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Weight cycling in competitive judokas Brewer, Paula E. 1992

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WEIGHT CYCLING IN COMPETITIVE JUDOKASbyPAULA E. BREWERB.Sc. in Biology, University of Victoria, B.C, 1988A THESIS SUBMITTED IN PARTIAL FULFILLMENT OFTHE REQUIREMENTS FOR THE DEGREE OFMaster of ScienceinTHE FACULTY OF GRADUATE STUDIESDIVISION OF HUMAN NUTRITIONSCHOOL OF FAMILY AND NUTRITIONAL SCIENCESWe accept this thesis as conformingto the required standardTHE UNIVERSITY OF BRITISH COLUMBIAApril,1992©  Paula E. Brewer, 1992In presenting this thesis in partial fulfilment of the requirements for an advanceddegree at the University of British Columbia, I agree that the Library shall make itfreely available for reference and study. I further agree that permission for extensivecopying of this thesis for scholarly purposes may be granted by the head of mydepartment or by his or her representatives. It is understood that copying orpublication of this thesis for financial gain shall not be allowed without my writtenpermission.Department of School of Family and Nutritional SciencesThe University of British Columbia^Vancouver, CanadaDate^DE-6 (2/88)ABSTRACTIt has been suggested that repeated cycles of weight loss, followedby weight gain (termed weight cycling) will lead to metabolic andphysiological adaptations which increase food efficiency and thus causeresistance to future weight loss. Athletes who compete in Judo (namedjudokas), were used as an athletic model of weight cycling. Some judokascut weight (lose weight) repeatedly, in order to meet specific weightcategories for competition, and may therefore represent a weight cyclingpopulation. Consequently it is important to determine if suggestedmetabolic and physiological adaptations associated with weight cyclingoccur in these athletes.Two groups, weight cyclers (n=9) and matched non-cyclers (n=9),were followed over a period of 10 months (including one competitiveseason). They followed similar training routines. Weight cyclers dieted(cut weight) in order to compete in a weight class below their usual bodyweight, because they believed that this would give them an advantage overtheir opponents. Dieting habits were characterized by food restrictionan average of 8.1±6.9 (mean±SD) days before their competition. Followingthe competition, weight was regained to baseline values.There was no significant difference in lean body mass, percentagebody fat, height, weight, age, or activity level between the two groupsat baseline. Measurements were recorded three times within a one yearperiod. The first pre-season (baseline) value was measured when thejudokas were training, but had not yet started to diet for competition.The second test session was during their peak season, at which point theweight cyclers had experienced episodes of weight reduction to meetiiABSTRACTcompetitive weight classes. The final test session was conducted duringthe off-season, at least three months after the Judo season had ended.Measurements included resting energy expenditure (REE), body composition(skinfolds), usual three day food intake (three day food records), andbiochemical parameters (fasting insulin, glucose and triiodothyronine).The weight cyclers lost 4.1±1.5 kg, 4.2±2.7 (mean±SD) times perseason, whereas the non-cyclers lost little or no weight throughout thestudy. Weight loss was achieved primarily through food restriction.There was no significant difference in metabolic or physiologicalparameters between the weight cyclers and the non-cyclers during any ofthe three test sessions. This study indicated that there were no effectsof weight cycling in this athletic population. It is possible thatregular physical activity protected against any suggested metabolicadaptations.iiiTABLE OF CONTENTSABSTRACT ^LIST OF TABLES ^ viiCHAPTER 1 1BACKGROUND ^  11.1 INTRODUCTION^  11.2 METABOLISM  21.2.1 METABOLIC EFFECTS OF DIETING^  41.2.2 METABOLIC EFFECTS OF WEIGHT CYCLING^  7ANIMAL STUDIES^  7HUMAN STUDIES: OBESE^  .10HUMAN STUDIES: NON-OBESE  13HUMAN STUDIES: ATHLETES  141.2.3 SUMMARY OF METABOLISM^  171.3 BODY COMPOSITION^  171.3.1 BODY FAT 18ANIMAL STUDIES  18HUMAN STUDIES^  191.3.2 FAT SELECTION 201.3.3 DISTRIBUTION  221.3.4 SUMMARY OF BODY COMPOSITION^  231.4 BLOOD PARAMETERS^ 241.4.1 INSULIN AND GLUCOSE^ 241.4.2 THYROID HORMONES 27MECHANISMS^ 301.4.3 SUMMARY OF BIOCHEMICAL PARAMETERS^ 321.5 HYPOTHESES^  331.6 SPECIFIC AIMS 34CHAPTER 2 ^ 35METHODOLOGY 352.1 SUBJECT SELECTION^  352.2 EXPERIMENTAL DESIGN 362.3 RESTING METABOLIC RATE 372.4 BODY COMPOSITION^ 382.5 BIOCHEMICAL MEASUREMENTS^  402.5.1 SERUM TRIIODOTHYRONINE  402.5.2 SERUM INSULIN DETERMINATION^ 412.5.3 SERUM GLUCOSE ANALYSIS  412.6 DIET ANALYSIS^  422.7 DATA ANALYSIS 43CHAPTER 3 ^ 45RESULTS 453.1 SUBJECTS^ 45ivTable of Contents3.1.1 IDENTIFICATION OF A WEIGHT CYCLER^ 453.1.2 SUBJECT MATCHING^  473.1.3 DIETING HABITS AND WEIGHT LOSS DURING THE SEASON^ 473.2 METABOLIC PARAMETERS  503.3 ANTHROPOMETRICS^  523.4 BIOCHEMICAL PARAMETERS^  543.5 DIET^  56CHAPTER 4 60DISCUSSION ^ 604.1 METABOLIC PARAMETERS^  604.1.1 HISTORY OF WEIGHT CYCLING: BASELINE VALUES^ 604.1.2 A SEASON OF WEIGHT CYCLING ^  624.1.3 REASONS FOR NO DIFFERENCES 64NO WEIGHT CYCLING EFFECTS  64NO DEFINITION FOR A WEIGHT CYCLER^ 64METHOD OF WEIGHT LOSS^ 66EXERCISE PREVENTS RMR DEPRESSION  67EXERCISE INCREASES RMR 68SMALL NUMBERS AND WIDE VARIABILITY^  70NON-RESTING ENERGY EXPENDITURE IS ALTERED^ 714.1.4 THYROID HORMONE^  724.2 ANTHROPOMETRICS^  734.2.1 REASONS FOR NO DIFFERENCES^ 74NO WEIGHT CYCLING EFFECTS  74SEVERITY OF WEIGHT CYCLING  74ACCURACY OF SKINFOLD MEASUREMENTS^  75EXERCISE MAINTAINS LEAN BODY MASS  76FAT SELECTION^  764.2.2 INSULIN^  774.2.3 FAT DISTRIBUTION  784.3 DIET ANALYSIS  78CHAPTER 5 ^ 80CONCLUSIONS AND RECOMMENDATIONS ^ 80BIBLIOGRAPHY ^ 83APPENDIX I. CERTIFICATE OF APPROVAL ^ 96APPENDIX II. WEIGHT CYCLING QUESTIONNAIRE ^ 98APPENDIX III. MEDICAL GRAPHICS CORPORATION SYSTEM 2001 ^ 105APPENDIX IV. PROCEDURE FOR ANTHROPOMETRIC MEASUREMENTS  108APPENDIX V. DURNIN AND WOMERSLEY LINEAR REGRESSION EQUATIONS ^ 111LIST OF TABLESTABLE 1The criteria required for male judokas to be classified as a weightcycler or a non-cycler and the ratings achieved by each group.46TABLE 2Physical characteristics of weight cycling and non-weight cyclingmale competitive judokas for the pre-season, baseline test...48TABLE 3Criteria for maximum differences allowable between matched weightcycling and non-weight cycling judokas for pre-season values andthe mean differences which were actually obtained^ 49TABLE 4The absolute and relative resting energy expenditures (REE) of weightcycling and non-weight cycling judokas at pre-, peak, and of . ^  51TABLE 5Anthropometric measurements of weight cycling and non-weight cyclingjudokas during pre-, peak, and off-season. ^  53TABLE 6Fasted serum values for insulin, glucose, and triiodothyronine inweight cycling and non-weight cycling judokas during pre-, peak,^and off-season   55TABLE 7Macronutrient and energy consumption, as determined by three day foodrecords for weight cycling and non-weight cycling judokas duringpre-, peak, and off-season.   57TABLE 8Predicted energy requirements, estimated energy requirements andestimated energy consumption of weight cycling and non-weightcycling judokas during pre-, peak, and off-season. ^ 58TABLE 9Definitions of weight cyclers for various weight cycling studies..65viCHAPTER 1BACKGROUND1.1 INTRODUCTIONDieting has become a common practice among many individuals today.Surveys show that over 50% of Canadians want to change their weightprimarily through weight loss and 70% of women at a "good weight-for-height" still want to lose weight. ' Athletes who must meet weightcategories for competition are also frequent dieters. One surveyindicated an average wrestler would "cut weight"(lose weight) 15 timesper season and 41% of those surveyed would have a weight fluctuationbetween 5.0 and 9.1 kg per week. 2Under normal circumstances, dieting can have beneficial healtheffects, specifically in obese individuals, who are at risk for coronaryheart disease, hypertension, Type II diabetes, and hypercholesterolemia. 3However, success of maintaining weight loss has been reported as verylow. Sjostrom4 specifically stated that a relapsing patient can beidentified in advance with high precision by predicting that everyonewill relapse. This necessitates further cycles of dieting which istermed "yo-yo dieting" or "weight cycling".Such a pattern of weight fluctuation has been correlated withcertain health risk factors. High individual variability in body massindex (BMI) accompanied by a high BMI, produced a 2.5 fold increased riskof coronary heart disease, compared to normal and stable BMI values. 5Ashley et al 6 studied subjects losing and gaining weight, and found thatweight loss was associated with a decrease in blood pressure, and weight1BACKGROUNDgain was associated with an increase in blood pressure. The increase inblood pressure was greater than the decrease, having a net detrimentaleffect. Additionally, severe protein catabolism associated with dietingmay result in myocardial protein loss and impairment of cardiac function.Cardiac atrophy is proportional to muscle atrophy, even when adiposetissue is present. 3Athletes are rarely obese, and usually are at low risk for coronarydisease, hypertension, and diabetes. However, athletes who must cutweight frequently to meet specific weight categories, may incurdeleterious metabolic consequences. The purpose of this study was todetermine if weight cycling in competitive judokas altered specificmetabolic and physiologic parameters. To accomplish this, restingmetabolic rate (RMR), serum triiodothyronine (T3), insulin and glucoselevels, as well body composition and fat distribution were examined.This study was approved by the Clinical Screening Committee at UBC(appendix I).1.2 METABOLISMDue to the high prevalence of obesity and a high failure rate ofdieting, it has been speculated that food restriction may havedetrimental metabolic consequences. It has been well documented thatchronic dieting leads to a reduction in resting energy expenditure as anadaptive response for energy conservation7-13 . This allows the body tominimize loss of weight, fat and lean body mass (LBM) 7 when food becomes2BACKGROUNDscarce, and it is a useful mechanism when famine may pose a threat toone's survival. It is however, a frustrating consequence when weightloss is desired.There are three main components to energy expenditure, all of whichmay be affected by the dieting process. The first and most importantcomponent is resting energy expenditure (REE) expressed per day. Whenexpressed as an hourly rate it is termed resting metabolic rate (RMR).It is the largest contributor to daily energy expenditure (70-75%) 14 andhas the most profound effect on daily caloric requirement if it isaltered. The REE is influenced by lean body mass, hormones, age,genetics and physical training. The second component of energyexpenditure is diet induced thermogenesis, which contributesapproximately 10% 14 . This is the energy required to digest, absorb, andassimilate nutrients. Of the three main nutrients, (carbohydrate (CHO),fat, and protein) protein has the highest thermogenic effect and fat hasthe lowest. The final component is exercise induced thermogenesis. Thisis the energy required to perform activity and it is dependent on theintensity and duration of the activity. It contributes approximately 20%to the daily energy expenditure in the average individual, but is veryvariable among individuals and can be considerably higher in athletes 14 .If caloric restriction reduces any of these three components, ashas been suggested by numerous studies, 7-13 it could make weight lossformidable. If such metabolic consequences were to persist when normalfood intake resumed, it would make weight maintenance difficult. This3BACKGROUNDcould initiate the recurring pattern of the cyclic dieter, especially ifthe effects of each diet were additive. For this reason it is importantto take an in depth look at metabolic consequences of dieting. Whetherit is in the case of obesity, eating disorders (anorexia nervosa), orcompetitive athletes cutting weight, if metabolic adaptations lead to areduced energy expenditure, the use of severe food restriction to achieveweight loss should be avoided.1.2.1 METABOLIC EFFECTS OF DIETINGProlonged calorie restriction results in a reduced RMR9 - 12 • Thecomposition of weight lost may influence this decrement. Under a weightreducing regime one would expect a loss of both fat and lean body mass(LBM). The percentage of weight lost as LBM is related to the severityof food restriction with losses being the greatest with completefasting.8 Studies have shown that RMR is highly correlated with LBM, 15as it is the most metabolically active component of the body. Althoughit still remains controversial as to what body measurement ie. fatweight, body weight or LBM is the best predictor of RMR,16 LBM valuescan be used to predict RMR from multiple regression equations. 14 It wouldtherefore be expected that weight reduction would result in a decline inRMR in proportion to the amount of LBM lost. 8 Furthermore, if weightloss was rapid (very low calorie dieting [VLCD] or fasting), thepercentage of LBM lost would increase, enhancing the depression ofmetabolic rate. This may be why so many individuals who have had4BACKGROUNDdifficulty losing weight, tend to regain lost weight 17 , or else requireless than normal energy intake to maintain reduced weight. 18Of the numerous studies that conclude RMR is reduced with caloricrestriction9 - 12 some have shown reduced rates beyond those whichcompensate for LBM losses. 7,8,11,13 Vansant8 et al demonstrated thatboth absolute RMR and RMR/LBM were significantly decreased in women on along term (6 months) protein sparing modified fast (PSMF) (2840-720kcal/day). However this effect was not observed during a short termfast of two weeks. Elliot13 et al demonstrated that obese womendieting for 10 to 20 weeks on a PSMF of 300 kcal/day (45g protein) hadRMR reduced by 22%. When corrected for LBM, the RMR was stillsignificantly lower than pre-diet values, indicating that loss of leantissue could not account for the entire reduction in RMR. 13 Barrows7 etal also concluded that factors other than reduced LBM must be involved indepression of RMR. They found that obese subjects restricted to 420kcal/day for 4-6 months had a decreased rate of weight loss by 3 monthsand the RMR per LBM had declined significantly.Whether reduced energy expenditure is sustained upon refeeding of aweight maintaining diet has been questioned. The obese women in thestudy of Elliot and co-workers maintained a stable reduced rate for twomonths and a sustained decrement in RMR persisted, despite an increasedcaloric consumption. 13 Geissler19 et al compared the metabolic rate ofpost obese subjects against matched lean controls and found that the postobese group had a 15% reduction in 24 hour energy expenditure. Only 10%5BACKGROUNDof the 15% reduction in energy expenditure could be attributed to adepressed basal metabolic rate (BMR). The other 90% reduction in energyexpenditure was identified during three different set levels of activity(from sedentary to aerobically active). Therefore it appears that themajority of the reducted 24 hour energy expenditure is due to a decreasein exercise induced thermogenesis and possibly diet inducedthermogenesis. 19 Whether such differences are caused by dieting, ornecessitate dieting has not yet been determined.Other studies have found no sustained effect of dieting on RMRbeyond that expected with reduction in LBM. Rattan20 et al showed thatsubjects on a VLCD for 8 weeks had a reduced RMR of 86% of their initialvalues, which recovered to 93% upon refeeding with a weight maintainingdiet (for another 8 weeks). The decrement could be accounted for by lossof LBM. A recent study demonstrated similar results. Wadden 21 et alstudied two groups of obese patients (9 in each group). One groupconsumed 1200 kcal/day for 48 weeks. The second group consumed 420kcal/day(VLCD) for 16 weeks and then switched to a conventional reducingdiet (1200 kcal/day) for the remaining 31 weeks (total 48 weeks). Whileon the VLCD the latter group had a decrease of RMR by 19.8%, but whenswitched to the 1200 kcal/day regime, their RMR was only depressed by8.3%. This was comparable to a 9.4% reduction in the group continuouslyconsuming 1200 kcal/day and could be accounted for by loss of LBM. 21The literature still remains controversial with respect to themetabolic effects of dieting. It is evident that there is a reduction in6BACKGROUNDdaily energy requirements when food restriction is severe enough, butwhether it is due to a decreased RMR, or a reduced diet or exerciseinduced thermogenesis has yet to be confirmed. Whether the RMR remainsdepressed over a longer time period is not known. Due to the variationin degree of caloric restriction, dietary composition, diet length andpopulations studied, it is difficult to compare experimental findings andreach a strong consensus.1.2.2 METABOLIC EFFECTS OF WEIGHT CYCLINGIf a single bout of dieting will result in a depressed RMR andincreased energy efficiency, then weight loss and regain which isrepeated several times could exacerbate this adaptation, resulting inresistance to weight loss. Miller and Parsonage22 found that women whowere resistant to weight loss had a long history of dieting. Jeffery23et al suggested that a history of dieting was a poor prognostic sign fortreatment. Metabolic effects of weight cycling which could explain thesefindings have been investigated in both animals and humans. Methods thathave been used to assess the metabolic effects of weight cycling includechanges in RMR, velocity of weight loss and weight regain from one cycleto the next, and the food efficiency ratio (FER) or weight gained/gram offood consumed.ANIMAL STUDIESWeight cycling was first studied in rodents. Brownell24 et al7BACKGROUNDstudied 21 week old male rats divided into three groups. One group werechow controls, fed ad libitum. The second group were obese controls, feda high fat diet (63% of energy as fat). The third group were obese"weight cyclers". In the first cycle the obese cycling rats wererestricted to 50% of the average intake of chow controls, until theyreached the weight of these controls. They were then refed the high fatchow until they reached the weight of the obese controls. The secondcycle was a repeat of this protocol. The number of days to lose andregain the weight in each cycle were compared. The desired weight lossin the first cycle required 21 days, but by the second cycle, weight lossoccurred at half the rate, requiring 46 days. Weight regain was threetimes as fast during the second cycle, despite an identical food intakeduring both cycles. Food efficiency (weight gain/g food) had increased 4fold when compared to the obese controls. Changes in metabolicefficiency as a result of increased age were controlled for. It wasconcluded that after two cycles of weight loss and regain, weight losswas slower and weight regain more rapid at the same level of energyintake.Cleary25 investigated the effects of weight cycling in 6 week oldlean and obese Zucker rats. Four groups were investigated; 1) ad libitumlean (AL), 2) restricted lean rats (RL), 3) ad libitum obese rats (AO),and 4) restricted obese rats (RO). The restricted groups had three weeksfeeding at half the amount of the respective ad libitum groups, followedby three weeks ad libitum. They underwent four similar cycles. The RL8BACKGROUNDrats gained three times the weight of AL rats on similar food intakes andthe RO rats gained 50% more weight than the AO rats, despite a lower foodintake (ad libitum) during the first refeeding episode. In thesubsequent cycles, both weight cycling groups lost and regained weight,were as the non-cycling groups maintained weight (similar intake torefeeding diet of weight cyclers). It is therefore evident that theeffect of weight cycling on energy efficiency occurs in both lean andobese rats. Food efficiencies were compared, and during the first andsecond refeeding period both restricted lean and obese rats had asignificantly increased FER as compared to their respective controls. Inthe last two refeeding periods the FER was greatest for the RO rats, andthen the RL rats, both being significantly greater than AL or AO rats. 25In contrast, Hill et a126 found no increase in energy efficiency inweight cycled adult male rats. The rats went through four cycles of 3days fasting (at either 100%,60% or 40% ad libitum) followed by 7 daysrefeeding. Similarly, Cleary 27 found four cycles of food restrictionfollowed by refeeding in both lean and obese female Zucker rats, had noeffect on food efficiency. A review of 18 weight cycling studies done inanimals27 led to the conclusion that no clear evidence suggesteddifficulty of future weight loss or ease of weight gain as a result ofweight cycling. Nor was there consistent evidence of increased totalbody fat or central adiposity, increased subsequent caloric intake,increased food efficiency, or decreased energy expenditure27 .Some of the inconsistencies in animal studies may be explained by9BACKGROUNDvariations in the age of the rodent used. Rodents restricted in a growthstage may undergo compensatory growth or catch up growth28 uponrefeeding. This results in an increased food efficiency ratio which isnot necessarily a result of weight cycling. Consequently, similarresults may not be demonstrated in adult rats under the same experimentalconditions. 