A lot of people who are interested in keeping fit have a complaint about some part of their body carrying extra fat. This is subcutaneous fat, such as the fat that hangs over your belt, flaps on your upper arms or hangs from your low back or upper back near the lats or latissimus dorsi muscles. The big question is how to get rid of it. The main school of thought from physiologists and personal trainers is that ‘spot reduction” (working hard on the specific region to rid fat in that region) does not work because the body metabolizes fat proportionately from all parts of the body at once. The resulting advice is that you have to do plenty of aerobic or cardio exercise to burn the fat, as well as train with weights. This just might not be true.
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There is some scientific evidence, that is not conclusive, but points to the possibility that ‘spot reduction’ DOES work. Immediately at the onset of exercise, blood flow is diverted from non-working muscles, the stomach or the kidneys and is directed as a priority to the working muscles. The whole body still experiences an increase in blood flow as the heart rate increases, but as your muscles begin to work, the sympathetic nervous system, a part of the automatic or autonomic nervous system stimulates the nerves to the heart (causing heart rate increase) and blood vessels (causing vasoconstriction). The vasoconstriction helps elevate blood pressure and reduces blood flow to tissues, except for the working muscles and nearby feeder arterioles, which experience an increase in blood flow. Metabolic byproducts (elevated by working muscles) override the sympathetic command and cause vasodilation. The whole physiological process helps increase the delivery of oxygenated blood and fuels, such as glucose and recently released fat byproducts to working muscles.
Now here is the connection with research that suggests that spot reduction might be successful. Maximal exercise causes a release of adrenaline and noradreanaline into the bloodstream (Brooks S, Burrin J, Cheetham ME et al). Adipose tissue displays a high, but transient (tachyphylaxia) sensitivity to noradrenaline, leading to stimulation of both lipolysis (fat breakdown) and blood flow rates (Quisth V, Enoksson S, Blaak E). You might deduce that the working muscle, feeder arteries and arterioles, and adjacent adipose tissue would have increased blood flow and an associated increase in reaction of lipolysis caused by noradrenaline. It’s not proof, but it is a strong lead.
Also, the regulation of skeletal muscle lipolysis is not fully understood, as reported in Quisth’s article. And, the exact cause of vasodilation in working muscle is not perfectly understood either. Elevated chemicals, such as adenosine, nitric oxide, lactic acid, potassium, hydrogen ion and other metabolic byproducts of the working muscles and the resulting lowered pH and hypoxia cause vasodilation, but scientists believe all of these factors work in a redundant system because individual factors can not be replicated in experiments (Clifford PS, Hellsten Y). It is also unkown what causes vasodilation in feeder arteries, not directly exposed to vasodilator substances in the interstitium. The discussion that these vasodilator substances are in the interstitium leads to the assumption that vasodilator substances might be reaching the adjacent adipose tissue, too. Therefore, does it seem reasonable to say without a doubt that spot reduction doesn’t work?
On top of that, here are some words of wisdom from the year 1985 from Arnold Schwarzenegger on page 506 of his book Encyclopedia of Modern Bodybuilding:
“Spot Reduction”
Many bodybuilders (and I am one of them) have always believed that doing a lot of abdominal training not only hardens and develops the abdominals but also seems to help eliminate fat in the area. However, physiologists and other experts keep assuring me that “spot reduction” — that is, burning up fat in a given area by strenuous use of adjacent muscles — just doesn’t work. According to the theory, when the body needs to use fat for energy it takes it proportionately from all the areas around the body where it is stored. Therefore, doing a lot of Sit-Ups or Leg Raises will not eliminate fat in the abdominal area any more than doing any other exercise which consumes calories.
But I have to take objection to this theory. I can’t say exactly what is going on physiologically during abdominal training, but I know from my own experience, and that of many other bodybuilders, that doing strenuous abdominal training does something to that area that makes it leaner, harder, and more defined. It may not actually be spot reduction, but it is enough like spot reduction so that I think a bodybuilder trying to get into contest shape would be making a serious mistake not working the abdominals to the maximum.
The important thing to note is that this ‘spot reducing’ exercise needs to be intense enough to get noradrenaline to respond. And Arnold? We hope we helped you say what might be happening physiologically. Try to find Arnold Schwarzenegger’s book on Amazon.com
SOURCES:
Brooks S, Burrin J, Cheetham ME, Hall GM, Yeo T, Williams C. The responses of the catecholamines and beta-endorphin to brief maximal exercise in man. Eur J Appl Physiol Occup Physiol. 1988;57(2):230-4.
Clifford PS, Hellsten Y. Vasodilatory mechanisms in contracting skeletal muscle. J Appl Physiol. 2004 Jul;97(1):393-403.
Quisth V, Enoksson S, Blaak E, Hagstrom-Toft E, Arner P, Bolinder J. Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo.
Diabetologia. 2005 May;48(5):946-53
ABSTRACTS BELOW:
Brooks S, Burrin J, Cheetham ME, Hall GM, Yeo T, Williams C. The responses of the catecholamines and beta-endorphin to brief maximal exercise in man. Eur J Appl Physiol Occup Physiol. 1988;57(2):230-4.
