effects of nandrolone decanoate on vo2max running econom

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Effects of Nandrolone Decanoate on VO2maxRunning Economy, and Endurance in RatsKATERINA N. GEORGIEVA and NICKOLAY P. BOYADJIEVDepartmentofPhysiology Medical University Plovdiv Plovdiv BULGARIA

ABSTRACTGEORGIEVA, K. N., and N. P. BOYADJIEV. Effects of Nandrolone Decanoate on VO 2,,,,x, Running Economy, and Endurance inRats. Med. Sci. SportsExerc., Vol. 36, No. 8, pp. 1336-1341,2004. Purpose: The aim of the present study was to determine the effectsof treatment with an anabolic androgenic steroid (AAS), nandrolone decanoate, on the submaximal running endurance (SRE),maximum oxygen consumption (O2ma,), running economy (VO2,Ub10=), and blood oxygen carrying capacity of endurance trained rats.Methods: Forty male Wistar rats were randomly allocated into two groups: a sedentary group and an exercising group training ontreadmill for 8 wk. Half of the trained and half of the sedentary rats received weekly either nandrolone decanoate (10 mg-kg-') orplacebo (P1) or the last 6 wk of experiment. SRE and V0 2m.. tests were performed several times for all four groups N = 10 each).Red blood cells parameters were measured at the end of the experiment. Results: The trained rats had increased their SRE comparedwith sedentary rats throughout the experiment. At the end of the trial, the trained rats receiving nandrolone decanoate ran 46 longerthan trained mts receiving P1 during the SRE test (P < 0.05). At the end of the experiment, trained rats had greater maximal time toexhaustion and higher V0 2 .,a than those of the sedentary rats but there were no differences in VO 2 .a., V02subl and red blood cellsparameters between the trained rats receiving nandrolone decanoate and those receiving PI. Conclusions: Nandrolone decanoate hasno effect on the SRE, V2 a and V2..bm.. of untrained rats. AAS treatment combined with submaximal training enhances SRE morethan training alone but exerts no additive effects on V02mx, running economy, and oxygen carrying capacity of blood. The resultssuggest that this improvement in SRE of trained rats is due to the impact ofAAS on other factors involved in exercise adaptation. KeyWords: MALE RATS, ANABOLIC ANDROGENIC STEROIDS, OXYGEN CONSUMPTION, RED BLOOD CELLS, SUBMAXI-MAL RUNNING,ENDURANCE

nabolic androgenic steroids (AAS), synthetic deriva-tives of the sex hormone testosterone, are used in,Alvarious sports to enhance athletic performance. Themajority of users are strength athletes in professional andamateur sports (8); however, there have also been reports ofsteroids taken by endurance athletes (e.g., swimmers, cyclists,runners) (14,29). Although there is much research on the effectof AAS on strength and power, there are few studies on theireffect on endurance exercise performance. Several potentialmechanisms have been suggested to cause the ergogenic ef-fects of AAS treatment on endurance trained subjects. One ofthe possible mechanisms is improvement of skeletal musclefunction by increasing protein synthesis (23,27). Another sug-gested mechanism is that AAS treatment counteracts the cat-

abolic action of high circulating corticosteroid concentrationsresulting from training 15). Another possibility is that AAS actthrough the central nervous system, allowing the subjects totrain harder (3,26).

Address for correspondence: Dr. Katerina Georgieva, Department of Phys-iology, Medical University Plovdiv, 15-A, Vasil Aprilov Blvd., 4000Plovdiv, Bulgaria; E-mail: [email protected] for publication August 2003.Accepted for publication March 2004.0195-9131/04/3608-1336MEDICINE SCIENCE IN SPORTS EXERCISE,Copyright 2004 by the American College of Sports Medicine