25 Further efforts must be made to conduct more controlledanimal experiments.HUMAN STUDIES: OBESEHuman experiments on weight cycling are limited and again,inconsistent. Such inconsistencies result from different diet treatmentsand/or levels of compliance, different degrees of obesity or leanness,different methods of collecting weight cycling data, and differentcriteria to define weight cycling. Sex specific differences, andindividual differences in response to weight cycling must also beconsidered. 29Blackburn29 et al investigated the metabolic efficiency ofinpatient and outpatient obese individuals by assessing the velocity ofweight loss over 2 successive diet cycles. In the inpatient group (n=13)it was concluded that the velocity of weight loss in a second cycle(after regaining 20% of cycle one weight) was slower than in the first(on PSMF). A similar decrease in velocity of weight loss was seen in theoutpatient group (n=40) on a second cycle following a 95% regain of lostweight. The authors suggested that chronic dieting leads to permanent10BACKGROUNDalterations in metabolic function which results in difficult weight lossand easy regain.29There were some limitations to this study. The length of timewhich had lapsed between diet cycles was as much as 9 years and changesin metabolism with aging must be considered. Secondly, those subjectswho weighed less by their second cycle would be expected to have adecreased velocity of weight loss due to reduced energy required forweight bearing activity and reduced lean body tissue.Beeson et a130 gave a brief report on the rate of weight loss inobese individuals (n=4) between 2 consecutive VLCD's (330 kcal/day and405 kcal/d respectively). They found that there was no change in therate of weight loss by the second cycle. The subjects had regainedbetween 0% and 83% of the lost weight in between the two cycles. Noinformation was given about the individuals' sex, dieting history, LBM, %fat and degree of obesity and there were only four subjects participatingin the study.In contrast Van Dale31 et al looked at absolute RMR following a 14week VLCD in obese weight cyclers and non-cyclers. Weight cyclers weredefined as those who were "frequently dieting", and had lost and regainedgreater than or equal to 10 kg in the past 5 years, more than once. Bodyweights were stable for the past 6 months. Half of each group wasrandomly assinged to an exercise program. The exercise program consistedof two days of aerobics, 1 day of fitness, and 1 day of jogging,11BACKGROUNDtotalling four hours of exercise at 60% V02 max per week. The weightreducing diet included three phases; (1) 5 weeks VLCD (722 kcal/day), (2)9 weeks VLCD (528 kcal/day + 312 kcal/day conventional foods), and (3) 2weeks VLCD (722 kcal/day). The RMR had decreased significantly frombaseline in all groups following the 14 week study period, but to asignificantly lesser extent in both weight cycling and non-cyclingexercise groups, when compared to non-exercising groups. There was nosignificant difference in RMR between the weight cyclers and non-cyclersin either exercising or non-exercising groups.The dieting history in this study may be questionable, as it isunlikely that an obese person would not have tried to diet at some pointin their life time. Only 5 years preceding the study were analyzed andit's possible that those that were not weight cycling had in fact dietedprior to the 5 years and were still suffering the metabolic effects. Thedefinition of a weight cycler is different from other experiments.A more recent study looked at the BMR of obese female cyclicdieters who underwent 3 cycles of 2 weeks on an 443 kcal/d diet followedby 4 weeks of ad libitum refeeding. 32 Classification as a weight cyclerrequired the subject to have lost 6 kg on 2 or more occasions. It wasfound that the absolute BMR was significantly different during allrestriction times, but when it was corrected for LBM, only the firstcycle showed a significant decrease in BMR. Furthermore the BMR returnedto normal following each 4 week refeeding period. At the end of thestudy there was no significant difference in absolute BMR and BMR/kg FFM.12BACKGROUNDBMR/kg had increased indicating loss of adipose tissue, with no excessiveloss of LBM. 32HUMAN STUDIES: NON-OBESEThere may be differences in metabolic responses between lean andobese individuals. One group 33 looked at non-obese females who had ahistory of cyclic dieting. This was defined as having dieted for greaterthan or equal to 7-10 days, 4 times in the last year. A diet wasconsidered to be an energy intake 1000 kcal/d below energy requirementfor weight maintenance. There were 11 weight cyclers who had lost anaverage of 3.5-8.2 kg on each diet and 12 non-cyclers who had no historyof weight loss through dieting. They found that the cyclic dietersweighed more and had more body fat. LBM was the same. The REE of theweight cyclers was compared to the matched controls and they found thatREE/kg was significantly reduced (this was because they had a higherpercentage fat which is less metabolically active) but that absolute REEwas the same (this is because they were matched for lean muscle masswhich is more metabolically active).The investigators also looked at exercise energy expenditure (EEE)to see if there was a difference in exercise induced thermogenesis in thetwo groups. EEE was estimated by measuring oxygen uptake whileexercising on a treadmill. Each subject followed a similar exerciseprotocol, walking at 4.8 km/h, with the treadmill grade increasing 2.5%every three minutes. Eight workloads were completed. They found that13BACKGROUNDEEE/kg was significantly reduced, but that the absolute EEE was the same(ie. there was no increase in energy required to move the excess weightof the heavier people as may be expected, even with no differences inLBM). Therefore they concluded that non-obese cyclers did not decreasebaseline metabolic rate but that they were more efficient in theirexercise, requiring less energy to move around a larger mass. 33 Over aperiod of a year this could have a significant effect on weightmaintenance.HUMAN STUDIES: ATHLETESWeight cycling is also common among athletes, especially those whocompete in certain weight classes (wrestling and judo) or those who arerequired to be lean for aesthetic purposes (gymnastics). Cutting weightoften requires athletes to go below their natural or usual weight.Following the set point theory, the body will try to defend its naturalweight, through changes in metabolism. 34 The effect of food restrictionwould be expected to be greatest among those furthest below their naturalweight and in those who have lost and regained numerous times in thepast. 2Wrestlers are a notable example of athletes who must "cut weight",and rapid, frequent weight loss is often necessary. One survey 2 showedthat of a group of collegiate wrestlers, an average wrestler would cutweight 15 times in a season, and 41% of those studied had a weightfluctuation between 5.0 and 9.1 kg every week. Because weight loss is14BACKGROUNDshort term and may be severe, it can result in loss of both fat and largeamounts of lean tissue. Furthermore weight regain is rapid, causingadded weight to potentially be deposited as fat rather than muscle. 2Steen35 et al compared the RMR of weight cyclers and non-cyclers inhigh-school wrestlers. A weight cycler was defined as one who cut weightgreater than or equal to 10 times per season, had a weekly loss greaterthan or equal to 4.5 kg and who was often or always cutting weight. Anon cycler would cut weight less than 5 times in a season, with a weightloss not more than 1.4 kg and considered frequency of weight cutting tobe never, rarely or sometimes. Cyclers and non cyclers had nosignificant difference in age, height, weight, body surface area,percentage body fat, or LBM. It was found that RMR was significantlylower (14%) in cyclers, even when corrected for differences in bodycomposition. The cyclers required 255 kcal/day less than the non-cyclersunder resting conditions.A more recent study on weight-cycling in wrestlers was conducted byMelby et al. 36 They designed a longitudinal study which looked atcollegiate wrestlers over a period of a year, to see if there was ametabolic effect after a season of cutting weight. The wrestlers werematched to physically active men who did not weight cycle and did nothave a history of dieting. The criteria for weight cyclingclassification included a loss of greater than or equal to 4.5 kg atleast 10 times in a season for at least the past 3 years. The three testperiods included pre-season, during the competitive season 24-48 hours15BACKGROUNDprior to a competition when food restriction, but not dehydration hadtaken place, and off season. This took place 5-6 weeks following thecompetitive season when weight had normalized and was stable.The results of the experiment indicated that at baseline thewrestlers in fact had a significantly greater absolute and relative RMRper kg and per fat free weight (FFW) than their matched controls. Thisindicates that there were no previous metabolic effects of weight cyclingin the wrestlers, which might be expected after three years of practisingsuch dieting habits. When the wrestlers were cutting weight, their RMRwas significantly decreased from pre-season values but was notsignificantly different from the controls. This depressed RMR is asexpected, due to food restriction. RMR/FFW and RMR/kg were alsosignificantly lower, indicating that RMR was decreased beyond that whichcompensates for loss of weight and lean tissue. This is also ademonstrated phenomenon of food restriction. The most significantfinding was that the absolute and relative RMR returned to baselinevalues 5-6 weeks after the competitive season. This was accompanied byan increase in LBM back to baseline values. The percentage fat didincrease slightly above baseline values but it was not significant.The subjects were not matched for type, duration, or intensity ofexercise, which can significantly affect RMR. Furthermore two differenttechniques for measuring body fat were used. Underwater weighing wasused for baseline values for the wrestlers, whereas skinfolds were usedfor the remainder of the data collection and for all control measures.16BACKGROUNDSince there is controversy over the variation between the two methods,the body composition and REE/LBM results may lack precision. 361.2.3 SUMMARY OF METABOLISMScientists have yet to establish if altered metabolism promotesweight cycling or if it is the result of weight cycling. Furthermore, itis not known whether only RMR is affected or if other components ofenergy expenditure are also affected. Applicability of animal studies tohumans is questionable due to different metabolic regulatory mechanismsand responses. The few human studies that have been done use differentpopulations with different weight cycling habits and classificationcriteria. Obese individuals, lean individuals and athletes may differwith respect to body composition and food intake, and may thereforerespond differently to repeated bouts of food restriction. Differentdegrees of restriction may be required for consequences to be realized.1.3 BODY COMPOSITIONAnother potential problem with weight cycling is a change in bodycomposition and fat distribution. It has been suggested that repeatedbouts of dieting may result in a higher percentage of body fat, whetherit is due to a large loss of lean body mass caused by severe caloricrestriction, or a tendency to regain lost weight as adipose tissue (orboth). The end result in any case may be a progressive loss ofmetabolically active tissue, which could be replaced by energy rich17BACKGROUNDadipose tissue. 81.3.1 BODY FATANIMAL STUDIESReview of the literature shows conflicting results regarding theeffects of weight cycling on body composition. Stock et al 37 found thatobese rats on a low calorie diet had an increased percentage fat and adecreased percent lean body mass following weight reduction, indicatingan excessive loss of LBM. Ozelci et a1 38 found that rats restricted to50% and 25% of ad libitum food intake for one week and then pair fed withan ad libitum control group for three weeks, had a body fat contentgreater than their ad libitum controls. The restricted rats demonstratedan increased propensity to convert food energy to body fat. This was notinfluenced by meal pattern and resulted with either a high carbohydrateor a high fat diet. The increased body fat was not demonstrated in ratsrestricted to 75% ad libitum food intake at the end of four weeks. Itwas concluded that weight gain and fat gain were more pronounced withincreased severity of caloric restriction. 38 Reed et a139 found thatrats that went through 3 cycles of dieting and refeeding were fatter andhad a greater number of adipocytes than chow controls despite a lowerbody weight.Other experiments show conflicting results indicating no change inbody composition with one cycle40 or repeated cycles41 f 42-44 of foodrestriction followed by refeeding. Lean female Zucker rats, age 1418BACKGROUNDweeks, were restricted for 22 days to 40% of the control food intake andwere refed ad libitum for 20 days. Lost fat was replaced on the sixthday and protein and body weight were recovered, but did not exceedcontrol rats fed ad libitum, by the 13th day of refeeding. When comparedto the control rats, the restricted rats were found to have similar bodyfat content. 40Gray et a142 found similar results in weight cycled adult femaleSprague-Dawley rats made obese by consuming a high fat diet. Those thatunderwent two cycles of restriction and refeeding ad libitum showed nodifference in weight or percentage body fat. Male Sprague-Dawley ratsstarved for three days had body weights, adipose tissue content and fatcell weights that had returned to control values upon refeeding. 43Three cycles of weight loss and regain in White-Footed Mice resulted inno significant differences in final weight or fat content. 44HUMAN STUDIESHuman studies are limited and equally controversial. An increasein adiposity as a result of food restriction was first demonstrated innormal weight young males who had lost 24% of their body weight during 24weeks of semi-starvation. 45 Upon refeeding the men recovered 93% oftheir body fat, yet only 60% of their body weight was regained. Althoughthe study has its limitations in that the physical activity and diet ofthe refed men were not observed, and weight was not 100% regained, ahigher proportion of lost body fat was recovered, as compared to leanbody mass. This may indicate that food restriction with subsequent19BACKGROUNDrefeeding results in an increase in percentage of body fat and areduction in lean body mass. 45 A cross sectional study conducted byManore et al33 found that non-obese females who had a history of cyclicdieting had a higher body weight and a higher percentage body fat thanwomen who had never dieted. Their LBM, however was the same as controls.Melby et a136 followed wrestlers through a season of cutting weightfor competitions and found that during the season they lost a significantamount of weight as both lean tissue and body fat. Upon refeeding LBMand percentage of fat returned to baseline values (pre-season). However,it is possible that the athletic population is resistant to an increasein adiposity as a result of regular exercise which protects against lossof LBM and accumulation of body fat.1.3.2 FAT SELECTIONChange in body fat may be related to diet composition. Foodrestriction has been suggested to result in an increased selection of fatupon refeeding39 46-48 and such a diet has been suggested to promotedeposition of adipose tissue, rather than lean body mass. 49-51 Withweight cycling there will be repeated episodes of weight regain and thepotential for repeated episodes of high fat selection, resulting inincreased fat stores. It should be noted that fat selection studies todate, have only been conducted in animals.Reed et al 39 found that female Sprague-Dawley rats restricted to25% of their baseline weight, and who were then allowed to self-selecttheir own diet upon refeeding, had a tendency to choose a diet high in20BACKGROUNDfat. These rats, compared to controls, who could self select throughoutthe experiment, had a fatter retroperitoneal and parametrial deposit, andheavier fat pad weights, despite a lower overall body weight. They alsohad a greater number of adipocytes in both fat pads. Fat cell size wassignificantly smaller, but a longer refeeding period may have resulted inincreased size as well (they were sacrificed at the end of theexperimental protocol).Weight cycled rats have shown a progressive increase in thepercentage of fat selected in the diet over two cycles. 