The terms “feel the burn”, “melting fat”, and “getting shredded” are all creative terms to describe using stored and dietary fat as energy but in fact, fat must be oxidized at a cellular level in the mitochondria by beta-oxidation. The majority of this cellular activity happens in the muscle which supports increasing exercise as a way to significantly use more fat, and the more muscle density means more cells to process fats at one time to energy. Simply, muscle is where fat is utilized but not disposed of.
Lipolysis is the term given to breaking down or splitting of fats into free fatty acids (FFA) to then be used as energy. Stored and dietary fats (triglycerides) need to be converted into free fatty acids (FFA) before they can be burned as fuel in the mitochondria. Lipolysis can happen in any cell but is most active in fat tissue. (1)
During exercise, free fatty acids mostly from stored fat are bound to circulating cholesterol (lipoprotein) LDL and VLDL and transported to the cell. Hormones catecholamines and insulin give signals for this to occur.
Catecholamines are better known as adrenaline or epinephrene. According to Professor Steve Boutcher, Head of the Health and Exercise Science program in the School of Medical Sciences at the University of New South Wales, increasing adrenaline is the key to losing belly fat. His research published back in 2007 was a landmark interval training study that compared super-short intervals of high intensity exercise against long cardio for fat loss. On the other hand, insulin from food in response to carbohydrates, stops lipolysis and fat breakdown, and the body will switch to using glucose as fuel rather than FFAs.(1)
Levels of adrenaline rise dramatically during exercise and even higher during high intensity, repetitive exercise which triggers lipolysis of stored fat to FFAs.
Caffeine has also shown to increase the rate of lipolysis by working with adrenaline to increase lipolysis and promote fattyacid oxidation.(2)
Stimulation of the adrenergic receptor stimulates the sympathetic nervous system, responsible for the “flight or fright” response, also triggered by exercise and fear. This response diverts blood flow to organs of need such as skeletal muscle and also mobilises energy. Hypertensive drugs such as beta-blockers block adrenergic receptors, and may well cause more of a challenge for weight loss.(3)
Studies have also shown that alcohol decreases adrenergic receptor stimulation, and maybe one of the drivers of weight gain associated with alcohol intake even when sugary beverages are not consumed.(4)
Getting FFAs to the working muscle for oxidation is a popular area of researched in an endeavor to understand mechanisms better. Since high intensity exercise can actually reduce blood flow around adipose tissue, low-to-moderate intensity exercise has shown to be optimal and therefore medium-intensity aerobic training might be best.(5)
Inside the cell, the mitochondria are the powerhouses that burn fat to ATP. Higher levels of muscle mean more power generators and potentially more fat fuel burned. Exercise increases two key signaling molecules, AMPK and PGC-1α (peroxisome proliferator-activated receptor γ coactivator 1α), both of which stimulate the mitochondria to burn fat and sugar more efficiently as long as there is no mitochondrial impairment as has been shown in obese patients to slow fat oxidation. (6) PGC-1 has been extensively described as a master regulator of mitochondrial biogenesis. However, its activity is not constant and can be finely tuned in response to different metabolic situations such as increased by fasting, exercise, cold temperatures, and certain natural compounds, and together in synergy with AMPK, they instruct the mitochondria to divide with the result of higher fat burning as opposed to fat storage.
There is great appeal for exploring along with exercise, nutrients, herbs, and botanicals which have shown to increase AMPK signaling, optimizing mitochondrial function and fat and sugar burning. Alpha-lipoic acid (ALA) in particular has been shown to increase AMPK signaling and fat burning in humans. Koh et al (n= 1,127) studied alpha-lipoic acid 1800 mg/d led to a modest weight loss in obese subjects which may be considered as adjunctive therapy for obesity. At the end of the study, participants reported a nine percent reduction in body mass, along with significant reductions in blood pressure and belly fat, compared to baseline. Korean researchers followed a similar approach and reported the high-dose overweight individuals lost significantly more belly fat and body weight than the placebo group on the same dietary intake. Other nutrients to potentially increase AMPK and maximize fat-burning are berberine, butyric acid, capsaicin (from chili peppers), chromium, curcumin, green tea polyphenols, genistein (soy), ginseng, quercetin, and resveratrol.(7)(8)
L-carnitine is a popular over the counter supplement promoted for fat loss. It functions as a transporter molecule binding FFAs formed from lipolysis and studies have suggested that FA transport is limited by L-carnitine availability. Shirali et al found L-carnitine was not a great fat loss agent by itself, but when combined with caffeine, green tea, and exercise, can help speed things along. How much and at what time should it be taken is debatable, but taken in a dose between 1,000-2,000 mg of L-carnitine with caffeine before aerobic exercise is suggested.
The critical aspects to consider here are that insulin needs to be scarce to promote lipolysis, high levels of anti-oxidatant’s increase signaling, L-carnitine acts as a shuttle, muscle density increases the capacity for burning fat and exercise increases the demand for energy.
1) Groop LC et al (1991) Role of free fatty acids and insulin in determining free fatty acid and lipid oxidation in man. J of Clin Invest; 87(1): 83–89.
2) Schubert MM et al (2014). Caffeine consumption around an exercise bout: effects on energy expenditure, energy intake, and exercise enjoyment. J Appl Physiol; 117(7): 745–754.
3) Sharma AM et al (2001). Hypothesis: Adrenergic receptor blockers and weight gain: a systematic analysis. Hypertens; 37(2): 250–254.
4) Siler SQ, Neese RA, and Hellerstein MK.(1999) De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption. Am J Clin Nutr; 70:928–36.
5) Haifeng Zhang et al (2017) Article Comparable Effects of High-Intensity Interval Training and Prolonged Continuous Exercise Training on Abdominal Visceral Fat Reduction in Obese Young Women. J Diabetes Research; Article ID 5071740.
6.) Consitt LA et al (2010) Peroxisome Proliferator–Activated Receptor-γ Coactivator-1α Overexpression Increases Lipid Oxidation in Myocytes From Extremely Obese Individuals. Diabetes; 59(6): 1407-1415.
7) Koh EH et al (2011) Effects of alpha-lipoic acid on body weight in obese subjects. Am J Med; 124(1): 85.e1–85.e8.
8) Carbonelli MG et al (2010) Alpha-lipoic acid supplementation: a tool for obesity therapy? Curr Pharm Des; 16(7): 840–846.
9) Shirali S et al (2016) Effect of Caffeine Co-Ingested with Carnitine on Weight, BodyFat Percent, Serum Leptin and Lipid Profile Changes in Male Teen Soccer Players: a Randomized Clinical Trial. Int J Pediatr; (4); 3685-3698.