Endurance exercise training improves maximum oxyconsumption VO2max) and running economy VO2subIwhich are considered key parameters in the improvemensubmaximal running performnance (17). AAS enhance erropoiesis and increase blood volume (21). As oxygenrying capacity is one of the factors determining VO nxsubmaximal running endurance (SRE) (4,11), it seems ta likely mechanism through which SRE can be increasedAAS (20). The combined effect of endurance trainingAAS treatment on these parameters is not well definedThe effect of AAS on submaximal running performais difficult to study in training athletes because of methological limitations and ethical considerations. One offirst animal studies investigating the effect of AASsubmaximal running performance was conducted on sptaneously running male rats (28). This study showedcombining AAS treatment with voluntary wheel runndelays fatigue during submaximal exercise and improSRE by 41 compared with wheel running. The improment in SRE could not be explained by either the increavoluntary training distance, the increased skeletal muoxidative capacity, or the increased skeletal muscle glygen concentration compared with trained controls. Italso found that AAS treatment had no effect on maxisprint speed and on SRE of untrained rats (28). These dsuggest that the increase of submaximal running permance is due to the impact of AAS on factors involvedexercise adaptation and not to the fact that subjects tr


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ing which improves SRE, running economy and VO2mx, ofrats similarly to the changes induced by the submaximaltraining on a treadmill (19). Treadmill-trained rats havebeen employed by other researchers to study the effects ofAAS on running performance, but the training and the testshave been performed using high exercise intensity (withadditional weight, high speed and high grade of the tread-mill belt) and changes in the SRE, V02max, running econ-omy, and blood oxygen carrying capacity have not beeninvestigated (25).Studying the changes these parameters undergo under thecombined influence of AAS treatment and endurance tread-mill training will provide new evidence about the AASeffect on endurance exercise performance and the possiblemechanisms causing this effect. To our knowledge, theeffects of AAS treatment on these parameters in submaxi-mal treadmill-trained rats have not been studied. Therefore,the aim of the study was to evaluate the separate andcombined effects of treatment with an anabolic androgenicsteroid and submaximal treadmill training on submaximalrunning endurance, maximum oxygen consumption, run-ning economy, and oxygen carrying capacity in rats. Wehypothesized that AAS can increase SRE, running econ-omy, and oxygen carrying capacity of endurance treadmill-trained rats.MATERIALS AND METHODSAnimals Forty male Wistar rats (200-220 g) were used

in this study. They were housed in individual metaboliccages and fed standard rat chow and water ad libitunt.Bodymass and the amount of food intake were measured daily.The rats were maintained at an ambient temperature of21-24C with a 12/12-h dark-light cycle. The experimentalprotocol was approved by the Ethical Committee on Humanand Animal Experimentation of Medical University, Plo-vdiv. Rat care and all experimental procedures employedwere in accordance with the policy statement of the Amer-ican College of Sports Medicine on research with experi-mental animals.Training program and steroid treatment. As run-ning on a treadmill is a skilled activity for rats, before theexperiment all rats were exercised on the treadmill (Colum-bus Instruments, Columbus, OH) at a speed of 27 m min- land 5 elevation for 5 min-d-', 3 d.wk-' for 2 wk. Suchworkload induces no training adaptations (18) but familiar-izes the rats with treadmill running and allows selection ofrats that run spontaneously. About 15 of the rats refusedto run on the treadmill and were discarded from the study atthe end of the preliminary stage.Compliant rats were randomized into two groups, seden-tary N = 20) and trained (N = 20). Trained animalsexercised on the treadmill at a speed of 27 m-min-1, 50elevation (which is about 70-75 5O2max ,.wk' for 8wk. The duration of the exercise was 20 min-d- l on the firstday and was increased by 5 min every second day. By theend of the second week, it reached 40 min-d-' and remainedso until the end of experiment. The untrained rats were