52 Female ratsafter one bout of food restriction were found to select 56% of theircalories from fat as compared to 44% in the ad libitum control rats.After the second cycle, fat selection had increased further to 73%,whereas the control rats had remained the same. Furthermore the weightcycled rats had an increased percentage body fat despite a lower bodyweight. 52 These results are difficult to interpret as the rats were ina growth stage. It might be expected that an even further increase inpercentage body fat may result in adult rats not experiencing catch-upgrowth.Conversely, Graham et al 53 found that lean female cycled rats(three cycles) given a high fat (60%), high caloric diet, only selectedthe number of calories required to match the reduced RMR caused by theweight cycling. In fact the control rats weighed more and were fattierthan the weight cycled rats. These rats showed no excessive intake ofcalories or fat resulting in an increased adiposity.21BACKGROUND1.3.3 DISTRIBUTIONAnother area of importance concerning body adiposity is fatdistribution. It has been suggested that repeated cycles of weight lossand regain may result in the redistribution of fat which can lead toincreased health risks.Studies have shown that android (upper body) fat is associated witha greater risk of coronary heart disease and that a high waist to hipratio (WHR) is a better predictor of diabetes and mortality from coronaryheart disease than body weight, body mass index and percentage body fat. 2Gynoid (lower body) obesity is associated with less risk of hypertensionand impaired glucose tolerance. 54These differences may be attributed to the different types ofreceptors located in these two areas. Beta-receptors located in theupper body enhance fat transfer. As a result, triglycerides in this areaare more readily mobilized and are available to form atheroscleroticplaques, which can subsequently increase blood pressure and increase therisk of coronary heart disease. Alpha-receptors in the gynoid regioninhibit fat transfer to and from the cell, making fat mobilizationdifficult. This fat is trapped and less available to contribute to suchhealth risks. 2Currently only one weight cycling study has investigated thequestion of fat distribution. 55 This was evaluated in non-pregnant, pre-menopausal women. A random sample of 87 normal weight women between theages of 21 and 40 were measured for WHR determination and identificationand rating of weight cyclers was achieved by questionnaire. It was found22BACKGROUNDthat a higher WHR was significantly associated with a higher degree ofweight cycling, controlling for age and parity. Normally this populationwould tend to have a higher deposition of fat in the gluteofemoralregion, but if excessive abdominal fat was present, a history of dietingmay be one explanation.Until further studies are done, it can only be speculated that fatredistribution to the upper body would occur with repeated bouts ofweight loss and weight gain in other populations.1.3.4 SUMMARY OF BODY COMPOSITIONCurrent studies have led to a number of inconsistent findings.Animal studies must be viewed with caution, as some use growing rats andothers use adult rats. These two groups may respond differently toweight cycling, as it is known that growing rats who are restrictedundergo compensatory growth in an attempt to catch up to their naturalgrowth pattern. As a result they require high caloric intakes for growthand fat deposition may not occur, even on a high fat diet. Furthermoreit is questionable as to whether rat studies are representative ofhumans, particularly with respect to eating behaviors such as fatselection. Rats tend to choose appropriately to increase their chance ofsurvival. Humans however, are influenced by psychological factors andnot simply physiological need. As a result they may be more or lesssusceptible to selecting higher fat diets, as well to consume morecalories than are required for weight maintenance.23BACKGROUND1.4 BLOOD PARAMETERS1.4.1 INSULIN AND GLUCOSEInsulin has an important function in the regulation of CHO, lipidand protein metabolism, and changes in hormone function can be seen withdiet manipulation and changes in body weight. In obesity, insulinresistance is quite prevalent. Under such conditions, mildhyperinsulinemia can occur as a result of reduced insulin receptors ontarget tissues. 56 As a result the ability of the target tissue torespond to insulin is reduced and glucose utilization is impaired. 57Post-receptor abnormalities can also occur in more severe cases,resulting in limited glucose transport and the possibility of developingdiabetes. Weight reduction usually reverses insulin resistance byincreasing the number of receptors on various tissues. A simultaneousfall in basal plasma insulin levels will occur. 56Fasting and caloric restriction also have a profound impact onplasma insulin concentrations and hormone function. Numerous studieshave shown that glucose and insulin levels are reduced with fasting inboth lean and obese individuals and a transitory loss of glucosetolerance has been observed. 58 Strubbe et a159 found that basal insulinlevels dropped in 24 hour fasted male rats, as a result of decreasedinsulin secretory responses of B-cells to glucose. Reduced insulinlevels would aid in the change in energy utilization from CHO to lipidmetabolism, an important adaptation to conserve glucose to fuel thecentral nervous system.24BACKGROUNDReduced levels of insulin result in enhanced lipolysis and reducedlipogenesis causing endogenous fat to be readily mobilized for fuel, andgluconeogenic precursors to be made available. " The lipogenic effectof insulin is inhibited with calorie restriction due to post receptorchanges, which alters transport and metabolism of glucose, and makes itunavailable as a glycerol-3-phosphate precursor for reesterification.Lipogenesis becomes unresponsive to insulin even at physiological levelsof glucose. 61Despite an obvious shift towards enhanced lipid mobilization,increased sensitivity to insulin's antilipolytic action has beendemonstrated during caloric restriction. 59 / 61 Arner et al61 studiedisolated human fat cells from obese females who had fasted for seven daysand found an enhanced antilipolytic action, by stimulating insulinreceptor binding. This may be a protective mechanism to prevent excesslipolysis and subsequent ketoacidosis. 59 Extreme protein losses arealso prevented by a preservation of insulin's role in proteolysisinhibition62 , ensuring that lean body mass is conserved.A decrease in plasma glucose and insulin is observed with fasting,however cyclic dieting appears to have a completely different effect.Cleary25 examined lean and obese Zucker rats that went through fourcycles of restriction and refeeding. They found that there was a trendtowards increased fasting serum insulin and glucose levels in comparisonto the control group (fed refeeding diet continuously), after the lastrestriction period and last refeeding period. The restricted obese ratshad even higher values than the restricted lean rats. Reed et al 39 also25BACKGROUNDdemonstrated that female rats that went through 3 weight cycling periods,had significantly higher basal plasma insulin values (after finalrefeeding period), although plasma glucose concentrations were similar tothe control group. It should be noted that retroperitoneal fat padweights and cell number accounted for 30% of the variance found in theinsulin values. The long term effects on insulin levels were not lookedat in either study, and therefore it remains unknown if this change waspermanent or temporary.In contrast Harris et a140 found that female adult rats restrictedfor 22 days and refed for 20 days ad libitum, showed no increase ininsulin values with refeeding.McCargar et a163 found that food restriction for 4 days(1000kcal), followed by over eating for 2 days (3000 kcal), produced agreater than normal postprandial rise in serum insulin in normal weightfemales. The fasting insulin values however were close to controlvalues. The overfeeding of a diet high in CHO may have stimulated suchan increase in insulin concentration. Once again, it was not determinedif the increased in postprandial rise in serum insulin was a temporary orpermanent change.These experiments may suggest that bouts of food restrictionfollowed by refeeding may lead to elevated insulin levels, especially ifovereating occurs. This could have important implications on lipid(adipocyte) metabolism, with enhanced lipogenesis, decreased lipolysis,and thus increased fat deposition at the time of refeeding. Whetherinsulin levels remain elevated has yet to be determined. Owens et a1 6426BACKGROUNDfound that fasting for 2 days and refeeding for 20 days produced alasting effect on basal and insulin stimulated metabolism of glucose inrats. Insulin stimulated glucose metabolism increased with refeeding.Although all three products of glucose metabolism were increased, theeffect on fatty acid synthesis was the greatest, followed by glucoseoxidation and glyceride-glycerol synthesis. This started on day three ofrefeeding and continued to increase to day 10. After this point itgradually returned to normal by day 20. They concluded that fastingfollowed by refeeding enhanced lipogenesis and insulin stimulation ofglucose metabolism. These changes in adipocyte metabolism are prolongedbeyond the restoration of size and adipose mass to prefasting conditions.These changes in insulin and glucose metabolism may help to explain anincrease in adiposity found in weight cyclers.1.4.2 THYROID HORMONESChanges in thyroid hormone levels may influence a reduction inresting metabolic rate as a result of weight cycling. Thyroid hormonesplay a role in metabolic regulation and have a calorigenic effect in avariety of tissues through the expression of membrane sodium-potassium(Na+-K+), adenosine triphosphatase (ATPase) and several mitochondrialenzymes. 65 The thyroid gland secretes thyroxine (T4) and a very smallamount of triiodothyronine (T3), under the influence of the pituitarygland and thyroid stimulating hormone (TSH). The majority of T3, whichis the most active form of the hormone, is produced in peripheral tissuesby the deiodination of T4. A small amount of T4 is also converted to27BACKGROUNDreverse triiodothyronine (rT3), which is metabolically inactive. Withintissue cells, T3 mediates its action by interacting with specific nuclearreceptors, there by inducing specific m-RNAs for gene expression of suchproteins as mitochondrial respiratory enzymes. It is through thisprocess that T3 has its calorigenic effect, 66 stimulating oxidativemetabolism and boosting BMR.Several studies have suggested that fasting and severe caloricrestriction will result in a decrease of both free and total serum T3,which is sometimes accompanied by an increase in rT3. T4 levels arevirtually unchanged with any degree of calorie restriction. 7 This mayhave important implications with respect to depressed RMR which oftenaccompanies food deprivation. Barrows et al7 conducted a study wheresubjects consumed a very low calorie diet (VLCD) (420 kcal/day) for 4-6months followed by a 5 week refeeding period. T3 levels decreasedsignificantly within the first 5 weeks of calorie restriction andremained depressed through the remainder of the diet. This depressionparalleled the decrease in BMR and decreased rate of weight loss. Uponrefeeding T3 levels increased but did not reach baseline values. Reversetriiodothyronine increased in the first 5 weeks, but dropped again by 10weeks and returned to baseline values with refeeding. Total and free T4levels remained unchanged. Barrows et a1 7 concluded that caloricrestriction resulted in decreased T3 levels. It is possible that such adecline is an adaptation which hinders weight loss, acting as aprotective mechanism against famine and may be linked to the diet-induceddecrease in BMR that is often observed.28BACKGROUNDJung et a1 67 also found a significant decline in T3 and asignificant increase in rT3 when obese women were placed on a low energydiet (9.2kcal/kg desirable weight) for 21 days. Upon refeeding with ahigh energy weight maintaining diet (40 kcal/kg), T3 had significantlyincreased within 72 hours, but did not reach predetermined baselinevalues (measured when subjects consumed the high energy diet for one weekprior to restriction diet). The rT3 had just begun to decline by 72hours. Carbohydrate (CHO) content of the diet may have been an importantfactor in the depressed T3 values, as energy restriction for the lowenergy diet was achieved by decreasing the carbohydrate content. 67Numerous studies have suggested such an effect. This however does notexplain why T3 does not return to baseline on a refeeding diet containingsufficient CHO.Spaulding et al65 postulated that carbohydrate was an importantfactor which regulated the production of T3. It was found that withcomplete fasting, serum T3 was reduced by 53%, and by 47% on ahypocaloric diet of 800 kcal containing no carbohydrate. There washowever, no change in T3 levels with an 800 kcal isocaloric dietcontaining 50g CHO. Other studies have shown that overfeeding with CHOin normal subjects produced increased serum T3 levels. 68 Azizi69 alsofound that following caloric restriction, depressed T3 levels wouldreturn to normal if refeeding consisted of a CHO or mixed diet, but notif the diet contained only protein and lipid. T3 production thereforeappears to be altered by CHO content of a diet, although the mechanism ofits influence is unclear.29BACKGROUNDReverse triiodothyronine did not follow the same trend. Reversetriiodothyronine levels did increase by 58% with total fasting, but withboth 800 kcal diets (100% CHO and no CHO) there was no significantincrease in rT3. 65 It would appear that rT3 production is more likelydependent on the severity of caloric deprivation, rather than CHOcontent.MECHANISMSTwo hypotheses have been suggested to explain how food restrictionmay alter normal T3 activity. Firstly, there may be a decline in T3production. This is a result of reduced transmembrane transport andtherefore availability of T4 within the cell, for T3 conversion.Secondly the number of nuclear receptors which can bind T3 may bediminished.The depression in T3 with caloric deprivation may result from adecreased production of the hormone. Vagenakis et al 70 determined theT4 and T3 production and metabolic clearance rates(MCR) in obesepatients undergoing prolonged starvation. They found that T3 MCR wasunchanged, thus indicating that T3 production rates must be substantiallyreduced, to account for depressed serum values. These findings wereconsistent with in-vitro studies of the livers of starved rats, where T4to T3 conversion was in fact decreased.Reduction in T3 production was first thought to be a result of analtered pathway for conversion of T4 to T3, diverting conversion to rT3production instead. This may be the case, as rT3 levels have been found30BACKGROUNDto increase in parallel with a T3 decline. However more recent studiesdid not show a similar relationship between the two hormones, and rT3showed variable responses to food deprivation.Possible mechanisms for decreased T3 and altered rT3 productionhave been postulated. It has been shown from liver homogenates of fastedrats that 5'-deiodinase enzyme activity is decreased, resulting indecreased T3 formation and diminished rT3 breakdown. 71 Further studyindicated that the transmembrane transport of T4, T3 and rT3, and masstransfer rates of T4 and T3 into tissue pools in humans were altered. 72Triiodothyronine had a 50% decrease in mass transport of which onlypartially could be accounted for by the decreased T3 production. Therewas an even more pronounced inhibition of T4 transport into tissuesresulting in less T4 within tissues. As a result of this decreasedtransmembrane transport of T4, there was a diminished 5'-deiodinaseenzyme occupation and thus decreased activity level.The cause of the transport inhibition is speculative, with thepossible suggestion that intracellular energy charge may be low withcaloric restriction, as is seen in profused fasted rat livers. T4, T3,and rT3 transport, although by two different pathways, both requireenergy (active transport mechanism). Another possibility is a decreasein Na+-K+ ATPase activity, which is caused by diet manipulation and canlead to attenuation of membrane fluidity. 72Another factor affecting thyroid hormone function, is a decrease inthe number of nuclear T3 receptors, which has been shown to result fromprolonged energy restriction. 