Bruce W. Craig, PhDColumn Editor

E-mail: Bcraig@gw.bsu.edu

summary

The ability to burn fat during exer-

cise is dependent on exercise inten-

sity and length of work out.

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If you have 6-pack abs, you arewell aware of one basic fact: youdid not obtain that anatomical

feature by employing a training tech-nique called spot reduction. In otherwords, performing just crunches orother abdominal exercises did not re-duce abdominal fat unless the exercis-

es were part of an overall trainingprogram. Fat is distributed in thebody based on genetics, with specificareas storing fat sooner than others.The usage of fat follows the sameprocess, and the area of subcutaneousfat that covers the stomach is not the

first area used. Along the same lines,the various exercise machines and

programs presented on TV or in mag-azines that claim a full aerobic and

anaerobic: workout in just 15 minutesper day are also questionable. Most ofyou know that these claims are un-substantiated, but do you really un-derstand the metabolic basis for

burning fat?

@ National Strength and Conditioning AssociationVolume 28, Number 5, pages 70-71

Bridging the Gap

FatBurningBruce W. Craig, PhDBall State University, Muncie,lndiana

Adenosine TriphosphateTurnoverDuring exercise, the muscle can use nu-merous fuels to supply its energy needs.The main fuel sources are carbohy-drates or fat, and their usage is set byexercise intensity. Muscle contractioninvolves 2 muscle proteins called actinand myosin, and when they interact themuscle fiber short-ens and movement

is produced. Theenergy for this short-enmg process comesfrom the metabolicbreakdown of a cel-

lular energy sourcecalled adenosine

triphosphate (ATP).The turnover rate

(production versusIusage) of ATP is one

of the primary deter-mining factors th~t -establishes the speed and force of con-traction (1) your muscles can generate.

teristics are attributable in part to theenzymes involved in ATP turnover ofthese fibers and the mitochondrial

number of each. In short, your type Ifibers have a slower chemistry thanyour type II fibers, and are the fiber ofchoice when the workload is lower.

Type I muscle fibers are classified asaerobic fibers and contain numerous

mitochondria. Mi-tochondria containa series of aerobic

enzymes that repre-sent a metabolic

pathway called theKrebs cycle (6). TheKrebs cycle withineach mitochondri-

on is able to pro-duce 1 ATP mole-

cule directly and 8hydrogen ions everytime it cycles. Thehydrogen ions this

system produces then enter the electrontransport system (5, 6) of the mito-chondria, and their energy is used to re-build the ATP broken down duringmuscle contraction. The metabolic

pathways of the mitochondria can sup-ply the ATP demands of the muscle atrest and during aerobic exercise if ade-quate oxygen is available. In the pres-

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Muscle Fiber Type SelectionThe fibers within your muscle can beclassified as either type I or type II(1-3). Type I muscle fibers produce lessforce than type II muscle fibers but aremore fatigue-resistant. These charac-

October 2006. Strength and Conditioning Journal

ence of oxygen, these 2 mitochondrialsystems can make 12 ATP molecules forevery turn of the Krebs cycle. The com-pound that starts the Krebs cycle iscalled acetyl-CoA, and it can be formedfrom either carbohydrates or fats. Thecarbohydrate your muscles metabolizeis a simple sugar called glucose, and it iseither imported (blood glucose fromdietary intake or liver) or taken from alocal storage form (muscle glycogen) asa modified version of glucose. Glucosemolecules consist of 6 carbons, and

their complete breakdown produces 2acetyl-CoA molecules. If both acetyl-CoA molecules enter the Krebs cycle,the ATP yield is 24. Fat, on the otherhand, contains a lot more carbon and

can produce more ATP than carbohy-drates. The fat your muscle uses cancome from many sources, such as plas-ma free fatty acids (FAs) and triglyc-erides, or the triglycerides stored with-in the muscle. Free FAs can be used

directly, but triglycerides need to bebroken down first. Triglycerides consistof a glycerol molecule (alcohol com-pound) and 3 FA molecules. When youexercise, the body releases hormonesthat activate a fat cell enzyme thatbreaks triglycerides into glycerol andFA (see "Fat Metabolism" below). TheFA molecules that are released follow-

ing this breakdown contain from 16 to18 carbons, and the metabolism of justone 16-carbon palmitic acid (saturatedFA) by the mitochondria will give you129 ATP molecules (5, 6). Given that

there are 3 FA molecules per triglyc-eride, fats represent a major source ofenergy (5, 6).