exercised on the treadmill 3 d.wk-' for 5 min at the samespeed and elevation as the training group to ensure famil-iarization with treadmill running. The treadmill speed wascalibrated before each training session.At the beginning of week 3, half of the trained anduntrained rats were given an anabolic androgenic steroid,nandrolone decanoate, (ND) 10 mg.kg' l wk- l intramuscu-larly (Retabolil, Gedeon Richter, Hungary) over a- imeperiod of 6 wk. The other half of the rats were given placebo(P1, oil vehicle) in the same dose and duration. The injectionwas administered after the day's training in m. gluteusmedius, applying it altermatively each week in the contralat-eral side. Nandrolone decanoate is a long acting steroid esterand the recommended therapeutic dose of ND in humansfalls within 50-100 mg (i.m.) range every 3-4 wk (about0.4 mg.kg-' -wk- ') (26). The supraphysiological dose of 10mg-k 1- wk- as used in the present study is consistentwith the high doses of AAS reported to have been used byathletes (14,20).As it is assumed that the AAS effect is more pronouncedin pretrained individuals (10), treatment with AAS startedafter the daily exercise reached a duration of 40 min. Todifferentiate exactly the effect of AAS, the absolute inten-sity and duration of the exercise of both training groups waskept constant from the beginning of treatment with ND/PIuntil the end of experiment. Thus, four experimental groupswere formed (N = 10): sedentary rats + PI (SP, controls);sedentary rats + ND (SND); trained rats + P1 (TP), andtrained rats + ND (TND). Two rats of the TP group droppedfrom experiment because of injuries and training protocolviolation.Submaximal running endurance test. Before thestart of training, after weeks 2 and 6,and at the beginning ofweek 9 all groups were subjected to a submaximal runningendurance test. SRE was determined in rats by having themrun at 27 m-min-, with 5 elevation of the belt until theycould no longer maintain their position on the treadmill belt.The time taken to reach this stage was assessed as SRE.

VO2max, VO2submax, and maximum time to ex-haustion assessment. At baseline, after week 6, and atthe beginning of week nine all groups were subjected toVO ax test according to Bedford et al. (5). The parameterswere measured using the Oxymax gas analyzing system forsmall animals (Columbus Instruments). The test was alwayscarried out after a 1-d recovery period. The volume of thesupplied air was 4.5 L-min- . The gas analyzers were cal-ibrated with a reference gas mixture before each test. TheO2maX test protocol involved stepwise increasing of thetreadmill speed and elevation as follows-I: 15 m min', 50elevation; II: 19 m min1, 100; ImI: 27 m min-1, 100; IV: 27m-min-1, 150; V: 30 m-min', 15; VI: 35 m-min', 15;and VII: 40 m-min-', 15. Each step of exercise was 3 min

long, and oxygen consumption (VO2) was measured atevery minute. Each rat was placed in the chamber 10 minbefore exercising, and the lowest value of those measuredduring the last 4 min was taken to be the rest consumption.The highest V02 measured at each workload was taken as ameasure of each rat's running economy (VO2,ubmax) for that


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workload, and at the last step, as 0nO2ma.Rats were removedfrom the test either when they could no longer maintain theirposition on the treadmill belt or in the plateau phenomenon (5).The time taken to reach V02max was defined as the maximumrunning time to exhaustion of each rat (18).Blood analysis. At the beginning of week 9, 10 d afterthe last administration of ND/PI and 23-25 h after the last''2max test, the rats were sacrificed under narcosis with 10mg.kg-' thiopental i.p. Mixed blood was collected intoheparinized tubes for investigation for amount of erythrocytes,mean corpuscular volume, hemoglobin and hematocrit. Allparameters were determined by a hematological analyzerCoulter T-660 (Coulter Electronics, Inc., I-ialeah, FL).Statistical analysis. To test for the two main effects(exercise training and AAS administration) and for the in-teraction between them, the results of all tests, which wererepeated several times during the experiment, were assessedby a two-way factorial analysis of variance for repeatedmeasures. The results obtained only at the end of the ex-periment were analyzed with a two-way factorial analysis ofvariance. The level of significance was set at P < 0.05.Tukey post hoc test was applied for intergroup differences.Data are presented as mean t SEM.RESULTS

Body mass and food intake. At baseline, all rats inthe groups had a similar body mass. During the experiment,the body weight of all rats gradually increased and at the endof the experiment the analysis failed to find any significantdifferences in their body mass: SP, 346.10 t 10.70 g; SND,323.30 10.70 g; TP, 323.25 11.96 g; TND, 340.40 10.70 g P > 0.05). There were no significant differencesbetween the groups in the amount of food taken during theexperiment (not shown).Submaximal running performance. At baseline, therats of all groups had similar SRE P > 0.05). Endurancetraining had a significant main effect on SRE measuredduring the study period (Fig. 1). The trained rats improvedsignificantly their SRE compared with baseline values (P