73 / 74 Moore et a174 found that obese31BACKGROUNDpatients on 1.34 MJ/day, for 12 weeks, showed a significant drop in rateof weight loss, RMR, serum T3 and the number of T3 receptors onperipheral lymphocytes. Since T3-nuclear receptor complex is requiredfor the hormonal effect of T3, this has strong implications on T3function. Schussler et a1 75 determined that fasted Spraque-Dawley ratshad a serum T3 drop of 50% and that receptors had decreased more so thanserum T3. Nuclear receptor affinity towards T3 was not found to bealtered. It was concluded that T3 serum concentration was not the causeof diminished hepatic nuclear receptor content, but rather had anindependent synergistic effect of fasting.Both the decrease in T3 serum concentrations and a decrease in thenumber of nuclear receptors may be important adaptive mechanisms duringfood deprivation, and could be strongly associated with the depressed RMRdemonstrated in such a situation. Repeated cycles of weight loss andregain may result in a prolonged or permanent alteration in T3 serumvalues and nuclear receptor numbers, which could have serious long termconsequences on metabolic rate. If such adaptations were to occur, itmay help explain the depression in resting energy expenditure which isexperienced by some weight cyclers.1.4.3 SUMMARY OF BIOCHEMICAL PARAMETERSWeight cycling may result in altered biochemical parameters such asfasting serum insulin, Glucose, and T3. It is well documented thatinsulin, glucose and T3 levels decrease with food restriction. Whatremains unknown however, is how these biochemical parameters respond to32BACKGROUNDrepeated cycles of weight loss and weight regain. It has been speculatedthat there will be an increase in serum insulin and a decrease in serumT3. Changes in these biochemical parameters may provide an explanation,even if only partially, to some of the changes that occur as a result ofweight cycling. Accordingly, they were examined in this study.1.5 HYPOTHESESAs described above, much remains to be learned about the metabolicand physiological effects of weight cycling. Competitive judokas, someof whom lose weight prior to each competition, may be a good model forstudying these effects. Accordingly, in this study competitive judokas,half of whom were weight cyclers, were followed for a period of 10months. The study period included three test sessions. The first testsession was conducted pre-season, when the judokas were training, but notyet dieting for competitions. The second test session was during thepeak season. At this point the judokas had been competing and thereforecutting weight for competitions. The third and final test session wasduring the off-season, when the judokas were no longer training for judoor dieting for competitions. The null hypotheses were as follows:1) There will be no difference in resting metabolic rate when the weightcycling judokas are compared to the non-weight cycling judokas at any ofthe three time periods.2) There will be no difference in body composition, specificallypercentage body fat, lean tissue, and waist to hip ratio when the weightcycling judokas are compared to the non-weight cycling judokas at any ofthe three time periods.33BACKGROUND3) There will be no difference in fasted serum insulin, glucose ortriiodothyronine when the weight cycling judokas are compared to the non-weight cycling judokas at any of the three time periods.4) There will be no difference in diet composition, specificallyproportions and amounts of macronutrients consumed and total caloriesconsumed at any of the three time periods when the weight cycling judokasare compared to the non-weight cycling judokas.1.6 SPECIFIC AIMSThe purpose of this research project is to determine what effect weightcycling in male competitive judokas has on the following parameters,during pre-season, peak season and off-season, when compared to non-weight cycling judokas:1) Energy metabolism: RMR2) Body composition: body fat content and fat distribution3) Biochemical indices: serum glucose, insulin, andtriiodothyronine.4) Dietary factors: macronutrient distribution andkilocalories consumed.34CHAPTER 2METHODOLOGY2.1 SUBJECT SELECTIONSubjects were recruited from the Men's Provincial Senior Judo Teamand the UBC Judo Team. Approximately 40 individuals were approached, ofwhom only twenty subjects were chosen on the basis of previous dietinghistory, as determined by a questionnaire (appendix II). Those that wereexcluded did not cut sufficient weight to fit necessary criteria.Subjects who were defined as weight cyclers were to answer specific keyquestions in the following manner:(a) frequency of dieting during competitiveseason?often or always(b) number of times weight is reduced in a givenseason?a 3 times(c) amount of weight lost during eachdieting session?a 4.0 kg(d) number of years cutting weight for Judo?a 2 yearsTen judokas matched these criteria.Control subjects who did not weight cycle were to answer rarely ornever to frequency of dieting during the competitive season, were to havecut weight no more than once for a competition the previous season, were35METHODOLOGYto cut less that 1.4 kg the previous season, and were to have had nohistory of cutting weight for judo. Ten judokas met these guidelines.They were matched as closely as possible to the weight cycling group withrespect to age, height, weight, percentage body fat, lean body mass andactivity level.One subject from each group could not complete the study due torelocation from the Vancouver area. Subject #105 was unable to haveblood taken, excluding himself and his matched weight cycler, 006, fromthe blood analysis. Subject #110 failed to complete any diet records,excluding himself and his matched weight cycler, /10, from the dietanalysis. Therefore the total number of subjects in each group becamenine.2.2 EXPERIMENTAL DESIGNAll subjects reported to the UBC Sports Medicine Clinic or theBuchanan Sports Laboratory three times within a 10 month study period.Height, weight, girth and body composition measurements were taken, RMRwas determined, and a fasting blood sample was taken at each of the threetest periods.The first test period (test session 1, pre-season) was at leastthree weeks into the training season, when the subjects were trained andin good physical condition, but had not yet started to compete or diet.This time period occurred from November 1990 to February of 1991. Thesecond test period (test session 2, peak season) occurred during thejudokas' peak competitive season, at least one week prior to their last36METHODOLOGYmajor competition. At this point they had been dieting intermittentlythroughout the season. The test was done prior to commencement of thelast dieting episode required for the final competition. The span ofthis test period was from March 1991 to June 1991. The third test period(test session 3, off-season) was during the off season when the subjectswere no longer competing and were therefore not dieting. This took placea minimum of three months following their last competition and last boutof caloric restriction. Testing during this period took place betweenJuly 1991 and October 1991. The judokas had variable competitionschedules and season lengths, resulting in the large time span of thetest sessions.2.3 RESTING METABOLIC RATEResting metabolic rate (RMR) was measured by indirect calorimetryusing the metabolic cart (Medical Graphics Corporation System 2001,Jostens Graphic Products, Chicago, IL) located in the UBC Sports MedicineCentre. Three subjects were tested at the Buchanan Sports Lab for allthree test sessions due to shortage of time on the metabolic cart at theSports Medicine Centre. All subjects reported to the centre early in themorning, after a 12 hour fast and having done no exercise the previousday. They were familiarized with the testing procedures and allowed torest for half an hour in the supine position. When ready for testing,the subjects were instructed to breathe through a mouth piece and a noseclip was put in place. A relaxation tape was played to put subjects atease. After an adjustment time of 5 minutes, RMR was measured for 2037METHODOLOGYminutes. Oxygen uptake and carbon dioxide production were determined,from which RMR and resting energy expenditure were derived using theNutritional Analysis Program (appendix III).Initially, an accurate test required the subject to be in a fastedstate, to have not exercised for 24 hours, to have rested for half anhour lying down, and to have an RQ below 0.88. It was later found thatthe metabolic cart at the Sports Medicine Centre gave elevated RQ valuesdue to elevated VCO2 levels. V02 levels were found to be accurate(personal communication). As a result an RQ value of 0.88 was excludedas a criteria and a test was considered valid when the remaining threecriterion were met. If the test was not valid it was repeated a weeklater. The same procedures were followed at the Buchanan Sports Lab, bututilizing a Beckman Metabolic Measurement Cart.2.4 BODY COMPOSITIONSkinfold measurements were used for indirect determination of bodycomposition. Studies have shown that skinfolds at four sites are ofsimilar accuracy as bioelectrical impedance, and hydrodensitometry. 76 I 77Brodie76 et al found comparable results of body fat determination withall three procedures. It has been found that bioelectrical impedance isvery sensitive to degree of hydration, and following a weight lossperiod, or a bout of strenuous exercise (when glycogen stores aredepleted), change in fat free mass may be underestimated. 78 Althoughcontroversy remains as to the precision of skinfold measurements forprediction of percentage body fat, repeated measurements have been found38METHODOLOGYto be consistent when a single trained observer conducts them. Thistechnique would therefore satisfy the requirements of this study, as itis the relative change in percentage body fat, and not absolute value,which was important. For this reason skinfolds at four different siteswere used to calculate the percentage of body fat using the Durnin andWomersley regression equations. 79 Equations were specific for men andage categories. The four sites measured include the bicep, tricep,subscapular and supra-iliac areas. Measurements were taken as describedin the Canadian Standardized Test of Fitness (appendix IV), using LangeCalipers (Cambridge Scientific Industries, Cambridge MD.). Allmeasurements were taken on the non-dominant side of the body and wererepeated twice. If the two measures were not within 0.4mm then a thirdmeasurement was taken. The two closest measurements were averaged and ifthey were equidistance apart, all three values were averaged. Subsequentskinfold tests were performed by the same individual in order to reducethe error caused by variability in technique. Percent body fat wasdetermined using linear regression equations79 which estimate bodydensity:Density = c - ( m x log skinfold)c and m values are specific for gender and age group, and wereobtained from tables in Durnin and Womersley79 (appendix V). Logskinfold is the log of a sum of the four skinfolds. From body density,Siri's equation80 was used to calculate percentage body fat:39METHODOLOGY% Fat = ((4.95/density - 4.5) x 100)Fat free body weight was calculated by:fat free body wt. = (present wt. - (present wt. x %fat/100))Girth measurements were taken using a measuring tape. The waist andhip measurements (Appendix IV) were used to calculate waist to hip ratio.2.5 BIOCHEMICAL MEASUREMENTSA 5-10 ml blood sample was taken from a vein in the arm by aqualified technician. Samples were centrifuged at 3000 RPM for 15minutes to separate the serum. The serum was then aliquoted and frozen(at-70 degrees C) for future analysis. T3 was analyzed at the Departmentof Laboratory Medicine, in UBC Hospital. Samples were delivered foranalysis in two batches; the first contained samples from test one andtest two, and the second contained samples from test three. Insulin wasanalyzed at the Endocrinology Department, Children's Hospital,Vancouver,B.C.. Samples for insulin were also delivered in two batchesas described above. Glucose was analyzed in the Division of HumanNutrition, at UBC, following each test session.2.5.1 SERUM TRIIODOTHYRONINETotal serum Triiodothyronine (T3) from blood samples wasdetermined by Microparticle Enzyme Immunoassay (MEIA), using an IMXSystem (IMx System, Abbott Diagnostics, Illinois). 81 Fordetermination, a blood sample and Anti-T3 Coated Microparticles are40METHODOLOGYplaced in a reaction cell were T3 binds the microparticles and anantibody-antigen complex is formed. The microparticles with boundantibody-antigen complexes are then transferred to a glass fibermatrix, where they bind irreversibly. Added T3 AlkalinePhosphatase Conjugate then binds to available Anti-T3 microparticlesites (not occupied by T3) and unbound materials are subsequentlywashed away. When substrate, 4-Methylumbelliferyl Phosphate, isadded to the matrix, a fluorescent product results and can bemeasured by the MEIA optical assembly of the IMx System. Fromthis, the concentration of T3 is calculated (nmols/L).2.5.2 SERUM INSULIN DETERMINATIONInsulin determinations in collected blood samples were carriedout using double antibody radioimmunoassay (RIA). 82 The insulin inthe blood competes with a known amount of 125I-labelled insulinfor specific antibody sites. Bound and free insulin are thenseparated with the addition of a second antibody immunoabsorbent.Centrifugation produces a radioactive pellet which gives a readinginversely proportional to the insulin quantity in the blood sample.2.5.3 SERUM GLUCOSE ANALYSISA Beckman Glucose Analyzer II (Beckman Instruments, Fullerton,CA) was used for blood glucose determinations.83 Ten microlitersof serum is placed in glucose oxidase enzyme, in the presence ofoxygen. A reaction forming gluconic acid and peroxide proceeds41METHODOLOGYwith a resultant depletion of oxygen that can be measured by anelectrode. Oxygen consumption is directly proportional to bloodglucose concentration and mg of glucose per 100m1 of blood wasdetermined.2.6 DIET ANALYSISAll subjects were asked to keep a dietary record for three daysduring each test period. They were thoroughly instructed on recordingtypes and weights or volumes of all foods (in form eaten) and liquidsconsumed. One of the three days was a weekend day. NutriCom(NutriCom,Smart Engineering LTD., Vancouver,B.C.) was used for dietrecord analysis.Three day food records were chosen, as they are believed to be asreliable in determining nutrient intake as seven day food records.Stuff84 et al found good agreement between three day and seven day foodrecords for estimating individual's nutrient intakes, and concluded thatthree day records were adequate for obtaining qualitative nutrient intakedata. Tremblay85 et al studied the reproducibility of three day foodrecords and found moderate to high agreement between two consecutiverecords. They concluded that three day records provided a reliableestimate of intakes for almost all nutrients. Other studies have alsofound a length of three days to be a sufficient time period to obtainacceptable estimates of nutrient intakes, particularly energy andmacronutrients (which are the main concerns of this study). 86 Basiotiset a187 found that in order to estimate true average energy intake for a42METHODOLOGYgroup of males, 3 dyas were required. Other nutrients however, requiredgreater than three days, and up to 39 days for vitamin A. It isconceivable that the 7 day food record accuracy may be compromised due tothe length of recording time required. People may find it tedious,resulting in reduced recording precision or inhibition of foodconsumption, underestimating true intake. 84 For these reasons 3 dayrecords were used.The overall accuracy of both three day and seven day diet recordsmust be considered. Other studies have indicated that numerous errorscan occur in the process of diet analysis. There may be incompletedietary recording, particularly with forgotten foods if recording isretrospective, and unrepresentative food selection. 88There may also be errors in coding and translation of foods intonutrients as well. 88 For this reason great care must be given ininstructing subjects on food recording in order to reduce possible errorand limitations must be realized to avoid inappropriate conclusions.2.7 DATA ANALYSISBaseline subject characteristics were analyzed by independent t-tests to determine any significant differences. Changes in meanindividual values for RMR, REE, fasted serum T3, insulin, blood glucose,percentage body fat, waist to hip ratio, and energy intake for all threetest periods were analyzed using an analysis of variance (ANOVA) for a 2(experimental and control group) x 3 (3 test sessions) factorialexperiment with repeated measures on the 2nd factor. Percentage body43METHODOLOGYfat, waist to hip ratio, % fat, % CHO, and % protein were arc sinetransformed for statistical analysis. When applicable, TUKEY Post-Hocanalysis was performed to determine statistical differences between testperiods. Results were presented as the mean ± S.D., with a level ofsignificance of p..g0.05.44CHAPTER 3RESULTS3.1 SUBJECTS3.1.1 IDENTIFICATION OF A WEIGHT CYCLERThe 9 judokas who met all criteria required for classification as aweight cycler were placed in the experimental group, and 9 judokas whomet the specifications of a non-cycler were placed in the control group.Table 1 indicates how well both groups matched their respective inclusioncriteria. The weight cyclers reported having lost an average of 4.0±0.9kgs, 5.0±2.9 (mean±SD) times within the season. The control groupreported having lost <0.15 kg (mean), 0.2±0.7 times (mean±SD) theprevious season. Five men in the experimental group reported that theyalways cut weight for competitions, and the remaining four said theyoften cut weight. None of them indicated having never, rarely orsometimes cut weight. The control group reported having never (6/9) orrarely (3/9) cut weight. None of them indicated having cut weightsometimes, often, or always.In regards to the history of weight loss (table 1), theexperimental group had lost a significantly greater amount of weight(p=0.00), losing 5 kg, 11.0 ± 9.2 times in the last 5 years, whereas thecontrol group had only lost 5 kg, 1± 1.5 times. The experimental grouphad been cutting weight for judo an average of 6.0 ± 5.0 years, whereasthe control group had never cut weight for judo (significant at p=0.00).45RESULTSTABLE 1: The criteria required for male judokas to beclassified as a weight cycler or a non-cycler andthe ratings achieved by each group.CYCLER (n=9)FACTOR CRITERIA CYCLERREQUIRED RATINGyears in judo a 2 8.0±6.1*years cutting weight for ndotimes cut in last 5 years a 2_ t 5.9±5.311.0±9.2 * i competitions last season a 2 5.0±2.0 *1 times weight cut last season 3 5.0±2.9 *ave. kgs lost per competition a 4 4.0±1.0 *NON-CYCLER (n=9)FACTOR CRITERIA NON-CYCLERREQUIRED RATINGyears in judoyears cutting weight for hdotimes cut in last 5 yearsa 2- ?6.5±5.1*0.0±0.01.0±1.5 *1 competitions last season a 2 2.5±1.3 *1 times weight cut last season 5 1 0.0±0.0 *ave. kgs lost per competition 5 1.4 0.0±0.0 *mean±SD* significant difference between weight cyclers and nonweight cyclers for given parameter at p50.05** the number of times greater than 5 kg were cut in thelast five yearst no criteria set46RESULTS3.1.2 SUBJECT MATCHINGThe experimental group was not significantly different from thecontrol group with respect to weight (kg), percentage fat, lean body mass(kg), height (cm), and age (years)(table 2) at baseline. There was alsono significant difference in hours of moderate to intense levels ofexercise at baseline or any other test session, as indicated by selfreported weekly records (8.6±5.9 and 7.5±5.3 for weight cyclers and non-cyclers respectively). Table 3 shows the mean differences between theexperimental group and their matched controls. It should be noted thatthe weight cycling group had competed more frequently than the controlgroup during the past season.3.1.3 DIETING HABITS AND WEIGHT LOSS DURING THE SEASONThroughout the season the experimental group lost significantlymore weight (4.1 ± 1.5 kg)(p=0.00), a significantly greater number oftimes (4.2 ±2.7 times) (p=0.00) than did the control group (no weight wascut foe) any competitions), as indicated by self reported weight cuttingepisodes. Examination of the difference between the competitive weightsand weight recorded during the second test session (peak season) verifiesthat approximately 4 kgs were lost for competitions. The maximum weightallowable in the competitive weight category for weight cyclers was anaverage of 77.1±11.9 (SD), with an average weight during the peak seasonof 81.3±11.8. The