Here’s what you need to know…
- Leptin is a hormone that decreases the appetite, increases the metabolism, and leads to leanness.
- The human body only responds to leptin if leptin receptors are working properly and telling the brain that leptin is high.
- 30 seconds of intense exercise, like bike sprints, will increase leptin signaling. But it only works in the absence of the hormone insulin, which is produced after meals.
- Fasted sprinting has shown to increase leptin signaling.
The Keys to Leanness
The body isn’t a simple, linear, or straightforward machine – it’s complex. And overcomplicating the fat-loss process usually backfires. But just because the physiology is messy, doesn’t mean your actions can’t be simple and effective.
Understanding more about the hormone leptin may help you uncover the answers to getting leaner.
First, here’s a short crash course on this important hormone.
Leptin was discovered by researchers in the ’50s. Fast forward to the ’90s when it was “rediscovered”, and many were predicting it would be the biggest weight loss breakthrough ever.
It’s a hormone that’s released primarily by fat cells (adipocytes) and works to regulate appetite, body fat mass, and basal metabolic rate.
Until just a few years ago, researchers thought that fat cells were only a storage place for unsightly body fat.
We know now that they’re very metabolically active, releasing and receiving a myriad of messenger hormones, one of which is leptin.
How Does Leptin Work?
Leptin travels up to the brain where it acts on receptors in the hypothalamus to inhibit appetite.
More leptin in your brain = less food intake.
This is great news for anyone looking to get leaner, since more leptin means you’ll be less likely to overeat. Leptin is your body’s way of putting the brakes on fat gain by decreasing appetite.
The chronic level of leptin you have is also a rough measure of the amount of fat you have on your body. Many things can affect leptin as shown in the table below:
Factors promoting leptin secretion
- Excess energy stored as fat (obesity)
- Inflammatory cytokines, including tumor necrosis factor and Interleukin-6 (acute effect)
Factors inhibiting leptin secretion
- Catecholamines and adrenergic agonists
- Thyroid hormones
- Low energy states with decreased fat stores (leanness)
- Peroxisome proliferator–activated receptor-agonists
- Inflammatory cytokines, including tumor necrosis factor (prolonged effect)
Obese Mouse Turned Lean
Researchers in ’90s did a series of mouse experiments to show that mice with messed up leptin became profoundly obese. Their metabolic rate was lower, they didn’t move as much, and they ate tons of food.
The mice didn’t make any leptin at all. To make the mice lean, they injected it with leptin, and voila – thin mice again!
The researchers thought this was the solution to the obesity problems: just inject humans with leptin and poof, thin humans. The problem is, it didn’t work.
Researchers measured blood levels of leptin in obese humans, and found that their leptin levels were sky high!
That wasn’t supposed to happen. Leptin levels were expected to be low since the humans were fat. As leptin increases, it tells the brain that the body has enough fat. So you see why they would expect low leptin levels in obese populations.
As you recall, when injected with leptin (thus increasing the level), the mice in the studies got thinner. But the obese humans already had high levels of leptin. Injecting more leptin was like pissing in the ocean to try to raise the water level.
Leptin 201: The Receptor
What researchers discovered was that the receptor for leptin may be what’s out of whack in the obese.
The receptor isn’t telling the brain that leptin is high. They may have tons of leptin, but the brain can’t tell since the receptor is broken. So the answer for leanness isn’t about increasing leptin, but increasing the body’s sensitivity to it.
Exercise that Increases Leptin Signaling
We already know that sprint training is a great way to burn fat, but it may have another benefit. Researchers in 2011 looked at sprints as a leptin signaling mimetic.
Unlike most research, this study used a group of fit people who were pretty lean (about 15% body fat) and young (23 years old). They split them into two groups: a fasting group, and a glucose group which ingested 75 grams of glucose an hour before sprints.
Both groups did one Wingate bike sprint for only 30 seconds.
If you’re not familiar with this set up, it’s like this: you hop on a bike with resistance set to a high workload (10% of body weight used here) and pedal like a rabid grizzly bear is chasing you.
What They Found
Subjects had a series of muscle biopsies done over the course of the study and researchers found that a single session of sprint training showed alterations in leptin signaling.
The sprints were jacking up leptin that, in theory, should cause obese to start dropping fat.
However, this was not seen in the group that ingested glucose before their sprint. Only the fasted group saw leptin alterations. It appears insulin may interfere with the leptin signaling to some degree.
The researchers said that sprints done while fasting elicited signaling like what was found in the rodents’ muscle after receiving leptin injections. But glucose ingestion before the exercise diminished the effect.