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line values (P < 0.001) and with the sedentary rats at week6 P < 0.01) and at the beginning of week 9 of experimentP < 0.001). We found no effect of ND treatment onmaximal endurance of both untrained and trained rats.Maximum oxygen consumption. Endurance traininghad a significant main effect on V02max. There were nodifferences between the groups in the VOmax measured atbaseline (P > 0.05) and after 6 wk P> 0.05) (Fig. 3). Atthe end of experiment the trained,rats VO2mCx was higherthan that of the sedentary rats by 4% (73.7 t 1.1mL-kg - minl vs 70.5 t 1.0 mL-kg -min'; P < 0.05).Between week 6 and the beginning of week 9, the TP andTND rats increased significantly their VO 2m.x (69.7 1.1mL.kg'- min-1 vs 74.1 1.2 niLkg'l-min-1, P < 0.01and 70.1 + 1.3 mL-kg- -min-1 vs 73.3 1.8mL.kg - min 1 , P = 0.01). ND treatment had no effect onVO?mo Of both untrained and trained rats.Running economy. At the end of experiment, the1O2submax measured in the first three steps during V2maxtest showed no differences between the groups. There was amain effect of training on running economy during thefourth step (27 m-min 1, 15 elevation) and the trained ratshad significantly lower V02submax than the sedentary rats(65.3 t 0.9 mL-kg- '-min- l vs 68.0 + 0.9 mL-kg7 1-min- ';P < 0.05). The V02subm. measured during the fifth, sixth,and seventh steps of exercise intensity were not analyzedbecause of the small and unequal number of measuredvalues in the groups. There was no effect of ND -treatmenton VO2submax of both untrained and trained rats in thedifferent steps of exercise intensity.There was a significant main effect of training onV02submax when it was analyzed as % O2 .ax (Fig. 4). Atthe first step the trained rats had lower values of %VO2maxthan sedentary by 5% P < 0.01), at the second step by 6%P < 0.05), at the third step by 7% P < 0.01), and at thefourth step by 9% P < 0.01). There was no effect of NDtreatment on %VO2max of both untrained and trained rats inthe different steps of exercise intensity.Oxygen carrying capacity. The results of the study ofblood oxygen carrying capacity assessed by the amount of

^80 -I.E 75E70 - s -S 2I

60 - -

4 50 -_ ,->45 _ _IT__

0 6 8Weeks

IOSP OSND 13TP *TND IFIGURE 3-Maximum oxygen consumption (mL-kg_1.min-1) of theinvestigated groups measured at the beginning of experiment and 6and 8 wk later. *P < 0.05 (trained vs untrained by 4 ).

erythrocytes, hemoglobin, hematocrit, and the mean corpus-cular volume of erythrocytes (MCV) are presented in Table1.All values of the red blood cells parameters measured inthe groups were within the physiologic reference values formale Wistar rats (6). There were no significant main effectsof training and AAS treatment on the erythrocyte count, butthere was a significant two-way interaction (P < 0.05). AAStreatment for 6 wk elevated the erythrocytes only in theSND group in comparison with SP P < 0.05), and therewas no effect on the TND group. Training resulted in higherred blood cell count only in TP in comparison with SP P 0.05). There was asignificant main effect of training on hemoglobin concen-tration and trained rats had higher hemoglobin than un-trained animals (161.56 1.42 g-L-1 vs 157.25 1.39g-L-1; P < 0.05). There was a significant main effect oftraining on hematocrit and trained rats had higher hemato-crit than sedentary rats (0.50 0.01 vs 0.47 0.01; P


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TABLE 1. Red blood cells parameters of the studied groups at the end of experiment; values are expressed as mean SEM.Variable SP N= 10) SND N 10) TP N = 8) TND N= 10 T vs S ND vs Pi T N

Erythrocytes 1012 1-) 7.86 + 0.18 * 8.67 0.22a , 8.78 0.21a 8.53 0.24 NS NSHemoglobin (g.L- ) 156.00 + 1.31 158.50 + 2.06 163.13 + 1.98 160.00 2.49 NS I NHematocrit (L.L- ) 0.47 0.01 0.47 0.01 0.51 0.01 0.49 + 0.01 ' NS NMCV tL) 59.70 0.98 55.04 0.72bc 59.19 + 1.14 58.61 0.64 NST vs S, rained vs sedentary main effect of training); ND vs PI, ND treated vs placebo treated main effect of ND treatment); T ND, two-way interaction.P< 0.05; ^,^ P< 0.01; IP 0.05 (in comparison with SP); bp 0.01 in comparison with SP); cp< 0.05 (in comparison with TP and TND).