As indicated above, type I fibers canmetabolize either carbohydrates or fats,and are more involved when exercise

intensity is at or below 70% of yourmaximal aerobic capacity (Vozmax). Ifaerobic exercise is above 70% of

Vozmax or you perform resistancetraining, the nervous system recruitsmore anaerobic muscle fibers (type II),which produce more force and metabo-lize more carbohydrates. Type II muscle

fibers do nor con rain as many mito-chondria as type I fibers and use muscleglycogen as their primary fuel, so theyare not as dependent on oxygen (4).The breakdown of glucose in type IIfibers is faster than its usage in type Ifibers because it occurs outside the mi-

tochondria and does not produce asmany acetyl-CoA molecules. The endresult of glucose metabolism in type IIfibers is lactic acid, and only 2 ATPmolecules are produced per molecule ofglucose. Therefore, when you increaseexercise intensity, the muscle tends toburn (metabolize) more carbohydratethan fat because of the type of musclefiber being used.

Fat Metabolism

If your ability to burn fat were depen-dent solely on its progression throughits metabolic pathways, 15 minutes ofaerobic exercise might be adequate.However, fat metabolism is also depen-dent on the delivery of FAs to an activemuscle, and the primary factor that in-fluences fat usage during exercise is thetime it takes to metabolize fats. The

mobilization of fat represents its releasefrom fat cells, and is hormonally regu-lated. Two hormones in particular, epi-nephrine from the adrenal gland andglucagon from the pancreas, are re-leased into the bloodstream at the onsetof exercise and activate hormone-sensi-

tive lipase (HSL) in fat cells and muscle(5, 6). Once activated, this enzymebreaks triglycerides into 3 FA mole-cules and glycerol, and the FA mole-cules enter the bloodstream (fat cells)or are available to the muscle (intra-

muscular triglyceride stores). Thebreakdown and usage of intramuscularstores of triglycerides during exercise isnot well understood, and estimates ofhow much fat the muscle uses from this

source are not possible with current re-search techniques. However, based onthe appearance of FAs in blood duringsteady-state aerobic exercise (70% ofVozmax) it takes approximately 20-30minutes to get FAs to an active muscle,which represents the time it takes to re-

October 2006' Strength and Conditioning Journal

lease the HSL-activating hormones, theaction of the HSL, and the transit time

required for FAs to reach the musclefrom fat cells. Even after FAs reach the

muscle, they must cross the cell mem-brane, enter the mitochondria, and be

converted into acetyl-CoA via a meta-bolic process called beta oxidation (5,6) before they can be metabolized inthe Krebs cycle. All of these steps in-crease the exercise time needed to uti-

lize fat for ATP production from an ex-ternal source. During this time, themuscle can use other fuels, and most

likely metabolizes intramuscular fat,any free FAs in the blood, or glucose,but does not utilize a high percentageof the fat within the fat cells that diets

and exercise programs target. There-fore, if your exercise goal is to reducefat, exercising aerobically at 60-70% ofyour Vozmax for at least 20 minutes perday is one way to achieve that goal.However, longer periods of aerobictraining or higher-intensity anaerobicprograms coupled with diet modifica-tion have also been shown to be effec-

tive, but that discussion will have towait for another time. .

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References1. CRAIG, B.W What is the scientific

basis of speed and agility? StrengthCond.j 26(3):13-14.2004.

2. CRAIG,B.W Does muscle pH affectperformance? Strength Cond j 26(6):24-25. 2004.

3. CRAIG,B.W What is the physiologicallimit of aerobic performance? StrengthCondj 27(3):57-58.2005.

4. HAFF,G.G., R. CHELTIN,B.W CRAIG,G. HUNTER, AND T. TRIPLETT.Roundtable discussion: Resistance

training and the older adult. StrengthCondj 27(6):48-69.2005.

5. ]EUKENDRUP,A.E. Modulation of car-

bohydrate and fat utilization by diet,exercise and environment. Biochem.

Soc. Trans.31:1270-1273,2003.6. WILMORE,].H. AND D.L. COSTILL.

Physiology of Sport and Exercise (3rded.). Champaign, IL: Human Kinetics,2004. pp. 120-131.

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