non-cyclers could not exceed an average weight of87.7±16.9 to meet their weight class. They had an average weight of86.1±13.1 (mean±SD) during the peak season. Each group participated in47RESULTSTABLE 2: Physical characteristics of weight cycling andnon-weight cycling male competitive judokas for the pre-season, baseline test.WEIGHT CYCLING JUDOKAS (n=9)SUBJECT AGE HEIGHT WEIGHT LBM* %FATNUMBER (yrs) (cm) (kg) (kg) (%)06 28 188 108.3 86.9 19.805 20 172 70.1 63.0 10.114 27 169 66.2 59.7 9.010 25 178 83.0 68.1 18.013 23 181 81.0 72.0 11.307 31 165 73.3 61.1 16.711 35 172 85.6 68.1 20.412 19 178 87.2 70.6 19.015 20 176 81.0 64.2 20.8MEAN 25 175 81.8 68.2 16.2SD 7.8 6.9 12.3 8.2 4.5P0.05 NS NS NS NS NSNON-WEIGHT CYCLING JUDOKAS (n=9)CODE AGE HEIGHT WEIGHT LBM* %FAT(Yrs) (cm) (kg) (kg) (%)105 26 203 103.0 89.9 12.7102 25 168 76.8 67.3 12.5101 22 168 64.6 58.7 9.1110 25 171 83.3 68.1 18.0103 34 189 86.6 75.0 13.4109 24 179 73.2 64.0 12.0106 30 187 92.4 74.2 19.7108 22 195 99.8 82.3 17.5111 19 175 86.5 73.6 14.9MEAN 25 182 85.1 72.6 14.4SD 4.5 12.6 12.4 9.5 3.4P0.05 NS NS NS NS NSM = lean body mass in kgs = [body weight(kg) - (bodyweight(kg) x % fat/100)]RESULTSTABLE 3: Mean differences between matched weight cyclingand non-weight cycling judokass for the pre-season values(test session 1)CHARACTERISTIC MEAN DIFFERENCES *(±SD)Age (yrs) 4.3±3.4Weight (kg) 4.9±3.9Height (cm) 9.2±6.4exercise (hrs/wk) 4.9±6.8% fat (%) 3.1±3.1LBM(kg) ** 2.5±2.4- n = 9 in each weight cycling and non-weight cyclinggroup* mean differences between matched weight-cyclers andnon-weight cyclers** LBM = lean body mass (kg) = [body weight(kg) - (bodyweight(kg) x % fat/100)]49RESULTSan average of 5.2±2.4 and 3.0±1.3 competitions respectively. The averagebody weight did however, show no significant change over time (ie. duringthe competitive season) as a result of weight cycling. This is due tothe fact that the second test was conducted one week before the lastmajor competition requiring weight reduction, and it was prior to thedieting episode required for the competition.3.2 METABOLIC PARAMETERSDuring REE determinations, the average RQ for the weight cyclerswas 0.86±0.07 and 0.88±0.07 for the non-cyclers, over the three testperiods. Table 4 shows the absolute and relative REE values for bothexperimental and control groups. There was no significant main effect ofgroup (weight cyclers versus non-weight cyclers) (F=0.16,p=0.68) andthere was no significant main effect of time (time 1 vs time 2 vs time3)(F=0.49,p=0.62) for absolute REE. There was also no group by timeinteraction (F=0.26,p=0.77). When REE was expressed relative to leanbody mass, body weight, or surface area there was still no main effect ofgroup (F=0.12,p=0.73; F=0.06,p=0.82; F=0.10,p=0.76 respectively), of time(F=0.64,p=0.54; F=0.22,p=0.80; F=0.47,p=0.63 respectively) or a group bytime interaction (F=0.20,p=0.82; F=0.08,p=0.92; F=0.35,p=0.70respectively). Therefore the experimental group did not demonstraterespectively). Therefore the experimental group did not demonstrate adifference in absolute or relative resting metabolism at any of the threetimes when compared to the control group. There did not appear to be anymetabolic consequences due to previous seasons of weight cycling, during50RESULTSTABLE 4: The absolute and relative resting energyexpenditures (REE) of weight cycling and non-weightcycling judokas at pre-, peak, and off-season.WEIGHT CYCLING JUDOKAS (n=9)METABOLIC^ TEST SESSIONSPARAMETERS 1^2^3(pre-season) (peak season) (off-season)REE* (kcal/day)^1610.5^1602.7^1622.9^± 306.0 ± 408.1 ± 0365.2REE* /Kg(kcal/kg)^19.7^19.9^20.0± 2.6 ± 5.3 ± 4.1REE*/LBM** (kcal/LBM)^23.5^23.3^23.9± 2.8 ± 5.2 ± 4.3RMRt (Kcal/m2 /hr)^34.0^33.9^34.1± 4.6 ± 8.2 ± 6.7NON-WEIGHT CYCLING JUDOKAS (n=9)METABOLIC^ TEST SESSIONPARAMETER 1^2^3(pre-season) (peak season) (off-season)REE* (kcal/day)^1625.9^1644.6^1728.1± 204.0 ± 276.1 ± 278.2REE */Kg(kcal/kg)^19.3^19.3^20.0± 2.7 ± 3.0 ± 1.5REE*/LBM** (kcal/LBM)^22.6^22.8^24.0± 3.0 ± 3.1 ± 2.0RMRt (Kcal/m2 /hr)^32.7^32.6^34.7± 4.9 ± 4.7 ± 3.6- non-significant at p value z 0.05* REE = resting energy expenditure in kilocalories** LBM = lean body mass = [body weight(kg) - (bodyweight(kg) x % fat/100)]RMR = resting metabolic rate in kilocalories51RESULTSa season of cutting weight or following a season of cutting weight, incomparison to the non-weight cycling group.3.3 ANTHROPOMETRICSThere was no significant main effect of group (F=0.57,p=0.46), maineffect of time (F=0.67,p=0.52), or group by time interaction(F=1.40,p=0.26) for body weight (table 5), indicating that body weight ofthe weight cycling group remained the same as that of the non-weightcycling group during the second and third test sessions. Measurementsduring the second test session were taken one week before the last majorcompetition requiring food restriction and weight loss. At this pointthe weight cyclers had not yet started to restrict food for the upcomingcompetition and were therefore not at their typical competing weight.For this reason the weight cyclers did not show a significant reductionin body weight during the competitive season, as may be expected. Thisdemonstrated that following a weight cutting episode the weight cyclinggroup regained weight back to pre-season, baseline values and reducedweight was only maintained for the duration of the competition.Furthermore when they were not cutting weight during the off season, theydid not tend to increase their body weight, remaining the same asbaselinevalues and similar to their control group.Analysis of body composition also demonstrated that there was nomain effect of group, main effect of time or group by time interactionfor percentage fat (F=0.00,p=0.99; F=0.02,p=0.98; F=1.56,p=0.23respectively), or amount of LBM (F=1.04,p=0.32; F=1.43,p=0.25; F=0.13,52RESULTSTABLE 5: Anthropometric measurements of weight cycling andnon-weight cycling judokas during pre-, peak, andoff-season.WEIGHT CYCLING JUDOKAS (n=9)ANTROPOMETRIC^ TEST SESSIONSPARAMETERS 1^2^3(pre-season) (peak season) (off-season)weight(kg)^81.8±12.3^81.3±11.8^81.6±10.8% fat(%) 16.2±4.5^15.5±4.6^14.6±6.5LBM(kg) *^68.2±8.2^68.5±8.2^67.5±7.9WHR** 0.87±0.05^0.88±0.04^0.87±0.05NON-WEIGHT CYCLING JUDOKAS (n=9)ANTHROPOMETRIC^ TEST SESSIONPARAMETER 1^2^3(pre-season) (peak season) (off-season)weight(kg)^85.1+12.4^86.1+13.1^86.5+13.9% FAT(%) 14.4±3.4^15.5±3.0^16.5±3.4LBM(kg) *^72.6±9.4^72.6±10.2^72.1±10.9WHR** 0.85±0.06^0.85±0.04^0.86±0.05... LBM = lean body mass(kg)=[body weight(kg)-(body weight(kg) - % fat/100)]** WHR = waist to hip ratio = waist(cm)/hip(cm)- non-significant at P0.05 for all parameters over time53RESULTSp=0.88 respectively) (table 5). The weight cycling group experienced noincrease in body fat or loss of LBM as a result of repeated dieting andthey were not significantly different than the non-cyclers. Because theywere matched in the beginning of the experiment it was not possible todetermine if they had experienced previous changes in body composition asa result of a history of weight cycling.There was no redistribution of body fat, as no significant maineffect of group (F=0.88,p=0.36), main effect of time (F=0.01,p=0.99), orgroup by time interaction (F=0.55,p=0.58) was found for the waist to hipratio. The weight-cycling judokas experienced no redistribution of bodyfat as a result of cutting weight and their WHR remained the same as thenon-cycling judokas through a season of cutting weight.3.4 BIOCHEMICAL PARAMETERSFasting blood samples showed no significant main effect of group(F=0.38,p=0.38), or group by time interaction (F=1.22,p=0.31) for T3values and they were all within the normal range (table 6).^The T3value of the weight cycling group had been the same as that of the non-weight cycling group at baseline, and throughout the study, experiencingno change as a result of weight cycling at any time. There was however amain effect of time (F=43.16,p=0.00). A Tukey Post Hoc revealed asignificant decrease at time two (p=0.00) and time three (p=0.00) whencompared to time one. Both groups experienced this drop, and it wassustained during the off season test session.Insulin and glucose values demonstrated no significant main effect54RESULTSTABLE 6: Fasted serum values for insulin, glucose,and triiodothyronine in weight cycling and non-weightcycling judokas at pre-, peak, and off-season.WEIGHT CYCLING JUDOKAS (n=8) *BLOOD^ TEST SESSIONSPARAMETERS 1^2^3(pre-season) (peak season) (off-season)Triiodothyronine^2.7±0.4a^2.0±0.3b^2.0±0.3b(umol/L)Insulin^39.1±23.6^51.6±23.4^52.1±15.7(pmol/L)Glucose 4.4±0.2^4.3±0.3^4.0±0.6(nmol/dL)NON-WEIGHT CYCLING JUDOKAS (n=8) *BLOOD^ TEST SESSIONPARAMETER 1^2^3Thyroid Hormone^2.7±0.2a^2.1±0.2b^2.2±0.3 b(nmol/L)Insulin^ 41.0±16.0^46.1±15.4 38.3±13.2(pmol/L)Glucose 4.3±0.5^4.3±0.3^4.2±0.3(nmol/L)* n is reduced from 9 to 8 do to the inability of subject105 to give blood, thus disqualifying his matched control,06- non-significant at p<0.05 unless marked a or b- a is significantly different than b at p=0.00- same letter superscript means non-significant55RESULTSof group (F=0.39,p=0.54; F=0.34,p=0.57 respectively), main effect oftime (F=2.03,p=0.15; F=3.01,0.07 respectively) or group by timeinteraction (F=0.96,p=0.40; F=0.59,p=0.56). Values were similar andwithin normal range at baseline and did not change over time for bothweight cycling and non-weight cycling groups.3.5 DIETTable 7 shows the average energy intake and proportions ofmacronutrients consumed. There was no significant main effect of group(F=1.06,p=0.32), main effect of time (F=0.53,p=0.60) or group by timeinteraction (F=0.05,p=0.95) for energy intake. The weight cycling groupwas not consuming fewer kilocalories due to a history of weight cyclingwhen compared to the non-cycling group. Nor were they consuming fewerkilocalories during the competitive season (in between the periods offood restriction for making weight) or following a season of cuttingweight.Table 8 shows the predicted kilocalories required per day(estimated by the Harris-Benedict equation and an activity level of 1.5),the estimated number of kilocalories required (as determined by REE andan activity level of 1.5) and the estimated number of kilocalories thatwere being consumed, at all three test periods. The activity level of1.5 was selected according to the British Columbia Diet Manual 89 whichstates BEE multiplied by 1.5 for weight maintenance and heavy activity.Mahalko et a190 also indicated an activity level of 1.5 for moderateactivity. Considering that the judokas were only required to attend56RESULTSTABLE 7: Macronutrient and energy consumption, asdetermined by three day food records for weight cyclingand non-weight cycling judokas at pre-, peak, and off-season.WEIGHT CYCLING JUDOKAS (n=8)DIET^ TEST SESSIONSPARAMETERS 1^2^3(pre-season) (peak season) (off-season)energy (kcal)^2137±608^2444±1154^2270±1219energy/kg* 27.1±6.6^30.9±13.8^27.8±13.3%**CHOt^ 47.6±12.0^48.6±10.7^42.9±11.0% protein 17.4±4.4^18.1±6.0^21.0±10.0% fat^ 32.5±10.5^32.1±6.4^35.6±10.5gramsSof CHOt^245.8±98.4^298.5±168^238.4±121.8grams of protein^91.0±33.6^99.3±47.7^98.1±46.7grams of fat^70.0±29.1^88.0±44.4^85.7±44.6NON-WEIGHT CYCLING JUDOKAS (n=8)DIET^ TEST SESSIONPARAMETERS 1^2^3_^...^-^• _energy (kcal)^2644±590^2773±798^2648±352energy/kg 31.6±8.8^32.7±10.7^30.9±4.6%**CHOt^ 52.9±7.2^49.8±7.0^47.6±5.0% protein 15.3±2.1^17.5±4.0^18.4±2.7% fat^ 31.7±5.5^33.0±5.5^31.4±2.8gramsSof CHOt^342.8±84.5^321.5±97.0^307.9±37.2grams of protein^105.0±30.9^116.9±40.0^116.5±28.9grams of fat^93.3±28.8^96.9±35.2^91.3±20.3 kg consumed per  o y weight** percentage of daily energy intake as the specifiedmacronutrientS CHO = carbohydrategrams of specified macronutrient consumed per day- non-significant at p50.0557RESULTSTABLE 8: Predicted energy requirements, estimated energyrequirements and estimated energy consumption of weightcycling and non-weight cycling judokas at pre-,peak, andoff-season.WEIGHT CYCLING JUDOKAS (n=8)*TEST SESSIONSPARAMETER^1^2^3(pre-season) (peak season) (off-season)A^predicted**^2837±297^2827±300^2833±179requirementB^actualt^2415±459^2403±612^2434±548requirementC^actualS^2137±608^2444±1154^2270±1219consumptionA vs B (p value)^0.04^0.04^0.02A vs C (p value) 0.02 0.40 0.20B vs C (p value)^0.12^0.70^0.76NON-WEIGHT CYCLING JUDOKAS (n=8)*TEST SESSIONPARAMETER^1^2^3(pre-season) (peak season) (off-season)D^predicted**^2939±339^2958±354^2967±372requirementE^actualt^2439±306^2466±414^2592±417requirementF^actualS^2644±590^2773±798^2648±352consumptionD vs E (p value)^0.002^0.006^0.001D vs F (p value) 0.24 0.50 0.03E vs F (p value)^0.37^0.32^0.80n is reduced from 9 to 8 matched subjects due to 1missing diet record* * the predicted caloric (kilocalorie) requirement asdetermined by the Harris-Benedict equation and anactivity level of 1.5.the actual caloric (kilocalorie) requirement asdetermined by REE determination and an activity levelof 1.5.the actual caloric consumption (kilocalorie) asdetermined by three day food records.58RESULTSpractice three days a week, the remainder of their activity would likelyfall within the moderate to sedentary range, particularily for thestudents. All judokas required significantly fewer kilocalories thanwere predicted by the equation at all three test times (p=0.04, p=0.04,and p=0.02 for weight cyclers at test 1, test 2, and test 3 respectively;p=0.002, p=0.006, and p=0.001 for the non-cyclers at test 1, 2, and 3).All groups showed no significant difference (at p50.05) between estimateddaily requirement (as determined by experimental REE and a 1.5 activitylevel) and estimated daily caloric intake (determined by dietanalysis)(table 8). When comparing the actual consumption to the actualrequirement, only test session 1 for the weight cyclers and test session3 for the non-cyclers indicated significant differences (table 8).There was no main effect of group, main effect of time or group bytime interaction for the percentages of CHO (F=1.09,p=0.32;F=2.78,p=0.08; F=0.10,p=0.91 respectively), fat (F=0.22,p=0.65;F=0.23,p=0.80; F=0.79,p=0.47) and protein (F=1.04,p=0.33; F=2.96,p=0.07;F=0.12,p=0.89) consumed. There was no main effect of group, main effectof time or group by time interaction for the grams of CHO (F=1.83,p=0.20;F=0.77,p=0.47; F=0.53,p=0.59), fat (F=0.66,p=0.43; F=0.76,p=0.48;F=0.56,p=0.58) and protein (F=0.86,p=0.37; F=1.35,p=0.28; F=0.09,p=0.92)consumed. There was no change in the composition of the diet consumed asa result of a history of weight cycling or during or following a seasonof weight cycling.59RESULTSCHAPTER 4DISCUSSIONIt has been suggested that repeated cycles of weight loss andregain will lead to physiological changes that can make subsequent weightloss difficult and weight regain rapid. Male judokas who had a historyof cutting weight to meet specific weight categories were followed for 10months (including one competitive season) to examine such physiologicaleffects.4.1 METABOLIC PARAMETERS4.1.1 HISTORY OF WEIGHT CYCLING: BASELINE VALUESAt baseline the judokas with a history of weight cycling showed nosignificant reduction in absolute or relative REE (REE/kg, REE/LBM, orREE/m2 ) when compared to judokas with no history of dieting.This is in contrast to a study on adolescent wrestlers whichdemonstrated that a history of cutting weight was associated with a lowerabsolute and relative REE (REE/LBM) 35 when compared to non dietingwrestlers. Both the study by Steen et a1 35 and the present study hadwell matched control groups who participated in a similar exerciseschedule. Discrepancies in RMR findings may be due to differences inweight cutting habits, such as the number of times that weight was lostand the amount of weight that was lost. The judokas did not compete asoften as the wrestlers, only having cut weight an average of 5.1±2.1times in the previous season. The wrestlers in Steen and coworkers'60DISCUSSIONstudy had previously cut weight an average of 18.7 times. Furthermorethe wrestlers had cut greater than or equal to 4.5 kg, with 64.3% cutting5.9-6.8 kg and 14% cutting even greater than 6.8 kg. The judokas onlycut an estimated 4 kg for each competition the season prior to the study.The number of years of cutting weight may also be significant, howeverthis was not reported in Steen's35 study and thus can not be compared.A more recent study found that collegiate wrestlers with a historyof weight cycling actually had a significantly higher RMR, when comparedto a physically active, non-cycling matched control group. 36 Theunexpected results of their study may be due to the fact that the twogroups were not matched for type of exercise. It has been found thathigh intensity exercise carried out for a long duration, such as thatexperienced by the wrestlers (approx 2 hours per session) may increaseRMR. On the other hand a shorter duration of moderately intense exercise(such as the 30-60 minutes in the physically active controls) may notaffect RMR. 91 This could explain the different findings when compared toSteen's group and the current judoka study.All judokas had an estimated REE that was significantly belowpredicted values (Harris-Benedict Equation) at baseline (p=0.00)(85% and83% for weight cyclers and non-cyclers respectively). Although it hasbeen suggested elsewhere92 that this equation overestimates REE, thesevalues are much lower than those demonstrated by other athletes, such asMelby's physically active controls (4% below predicted), their weightcyclers (112% max and 96% min) and Steen's non-cycling wrestlers (also4% below predicted), using the same equation. In fact the values61DISCUSSIONobtained for all judokas were in line with the reduced REE experienced bySteen's weight cycling wrestlers (85% of predicted).4.1.2 A SEASON OF WEIGHT CYCLINGDuring a season of cutting weight there was no decrease in absoluteor relative RMR. Off season values also remained constant, despite areduction or cessation of training for judo. Some studies have suggestedthat weight cycling leads to increased metabolic efficiency and decreasedREE.4,25,29,32,33,35 It is difficult however, to compare male judokas toanimal studies and different human populations, such as obeseindividuals, lean individuals, females and even lean-non active males,due to the possibility of wide variations in metabolic function.The only other longitudinal study recorded in the literature, whichlooked at male collegiate wrestlers, found no detrimental decrease in RMRduring or following a season of cutting weight. 