training used and/or the treatment with AAS did not impairthe natural growth of the rats, and this is consistent with theresults reported by Van Zyl et al. (28).To our knowledge, this is the first study to show thatanabolic androgenic steroid treatment combined withendurance treadmill training in rats delays fatigue duringsubmaximal exercise. Our results have shown clearly thatsupraphysiological doses of nandrolone decanoate ad-ministered together with submaximal treadmill trainingimprove the SRE of male rats better than the trainingalone does. This was proved by the different magnitudeof SRE improvement of the two trained groups subjectedto a stable training identical in intensity and durationduring the treatment with AAS/placebo. These resultscorroborate the findings of a study on the combined effectof AAS and training on SRE of spontaneously runningmale rats (28).In contrast to AAS effect on SRE, treatment with nan-drolone decanoate did not increase the maximal runningtime to exhaustion to a greater extent than training alone.These different effects can be accounted for by the fact thatperformance SRE and maximal running time are dependenton different mechanisms. Davies et al. 9) report that sprinttraining in rats increases their maximal endurance and max-imal sprint speed, whereas it has no affect on muscle oxi-dative capacity or SRE. Differences in the degree and rate ofchange of both parameters in rats have been reported also insubmaximal training on treadmill (18).These results, supporting previous research (1), show thatAAS treatment does not increase the aerobic power either ofuntrained or endurance trained animals. The values ofVO2max we measured in the study are consistent with thedata about the Wistar male rats in the methodological studyof Bedford et al. 5) and to the established time parametersof change in rats. No change of VO2 .. x was found after 8wk of treadmill training (18), but increases of 14-18% havebeen reported with 10-12 wk of training (18,22). The 4%increase of V02max we established in this study at thebeginning of week 9 of training suggests that initial changeshave been registered in this parameter. We only observedthe plateau phenomenon in three rats tested. There are otherauthors reporting similar absence of plateau in the V02.axtest in part 5) or in all studied rats (18).The training protocol in this study exerted different ef-fects on the rate and extent of improvement in SRE andV02... In the trained rats, SRE increased significantly asearly as during the second week of training whereas the firstsignificant differences in VO2m X were found only at thebeginning of week 9 of experiment. The slight increase of

trained rats at the end of experiment suggests that chain VO2max cannot serve as an accurate predictor ofimprovement (18). Thus, the combined effect of submmal training and AAS treatment on SRE cannot beplained by changes in VOmax.Our results indicate that treatment with AAS doeschange running economy to a greater degree than trainalone. Higher running economy (lower VO2 at a specintensity of submaximal exercise) is considered an adtage in endurance sports as it leads to utilization of lopercentage of VO2max (17). This increases the running spat. equal 000 2 .nX and improves sports achievementssessed by the time (speed) needed to run a specific distaeven for trained athletes with similar values for VO2(4,7). Our results for VO2,Ubmax presented as VO2showed that submaximal training induced a better adation of the trained rats and lowered the degree of utilizaof their oXygen capacity in comparison with the untrairats subjected to exercise at the same absolute intensThere is a clear tendency towards increasing the differenin VOmax between the untrained and trained rats withincrease of exercise intensity. The absence of difference /VO2mnxbetween the two trained groups in this experimsuggests that although AAS improve the SRE of trainedthis might not improve performance assessed by the (speed) needed to run a definite distance in a greater dethan the training alone.A 6-wk treatment with AAS did not increase the bloxygen carrying capacity of the untrained rats, nor dincrease that of the trained rats, which shows that the efAAS have on SRE cannot be due to the increase of boxygen capacity. Our findings agree with the resultsstudies conducted with humans (2) and trained horsesin which at least 3 months of AAS treatment are requireincrease hemoglobin and/or red cell volume. As oxycarrying capacity is one of the factors determining V02(4) these data are consistent with the absence of differenin the values Of V02max we found between the TP and Tgroups at the end of experiment.Our results show that AAS treatment can increase Sonly in combination with endurance training. Although ndrolone decanoate failed to have any effects on SREuntrained rats, the interaction with training can be inpreted as AAS speeding up the adaptation processes cauby the training itself. The combined effect of NDtraining on SRE is not related to changes in variablestermining 02 transport to the working muscles. Therefour findings suggest that the improvement of SRE is duthe impact of AAS on 'exercise induced peripheral al


