses ageing process

Telomerase reverses ageing process

Dramatic rejuvenation of prematurely aged mice hints at potential therapy.

Premature ageing can be reversed by reactivating an enzyme that protects the tips of chromosomes, a study in mice suggests.

Mice engineered to lack the enzyme, called telomerase, become prematurely decrepit. But they bounced back to health when the enzyme was replaced. The finding, published online today in Nature1, hints that some disorders characterized by early ageing could be treated by boosting telomerase activity.

It also offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working, says Ronald DePinho, a cancer geneticist at the Dana-Farber Cancer Institute and Harvard Medical School in Boston, Massachusetts, who led the new study. "This has implications for thinking about telomerase as a serious anti-ageing intervention."

Other scientists, however, point out that mice lacking telomerase are a poor stand-in for the normal ageing process. Moreover, ramping up telomerase in humans could potentially encourage the growth of tumors.
Eternal youth

After its discovery in the 1980s, telomerase gained a reputation as a fountain of youth. Chromosomes have caps of repetitive DNA called telomeres at their ends. Every time cells divide, their telomeres shorten, which eventually prompts them to stop dividing and die. Telomerase prevents this decline in some kinds of cells, including stem cells, by lengthening telomeres, and the hope was that activating the enzyme could slow cellular ageing.

Two decades on, researchers are realizing that telomerase's role in ageing is far more nuanced than first thought. Some studies have uncovered an association between short telomeres and early death, whereas others have failed to back up this link. People with rare diseases characterized by shortened telomeres or telomerase mutations seem to age prematurely, although some tissues are more affected than others.

“They are not studying normal ageing, but ageing in mice made grossly abnormal.”

David Harrison
Jackson Laboratory, Bar Harbor, Maine

When mice are engineered to lack telomerase completely, their telomeres progressively shorten over several generations. These animals age much faster than normal mice — they are barely fertile and suffer from age-related conditions such as osteoporosis, diabetes and neurodegeneration. They also die young. "If you look at all those data together, you walk away with the idea that the loss of telomerase could be a very important instigator of the ageing process," says DePinho.

To find out if these dramatic effects are reversible, DePinho's team engineered mice such that the inactivated telomerase could be switched back on by feeding the mice a chemical called 4-OHT. The researchers allowed the mice to grow to adulthood without the enzyme, and then reactivated it for a month. They assessed the health of the mice another month later.

"What really caught us by surprise was the dramatic reversal of the effects we saw in these animals," says DePinho. He describes the outcome as "a near 'Ponce de Leon' effect" — a reference to the Spanish explorer Juan Ponce de Leon, who went in search of the mythical Fountain of Youth. Shriveled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver and intestines, recuperated from their degenerated state.

The one-month pulse of telomerase also reversed effects of ageing in the brain. Mice with restored telomerase activity had noticeably larger brains than animals still lacking the enzyme, and neural progenitor cells, which produce new neurons and supporting brain cells, started working again.

"It gives us a sense that there's a point of return for age-associated disorders," says DePinho. Drugs that ramp up telomerase activity are worth pursuing as a potential treatment for rare disorders characterized by premature ageing, he says, and perhaps even for more common age-related conditions.
Cancer link

The downside is that telomerase is often mutated in human cancers, and seems to help existing tumors grow faster. But DePinho argues that telomerase should prevent healthy cells from becoming cancerous in the first place by preventing DNA damage.

David Sinclair, a molecular biologist at Harvard Medical School in Boston, agrees there is evidence that activating telomerase might prevent tumors. If the treatment can be made safe, he adds, "It could lead to breakthroughs in restoring organ function in the elderly and treating a variety of diseases of aging."

Spotlight on Nature Photonics

Other researchers are less confident that telomerase can be safely harnessed. "Telomere rejuvenation is potentially very dangerous unless you make sure that it does not stimulate cancer," says David Harrison, who researches ageing at the Jackson Laboratory in Bar Harbor, Maine.

Harrison also questions whether mice lacking telomerase are a good model for human ageing. "They are not studying normal ageing, but ageing in mice made grossly abnormal," he says. Tom Kirkwood, who directs the Institute for Ageing and Health at Newcastle University, UK, agrees, pointing out that telomere erosion "is surely not the only or even dominant, cause" of ageing in humans.

DePinho says he recognizes that there is more to ageing than shortened telomeres, particularly late in life, but argues that telomerase therapy could one day be combined with other therapies that target the biochemical pathways of ageing. "This may be one of several things you need to do in order to extend lifespan and extend healthy living," he says.

Thursday, December 2, 2010