36 These findings concurwith the findings of the judoka study, however there were somesignificant differences. Firstly, the wrestlers in Melby's study in facthad a significantly greater absolute and relative RMR (11% above thevalue predicted by Harris-Bennedict Equation) at baseline, when comparedto a non-cycling physically active control group (4% below predicted).In the present study, both weight cycling and non-weight cycling judokashad a similar RMR, 85% and 83% of the predicted value respectively.As previously mentioned, this may be explained by differences inthe exercise regime. The wrestlers trained for 2 hours per session, butthe number of sessions per week is not mentioned. Because the judokas do62DISCUSSIONnot compete as often (average 5 times a season) they may not have had asintense a training session. Practice sessions were conducted for 1-1 1/2hours 3 times per week. They did engage in other forms of activity,although intensity is very subjective and may not have been accuratelyidentified, making exact quantification difficult.Secondly, during the competitive season the wrestlers' absolute andrelative RMR which was measured in the food restricted state, but not yetdehydrated state, demonstrated a significant drop from their baselinevalues. Such a drop was not experienced by the judokas. This may beexplained by differences in methodology between the two studies. In thejudoka study, RMR was measured the week prior to the last majorcompetition which required food restriction. The measurement was takenhowever, before the food restriction episode had begun. On the otherhand, the wrestlers in Melby's study were measured during the actualprocess of cutting weight. It has already been established that RMRdecreases when food restriction occurs. 7-13 The methodology used for thejudoka study would indicate whether a reduced RMR due to a dietingepisode was sustained when normal food intake resumed.The most important finding of Melby's study36 was that the RMR ofthe weight cycling wrestlers returned to baseline values, suggesting nosustained effect of cutting weight. The judoka study and Melby's studythus suggest the same outcome; there was no evidence of a sustaineddecrement in either absolute or relative REE as a result of repeatedcycles of weight loss and weight regain. A follow-up study conducted byMelby's group further showed no effect of weight cycling on REE after two63DISCUSSIONyears. 934.1.3 REASONS FOR NO DIFFERENCESNO WEIGHT CYCLING EFFECTSThere are several possibilities which may explain the lack ofsignificant differences between the two groups. Firstly it is possiblethat there are, in fact, no effects of weight cycling. There have beenstudies conducted which show that weight cycling does not result in anychange in metabolic rate. 30-33 ' 36 There are however studies that dosuggest physiological effects. 2425 I 2935NO DEFINITION FOR A WEIGHT CYCLERAn important element of all weight cycling studies which must beconsidered when comparing and interpreting data, is that there is a widevariation in the description of a weight cycler. As indicated by table9, no two studies share the same definition. This inconsistency indefining weight cyclers along with the use of metabolically differentpopulations could result in inappropriate application to otherpopulations. Studies that show no metabolic consequences may not in factrepresent a true weight cycling population.This must be considered in the judoka study. It is possible thatthe duration of food restriction, degree of food restriction and numberof times weight was cut were not sufficient in this study and in otherstudies (ie.Melby et a1 36 ) to show an effect. The Melby study 36 and the64DISCUSSIONTABLE 9: Definitions of weight cyclers from various weightcycling studies.GROUP DEFINITION FINDINGSteen et al,adecreased1988(wrestlers)- lost wt > 10 times duringa season- > 4.5 kg loss/wk- often of always cutting wt-RMRVan Dale et al,bchange1989(obese women)- frequently dieting- lost & gained^to 10kgin past 5 yrs more than once- often or always cutting wt.- noin RMRBlackburn et al,b- wt. regain of a min. ofvelocity1989^20% of cycle 1 loss duringloss(obese patients)^inter-diet period-of wtslowerBeason et al,bchange1989veloc.(obese patients)loss- no definition given- dieted - refed - dieted- noinof wtMelby et al,beffect1990(wrestlers)- lost^4.5 kg at least10 times a season-^3 seasons of cutting wt- noon RMRJebb et al,b1991sustained(obese females)in- lost^6 kg^2times- self reported history of yoyodieting- nodropRMRManore et al,aeffect1991RMR(lean females)- dieted^10 days, 4 timesin last year- dieting was considered1000 kcal/d below energyrequirement for wt maint.- noonndicates cross sectional studiesindicates longitudinal studies65DISCUSSIONjudoka study had similar definitions of a weight cycler (except number oftimes weight was to be cut) and no significant results were found. Thedefinition for weight cycling for wrestlers in Steen's study 35 was alsosimilar but actual weight loss during the competitive season was moresevere (a 5.9-6.8 kg and some greater that 6.8 kg). These weight cyclersdid not represent the specified definition given, but rather more severefood restricters than the latter wrestler study and the judoka study(hence possible reason for significant findings). Furthermore thejudokas cut weight half as many times as both wrestling populations,further increasing the possibility of insignificant findings.A clear definition of a weight cycler is required before any solidconclusions will be reached. It is likely that this will not be onespecific definition, but rather a wide range of definitions for eachspecific population. For example small amounts of weight lost andregained, several times in a year (Steen et a1 35 ) may be just asdetrimental as one large weight loss and regain, once a year (Blackburnet al29 ). Degree of food restriction, composition of the diet, and thespecific population must also be considered. Thus, it becomes evidentwhy defining a weight cycler is such a difficult task and has not yetbeen accomplished.METHOD OF WEIGHT LOSSThe method of weight loss, whether through food restriction,dehydration, or exercise, is also an important consideration in studiesof weight cycling. Weight loss practices of wrestlers have been found to66DISCUSSIONbe a combination of both dehydration and food restriction. 94 Steen eta135 did not mention the wrestlers' method of weight loss. This couldlead to erroneous identification of the actual weight lost as LBM andfat, if a large proportion was actually water. Melby et a1 36 identifiedweight loss before dehydration. All of the judokas achieved their weightloss primarily by food restriction for an average of 8.1±6.9 days, asindicated by self reported records. Since both judoka groups had similarexercise regimes, and the non-cyclers remained weight stable, it is notlikely that weight loss was achieved through exercise.EXERCISE PREVENTS RMR DEPRESSIONIt is possible that exercise played a protective role against areduced RMR expected with weight cycling. It has been suggested thatexercise may prevent the drop in RMR experienced with caloricrestriction, although studies are controversial and inconclusive. Whenobese individuals engage in regular exercise while restricting food,exercise has been found to counteract the depression in RMR that oftenaccompanies dieting. 95-97 Similar results were found in obeseindividuals who were weight cyclers. 31 Mole et a197 however found thatthis protective effect was removed as soon as exercise ceased. Incontrast Phinney98 found that dieting with exercise had the exactopposite effect, decreasing RMR three fold below baseline values whencompared to dieting alone (10% decreased RMR). He postulated that thiswas a protective mechanism to compensate for the additional negativeenergy balance.67DISCUSSIONFew studies on the effect of exercise on metabolic rate have beendone in lean athletes. Steen et al35 found no protective effect ofexercise on depressed RMR in the adolescent wrestlers. Melby et al 36also demonstrated that wrestlers cutting weight experienced a significantdrop in RMR from their baseline (pre-dieting) values, despite an intenseexercise schedule. This suggests no protective effect, although RMRvalues were only 4% below predicted values and did return to baselinewhen weight cycling ceased. Exercise may have resulted in, or helped REEbounce back to normal. It is possible that exercise protected thejudokas from a drop in RMR due to caloric restriction.Exercise may prevent a drop in RMR in two ways. It may lead to ashort-term increase in RMR following activity and it may also increaseRMR over the longer-term by maintaining or increasing LBM, which is amain determinant of RMR. Exercise may have protected against a drop inRMR in the judokas through both of these mechanisms. Effects of weightcycling on LBM will be discussed under anthropometrics.EXERCISE INCREASES RMRExercise may prevent a drop in REE caused by energy restriction,but it can also increase REE above normal predicted values, in bothdieting and non-dieting individuals. This effect must be considered as apossible confounding factor in metabolic determinations. Numerousstudies have shown that highly trained athletes have a significantlyincreased REE (absolute and per LBM) when compared to sedentaryindividuals. 91 ' 99-101 This is controversial however, as some have in68DISCUSSIONfact found REE to decrease with training. 102The type, duration, and intensity of exercise has importantimplications on the effect exercise has on RMR. Intense exercise (11-16hours per week) has been shown to increase RMR whereas moderate exercise(6-10 hours per week) has no effect.91 This phenomenon was suggested inpre-season (baseline) values of collegiate wrestlers (Melby et al) whoexhibited a RMR significantly higher (11% higher) than predicted valuesand 15% higher than their physically active, matched controls. Thediscrepancy in RMR's may be explained by differences in trainingschedules. The wrestlers trained for a longer duration of time (2 hrsper session), whereas the control group only exercised between 30 and 60minutes per session three times per week.The hours of moderate to intense exercise between the weightcycling and non-cycling judokas was not significantly different,averaging 8.6±5.9 and 7.5±5.3 hours per week respectively. Exercise wasrecorded on a weekly basis and duration of each exercise episode was notidentified. Furthermore, judokas only indicated whether exercise wasmoderate or intense, which may be too subjective to obtain quantitativedata. As a result it is difficult to interpret the impact exercise mayhave had on RMR.It should be noted also, that 10 hours a week, which is consideredmoderate exercise, has been found to have no prolonged effect on RMR.91The weight cycling and non-cycling judokas averaged 8.6±5.9 and 7.5±5.3hours per week respectively. It has also been found that 90 minutes ofexercise (stationary bike at 175 watts) the evening before, has no effect69DISCUSSIONon RMR the next morning. 103 Furthermore, an increased RMR due toexercise, was not sustained when the exercise was discontinued for threedays. 104 The point at which RMR returned to normal was not known but itcould be as soon as a day following the exercise. In the present study,all subjects were asked to refrain from any form of exercise for 24 hoursbefore the test day. Furthermore, an RMR 15-16% below predicted valuesdoes not likely indicate an elevated RMR due to exercise. It istherefore unlikely that such an effect on RMR would significantly alterthe results of this study.Although there is evidence to support that there was no impact ofexercise on RMR with the judokas, there is controversy in the literatureregarding this subject. Discrepancies arise in the classification ofathletes, classification of "trained state" and the lack ofacknowledgement that there is a wide spectrum of trained athletes. Theduration, type and intensity of training are all factors which must beconsidered in these studies, yet very few have controlled for all ofthem. This makes it very difficult to classify the judokas in thecurrent study.SMALL NUMBERS AND WIDE VARIABILITYThe number of subjects in the study was very small due tounavailability of weight cycling judokas. A small subject populationwith large individual variability may contribute to lack of significantdifferences in RMR. Large variabilities in RMR can be found due todifferent genetic and environmental influences. This is an issue in70DISCUSSIONnumerous weight cycling studies. In the studies of wrestlers, Steen eta135 had 13 matched cyclers and Melby 36 had 12 matched cyclers. Manoreet a133 had 11 non-obese weight cycling women, Jebb et a1 32 had 11 obesecycling women and Beeson30 had only 4 obese weight cycling women. Muchlarger numbers may be required in order to obtain consistent results.Furthermore, if there is a small subgroup of individuals who areparticularly susceptible to weight cycling, as has been suggested byBrownell et all2 they will be missed in studies with a small sample size.Attempts must be made to identify those people who are specificallysusceptible.NON-RESTING ENERGY EXPENDITURE IS ALTEREDIt is possible that adaptation to food restriction is notmanifested in a reduced RMR but rather results in an alteration of non-resting energy expenditure. There may be a decrease in the thermogeniceffect of food, the thermogenic effect of exercise, or both. Geissler eta119 found that post obese subjects had a 15% decrease in 24 hour energyexpenditure, when compared to lean counterparts, with no history ofdieting. They found that energy cost of sleep (ie. no effect of food andexercise thermogenesis) in the post obese subjects could only account forone tenth of the 15% drop below controls. The remaining 90% of the 15%reduction in 24 hour energy expenditure occurred during the day, undervarying exercise regimes. This indicated that differences were due to areduction in thermogenesis, as well as BMR. Furthermore, an elevation inmetabolic rate seen in the controls following an episode of exercise, did71DISCUSSIONnot occur in the post-obese subjects. Manore et a1 33 found that leanfemales had no change in RMR as a result of weight cycling, but theamount of energy expended for a given body weight (thus work load) wasless than lean matched controls.Evaluation of exercise and food thermogenesis in the judokas mayhave identified adaptations due to their weight cutting habits. It mustalso be considered that the judokas who weight cycle may have aninherently reduced thermogenesis which necessitated weight cycling.4.1.4 THYROID HORMONEIn studies where the REE and REE/LBM have decreased due to repeatedcycles of weight loss and regain, possible mechanisms for this decreasemust be indicated. This study investigated the possibility of areduction in T3 to explain the depressed REE. No drop in REE was foundand no change in T3 as a result of weight cycling occurred. As with REE,more dramatic food restriction, for a longer period of time may berequired to show a sustained effect on T3. Studies which havedemonstrated a sustained decrease in T3 values have used very low caloriediet (VLCD) (420-600 kcal/day) for 21 days and up to 3-4 months. 7 ' 67 Adecreased RMR accompanied these decreases in T3. 67The significant drop in T3 values which occurred for both groupsfrom pre-season to peak season and off-season must be explained bysomething other than weight cycling. Seasonal changes may explain thedrop in T3, since pre-season values were obtained in the winter time andthe remaining test sessions occurred in the spring through late summer,72DISCUSSIONinto the first part of fall. Increases in T3 have been seen duringwinter in Japanese individuals living in Kijimadaira, however they wereliving in houses with temperatures between minus three degrees and sixdegrees Celsius (15-20 degrees in summer). No changes were seen inindividuals living in heated rooms with outside temperatures betweenminus three and plus six degrees Celsius. 105 It is therefore unlikelythat the judokas would experience a drop in T3 as a result of climatechange.It is also possible that vigorous exercise may result in anincrease in T3. Chronic voluntary exercise in mice demonstrated a risein serum T3. 106 Athletes may have been training vigorously during theirfirst test session, when their serum T3 levels were high, and lessvigorously during their competitive and off-season, when T3 levelsdropped. It should be noted however, that there was no significantdifference in exercise during any of the test sessions. The reason for adrop in serum T3 remains unknown.4.2 ANTHROPOMETRICSOne negative consequence of weight cycling that has been postulatedis an increase in percentage body fat and a decrease in LBM. Because LBMis a good predictor of REE, loss of LBM could potentially explain adecrease in absolute REE. Furthermore increased adiposity has beenrelated to increased health risks for coronary heart disease and highblood pressure. There was no evidence in this study of an increase inbody weight, percentage body fat or a decrease in LBM as a result of73DISCUSSIONweight cycling.4.2.1 REASONS FOR NO DIFFERENCESNO WEIGHT CYCLING EFFECTSThis may indicate that there is no effect of weight cycling on bodycomposition. Both animal studies and human studies have indicated thatthere is no increase in adiposity with repeated cycles of weight loss andregain. 41,35,42 -44 In contrast however, other studies have indicatedincreased adiposity with one cycle 45 or repeated cycles of weight lossand regain. 33 f 38 There are several possible explanations as to why noeffects were demonstrated in this study, and possibly other studies.SEVERITY OF WEIGHT CYCLINGWeight cycling may not have been severe enough to invoke suchchanges. Changes in body composition may be related to the degree ofcaloric restriction, the duration of caloric restriction, and the numberof times caloric restriction occurs. Ozelci et al 38 demonstrated thatrats restricted to 50% or 25% of their ad libitum food intake for oneweek had an increase in body fat following refeeding. This however wasnot demonstrated in rats restricted to 75% of ad libitum intake. It ispossible that restriction was not severe enough to incur large changes inbody fat and LBM. In humans, an increase in adiposity and decrease inLBM was seen in normal weight young males after weight regain. However,they had undergone semi-starvation, losing 24% of their body weight in 2474DISCUSSIONweeks. 45 The athletes in this study lost an average of only 4.1±1.5 kgper competition and the duration of food restriction was only an averageof 8.1±6.9 days.It is possible that the judokas did not cut weight enough times toinfluence the body fat to lean ratio (only cutting an average of 5.2±2.4times). However the wrestlers in Melby et al's study, who underwentsimilar weight cycling habits, but cut weight more frequently (11times,range9-13), also showed no increase in body fat following a seasonof cutting weight.ACCURACY OF SKINFOLD MEASUREMENTSAnother limitation of small weight losses, is that skinfold changesmay have been too small to detect, considering the method of body fatdetermination. Although numerous studies report that skinfolds are asaccurate as bioelectrical impedance and hydrodensitometry, and have goodreproducibility76-78 this still remains controversial. Skinfolds havebeen indicated to be accurate within 3%• 79 The same trained observerconducted all skinfold measurements and repeated them 3 times, whichincreases the precision of the recorded measurement. 