So it appears that fasted sprint training can pinch hit for leptin and sensitivity to it.
Sprint Sample Workout
Get on a bike and work up to one maximum, all out, pedal-as-hard-as-you-can sprint for 30 seconds.
The tension should be relatively high, but the goal is to keep your pedaling at a fast pace for the entire 30 seconds. If you slowed to a snail pace 20 seconds in, go to a lighter workload.
Do this in a fasted condition, like first thing in the morning.
Don’t have a bike? While the study didn’t look at running, it may elicit the same response as the pathways are very similar.
It sounds ridiculously simple, but my purely anecdotal experience with my athletes shows that this does seem to help speed fat loss.
- More leptin production is associated with less food intake, but only in those who’s body responds to leptin properly.
- Some may have a leptin receptor issue where it’s not responding to the amount of leptin floating around.
- Science isn’t at the point yet where we can always tell who has a receptor issue, but the more overweight you are, the more likely you are to having broken leptin receptors.
- Doing just one sprint in a fasted state works to pinch hit for leptin, putting you on the road to leanness. Non-fasted training doesn’t have the same effect.
- Fasted sprints can be done any time on a fasting day or done before breakfast. This way it’s unlikely to interfere with your normal training session.
While we don’t have a long-term study to show how much this will help your body composition, it’s simple enough to try and study the results on your own body.
- Everard, A., Lazarevic, V., Derrien, M., Girard, M., Muccioli, G. G., Neyrinck, A. M., Cani, P. D. (2011). Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes, 60(11), 2775-2786. doi:10.2337/db11-0227
- Finocchietto PV, Holod S, Barreyro F, Peralta JG, Alippe Y, Giovambattista A, Carreras MC, Poderoso JJ. Defective leptin-AMP-dependent kinase pathway induces nitric oxide release and contributes to mitochondrial dysfunction and obesity in ob/ob mice. Antioxid Redox Signal. 2011 Nov 1;15(9):2395-406. Epub 2011 Jun 28.
- Galgani, J. E., Greenway, F. L., Caglayan, S., Wong, M. L., Licinio, J., & Ravussin, E. (2010). Leptin replacement prevents weight loss-induced metabolic adaptation in congenital leptin-deficient patients. The Journal of Clinical Endocrinology and Metabolism, 95(2), 851-855. doi:10.1210/jc.2009-1739
- Guerra, B., Olmedillas, H., Guadalupe-Grau, A., Ponce-Gonzalez, J. G., Morales-Alamo, D., Fuentes, T., . . . Calbet, J. A. (2011). Is sprint exercise a leptin signaling mimetic in human skeletal muscle? Journal of Applied Physiology (Bethesda, Md.: 1985), 111(3), 715-725. doi:10.1152/japplphysiol.00805.2010
- Ho, J. N., Jang, J. Y., Yoon, H. G., Kim, Y., Kim, S., Jun, W., & Lee, J. (2012). Anti-obesity effect of a standardised ethanol extract from curcuma longa L. fermented with aspergillus oryzae in ob/ob mice and primary mouse adipocytes. Journal of the Science of Food and Agriculture, doi:10.1002/jsfa.5592; 10.1002/jsfa.5592
- INGALLS, A. M., DICKIE, M. M., & SNELL, G. D. (1950). Obese, a new mutation in the house mouse. The Journal of Heredity, 41(12), 317-318.
- Kelesidis, T., Kelesidis, I., Chou, S., & Mantzoros, C. S. (2010). Narrative review: The role of leptin in human physiology: Emerging clinical applications. Annals of Internal Medicine, 152(2), 93-100. doi:10.1059/0003-4819-152-2-201001190-00008
- Kowalik, S., & Kedzierski, W. (2011). The effect of interval versus continuous exercise on plasma leptin and ghrelin concentration in young trotters. Polish Journal of Veterinary Sciences, 14(3), 373-378.
- Plinta, R., Olszanecka-Glinianowicz, M., Drosdzol-Cop, A., Chudek, J., & Skrzypulec-Plinta, V. (2011). The effect of three-month pre-season preparatory period and short-term exercise on plasma leptin, adiponectin, visfatin and ghrelin levels in young female handball and basketball players. Journal of Endocrinological Investigation, doi:10.3275/8014
- Wolsk, E., Mygind, H., Grondahl, T. S., Pedersen, B. K., & van Hall, G. (2011). The role of leptin in human lipid and glucose metabolism: The effects of acute recombinant human leptin infusion in young healthy males. The American Journal of Clinical Nutrition, 94(6), 1533-1544. doi:10.3945/ajcn.111.012260
- Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372(6505), 425-432. doi:10.1038/372425a0