Time Course of Performance Changes and Fatigue Markers During Intensifed Training in Trained Cyclists

8/12/2019 Time Course of Performance Changes and Fatigue Markers During Intensifed Training in Trained Cyclists

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doi:10.1152/japplphysiol.01164.200193:947-956, 2002. First published Apr 5, 2002;Journal of Applied Physiology

Gleeson, David A. Jones and Asker E. JeukendrupShona L. Halson, Matthew W. Bridge, Romain Meeusen, Bart Busschaert, Michaelmarkers during intensified training in trained cyclistsTime course of performance changes and fatigue

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Time course of performance changes and fatigue markersduring intensified training in trained cyclists

SHONA L. HALSON,1,2 MATTHEW W. BRIDGE,1 ROMAIN MEEUSEN,3 BART BUSSCHAERT,3

MICHAEL GLEESON,1 DAVID A. JONES,1 AND ASKER E. JEUKENDRUP11Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham,

Edgbaston, Birmingham, B15 2TT, United Kingdom; 2School of Human Movement Studies,

Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia; and 3Department

of Human Physiology and Sportsmedicine, Vrije Universiteit Brussel, B-1050 Brussels, Belgium

Received 26 November 2001; accepted in final form 3 April 2002

Halson, Shona L., Matthew W. Bridge, RomainMeeusen, Bart Busschaert, Michael Gleeson, David A.Jones, and Asker E. Jeukendrup. Time course of perfor-mance changes and fatigue markers during intensified train-ing in trained cyclists. J Appl Physiol 93: 947956, 2002.First published April 5, 2002; 10.1152/japplphysiol.01164.

2001.To study the cumulative effects of exercise stress andsubsequent recovery on performance changes and fatigueindicators, the training of eight endurance cyclists was sys-tematically controlled and monitored for a 6-wk period. Sub-

jects completed 2 wk of normal (N), intensified (ITP), andrecovery training. A significant decline in maximal poweroutput (N 338 17 W, ITP 319 17 W) and a significantincrease in time to complete a simulated time trial (N 59.4 1.9 min, ITP 65.3 2.6 min) occurred after ITP inconjunction with a 29% increase in global mood disturbance.The decline in performance was associated with a 9.3% re-duction in maximal heart rate, a 5% reduction in maximaloxygen uptake, and an 8.6% increase in perception of effort.Despite the large reductions in performance, no changeswere observed in substrate utilization, cycling efficiency, and

lactate, plasma urea, ammonia, and catecholamine concen-trations. These findings indicate that a state of overreachingcan already be induced after 7 days of intensified trainingwith limited recovery.

cycling; overtraining; overreaching; overload

THE BALANCE BETWEEN TRAININGand overtraining is oftena very delicate one. Many athletes incorporate hightraining volumes and limited recovery periods intotheir training regimes. This may disrupt the fragilebalance, and the accumulation of exercise stress mayexceed an athletes finite capacity of internal resis-tance. Often this can result in overreaching, defined as

an accumulation of training and/or nontraining stressresulting in a short-term decrement in performancecapacity, in which restoration of performance capacitymay take from several days to several weeks (17). It isgenerally believed that if the imbalance between train-ing and recovery persists, this may result in an accu-mulation of training and/or nontraining stress result-

ing in a long-term decrement in performance capacity,in which restoration of performance capacity may takeseveral weeks or months. This condition is termedovertraining (17).

Increased exercise stress is manifested in physiolog-ical and biochemical changes and is often in conjunc-tion with psychological alterations, all of which resultfrom an imbalance in homeostasis (10). However, thequantity of training stimuli that results in either per-formance enhancement or a chronic fatigue state ispresently unknown. Of the current information regard-ing training regimes and protocols, most is derivedfrom conjectural or experiential sources and has littleresearch support. Because it is difficult to ascertain thevolume of training that will result in overreaching orovertraining, it is necessary to identify markers thatdistinguish between acute training-related fatigue andoverreaching.

Similarly, much of our knowledge about overtraining

is derived from cross-sectional studies and anecdotalinformation (2, 14). Although a number of studies haveused a longitudinal approach (8, 19, 22, 24, 27), inmany cases failure to adequately monitor performancemeans we know little about the time course of changesof potential indicators of overreaching and earlyphases of the overtraining syndrome.

The aim of this investigation was to identify the timecourse of changes in selected physiological, biochemi-cal, and psychological parameters during 2 wk of in-tensified training and 2 wk of recovery in trainedcyclists. To ascertain the time course and fluctuationsof these changes, repeated performance tests were con-ducted. To our knowledge, this is one of the first at-

tempts to systematically induce a state of overreachingwhile monitoring training stress and performance in asupervised and highly controlled environment. We hy-pothesize that the intensified training program em-ployed will result in a state of overreaching, identifiedby a reduction in performance and an increase in globalmood disturbance. In addition, we hypothesize that the

Address for reprint requests and other correspondence: A. E.Jeukendrup, Human Performance Laboratory, School of Sport andExercise Sciences, Univ. of Birmingham, Edgbaston, B15 2TT Bir-mingham, UK (E-mail: [email protected]).

