25 April 2019


by Jackson Peos 0

Excuse the title, but no we didn’t eat any rats and that in itself is kinda NEAT! During hypocaloric periods (calorie deficits) we observe decreases in body weight, we also observe decreases in energy expenditure (with lower body weight comes decreased energy need). This response is not surprising given that weight loss is driven by…

Excuse the title, but no we didn’t eat any rats and that in itself is kinda NEAT!

During hypocaloric periods (calorie deficits) we observe decreases in body weight, we also observe decreases in energy expenditure (with lower body weight comes decreased energy need). This response is not surprising given that weight loss is driven by reductions in metabolically active tissue (fat free mass and fat mass). However, what we find is that energy expenditure falls beyond what would be predicted for a smaller body size, and we term this response adaptive thermogenesis (AT). As AT takes hold…future weight loss becomes more difficult, and the potential for weight regain post-diet intensifies.

While most in the fitness community will refer to AT as a “slowing down of the metabolic rate”, this is an oversimplification. Yes, significant AT occurs in resting energy expenditure, but we also see at least part of this adaptation in non-resting components, and this is often underappreciated. For example, in a 2003 study by Rosenbaum and colleagues, 10% weight loss caused an increase in participant muscle work efficiency, meaning they can now use less calories to perform the same activity, and this response was still evident when they accounted for the loss of tissue mass. In 1995 Liebel and colleagues showed that in obese individuals who maintained a reduced body weight, non-resting energy expenditure (activity calorie burn) is suppressed proportionally more than resting energy expenditure as the magnitude of weight loss increases. In another study by Rosenbaum and Liebel in 2016 the authors concluded that adaptive thermogenic responses can be even further pronounced and more susceptible to suppression in non-resting components of our energy expenditure, NOT our resting energy expenditure. Finally, a 1999 study by Levine and colleagues also demonstrated a certain component of our non-resting energy expenditure which involves low-to-moderate intensity incidental activity – termed NEAT (non-exercise activity thermogenesis) – is predictive of the amount of fat gain in response to overfeeding.

So…we know that a large decrease in calories expended during activity (including non-exercise activity) is more to blame for weight loss stalls and post-diet regain than a “slow down” of our resting energy expenditure like some people assume.

With this being a hot area of research, investigators recently completed a weight loss study in rats to investigate the relative contributions to reduced energy expenditure after a 3-week diet with a 50% caloric deficit. The 3-week diet caused a 19% decrease in body weight and a 42% decrease in daily exergy expenditure. AT in energy expenditure occurred, with resting energy expenditure decreasing by 39%, and non-resting energy expenditure having a more severe decline, decreasing by 48%. The researchers observed reduced muscle heat dissipation, suggesting that thermogenic mechanisms may be responsible. Importantly, moderate-intensity activity was able to increase muscle thermogenesis and partly counteract the decline. Thus, this finding suggests we have a potential avenue to counter AT and promote continued weight loss by implementing periods of at least moderate intensity exercise to produce skeletal muscle thermogenesis. As the authors state, “the capacity to increase activity energy expenditure in response to a stimulus (e.g. exercise) is retained” despite an energy deficit.

So, what can we make of all this, and how can we translate these studies into practice?

It seems wise to increase levels of moderate intensity exercise during a diet phase, or during the post-diet period. Increasing skeletal muscle thermogenesis may help to counteract the typical decline and reduction in muscle heat dissipation. Mitigating reductions in activity expenditure will also likely lead to greater weight loss efficiency (amount of weight lost per unit of caloric restriction).
Research suggests that levels of NEAT can also be severely suppressed during a diet phase. Thus, it seems wise to be proactive in attempting to increase levels of NEAT to counteract the usual decline via increased locomotion efficiency and reduced skeletal muscle thermogenesis. Practical examples could include parking the car further away from the entrance to walk further, walking the dog for 10 minutes longer than usual, or wearing an activity monitor like a FitBit.
Understand that after a significant amount of weight loss, due to AT and decreases in energy expenditure, you will need to eat LESS than expected (or predicted by loss of tissue mass) to keep the weight off.
Given the substantial AT and decline in daily energy expenditure after just 3 weeks in a severe caloric deficit, this brings into question the utility of aggressive mini-cuts. Often an individual will implement a 3-6 period of aggressive dieting during a longer offseason with the assumption that this hypocaloric period is too short to observe marked alterations in metabolism. The study by Almundarij suggests this may not be the case, and may warrant more moderate less aggressive (albeit “mini”) cuts, however we are limited by the rodent nature of this study.
It has been speculated that an individual will not require a refeed or diet break during a weight loss phase until substantial scale movement has been made, until the individual is lean, or until the individual has been dieting for a couple of months. Given the rapid decline in energy expenditure during just 3 weeks of dieting and given that the rationale of refeeds and diet breaks is to mitigate declines in energy expenditure, it seems plausible that these techniques may have utility much earlier in the dieting phase than originally thought.

Rosenbaum M., Vandenborne K., Goldsmith R., Simoneau J. A., Heymsfield S., Joanisse D. R., et al. 2003. Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects. Am. J. Physiol. Regul. Integr. Comp. Physiol. 285:R183–R192.

Leibel R. L., Rosenbaum M., and Hirsch J.. 1995. Changes in energy expenditure resulting from altered body weight. N. Engl. J. Med. 332:621–628.

Rosenbaum M., and Leibel R. L.. 2016. Models of energy homeostasis in response to the maintenance of reduced body weight. Obesity (Silver Spring) 24:1620–1629.

Levine J. A., Eberhardt N. L., and Jensen M. D.. 1999. Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science 283:212–214.

Almundarij, T. I., Gavini, C. K., & Novak, C. M. (2017). Suppressed sympathetic outflow to skeletal muscle, muscle thermogenesis, and activity energy expenditure with calorie restriction. Physiological reports, 5(4), e13171.

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