79 Furthermore,skinfolds on lean individuals are known to produce more accurate results,as compared to obese individuals. 107 Even if the actual fat percentagewas not valid, the change in percentage fat relative to baseline valueswas determined with validity. Since the relative change in percentagefat was important, and not the absolute values, the method wasappropriate.75DISCUSSIONEXERCISE MAINTAINS LEAN BODY MASSExercise may have maintained LBM and prevented the accumulation offat. Studies have shown that exercise can prevent the loss of LBM and caneven increase it during weight loss. 5 Weight regained while exercisingis more likely to be regained as lean tissue rather than fat. 5 Differenttypes of exercise will have different effects on body composition.Weight lifting will increase LBM whereas sustained aerobic exercise willdecrease body fat. Exercise may have prevented any decline in LBM andany accumulation of body fat in the judokas, which may have occur in thesedentary individual. Melby et a1 36 found that there was no proportionalloss of LBM or increase in percentage fat in their wrestlers when weightwas regained.FAT SELECTIONAn increase in fat selection following a period of food restrictionhas been suggested to occur, 39,46-48 resulting in an increase inadiposity. 49-51 There was no suggestion of an increase in fat selectionin this study possibly preventing an increase in percentage body fat. Itshould be noted however that if there was an increase in fat selection,it would most likely occur immediately following food restriction. Dietrecords were not kept during a refeeding period and if an increase in fatselection had occurred it would have to be maintained throughout theseason to be detected. Off-season diet records did not indicate thatathletes increased the percentage of fat in their diet when they were nolonger required to watch their caloric intake.76DISCUSSION4.2.2 INSULINFasting serum insulin and glucose levels of weight cycling judokaswere no different from non-cycling judokas at baseline and did not changefollowing a season of weight cycling. There did not appear to be aprolonged effect of weight cycling on insulin or glucose values. Somestudies have suggested that refeeding following a period of calorierestriction can result in a rise in serum insulin levels, 25 f 39163,64especially if overfeeding occurs. 63 Such changes may have explained inpart, any increases in body fat, through promotion of lipogenesis and fatstorage.It should be noted however, that measurement of fasting insulinvalues may not have been appropriate if there were only changes inpostprandial insulin levels, as indicated by McCargar et al. 63 Fastingserum insulin levels were normal in normal weight 4 day food restricted,2 day overfed females, and only the insulin response (2 hourspostprandial) to glucose in a meal was exaggerated, rising above normal.Owens et al 64 found that an effect on insulin and glucosemetabolism following 2 days of food restriction, remained up to 10 days,after which time, values would return to normal. The judokas were notmeasured immediately after a bout of dieting.Once again it should be noted that the duration, frequency andlevel of calorie restriction may not have been sufficient to cause anyalteration in serum insulin and glucose levels.77DISCUSSION4.2.3 FAT DISTRIBUTIONDistribution of body fat is also an important factor in relation tohealth. Android fat has been associated with increased risk of coronaryheart disease whereas gynoid fat has not2 . It has been suggested thatweight cycling may lead to a redistribution of body fat to the abdominalregion. 55 Results of this study however do not indicate any such change.The WHR of the experimental group remained the same during all testsessions, and was never significantly different than the control group.The WHR measurements of this population were well below levels that wouldbe considered a "risk factor" at all times points during the study.Once again, it is possible that the severity and duration of weightloss was not enough to mobilize significant amounts of fat to beredistributed. There may not have been enough cycles of weight loss andregain to show such effects. It is possible that repeated seasons ofweight cycling may be required to detect an increase in WHR, however thejudokas did have a history of weight cycling (average 6.0±5.3 years) andshowed no increase in WHR as compared to non-cycling judokas.4.3 DIET ANALYSISThe weight cycling judokas did not consume significantly fewercalories at any test time as a result of cutting weight. This wouldsuggest that they did not require fewer calories at baseline (pre-season), or following a season of cutting weight, to maintain weight.Diet analysis at peak season did not occur during an episode of foodrestriction, and thus did not reflect the caloric intake during weight78DISCUSSIONreduction.Diet analysis at baseline also demonstrated that weight cycling andnon-cycling judokas were consuming 25% and 11% fewer calories thanpredicted by the Harris-Bennedict Equation, respectively (table 8). Thistrend continued throughout remaining test sessions. Once again it hasbeen suggested that the Harris-Benedict Equation overestimates REE, 92although this appears to be extreme.It is possible that energy consumption was underestimated due tothe limitations of three day food records. A recent study by Livingstonet a1 108 indicated that energy intakes determined by seven day foodrecords were only about 80% of outputs, as indicated by use of doublylabeled water, for a period of two weeks. Underreporting was suggestedto occur in all subjects (not just obese individuals as previouslysuggested109 ) and was a result of failure to record snack items andalcohol, as well as an alteration in habitual intake to avoid weighingand recording tasks.1"There was no significant change in the percentage or absoluteamounts of macronutrients consumed in both groups. This indicates, asmentioned earlier, that there was no sustained increase in fat selectionas a result of food restriction. The consumption of protein was nevercompromised, being in excess of the calculated requirements for athletesbased on body weight for both non-cycling and cycling groups.79CHAPTER 5CONCLUSIONS AND RECOMMENDATIONSIt is very difficult to study the metabolic effects of weightcycling. Populations which are metabolically different, such as theseverely obese, the moderately obese, the mildly obese, the sedentarylean, the active lean and the very athletic lean, may all respond toweight cycling differently. How they respond will depend on theseverity, duration and frequency of food restriction and their metabolicdifferences. For these reasons it has been difficult to devise aclassification system for weight cycling. A different classificationscheme may even be required for each individual population. Furthermore,there is wide individual variability in metabolism and there may be widevariability in response to weight cycling, even within the samepopulation. Any solid conclusions with respect to the effects of weightcycling will require a clear definition. Factors which identifyindividuals who are particularly susceptible to weight cycling, will alsohave to be defined.Recently there have been numerous additional studies looking at theeffects of weight cycling on RMR and body composition in humans. Todate, few are showing detrimental effects of weight cycling. Inparticular, there appears to be no reduction in RMR beyond that expectedfor loss of LBM. This may be due to the fact that only a select few aresusceptible to the effects of weight cycling. Since the currentliterature consists of studies of quite small numbers, the susceptiblefew would not be identified. Furthermore it is possible that the main80CONCLUSIONS AND RECOMMENDATIONSdetrimental effect of weight cycling is a disproportionately large lossof LBM due to rapid weight loss and rapid weight regain, and not anactual reduction in RMR/LBM. Further study with larger sample sizes anddefined weight cyclers will have to confirm this.Another important issue to consider is that weight cycling maycause a reduction in non-resting components of RMR, such as diet orexercise induced thermogenesis. This may be with or without a reductionin RMR. Most studies fail to measure these parameters, therefore missingany such effect.The judoka weight cyclers showed no decrease in absolute orrelative RMR. There was no increase in percentage body fat or decreasein lean tissue. The distribution of body fat also remained unchanged.Serum triiodothyronine, insulin and glucose all remained within thenormal range and did not change significantly as a result of weightcycling. There was no change in caloric consumption or macronutrientdistribution. Additionally no increase in fat selection was observed.No detrimental effects of weight cycling were identified in this study.Some changes in experimental protocol may have helped to enhancethe conclusions. More precise exercise records (hours per day, type ofexercise, intensity) may account for any possible variation in RMR as aresult of change in type, intensity or duration of exercise. This wouldbe difficult, due to unavailable classification schemes for exercise.Furthermore it would have been difficult to get the athletes to keep suchdetailed and complete records, requiring daily phone calls to ensureaccurate recording or any recording at all.81CONCLUSIONS AND RECOMMENDATIONSIt would have been useful to record diets at different periodswithin the peak season. These may include their diet while not cuttingweight for a competition, exact diet while cutting weight forcompetition, and the diet immediately following the competition. Thesewould give a good indication of the changes in eating behaviors. Thiswould also identify imbalances or deficiencies in the restrictive dietand the composition of the refeeding diet (ie did they over eat, howmuch, for how long, did they consume excess fat, or excess CHO?).Duplicate or triplicate diet records would also verify the accuracy ofrecording or the accuracy of the diet analysis itself.Lipid profiles may have been a useful addition to biochemicalparameters studied. Although it would not have helped explain changes inbody composition and insulin metabolism, it may have indicated additionaleffects of weight cycling, such as elevated lipid and cholesterol levels.The results of this study indicate that judokas who cut an averageof 4 kg, an average of 4 times a season, will experience no reduction inRMR, and no alteration in body composition, fat distribution, and fastingserum insulin, glucose and T3 levels. 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The myth of theyo-yo: consistent rate of weight loss with successive dieting byVLCD. Inter J Obes 13: 135-139.31. Van Dale, Djoeke, and Saris, H.M. 1989. Repetitive weight loss andweight regain: effects on weight reduction, resting metabolic rate,and lipolytic activity before and after exercise and/or diettreatment. Am J din Nutr 49: 409-416.32. Jebb, Susan A, Goldberg, GR, Coward, WA, Murgatroyd, PR, andPrentice, AM. 1991. Effects of weight cycling caused byintermittent dieting on metabolic rate and body compostion in obesewomen. Inter J Obes 15: 367-374.33. Manore, Melinda M, Berry, TE, Skinner, JS, and Carroll, SS. 1991.Energy expenditure at rest and during exercise in nonobese femalecyclical dieters and in nondieting control subjects. Am J din Nutr54: 41-46.34. Keesey, RE. 1986. A set-point theory of obesity. in Handbook ofEating Disorders: Physiology, Psychology and Treatment of Obesity,Anorexia, and Bulimia, K.D. Brownell and J.P. Foreyt, editors. NewYork: Basic Books, pp 63-87.35. Nelson Steen, Suzanne, Oppliger, Robert A, and Brownell, Kelly D.1988. Metabolic effects of repeated weight loss and regain inadolescent wrestlers. J Am Med Assoc 260: 47-50.8636. Melby, Christopher L, Schmidt, WD, and Corrigan, D. 1990. Restingmetabolic rate in weight-cycling collegiate wrestlers compared withphysically active, noncycling control subjects. Am J din Nutr 52:409-414.37. Stock, MJ. 1989. Effects of low (LCD) and very low (VLCD) energydiets on metabolic rate and body composition in obese (fa/fa)zucker rats. Inter J Obes 13: 61-65.38. Ozelci, Aysel, Romsos, Dale R, and Leveille, Gilbert A 1978.Influence of initial food restriction on subsequent body weightgain and body fat accumulation in rats. J Nutr 108:1724-1732.39. Reed, Danielle R, Contreras, Robert J, Maggio, Carol, Greenwood, MRC,and Rodin, Judith. 1988. Weight cycling in female rats increasesdietary fat selection and adiposity. Physiol Behav 42: 389-395.40. 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Gerardo-Gettens, Theresa, GD Miller, GD, Horwitz, BA McDonald, RB,Brownell, KD, Greenwood, MRC Rodin, J and Stern, JS. 1991.Exercise decreases fat selection in female rats during weightcycling. Am J Physio 260: R518-R524.8853. Graham, Brent, S Chang, S Lin, I, Yakubu, F and Hill, JO. 1990.Effect of weight cycling on susceptibility to dietary obesity. Am JPhysio 259: R1096-R1102.54. Kissebah, AH, Vydelingum, N, Murray, R, Evans, DJ, Harts, AJ,Kalkhoff, RK, and Adams, PW. 1982. Relation of body fatdistribution to metabolic complications of obesity. J dinEndocrinol Metab 54: 254-260.55. Rodin, Judith, N. Radke-Sharpe, N, Rebuffe-Scrive, M and Greenwood,M. 1990. Weight cycling and fat distribution. Inter J Obes 14:303-310.56. Baxter, P, Stanton, J, Lazarus, NR, et al. 1978. _The relationbetween insulin and adipocyte insulin receptors during treatment ofhuman obesity. J din Invest 8: 361-372.57. Schemmel, Rachel. 1980. Nutrition, Physiology and Obesity. CRC PressInc. Boca Roton, Florida.58. Kolterman, OG, Insel, J, Saekow, M et al. 1980. Mechanism of insulinresistance in human obesity: Evidence for receptor and postreceptor defects. J Clin Invest 65: 1272-1282.59. Strubbe, JH and Alingh Prins, AJ. 1986. Reduced insulin secretionafter short-term food deprivation in rats plays a key role in theadaptive interaction of glucose and free fatty acid utilization.Physiol Behav 37: 441 -445.60. Klein, Samuel,Holland, 0 Bryan, and Wolfe, Robert R. 1990.Importance of blood glucose concentration in regulating lipolysisduring fasting in humans. Am J Physiol 258: E32-E39.61. Arner, Peter and Engfeldt, Peter. 1987. Fasting-mediated alterationstudies in insulin action on lipolysis and lipogenesis in obesewomen. Am J Physiol 253: E193-E201.8962. Jensen, Michael D, Miles, John M, Gerich, John E, Cryer, Philip E,and Haymond, Morey W 1988. Preservation of insulin effects onglucose production and proteolysis during fasting. Am J Physiol254: E700-E707.63. McCargar, Linda J, Clandinin, Michael T, and Fawcett, David M. 1988.Short-term changes in energy intake and serum insulin, neutralamino acids, and urinary catecholamine excretion in women. Am Jdin Nutr 47: 932-941.64. Owens, Jeanna L, Thompson, D, Shah, N and DiGirolamo, M. 1979.Effects of fasting and refeeding in the rat on adipocyte metabolicfunctions and response in insulin. J Nutr 109: 1584-1591.65. Spaulding, Stephen W, Chopra, Inder J, Sherwin, Robert S, Lyall,Santokh S. 1976. Effect of caloric restriction and dietarycomposition on serum T3 and reverse 73 in man. J din EndocrinoIMetab 42: 197-200.66. Nunez, J. Mechanism of action of thyroid hormone. 1988. in Hormonesand their Actions Part I. Cooke, BA, and RJ, King, B, Vander Molen,HJ editors. New York: Elsevier Science Publishers.BiochemicalDivision, pgs 1-38.67. Jung, RT, Shetty, PS, and James, WPT. 1980. The effect of refeedingafter semistarvation on catecholamine and thyroid metabolism. InterJ Obes 4: 95-100.68. Danforth, E, Jr, Sims, EAH, Horton, ES, and Goldman, RS. 1975.Correlation of serum triiodothyronine concentrations (T3) withdietary composition, gain in weight and thermogenesis in man.Diabetes 24: 406 (abstract).69. Azizi, F. 1978. Effect of dietary composition on fasting inducedchanges in serum thyroid hormones and thyrotropin. Metab 27: 935-942.9070. Vagenakis, AG, Portnay, GI, O'Brian, JT, Rudolph, M, Arky, RA,Ingbar, SH, and Braverman, LE. 1977. Effect of starvation on theproduction and metabolism of thyroxine and triiodothyronine ineuthyroid obese patients. J Clin Endocrinol 45: 1305-1309.71. Harris, ARC, Fang, SL, Vagenakis, AG, and Braverman, LE. 1978.Effect of starvation, nutrient replacement, and hypothyroidism onan in vitro hepatic T4 to T3 conversion in the rat. Metab 27: 1680-1690.72. Van der Heyden, JTM, Docter, R, Van Toor, H, Wilson, JHP., Hennemann,G, and Krenning, EP. 1986. 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Bodycomposition analysis: A defense of anthropometry in overweightfemale dieters and controls. Inter J Obes 13: 155-156.9178. Deurenberg, Paul, Weststrate, Jan A, and Hautvast, Joseph GAJ. 1989.Changes in fat free mass during weight loss measured bybioelectrical impedance and by densitometry. Am J din Nutr 49: 33-36.79. Durnin, JGVA and Womersley, J. 1974. Body fat assessed from totalbody density and its estimation from skinfold thickness:measurements on 481 men and women aged from 16 to 72 years. Brit JNutr 32: 77-96.80. Sin, WE. 1956. The gross composition of the body. Adv Biol Med Phys4; 239-280.81. Groskopf, WR, Hsu, S, and Sohn L. A fully automated assay for totalT3 utilizing the Abbott IMxTM Analyzer. in: IMx System Manual,Abbott Laboratories, Abbot Park, IL.82. Livesey, JH, Hodgkinson, SC, Roud, HR, and Donald, RA. 1980.Pharmacia Insulin RIA 100 Radioimmunoassay. din Biochem 13: 151.83. Kadish, AH and Sternberg, JC. 1969. Determination of urine glucoseby measurement of rate of oxygen consumption. Diabetes 18: 467-470.84. Stuff, Janice E, Garza, K Cutberto, O'Brian Smith, E, Nichols, BufordL, and Montandon, Corinne M. 1983. A comparison of dietary methodsin nutritional studies. Am J Clin Nutr 37: 300-306.85. Tremblay, Angelo, Sevigny, Jeannine, Leblanc, Claude, and Bouchard,Claude. 1983. The reproducibility of a three-day dietary record.Nutr Res 3: 819-830.86. Heady, JA. Development of a method of classifying the diets ofindividuals for use in epidemiological studies. J Roy Stat Soc 124:336-360.9287. Basiotis, PP, Welsh, SO, Cronin FJ, Kelsay, JL, and Mertz, W. 1987.Number of Days of food intake records required to estimateinduvidual and group nutrient intakes with defined confidence. JNutr 117; 1638-1641.88. Dwyer JT. 1988. Assessment of dietary intake. in: Modern nutritionin health and disease, 8th ed., Shils ME, Young VR, eds.Philadelphia: Lea & Febiger, pg 887-905.89. The British Columbia Diet Manual: a nutritional care manual. 