The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorized treadmill, the mean power output (mean +/- SD) was 424.8 +/- 41.9 W, peak power 653.3 +/- 103.0 W and the distance covered was 167.3 +/- 9.7 m. In response to the exercise blood lactate concentrations increased from 0.60 +/- 0.26 to 13.46 +/- 1.71 mmol.l-1 (p less than 0.001) and blood glucose concentrations from 4.25 +/- 0.45 to 5.59 +/- 0.67 mmol.l-1 (p less than 0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38 +/- 0.02 to 7.16 +/- 0.07 (p less than 0.001) and the estimated decrease in plasma volume of 11.5 +/- 3.4% (p less than 0.001). The plasma catecholamine concentrations increased from 2.2 +/- 0.6 to 13.4 +/- 6.4 nmol.l-1 (p less than 0.001) and 0.2 +/- 0.2 to 1.4 +/- 0.6 nmol.l-1 (p less than 0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid beta-endorphin increased in response to the exercise from less than 5.0 to 10.2 +/- 3.9 p mol.l-1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise beta-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS
Clifford PS, Hellsten Y. Vasodilatory mechanisms in contracting skeletal muscle. J Appl Physiol. 2004 Jul;97(1):393-403.
Skeletal muscle blood flow is closely coupled to metabolic demand, and its regulation is believed to be mainly the result of the interplay of neural vasoconstrictor activity and locally derived vasoactive substances. Muscle blood flow is increased within the first second after a single contraction and stabilizes within approximately 30 s during dynamic exercise under normal conditions. Vasodilator substances may be released from contracting skeletal muscle, vascular endothelium, or red blood cells. The importance of specific vasodilators is likely to vary over the time course of flow, from the initial rapid rise to the sustained elevation during steady-state exercise. Exercise hyperemia is therefore thought to be the result of an integrated response of more than one vasodilator mechanism. To date, the identity of vasoactive substances involved in the regulation of exercise hyperemia remains uncertain. Numerous vasodilators such as adenosine, ATP, potassium, hypoxia, hydrogen ion, nitric oxide, prostanoids, and endothelium-derived hyperpolarizing factor have been proposed to be of importance; however, there is little support for any single vasodilator being essential for exercise hyperemia. Because elevated blood flow cannot be explained by the failure of any single vasodilator, a consensus is beginning to emerge for redundancy among vasodilators, where one vasoactive compound may take over when the formation of another is compromised. Conducted vasodilation or flow-mediated vasodilation may explain dilation in vessels (i.e., feed arteries) not directly exposed to vasodilator substances in the interstitium. Future investigations should focus on identifying novel vasodilators and the interaction between vasodilators by simultaneous inhibition of multiple vasodilator pathways.
Quisth V, Enoksson S, Blaak E, Hagstrom-Toft E, Arner P, Bolinder J. Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo.
Diabetologia. 2005 May;48(5):946-53
AIMS/HYPOTHESIS: The regulation of skeletal muscle lipolysis is not fully understood. In the present study, the effects of systemic and local noradrenaline administration on lipolysis and blood flow rates in skeletal muscle and adipose tissue were studied in vivo. METHODS: First, circulating noradrenaline levels were raised tenfold by a continuous i.v. infusion (n=12). Glycerol levels (an index of lipolysis) were measured in m. gastrocnemius and in abdominal adipose tissue using microdialysis. Local blood flow was determined with the (133)Xe clearance technique and whole-body lipolysis rates assessed with a stable glycerol isotope technique ([(2)H(5)] glycerol). Second, interstitial glycerol levels in m. gastrocnemius, m. vastus and adipose tissue were measured by microdialysis during local perfusion with noradrenaline (10(-8)-10(-6) mol/l) (n=10). Local blood flow was monitored with the ethanol perfusion technique. RESULTS: With regard to systemic noradrenergic stimulation, no change in fractional release of glycerol (difference between tissue and arterial glycerol) was seen in skeletal muscle. In adipose tissue it transiently increased twofold (p<0.0001), and the rate of appearance of glycerol in plasma showed the same kinetic pattern. Blood flow was reduced by 40% in skeletal muscle (p<0.005) and increased by 50% in adipose tissue (p<0.05). After noradrenaline stimulation in situ, a discrete elevation of skeletal muscle glycerol was registered only at the highest concentration of noradrenaline (10(-6) mol/l) (p<0.05). Adipose tissue glycerol doubled already at the lowest concentration (10(-8) mol/l) (p<0.05). In skeletal muscle a decrease in blood flow was seen at the highest noradrenaline concentrations (p<0.05). CONCLUSIONS/INTERPRETATION: Lipolysis and blood flow rates are regulated differently in adipose tissue and skeletal muscle. Adipose tissue displays a high, but transient (tachyphylaxia) sensitivity to noradrenaline, leading to stimulation of both lipolysis and blood flow rates. In skeletal muscle, physiological concentrations of noradrenaline decrease blood flow but have no stimulatory effect on lipolysis rates.