Understanding Metabolic Damage And Adaptation

Daniel DeBrocke

Calgary, Alberta, Canada

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The term metabolic damage has gained lots of traction over the years. Researchers1 initially observed a reduced metabolic rate in subjects who had lost a substantial amount of weight. This reduction is far from shocking since lowering an individual's body weight will simultaneously reduce their energy demands.

 

However, what was unique in this case was that some individuals' metabolic rates were far lower than what the researchers projected.

 

 

These findings became popular within various fitness circles and were quickly given the label of metabolic damage. However, at the moment, there isn’t any convincing evidence to support the existence of metabolic damage within this context. What researchers were observing is more accurately defined as metabolic adaptation and adaptive thermogenesis.1

 

During a period of caloric restriction accompanied by a reduction in body weight, your body undergoes several physiological changes to adapt to the changing environment—both internal and external.

 

Changes in Hormones Accompany Fat Loss

Leptin is a hormone whose primary function is regulating energy balance and maintaining bodyweight.

 

  • Often called the satiety hormone, it helps regulate an individual's drive to consume food. Because leptin synthesizes in adipocytes, leptin is sensitive to body fat stores.2
  • When we lose body fat during a period of caloric restriction, serum leptin concentrations decrease. This reduction in leptin concentration accompanies a cascade of neurochemical alterations that can significantly increase hunger and reward-seeking behavior.3
  • Various other hormones, including the thyroid, are also impacted. The thyroid hormone has been demonstrated to be an essential variable in determining energy expenditure and Basal Metabolic Rate (BMR).4

 

Observations show that fat loss during a sustained caloric deficit can reduce thyroid values, thereby decreasing basal BMR.5

 

Fat Loss Affects Physiological Energy Processes

Additionally, Adenosine Triphosphate (ATP) synthesis becomes more efficient. Typically ATP synthesis is roughly 40% efficient, which means approximately 60% of energy is lost via thermogenesis.6 However, in low energy availability and reduced body fat, mitochondrial efficiency increases.

 

Proton leak, a process regulated by uncoupling proteins, causes energy to be lost as heat. But increased mitochondrial efficiency reduces proton leak and increases ATP synthesis as an adaptive response.7

 

We also see other aspects of our physiology, such as muscular work efficiency, increase as calories are restricted, and reduced weight.8

 

 

As these adaptations occur, we also see a reduction in Non-Exercise Activity Thermogenesis (NEAT). This reduction is associated with spontaneous, nonexercise-related physical activity and accounts for most energy expenditure.9

 

Researchers have observed that caloric restriction and loss of body weight can reduce an individual's NEAT significantly. Unfortunately, this is mainly unconscious, so there’s not much that you can do.

 

Adopting a daily step count is a common practice to keep an account of and regulate energy expenditure.

 

However, because this is for the explicit purpose of expending calories, it’s not technically NEAT. It’s exercise activity thermogenesis. But I digress.

 

Researchers have found that our bodies like consistency. Enter the settling point theory. As one paper described it,

 

 

“The set point model is rooted in physiology, genetics, and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain.”10

 

 

Although this does not account for all relevant variables, it does explain to some degree the body's desire to preserve homeostasis from the body weight and energy availability standpoint.

 

Essentially as energy availability from external, like food, and internal, as in body fat stores, sources decrease, our body tries to resist this change via several physiological and neurochemical changes.

 

As mentioned previously, changes in thyroid, leptin, and even increased hedonic dive for food are just some of the numerous adaptive responses.

 

As you reduce your body weight, the energy requirement for locomotion decreases accordingly.11 NEAT may vary between individuals of the same size by 2,000 kcal per day.12

 

In a previous article, I wrote for Kabuki Strength,

 

I mentioned “A paper by Rosenbaum and colleagues cited a reduction in Total Energy Expenditure (TEE) of 10-15% which was unexplained by body composition changes. Of this 10-15% reduction, roughly 85% could be explained by reductions in nonresting energy expenditure of which NEAT is the largest contributor.”13,14

 

 

Once we account for these changes, the vast majority of discrepancies are accounted for between estimated BMR and actual BMR.

 

So, is metabolic adaptation an issue? Absolutely. But does it suggest some form of damage? Well, at the moment, there doesn’t seem to be strong supporting evidence of this.

 

What can you do to manage some of these adaptive responses to maintain your new body weight composition successfully? One potential approach is utilizing a high energy flux approach.15

 

Increase Physical Activity

Researchers have consistently found that regular physical activity is strongly associated with successful weight management.