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provement of SRE is not due to the higher skeletal muscleoxidative capacity because data from other studies suggestthat AAS treatment on endurance-trained male rats does notincrease the mitochondrial enzyme activity (24,28) and theutilization of fats (13) in a greater degree than trainingalone. Although the physiological mechanisms for the AA Sinduced increase of the submaximal running endurance can-not be determined from the data presented here, some po-tential mechanisms can be suggested. Data from recentstudies show that nandrolone decanoate treatment in endur-ance treadmill-trained male rats improves contractile re-sponses of skeletal muscles (30) and may improve thetolerance to exercise training by increasing the levels ofstress protein HSP72 in fast-twitch fibers (12) more thantraining alone. Further studies are necessary to investigatewhether these effects of nandrolone decanoate on skeletalmuscles of trained male rats are related to the improvementof SRE. Although the present investigation demonstrates theimprovement of SRE of endurance-trained subjects after

treatment with supraphysiological doses of nandrolone de-canoate, care should be taken when one extrapolates datafrom animal models to humans. The abuse of high doses ofAAS by athletes is associated with many somatic and psy-chic adverse effects on health (20,29).In conclusion, the present findings show that treatmentwith AAS administered in combination with submaximalexercise on a treadmill enhances the SRE of male rats to agreater degree than does the training alone. AAS does notincrease V02max, and the oxygen carrying capacity and doesnot improve running economy more than training alone;therefore, these parameters cannot explain the improvementof SRE. These results suggest AAS treatment effects otherfactors not measured in this study to induce adaptationsleading to the increase of submaximal running endurance.

The authors thank Dr. P. Pavlov, Department of Clinical Chem-istry, Medical University Plovdiv, for his assistance with the study.This study was supported by grant 05/2001-02 from MedicalUniversity Plovdiv, Plovdiv, Bulgaria.REFERENCES

1. AMERICAN COLLEGE OF SPORTS MEDICINE. Position statement on theuse and abuse of anabolic-androgenic steroids in sports Med. SciSports Exerc. 19:534-539, 1987.

2. ANDERSON F. H., R. M. FRANcIs, and K. FAULKNER. Androgensupplementation in eugonadal men with osteoporosis: effects of 6months of treatment on bone mineral density and cardiovascularrisk factors. Bone 18:171-177, 1996.

3. ARIEL G., and W. SAVILLE. Anabolic steroids: the physiologicaleffects of placebos. Med. Sci. Sports 4:124-126, 1972.4. BAssEr, D. R., JR., and E. T. HOWLEY. Limiting factors for max-imum oxygen uptake and determinants of endurance performance.Med. Sci. SportsExerc. 32:70-84, 2000.5. BEDFORD, T. G., C. M . TiProN, N. C. WILSON R. A. OPPLIGER andC. V. GISOLR. Maximum oxygen consumption of rats and itschanges with various experimental procedures. J. AppL PhtysioL47:1278-1283, 1979.

6. BOYADJIEv N. Increasing of the aerobic working capacity of theorganism in submaximal training through the diet. DoctoralDis-sertation,Medical University, Dept. of Physiology, Plovdiv, Bul-garia, July 1996.7. CONLEY, D. I., and G. S. KRAHENBUHL. Running economy anddistance running performance of highly trained athletes. Med. Sci.Sports Exerc. 12:357-360, 1980.

8. COUNCIL oF SCIENTrlFC AFrAIRs. Medical and nonmedical uses ofanabolic-androgenic steroids. JAMA 264:2923-2927, 1990.9. DAVIES K. J. A., L. PACKER and G. A. BROOKS. Exercise bioen-ergetics following sprint training. Archt. Bioclein Bioplhys. 215:260-265, 1982.