The costs of publication of this article were defrayed in part by thepayment of page charges. The article must therefore be herebymarked advertisement in accordance with 18 U.S.C. Section 1734solely to indicate this fact.

J Appl Physiol93: 947956, 2002.First published April 5, 2002; 10.1152/japplphysiol.01164.2001.

8750-7587/02 $5.00 Copyright 2002 the American Physiological Societyhttp://www.jap.org 947


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intensified training will result in a decrement in per-formance during the initial period of training; however,consistent elevations in mood disturbance will not oc-cur until later during the intensified training period. Itis hypothesized that laboratory-assessed performancewill continue to decline throughout the intensifiedtraining period and will return to baseline or abovebaseline levels on completion of a recovery period.Changes in performance will occur along with changesin maximal physiological parameters [i.e., heart rate,oxygen consumption (V O2)]; however, substrate utiliza-tion, cycling efficiency, and other biochemical indica-tors will remain unchanged.

METHODS

Subjects. Eight endurance-trained male cyclists volun-teered for this study. All subjects had competed for at least 2yr and were training a minimum of 3 days/wk. The study wasapproved by the South Birmingham Local Research EthicsCommittee. Before participation, and after both comprehen-sive verbal and written explanations of the study, all subjectsgave written, informed consent. Subject characteristics arepresented in Table 1.

Experimental protocol. Subjects were familiarized to thetest procedures by completing both a maximal cycle ergome-ter test (MT) and a time trial (TT) in the week preceding thestudy commencement. No subjects exhibited signs or symp-toms of overreaching or overtraining on the basis of the

previously mentioned definitions (18); i.e., during the 2 wk ofbaseline training maximum power output was unchangedand mood state was within normal ranges for athlete popu-lations.

The training of each subject was then controlled and mon-itored for a period of 6 wk in total, which was divided intothree distinct phases each of 2-wk duration (Fig. 1). The firstphase consisted of moderate training with a small numberexercise testing sessions. Subjects completed their normal orusual amount and type of training (Fig. 1).

The second phase consisted of an increase in trainingvolume and intensity (Fig. 1) as well as the number ofexercise tests performed. Subjects trained 7 days/wk forthese 2 wk in addition to the laboratory tests. A similarprotocol has previously been shown to induce a state of

overreaching in the time frame specified (15). The thirdphase of the study was one of reduced training (Fig. 1) andaimed to provide subjects with a period of recovery.

To describe the time course of the changes in performanceand potential indicators of overreaching, subjects performedthree different exercise tests at regular intervals during theexamination period (Fig. 1). Each individual test was per-formed at the same time of day. A total of 20 exercise testswere performed per subject, 10 of which were in the over-training phase. In total, subjects underwent six MTs, six TTs,and eight intermittent tests (ITs).

Training quantification. Each subject received a PolarVantage NV heart rate monitor (Polar Electro, Kempele,

Finland) for the duration of the study. Each subject wasgiven a training diary to record duration of training, distancecovered, average heart rate, maximal heart rate, andweather conditions. Subjects recorded all training sessions,which were downloaded to a computer using the Polar Inter-face (Polar Electro). From this information, average heartrate, maximal heart rate, and time spent in each of the heartrate zones could be calculated and verified against the train-ing diary.

The majority of subjects performed their training outdoors;however, on occasion, subjects trained inside the laboratory ifweather conditions prevented them from training outdoors.Subjects were encouraged to consume a carbohydrate-richdiet and to remain euhydrated during the entire experimen-tal period.

After each maximal test, subjects training zones werecalculated from their individual lactate and heart ratecurves. Lactate threshold was determined by using the max-imal distance (Dmax) method as described elsewhere (4).Five training zones were calculated and expressed as per-centages of individual maximum heart rate. The trainingzones for the eight subjects before the intensified trainingperiod were, on average, as follows: zone 1 69% maximalheart rate; zone 2, 6981% maximal heart rate; zone 3,82 87% maximum heart rate;zone 4,8894% maximal heartrate; zone 5, 94% maximal heart rate.

Subjects training programs for the intensive trainingweeks were based on their current amount of training in the2-wk baseline period. In the 2 wk of intensive training, theresearchers aimed to increase the amount of time the sub-

jects trained in zones 3, 4, and 5. This was achieved bydesigning individual training programs that doubled normal

Fig. 1. Study design. MT, maximal cycle ergometer tests (maximaloxygen uptake); TT, time trial; IT, intermittent test; shaded areas,moderate- to high-intensity training.

Table 1. Selected characteristics of the subjects at week 1

Age, yr Height, cm Body Mass, kg Body Fat, % V O2 max, ml kg1 min1

Mean SE 27.13.0 179.71.9 73.72.5 14.61.1 58.01.7

V O2 max, maximal oxygen consumption.

948 TRAINING AND PERFORMANCE

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training volumes. The majority of the increase in trainingvolume was in the form of high-intensity training, i.e., abovethe lactate threshold (Fig. 2).

