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science nutrition <strong>blog</strong>

The most well-established exercise paradigm for fat loss asserts that exercise consumes energy that is replenished when the body oxidizes stored carbohydrates or fat. The oxidation of these macronutrients converts them into the energy required to pay for the energy deficit created by exercise. As a result, the more calories burned during exercise results in more body fat burned to restore energy. So you might assume, based on this knowledge, that burning as many calories as possible with more cardiovascular exercise would improve your physique more rapidly-making you leaner in no time at all. Well, unfortunately that isn't the case, as once again, theory and reality don't exactly agree. The major deficiency with this approach being that extensive cardiovascular training drives your biochemical system into a catabolic state that drastically reduces the ability to pack on muscle mass.

HIIT Drives Fat Loss Without Compromising Muscle Size

Fortunately, there are other ways to burn plenty of calories and body fat without promoting muscle breakdown, such as high-intensity interval training (HIIT). HIIT involves extreme interval training for approximately 15-30 minutes that entails working at 80-90 percent of your maximum heart rate for roughly one minute, accompanied by less-intense recovery periods such as walking at 40-50 percent of your maximum heart rate, also for approximately one minute. This approach is in sharp contrast to the typical cardiovascular exercise that is mostly done at a moderate intensity, for instance walking at 60-70 percent of your maximum heart rate. Interestingly, studies have found that subjects performing HIIT burned significantly more body fat than those who did standard cardio programs1 while also promoting an anabolic environment that supports muscle growth. For example, one study by Boutcher et al.2 showed that HIIT increases testosterone levels whereas standard cardio has the reverse effect.

HIIT Raises PGC1-alpha

In addition to HIIT burning fat while supporting a more robust anabolic environment in the body, additional research has shown that HIIT also increases the level and activity of the transcriptional co-activator PGC-1 alpha.3 PGC1-alpha normally functions by increasing the expression of genes involved in mitochondrial biosynthesis in response to endurance exercise.4,5 Interestingly, this study also showed that the increase in PGC-1 alpha from HIIT also increased expression of mitochondrial proteins and enzyme activity, clearly demonstrating that an acute bout of HIIT activates mitochondrial biogenesis through a mechanism involving increased PGC-1 alpha. Because mitochondria are the power-producing organelles within the cell, the ability of PGC-1 alpha to enhance their quantity and function directly increases muscle cell energy, resulting in increased endurance.

Increased PGC-1 alpha in Muscle Increases BAT Thermogenesis

In response to exercise, PGC-1 alpha is induced in several tissue types, including fat and muscle, which locally stimulates many positive effects associated with exercise only within the cells with greater PGC-1 alpha levels. However, exercise induction of PGC-1 alpha in muscle has additional non-local effects outside of the muscle cell where it directly influences adipose tissue. This was shown in a study by Boström et al.6 where increased levels of muscle cell PGC-1 alpha induced the expression of a newly identified protein known as irisin, which binds to receptors on the surface of white adipose tissue (WAT). This results in the induction of BAT-associated proteins such as UCP-1, which is the protein that drives thermogenesis in BAT. Thus, irisin functions as a muscle-derived signal that directly makes WAT more similar to BAT- resulting in a significant increase in total-body energy expenditure and a greater ability to burn body fat. Thus, altogether these results suggest that exercise protocols such as HIIT, that effectively induce PGC-1 alpha in muscle tissue, likely prompt the expression of irisin- driving BAT-like activity for greater fat loss.

Water-Induced Thermogenesis Boosts Fat Loss

Drinking a lot of water is routinely put forward as a potential weight-loss method. However, very few studies have investigated the specific aspects of water consumption that might trigger fat loss. As strange as this might appear, a few recent studies have shown that water consumption provided a sympathetic nervous system stimulus, which increased the metabolic rate by activating thermogenesis, which in turn boosted total-body energy expenditure.7 Furthermore, another study looked at whether water-induced thermogenesis translated into actual weight loss, where researchers specifically looked at the influence of drinking roughly six additional cups of water per day on thermogenesis and fat loss.8 Interestingly, each subject demonstrated a significant improvement in bodyweight, body mass index and body composition at the end of the study, establishing the positive role of water-induced thermogenesis on weight loss. 

High-Intensity Exercise Increases Noradrenaline, Which Drives BAT Thermogenesis

Noradrenaline is a hormone produced by the adrenal glands that is well known for supporting the "fight or flight" response that occurs when we get scared, or deal with different forms of stress. During periods of stress, such as HIIT9, noradrenaline is secreted and binds to the adrenergic receptor embedded in the muscle cell membrane. This interaction between noradrenaline and the adrenergic receptor activates a complex signaling cascade that ultimately converts glycogen into glucose, providing a large source of energy for the muscle cell during intense exercise. In addition to noradrenaline liberating energy within the muscle cell, noradrenaline also binds to the beta-adrenergic receptor embedded within the cellular membranes of BAT and turns up thermogenic fatty acid oxidation. 

In conclusion, while most cardiovascular training regimens increase PGC-1 alpha levels, exercise protocols like HIIT induce PGC-1 alpha without causing muscle loss. In addition, amplified PGC-1 alpha levels from HIIT locally increase fatty burning for energy production, offering greater endurance while also producing a systemic effect that induces BAT-driven thermogenesis for an additional means of scorching body fat. The enhanced thermogenic effect associated with HIIT combined with the potent thermogenic-enhancing Thermo-Heat combined with a caloric-restricted diet should further catapult fat reduction. For more on the potent fat-burning product Thermo-Heat, see my Nutrition Performance article in this issue of MD. Furthermore, additional studies suggest that consuming more water throughout the day may additively stimulate thermogenesis, suggesting that uniting all three approaches ought to yield an exceptional amount of fat loss that provides a clear-cut path to ripped, lean muscle.

For most of Michael Rudolph's career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a Research Scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biology of exercise as a fellow at Harvard Medical School and Columbia University for over eight years. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK- leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a scientist working at the New York Structural Biology Center doing contract work for the Department of Defense on a project involving national security.

References:

1.Tremblay A, Simoneau JA and Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism 1994;43, 814-818.
2. Boutcher SH. High-intensity intermittent exercise and fat loss. J Obes 2011;868305.
3. Little JP, Safdar A, et al. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1alpha and activates mitochondrial biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol 2011;300, R1303-1310.
4. Arany Z. PGC-1 coactivators and skeletal muscle adaptations in health and disease. Curr Opin Genet Dev 2008;18, 426-434.
5. Short KR, Vittone JL, et al. Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity. Diabetes 2003;52, 1888-1896.
6. Bostrom P, Wu J, et al. A PGC1-alpha-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature 2011;481, 463-468.
7. Boschmann M, Steiniger J, et al. Water-induced thermogenesis. J Clin Endocrinol Metab 2003;88, 6015-6019.
8. Vij VA and Joshi AS. Effect of "water induced thermogenesis" on bodyweight, body mass index and body composition of overweight subjects. J Clin Diagn Res 2013;7, 1894-1896.
9. Bracken RM, Linnane DM and Brooks S. Plasma catecholamine and nephrine responses to brief intermittent maximal intensity exercise. Amino Acids 2009;36, 209-217.