Work Out 'Till You Drop: After 1h+ of Intense Exercise or an Energy Equivalent of >800kcal Leptin Begins to Plummet!

Image 1: Losing consciousness is very different from losing body fat and while the former may require "burning" more than 800kcal, the latter does not.

Sometimes you read an abstract like that by Mahmoud Hesar Koushki et al. and think "Hmm... that sucks!" Then, you come to think about it and realize "Yeah! That really sucks!" And the thing that sucks in this particular case is the message studies like that are sending out to the public, when they end on statements like "Rising the energy costs of the exercise through increasing the exercise duration, can be one of the factors affecting negative energy balance, leading to positive changes in leptin concentrations." (Hesar Koushki. 2012).

What's good for your obese neighbor...

... must not be good for you! I know, I am repeating myself here, but in view of the fact that my voice obviously has not been heard in Iran, as of yet, I will repeat my novel mantra as often as it takes for people to get it into their stup... ah, I mean stubborn heads and stop sending healthy people into misery.

Figure 1: This is what the study particpants in the Hesa Koushki study had to endure - a "exhaustion exercise session" on the treadmill (Hesar Koushki. 2012)

A good way to achieve that is known as "exhaustive running session" (cf. figure 1), but as you have heard before was still "insufficient" to induce significant decreases in leptin levels in the 23 male students (age 19.58 ± 2.12 yr, BMI 1.63 ± 2.7 kg/m²) who volunteered to participate in this study (cf. figure 2):

Figure 2: Serum leptin, insulin, blood glucose, cortisol and lactate levels of young healthy, but untrained men before and after exhaustive exercise session (Hesar Koushki. 2012)

But what does that tell us? If we were dealing with women, it would probably mean that this type of exercise was insufficient to induce amenorrhea (Chou . 2011), that, when performed once(!), it was not excessive enough to induce a profound enough starvation signal to trick the bodies of athletes or gymrats to believe that they were running the risk of becoming underweight (Köpp. 1997) and that it was not the first step towards muscle and bone loss (Kaufman. 2002). But does this mean that it's safe and effective?

When much is not yet too much, more must not be better either!

Figure 3: If you don't want to burn more energy, more glucose, more fat, and reduce your intramuscular and liver triglyceride stores to ramp up insulin sensitivity and ward off NAFLD, you better stick to 60min+ exercise and 800kcal+ energy expenditure per workout - without eating any carbs, at all, of course! After all, those could negate these "beneficial effects" *sarcasm mode off!*

If we apply standard paradigma of "working out to lose weight" to the finding that short-term intense exercise with an energy expenditure way below 800kcal did not reduce circulating leptin levels and switch off our brains, the (un!)reasonable conclusion would be that

"According to the findings of this study [...] exercise longer than 60 minutes with energy expenditure higher than 800 kcal can be recommended for the reduction of leptin concentration in non-athletes." (Hesar Koushki. 2012)

If we use our brains, though, the take home message would be very different an should rather read like:  "NEVER! Expend more than 800kcal in one workout if you are not leptin resistant and want to make sure that you don't forestall fat loss and mess up your endocrine system." (Dr. Andro ;-)

Fat loss training for non-obese individuals should focus on keeping leptin levels steady!

Once you acknowledge the importance of normal leptin levels for fat loss and overall metabolic health in lean, not leptin resistant individuals, the same review (Bouassida. 2010) the Iranian scientists cite to support their (misleading!) conclusion that it would be basically nonsensical to do intense short bouts of exercise, since those do not reduce circulating leptin levels has to be interpreted in a completely different way.

Just as the complete failure to produce insulin would not just hamper your gains, but have you literally shrivel away, lowering leptin levels in an already lean, if not very lean individual even further will sooner or later whack your metabolism and endocrine system (infertility, low testosterone, amenorrhea, you name it...). Not to mention that you will obviously not be able to derive any of the metabolic benefits of adequate leptin levels and receptor activity (figure 3).

So what can or must be done to keep healthy leptin levels and sensitivity?

Lean, athletic individuals should thus focus on shorter (below 1h), intense and glycolytic workouts (HIIT, lifting weights) and regenerative 'cardio' work in the << 800kcal energy expenditure range and make sure that they...

• get enough sleep - even a moderate sleep debt will increase the production and systemic circulation of TNF-alpha and IL-6 and reduce the expression of adiponectin and leptin in the adipose tissue (Padilha. 2011)
• strategically cycle & refeed on carbohydrates - it stands out of question that a reduction in carbohydrate intake is an effective means to get rid of body fat, but it will work optimally only, if you strategically cycle (higher carb intake on workout, lower carb intake on non-workout days) your carbohydrate intake, integrate regular refeeds (with a 20% caloric deficit every other week) and always eat as much green leafy veggies as it takes to fill you up without ever counting their quasi non-existent carbohydrate content

And while there is some evidence (Teta. 2007, Rodríguez-Carmona. 2012) that would suggest that sodium bicarbonate (baking soda, NaHCO3) to counter the reduction in leptin expression and the use of 12g of ALCAR /day to increase leptin sensitivity (particularly, in older people; cf. Iossa. 2002) could help, as well. Working and eating right for your current metabolic needs will always be the most important factors.

References:

1. Bouassida A, Chamari K, Zaouali M, Feki Y, Zbidi A, Tabka Z. Review on leptin and adiponectin responses and adaptations to acute and chronic exercise. Br J Sports Med. 2010 Jul;44(9):620-30.
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3. Coope A, Milanski M, Araújo EP, Tambascia M, Saad MJ, Geloneze B, Velloso LA. AdipoR1 mediates the anorexigenic and insulin/leptin-like actions of adiponectin in the hypothalamus. FEBS Lett. 2008 Apr 30;582(10):1471-6.
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8. Köpp W, Blum WF, von Prittwitz S, Ziegler A, Lübbert H, Emons G, Herzog W, Herpertz S, Deter HC, Remschmidt H, Hebebrand J. Low leptin levels predict amenorrhea in underweight and eating disordered females. Mol Psychiatry. 1997 Jul;2(4):335-40.
9. Padilha HG, Crispim CA, Zimberg IZ, De-Souza DA, Waterhouse J, Tufik S, de-Mello MT. A link between sleep loss, glucose metabolism and adipokines. Braz J Med Biol Res. 2011 Oct;44(10):992-9. Epub 2011 Sep 2.
10. Punyadeera C, Zorenc AH, Koopman R, McAinch AJ, Smit E, Manders R, Keizer HA, Cameron-Smith D, van Loon LJ. The effects of exercise and adipose tissue lipolysis on plasma adiponectin concentration and adiponectin receptor expression in human skeletal muscle. Eur J Endocrinol. 2005 Mar;152(3):427-36. 
11. Rodríguez-Carmona A, Pérez-Fontán M, Guitián A, Peteiro J, García-Falcón T, López-Muñiz A, García-Buela J, Cordido F. Effect of low-GDP bicarbonate-lactate-buffered peritoneal dialysis solutions on plasma levels of adipokines and gut appetite-regulatory peptides. A randomized crossover study. Nephrol Dial Transplant. 2012 Jan;27(1):369-74.
12. Teta D, Maillard M, Tedjani A, Passlick-Deetjen J, Burnier M. The effect of pH-neutral peritoneal dialysis fluids on adipokine secretion from cultured adipocytes. Nephrol Dial Transplant. 2007 Mar;22(3):862-9.
13. Wolkowicz P, Grenett H, Belousova M, Urthaler F. Activation of leptin expression by an inhibitor of carnitine palmitoyltransferase-1. Int J Obes Relat Metab Disord. 2004 Apr;28(4):649-51.