10. ELAsHioFF J. D., A. D. JACKNOW S. G. SHAIN and G. D. BRAUN-srAIN. Effects of anabolic-androgenic steroids on muscularstrength. Ani. Intern. Med. 115:387-393, 1991.11. GREGG S. G., W. T. WILLIS and G. A. BROOKS. Interactive effectsof anemia and muscle oxidative capacity on exercise endurance.J Appl. Plhysio. 67:765-70,1989.12. GONZALES B., R. HERNANDO and R. MANSo. Anabolic steroid andgender-dependent modulations of cytosolic HSP70s in fast- andslow-twitch skeletal muscle. J Steroid Bioclhem. Mol. Bio. 74 :63-71, 2000.

13. GuzmAN, M., A. SABORIDO J. CAsTRo, F. MoLANo, and A. MEGIAS.Treatment with anabolic steroids increases the activity of themitochondrial outer carnitine palmitoyltransferase in rat liver andfast-twitch muscle. Biochetn PlharmacoL 41:833-835, 1991.

14. H-JALLAGAN J. B., L. F. HALLAGAN and M. B. SNYDER. Anabolic-androgenic steroid use by athletes. N. Engl. J Med. 321:1042-1045, 1989.

15. HICKSON R. C., S. M. CZERWINSKI M. T. FALDUTO and A. P.YOUNG. Glucocorticoid antagonism by exercise and androgenic-anabolic steroids. Med. Sci. Sports Exerc. 22:331-340, 1990.16. HYYPPA S., L. A. RaSXNEN S. G. B. PERSSON and A. R. Pos6.Exercise performance indices in normal and anabolic steroidtreated trotters. Equiine Vet. J. 18(Suppl.):443-447, 1995.17. JONES A. M., and H. CARTER. The effects of endurance training onparameters of aerobic fitness. Sports Med. 29:373-386, 2000.18. LAMBERT M. I., and T. D. NOAKES. Dissociation of changes inVO 2 ,,., muscle Q02, and performance with training in ratsJ. Appl. PlhysioL 66:1620-1625, 1989. i19. LAMBERT M. 1. and T. D. NOAKES. Spontaneous running increasesVO2.,, and running performance. J. Appl. Phiysio . 68:400-403,1990.20. LuKAs, S. E. Current perspectives on anabolic-androgenic steroidabuse. Trends Pharmacol. Sci. 14:61-68, 1993.21. MOORADIAN A. D., J. E. MouLr.y, and S. G. KoRENMAN. Biologicalactions of androgens. Endocrinol. Rev. 8:1-29, 1987.22. POWERS S. K. J. LAWLER D. CRISWELL F.-K. LiEu, and D. MARTIN.Aging and respiratory muscle metabolic plasticity: effects of en-durance training. J.AppL Phiysio . 68:2114-2118, 1992.23. RoGozKIN V. Metabolic effects of anabolic steroid on skeletamuscle. Med. Sci. Sports 11:160-163, 1979.24. SABORIDo A., J. VILA F. MOLANO and A. MEGIAS. Effect oanabolic steroids on mitochondria and sarcotubular system oskeletal muscle. J Appl. Phtysio. 70:1038-1043, 1991.25. STONE M. H., and H. LIPNER. Responses to intensive training andmethandrostenolone administration. 1. Contractile and performance variables. PflutgersArch. 375:141-146, 1978.26. TAMAKI T., T. SHlRAIstH H. TAKEDA T. MATSUMIYA, R. R. Royand V. R. EDERTON. Nandrolone decanoate enhances hypothalamic biogenic amines in rats. Med. Sci. Sports Exerc. 35:32-382003.27. TAMAKI T., S. UCHIYAMA Y. UCHIYAMA A. AKATsuKA R. R. Royand V. R. EDGERTON. Anabolic steroids increase exercise toleranceAm. J. Physiol. Endocrinol Metab. 280:E973-E981, 2001.28. VAN ZYL, C. G. T. D. NOAKES, and M. 1. LAMBERT. Anabolicandrogenic steroid increases running endurance in rats. Med. SciSports Exerc. 27:1385-1389, 1995.

29. YESALIS, C. E., and M . S. BAHRKE. Anabolic-androgenic steroidsSports Med. 5:326-340, 1995.30. YOUMAA W. H., and C. LEory. Differential effects of nandrolonedecanoate in fast and slow rat skeletal muscles. Med. Sci. SporExerc. 33:397-403, 2001.


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TITLE: Effects of Nandrolone Decanoate on VO2max, Running

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effects of nandrolone decanoate on vo2max running econom

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