 

  • By increasing energy intake in proportion to energy expenditure, we can offset some of the adaptive responses of dieting and increase energy intake while staying within a predetermined bodyweight range.
  • Increasing calories can reduce hunger, improve the thermic effect of food, and help decay psychological fatigue accumulated throughout your diet.
  • Adopting a more gradual approach to weight loss such as 1% of your body weight loss per week may delay some of these adaptive responses since the acute change in energy availability is not dramatic.
  • Additionally, it’s important to establish clear timelines and end dates for your diet periods.
  • Dieting for more than three months is typically not recommended since you often see diminishing returns beyond that point.
  • Utilizing maintenance phases to slowly increase your energy intake while remaining weight stable will set you at a higher caloric starting point at the onset of the next diet phase.

 

Metabolic damage doesn’t appear to have strong supporting evidence at this time. What we typically observe instead is metabolic adaptation.

 

These adaptations are entirely reversible in the vast majority of cases.

 

When done correctly, dieting can be an important aspect of healthy eating and optimizing body composition.

 

References

1. Michael Rosenbaum and Rudolph L. Leibel, “Adaptive thermogenesis in humans.” International Journal of Obesity, London. 2010 Oct; 34(0 1): S47–S55.

2. R V Considine 1, M K Sinha, M L Heiman, A Kriauciunas, T W Stephens, M R Nyce, J P Ohannesian, C C Marco, L J McKee, T L Bauer, et al., “Serum immunoreactive-leptin concentrations in normal-weight and obese humans.” New England Journal of Medicine. 1996 Feb 1;334(5):292-5.

3. Miguel Alonso-Alonso, Stephen C. Woods, Marcia Pelchat, Patricia Sue Grigson, Eric Stice, Sadaf Farooqi, Chor San Khoo, Richard D. Mattes, and Gary K. Beauchamp. “Food reward system: current perspectives and future research needs.” Nutrition Review, 2015 May; 73(5): 296–307. Published online Apr 9, 2015.

4. Brian Kim, “Thyroid hormone as a determinant of energy expenditure and the basal metabolic rate.” Thyroid, 2008 Feb;18(2):141-4.

5. Edward P. Weiss, Dennis T. Villareal, Susan B. Racette, Karen Steger-May, Bhartur N. Premachandra, Samuel Klein, and Luigi Fontana. “Caloric Restriction But Not Exercise-Induced Reductions in Fat Mass Decrease Plasma Triiodothyronine Concentrations: A Randomized Controlled Trial.” Rejuvenation Res. 2008 Jun; 11(3): 605–609.

6. Sunil Nath, “The thermodynamic efficiency of ATP synthesis in oxidative phosphorylation.” Biophys Chemistry. 2016 Dec; 219: 69-74. Epub 2016, Oct 15.

7. Martin Jastroch, Ajit S. Divakaruni, Shona Mookerjee, Jason R. Treberg, and Martin D. Brand, “Mitochondrial proton and electron leaks.” Essays Biochem, 2010; 47: 53–67.

8. Michael Rosenbaum 1, Krista Vandenborne, Rochelle Goldsmith, Jean-Aime Simoneau, Steven Heymsfield, Denis R Joanisse, Jules Hirsch, Ellen Murphy, Dwight Matthews, Karen R Segal, Rudolph L Leibel, “Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects.” Am J Physiol Regul Integr Comp Physiol. 2003 Jul; 285(1): R183-92. Epub 2003, Feb 27.

9. Christian von Loeffelholz, M.D. and Andreas Birkenfeld. “The Role of Non-exercise Activity Thermogenesis in Human Obesity.” Endotext, {Internet}. Last updated Apr 9, 2018.

10. John R. Speakman, David A. Levitsky, David B. Allison, Molly S. Bray, John M. de Castro, Deborah J. Clegg, John C. Clapham, Abdul G. Dulloo, et al., “Set points, settling points, and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity.” Disease Model Mech, 2011 Nov; 4(6): 733–745.

11. Michael Rosenbaum 1, Krista Vandenborne, Rochelle Goldsmith, Jean-Aime Simoneau, Steven Heymsfield, Denis R Joanisse, Jules Hirsch, Ellen Murphy. Dwight Matthews, Karen R Segal, Rudolph L Leibel, “Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects.” Am J Physiol Regul Integr Comp Physiol. 2003 Jul; 285(1): R183-92. Epub 2003 Feb 27.

12. Christian von Loeffelholz, M.D. and Andreas Birkenfeld. “The Role of Non-exercise Activity Thermogenesis in Human Obesity.” NCBI, Endotext {Internet}. Last updated Apr 9, 2018.

13. Debrocke, Daniel, “Preventing Weight Regain After A Diet.” Kabuki Strength, Apr 24, 2020. Accessed Feb 25, 2021.

14. Michael Rosenbaum and Rudolph L. Leibel, “Adaptive thermogenesis in humans.” Int J Obes (Lond). 2010 Oct; 34(0 1): S47–S55.

15. Gregory A Hand and Steven N Blair, “Energy Flux and its Role in Obesity and Metabolic Disease.” Eur Endocrinol. 2014 Aug; 10(2): 131–135. Published online 2014, Aug 28.

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