1984.published by Hospital Programs, Vancouver B.C. pg 24.90. Mahalko, Janet R. 1980. Accuracy of predictions of long-term energyneeds. J Am Diet Assoc 77; 557-561.91. Tremblay, Angelo, Fontaine, E, and Nadeau, A. 1985. Contribution ofpostexercise increment in glucose storage to variations in glucose-induced thermogenesis in endurance athletes. Can J PhysiolPharmacol 63: 1165-1169.92. DuBois, Eugene F. 1936. in Basal Metabolism in Health and DiseasePhiladephia: Lea & Febiger, pp 166.93. Schmidt, W Daniel, Melby, CL and Corrigan, D. 1991. Two consecutiveseasons of weight cycling does not lower resting metabolic rate incollege wrestlers. Med Sci Sports Exer 23: 53 (abstract).94. Nelson Steen, Suzanne, and Brownell, KK. 1990. Patterns of weightloss and regain in wrestlers: has the tradition changed? Med SciSports Exer 22: 762-768.95. Lennon, Boris, Nagle, Francis, Stratman, Frederick, Shrago, Earl andDennis, Susana. 1985. Diet and exercise training effects onresting metabolic rate. Inter Obes 9: 39-47.9396. Donahoe CP, Lin, DH, Kirschenbaum, DS, and Keesey, RE. 1984.Metabolic consequences of dieting and exercise in the treatment ofobesity. J Consult din Psychol 5: 827-836.97. Mole, Paul A, Stern, Judith S, Schultz, Cynthia L, Bernauer, EdmundM, and Holcomb, Bryan J. 1989. Exercise reverses depressedmetabolic rate produced by severe caloric restriction. Med SciSports Exer 21: 29-33.98. Phinney, S.D. 1985. The metabolic interaction between very lowcalorie diet and exercise. in Management of Obesity by SevereCaloric Restriction, Blackburn GL and Bray, G.A., editors.Littleton, MA: PSG Company, pp 99-105.99. Poehlman, ET, Melby, CL and Badylak, SF. 1988. Resting metabolicrate and postprandial thermogenesis in highly trained and untrainedmales. Am J Clin Nutr 47: 793-798.100. Poehlman, Eric T, Melby, CL, Badylak, SF and Calles, J. 1989.Aerobic fitness and resting energy expenditure in young adultmales. 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Proc Nutr Soc 47;259-68.95APPENDIX ICERTIFICATE OF APPROVAL96CERTIFICATE OF APPRCThe University of British Columbia^C89-009Office of Research ServicesCLINICAL SCREENING COMMITTEE FOR RESEARCHAND OTHER STUDIES INVOLVING HUMAN SUBJECTSCERTIFICATE^of APPROVALINVESTIGATOR: McCargar, L.UBC DEPT:^Family & Nutr SciINSTITUTION: FMSCTITLE:^Metabolic consequences of recurrent dieting(Amended 16 September 1990)NUMBER:^C89-009APPROVED: SEP 25 1990The protocol describing the above-named project has beenreviewed by the Committee and the experimental procedures werefound to be acceptable on ethical grounds for researchinvolving human subjects.DrCl^ esTHIS CERTIFICATE OF APPROVAL IS VALID FOR THREE YEARSFROM THE ABOVE APPROVAL DATE PROVIDED THERE IS NOCHANGE IN THE EXPERIMENTAL PROCEDURES97APPENDIX IIWEIGHT CYCLING QUESTIONNAIRE98WEIGHT CYCLING QUESTIONNAIRE Date ^ OFFICE USE ONLY personal Data^ No. ^BMI Age^ Sex  ^VHR Height Weight ^Waist  ^Hip ^Eating and Weight Patterns 1. Have you ever tried to lose weight by dieting, 1.e.,restricting food intake to a level less than usual? (pleasecircle the number of your answer)1 NO, NEVER^IF NO, GO TO QUESTION 22 YES, ONCE3 YES, MORE THAN ONCEA. How often are you dieting to lose weight? (circle number)I NEVER2 RARELY3 SOMETIMES4 OFTEN5 ALWAYSB. Have you tried the following weight loss diet programs ormethods to lose weight in the past five years? (pleasecheck either yes or no) Yes NoWeight WatchersDiet CenterTOPSNutrisystemHerbalifeformula diets (specify)diet books (specify)hospital program (specify)Overeaters Anonymousdiet pillsdiuretics/emeticsother (please specify) ^99C. How many times have you tried to lose weight in the past.,year? (circle number of your answer)102 1-23 3-54 6-95 10 OR MORED. For what reason(s) have you dieted to lose weight? (circleall that apply)1 A SPORT OR ATHLETIC EVENT, ON THE ADVICE OF A COACH2 A SPORT OR ATHLETIC EVENT, WITHOUT A COACH'S ADVICE3 TO LOOK MORE ATTRACTIVE4 HEALTH REASONS, ON THE ADVICE OF A DOCTOR5 HEALTH REASONS, WITHOUT A DOCTOR'S ADVICE6 OTHER (please specify) ^Z. When was the last time you started a diet to lose weight?(circle number of your answer)1 WITHIN THE LAST TWO WEEKS2 WITHIN THE LAST MONTH3 WITHIN THE LAST SIX MONTHS4 WITHIN THE LAST YEAR5 MORE THAN ONE YEAR AGOF. How much weight did you want, to lose on your most recentdiet?^lbs.G. How much weight 414 you lose on your most recent diet?^ lbs.H. How long did you stay on your most recent diet? ^I. How old were you when you first dieted to lose weight?J. Are you a yo-yo dieter (that is, do you experience frequentweight losses and regains)? (circle number of your answer)1 YES2 NO2. What is the maximum amount of weight you have ever lostwithin one week, not due to illness or pregnancy? ^ lbs1003. What Is your maximum weight gain within a week? lbs4. When you gain weight, where do you gain it? (check all thatapply)^ AROUND THE MIDDLE (WAIST, ABDOMEN)HIPS, THIGHS AND BUTTOCKS^ ALL OVERELSEWHERE (please specify) ^NOT APPLICABLE--MY WEIGHT GAIN IS MINIMALS. When you lose weight, where do you lose it? (check all thatapply)^ AROUND THE MIDDLE (WAIST, ABDOMEN) HIPS, THIGHS AND BUTTOCKSALL OVERELSEWHERE (please specify) ^NOT APPLICABLE--MY WEIGHT LOSS IS MINIMAL6. How many times in the oast 5 years , would you estimate youhave lost the number of pounds shown below, excluding preg-nancy/post-partum? (write in number of times)Weight loss^Number of times 1-5 lb6-10 lb11-20 lb21-30 lb31-50 lb51♦ lb7. Describe your weight between the ages: (check where appropri-ate) 6-10years 11-13years 14-17years 16-25years 26+yearsExtremely thin (^) ( ) ( ) ( ) ( )Very thin ( ) ( ) ( ) ( ) ( )Somewhat thin ( ) ( ) ( ) ( ) ( )Average ( ) ( ) ( ) ( ) ( )Somewhat overweight ( ) ( ) ( ) ( ) ( )Very overweight ( ) ( ) ( ) ( ) ( )Extremely overweight ( ) ( ) ( ) ( ) ( )1011 YES2 NO^IF NO, GO TO QUESTIO11-1312. How often do you vomit to control weight?e. What has been your minimum weight as an adult (>25 yearsold)?^lbs9. What has been your maximum non-pregnant weight ever?'^lbs10. Have you ever purged (used self-induced vomiting,laxatives, diuretics) to control your weight? (circlenumber of your answer)1 YES2 NO^IF NO, GO TO QUESTION 17-11. Have you ever used emetics or vomitted to control weight?1 LESS THAN ONCE PER MONTH2 1-3 TIMES PER MONTH3 ONCE PER WEEK4 2-6 TIMES PER WEEK5 DAILY6 MORE THAN ONCE PER DAY13. Have you ever used laxatives to control weight?1 YES2 NO^IF NO, GO TO QUESTION 1514. How often do you use laxatives to control weight1 LESS THAN ONCE PER MONTH2 1-3 TIMES PER MONTH3 ONCE PER VESA4 2-6 TIMES PER WEEK5 DAILY6 MORE THAN ONCE PER DAY15. Have you ever used diuretics to control weight?1 YES2 NO^IF NO, GO TO QUESTION 1710216. How often do you use diuretics to control weight?1 LESS THAN ONCE PER MONTH2 1-3 TIMES PER MONTH3 ONCE PER WEEK4 2-6 TIMES PER WEEKS DAILY6 MORE THAN ONCE PER DAY17. How satisfied are you with your current body size and shape?(circle number)1^2^3^4^5^6^7NOT AT ALL MODERATELY EXTREMELYSATISFIED SATISFIED SATISFIED18. What do you consider to be your ideal weight? ^ lbsExercise Patterns 19. How many hours per week do you engage in vigorous physicalactivity (e.g. running, swimming, cycling, brisk walking)?(circle number)1 0-1 hour2 1.1-3 hours3 3.1-5 hours4 5.1-8 hoursS 8.1-11 hours6 More than 11 hoursPlease specify the activities in which you participate:20. How many years have you been exercising vigorously (working^out at least three days per week)? ^ yearsNot applicable 21. Please list any medications that you are currently using:Thank you for completing this questionnaire.103JUDO SUBJECT  QUESTIONNAIRE (1) How many years have you been In competitive Judo?^(2) How many years have you been cutting weight for Judocompetitions?...(3) What is your normal weight range off -season?_(4) What is your normal weight during the competitiveseason?(5) What is your competing^ _(6) How frequently would you say you reduce weight forcompetitions?(circle one):never^rarely^sometimes^often^always(7) Estimate how many times you reduce weight in a givenseason.(8) How many competitions, where meeting your competitiveweight is necessary, can you estimate this season?_(9) How much weight would you lose each dietingsession?(circle one):<1.4 kg^1.5-2.9 kg^3.0-3.9 kg^4.0-4.9 kg^=>5 kg(10) What is involved in your Judo training?:(a)strength training:^high^moderate^low(b)cardiovascular training:^high^moderate^low(11) What forms of vigorous exercise do you do:(a)pre-season_^ total  hrs/wk_(b)during season_ _total hrs/wk(c)off-season_ _total(12) Have you found losing weight is getting harder to do?:(a)from season to season?^yes^no(b)with in a season?^yes no______(13) Have you found that you regain weight more rapidly orwith greater ease:(a)from season to season?^yes_^no__(b)within a season?^yes no(14) Off season, do you:(a)regain to previous off season weight?^yes^no_(b)gain more than your off season weight? yes no____(c)remain the same weight'^ yes____ no104APPENDIX IIIMEDICAL GRAPHICS CORPORATION SYSTEM 2001105Medical Graphics Corporation System 2001 RMR will be determined using the System 2001 metabolic cartlocated in the Sports Medicine Center. It utilizes open circuit,indirect calorimetry, which allows energy expendituredetermination by measuring oxygen(02) consumption and carbondioxide(CO2) production. -Air expired by the subject is directed through a hose intothe System 2001, and flow rate and volume is measured by heatedlinear pneumatach. these measurements are then amplified andsent to a wave form analyzer. This analyzer will compute thefollowing:- relative time since start of collection (min.sec.)- inspiratory time of breath(sec)- total time of breath(sec)- tidal volume(al)- frequency of breathing(br/min)- minute ventilation(L/min)- volume of CO2 in breath(m1)- end tidal CO2(%)- inspired CO2(%)- volume of 02 in breath(m1)- end tidal 02(%)- inspired 02(%)- heart rate106METABOLICThe computer will recieve this data to calculate energyexpenditure, respiratory quotient, and percentage of each fuelsource utilized(CHO, protein, and fat) during the time oftesting.The testing conditions stated by the Systems 2001 manual areas follows:- rest 20-30 minutes prior to testing- fast 2 to 4 hours prior (12 hour fast will be used)- early morning measurements(before breakfast)- thermoneutral and quite environment- 15 to 20 minute data collectionThe conditions under which RMR will be tested in this study havebeen indicated in the methods section.107APPENDIX IVPROCEDURE FOR ANTHROPOMETRIC MEASUREMENTS1080) Waist (Abdomen) GirthThe participant stands erect Theappraiser uses a cross-handed tech-nique to position the tape horizontally atthe level of noticeable waist narrowingThe tape is then placed in the recordingposition and the measurement is rna0eat the end of a normal expiration Insome Participants an indeterminatewaist can be approximated by taking thegirth at the estimated lateral level of thetwelfth or lower floating ribis) Right Thigh GirthThe participant stands erect feet slightlyapart The tape is positioned around theright thigh to a level one centimeterbelow the glutea1 linec) Hip (Gluteal) GirthThe participant stands erect with feeltogether The tape is positioned woundthe hips at the level of the symPhYsispubis and the greatest gluteal pro-tuberance.109P.ROCEDURE FOR ANTEROPOMETRIC MEASURE4.3.4 Veilfold ApfeeSure/710ndSee section 5 2 - BOOY WEIGHT.ADIPOSITY AND FAT OISTRIBUTH(regarding use of the skolold meamentS)Equipment: Harpenden or LangeipersDo one complete rcund delete skimeasurements before repeating Me Icecture to obtain a second skinfodo nsurement for each see. AN measurenare taken only on the right side at IvbodyGene'rei ProcedureDuring skinlold measurements. kessential that the participant relax 0underlying musculature as much assible. When the site of the skintold Ibeen determined, a told of skin pitounderlying tat is grasped betweenthumb and forefinger with the backthe hand facing the appraiser Keepthe jaws of the calipers *ways at ricangles to the body surface. tie confaces of the calipers are placed onecentimeter below the point where thiskinfold is raised. While maintainingpressure of the fingers on the skinblthe trigger of the calipers is fullyreleased and the measurement is tatThe measurement is noted when theindicator stabilizes which is approod-rnately two seconds after the fullsure of the caliper jays is apØed toskinfold. The reading is recorded to Inearest 0.2 millimetres; ..9.11 18 :8Complete the first set of skintold measurements for all sites. Then. repeal tprocedure to obtain a second set ofmeasurements for each skinfold site.Record the mean of the two measure:unless the difference between the firSand second measure of that parlicutaskinfold site is found to be greater thg0.4 mm. If SO. take a third meaSulethat skinfold site and choose hamamong the three values, the two mea-sures which most closely match eachother in value. Determine the mean ofthose two measures. Should the threemeasures be equidistant. e.g. 18.6 1919.8 determine the mean of aN threevalues.I should be noted that the accuracy ofskinfold measurements &pen& on:•precise identlicablxi of 'he sea of theslcinioick• tenting Su *inked prior he tie appacaNon of the caliper jeers:• tie standardization of the afignment atihe Witold cost• naintenanct of the plenum by to fin-gers on So *Mold when 1winsaase-mint is titan•complete Mose of Nu caper jawPROCISDORE^ainwitoPomariac ltEASC4a) Triceps SkintoldThe participant stands with the armsrelaxed by the sides The triceps skinfoldis !aken on the back of the right arm atthe poont midway between the tip of the&on:rub/1 (right shoulder) and the tip ofthe Ofecranon thght elboo) The midpointdetermined by placing the fifth lingerof the left hand on the tip of the acro-macn (right Shoulder). the fifth linger ofate right hand on the tip of the olecranon(right &bow) and then the thumbs arepiac0d together to determine the mid-sxvntThe skinfold is then raised at the mid-arm point. so the told runs verticallyalong the midline of the back of the arm.b) Biceps SkinfoldThe biceps skinfold is measured on theright extended upper arm Goer thebiceps at the same 'eves as the mid-armpont for the triceps The skofol0 is thenraised at the mid-arm pont so the foldruns vertically along the midline Of thefront of the arme) Subscaputar SkinfoldThe participant stands with the shoul-ders relaxed and the arms by the sides.The skinfold is raised so it can be mea-sured on a diagonal line coming horn thevertebral border of the scapula so a pointcm. beneath the intro. angle. TheWonted runs downward and outward atan angle of approximately 45 degrees tothe spine.d) Iliac Crest SkinfoidThe participant stands in a normal erecPosition Have the participant raise the•ight arm to the side so that it a hOrIZOg!al and dace the right hand on the richshoulder If the participant 3 unable 10Place hand on shoulder, keep the hori-zontal arm extended The skinfold is themeasured three centimetres above thecrest of the ilium at the midline of thebody so that the fold runs forward andSlightly downward.e) Medial Call SkinfoldHave the participant place theunweighted (relaxed) right tot flat on astep so that the knee is at 90*. The skin-told is raised on the inside of the rightcalf just abows the level al the maximumcalf girth so that the fold runs verticallyalong the midline.TIM(: CANADIAN STANDARDIZED TEST OF FITNESS, entAtriES MANUAL 1986•110APPENDIX VDURNIN AND WOMERSLEY LINEAR REGRESSION EQUATIONS111!MANZI AND WOMERSLET LINEAR REGRESSION EQUATIONSJ. V. G. A: DURNIN AND J. WOMERSLEYTable S. Linear regression equations for the estimation of body density x io 3 (kelm 3)froftthe logarithm of the shinfold thickness: density^c - m x log skinfold(o) MalesAge (years)^--Skinfold 17-19 20-29 30-39 4*--49 50+ 17-72Biceps^ c 1'1066 1.1015 10781 1'0829 3'0833 1.0997in 0-0686 o•o616 0.0396 •0.0508 0.06:7 0.0659Triceps c 1'1252 1.31 31 1'434 1.1041 1.3027 1'1143nt 0.0625 0.0530 0.0361 0.0609 0.0662 0•0618Subscapular^c 1.3372 3.3360 10978 1.3246 1'1334 1'1369771 0.0670 0.0700 0.0416 0-0686 0.0760 00741Supra-iliac c 1.1092 1.31117 11047 1.3029 1'3193 1'1171on...0-0420 00431 00432 0.0483 00652 00330Biceps+ triceps^c 1'1423 1.1307 3'0995 3.1374 1'1185 11336in 0-0687 0.0603 0.0431 0.0614 0'0683 00700Biceps +subscapular^c 1'1437 1.1469 1'0733 3'1341 v1427 3'1490m 0.0707 00709 0.0445 0.0680 420762 00759Biceps+ supra-iliac^C 1'1247 1.1259 1'3174 3-1371 I.3307 11333113 00501 00502 0046 00539 0-0678 00601Triceps + subscapular^c 1'1361 1'1525 3.1165 3.1539 3°1527 1'1625nt 0.0711 0.0687 00484 0-0771 0'0793 00797 .Triceps+ supra-iliac^C 1.1370 1'3362 1-1273 1.1383 1.1435 1'1463^'In 0'0545 0.0538 0.0331 o-c660 0.0718 00656Subscapular+ supra-iliac^c 3.3374 11429 1.3260 1.1392 z.1582 1'15223n 0.0544 00573 0.0497 0.0633 00771 00671Biceps + triceps +subscapular c 1.1643 3'1393 1.1233 11530 1.1569 3.1689371 0-072 7 00694 00487 0.0730 0.0780 0.0793Biceps + triceps + supra-iliac^c 3- t 466 1'1431 1.1332 1.1422 11473 3.1536m 0.03114 •0572 00542 0'0647 00733 00663Biceps + subscapular+^C 1.1469 1.1508 11335 1452 1.1626 I.1605supra-iliac^M 00583 0.0599 00530 0.0640 0.0768 00694Triceps+ subscapular+^c 1'1555 3'3575 111393 3.1604 3'3409 1.3704supra-iliac m 0.0607 0.0637 0-0544 0-0736 00787 0-0731All four skinfolds^c 1.3620 3.1631 1'1422 3-1620 3'3735 1.1765m 0.0630 0.o632 00544 0.0700 0'0779 co.0744112DORNIN AND VONERSLEY LINEAR REGRESSION EQUATIONSBody fat and skinfoldsTable s (cont.)(b) FemalesAge (years)Sk in fold0^-16-19 20-29 30-39 40-49 50 + :6-68Biceps e t-o889 11'0903 zo117 z10794 t•o736 3•068: -m o-o553 o•o6ot o-o5 I t 00492 o •os toTriceps C "159 11319 11176 11121 I•I 160 :9:::738in o-o648 0-0776 o-o686 0-069 t 400762 0-0775Subscapular t • so8 tc vita; 10979 t -o86o t •o899 vztooin o -o6a t crop 6 0-0567 o-osos 0•0590 0-0669Supra-iliac c 1'0931 10923 t -086o 1.0691 i -o656 1.0884in 00470 0•0509 0•0497 00407 °I); t 9 o•os t 4Biceps + triceps c t •1290 p 1398 11343 1 1230 •:1226 12362m 0-0657 00738 0'0646 0•0672 crop° 00740Biceps + subscapular c 11241 1-1314 1'1120 1•1031 11029 11245in 00643 00706 0•058 t 0'0549 0-0592 0'0674Biceps + supra-iliac c 11113 11112 I•1020 1'0921 10857 1'1090m o-o337 o•o568 o•osa8 0'0494 00490 00577Triceps + subscapular e 11468 t-t Oa 12336 11230 11347 1•1507m 0-0740 0•0813 o•o68o 0'0635 o•civia 00785Triceps + supra-iliac c 1'1311 1'1377 1•1281 21:98 1•1158 1-1367... in 0-0624 0-0684 00644 o•co63o cro635 0r0704Subscapular + supra-iliac c t• :278 t• 128oi:ll 1010997 10963 11234m oo6•^t 6 0'0640 o51: 0-0509 043523 00632Biceps + triceps + subscapular c : -1509 i -16o5 1'1385 r z3o3 2•1372 11543in crop 5 0-0777 00654 00635 crop o 0•0756Biceps + triceps + supra-iliac c t • t382 2•1441 11319 11267 1'1227 11432in 0-0628 cr068o 0-0624 040626 0-0633 0•0696Biceps + subscapular + c 1'1355 : • t 366 11212 I. t to8 1.1063 1'1530supra-iliac in o-o62a 0•0648 0•0570 0•0536 0'0544 0-0727Triceps + subscapular + c 1-1517 1•1566 1.1397 1.1:78 11298 1'1327supra-iliac in 00689 00728 0'0646 0•0609 o-065o 0-0643All four slinfolds c 11349 11399 1'1433 1'1333 11339 1'1567In 0'0678 0-0717 00632 0-06 :a 0-0643 own113

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