MT. Subjects arrived at the laboratory after an overnight

fast, and a Teflon catheter (Becton-Dickinson, Quickcath)was inserted into an antecubital vein. After this, the subjectsperformed an incremental test to exhaustion on an electri-cally braked cycle ergometer (Lode Excalibur Sport, Gro-ningen, The Netherlands) to determine maximal power out-put (Wmax), submaximal and maximal V O2, and heart ratethroughout the test.

Resting data were collected before subjects began cyclingat 95 W for 3 min. The load was increased by 35 W every 3min until volitional exhaustion. Expiratory gases were col-lected and averaged over a 10-s period, by using a comput-erized on-line system (Oxycon Alpha, Jaeger, Bunnik, TheNetherlands). Wmax was determined using the equation

Wmax Wfinal (t/T) Winc (1)

where Wfinal (W) is the power output during the final stagecompleted, t (s) is the amount of time reached in the finaluncompleted stage, T(s) is the duration of each stage, andWinc (W) is the workload increment.

Heart rate was recorded throughout the exercise test usinga heart rate monitor (Polar Vantage NV). Rating of perceivedexertion (RPE) was recorded at the end of each stage, byusing the modified Borg scale (3).

Blood samples were collected at rest, in the last 30 s of eachstage, and immediately after the cessation of the test for thedetermination of blood lactate, plasma urea, plasma ammo-nia, and catecholamine concentrations. Blood samples wereimmediately analyzed for lactate (YSI 2300 STAT Plus, Yel-

low Springs Instruments, Yellow Springs, OH). Heparinizedblood samples were centrifuged for 10 min at 1,500 g. Plasmawas stored at 20C and analyzed for ammonia (model171-UV, Sigma Chemical, Poole, UK) and urea (model 640,Sigma Chemical).

Plasma epinephrine, norepinephrine, and dopamine weremeasured by HPLC with electrical detection (BioRad, Naz-areth, Belgium). Interassay coefficients of variation for epi-nephrine and norepinephrine were 7.8 and 4.2%, respec-tively.

From carbon dioxide production and V O2, rates of carbohy-drate and fat oxidation were calculated by using stoichiomet-ric equations (6).

Gross efficiency (GE) was calculated by using the for-mula (11)

GE (power/EE)100% (2)

where EE is energy expenditure.Cycling economy was calculated by using the formula (28)

Economy (J/l) power

V

O2

(3)

TT. After a 5-min warm-up at 50% Wmax, subjects per-formed a simulated TT in which a target amount of work wasto be completed in as short a time as possible. The amount ofwork to be performed was calculated by assuming that sub-

jects could cycle at 75% of their Wmax for 60 min, and thusthese TTs lasted 60 min for all subjects. The formula forthis is described elsewhere (16) and is as follows

Total amount of work 0.75Wmax3,600 s (4)

For each of the TTs, the ergometer was set in the pedaling-dependent mode so as to replicate as accurately as possible aTT in a field setting. Thus power varies with cadence (rpm)and is represented by the following formula

W L (rpm)2 (5)

Hence, the work rate (W) measured in watts is equal to thecadence squared [(rpm)2] multiplied by the linear factor (L).

L was based on each subjects Wmax and calculated so that75% Wmax was produced at a pedaling rate of 90 rpm. Withuse ofEq. 5, L could be calculated by W/(rpm)2.

A computer was connected to the ergometer, and work,power, and time were recorded. However, subjects receivedlittle information other than the amount of work performedand the present amount of work relative to the total to becompleted. Subjects received no feedback on time, W, ca-dence, or heart rate. Any changes in TT performance inresponse to the intensified training were determined by ex-amining changes in time taken to complete the set amount of

work for each subject.Subjects were required to fast for at least 3 h before each

test. Blood samples were taken before and immediatelyafter each test and were analyzed for lactate. Heart ratewas monitored continuously throughout the test (Polar

Vantage NV).IT. Unlike the TT, the IT was of a set duration and a

change in work production was assessed. Subjects completeda 5-min warm-up at 50% Wmax followed by two 10-min boutsof maximal exercise. Each subject was given a 5-min restbetween bouts.

Subjects were asked to cycle ashardas possible for eachof the 10-min bouts. Similar to the TT protocol, the ergometerwas set in the pedaling-dependent rate mode. However, inthis case the W was set as 90% Wmax. The ergometer was

again connected to a computer as in the TTs; however, sub-jects only received information on time and power indicatedgraphically. Heart rate was recorded continuously through-out the test (Polar Vantage NV).

Any changes in IT performance over time were analyzed byexamining both work and power for each of the bouts. Sub-

jects again fasted for at least 3 h before testing. Bloodsamples were taken before the test and on completion of thesecond exercise bout and were assayed for lactate concentra-tion.

Questionnaires.Every day for the duration of the study,subjects completed both the Daily Analysis of Life Demandsof Athletes (DALDA) (29) and the short form of the Pro file of

Fig. 2. Changes in time spent in heart rate zones during normaltraining (N), intensified training (ITP), and recovery (R).

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Mood States (POMS) questionnaire (POMS-22) (25). TheDALDA is divided into parts A and B, which represent thesources of stress and the manifestation of this stress in theform of symptoms, respectively. Subjects were asked to com-plete these questionnaires at the same time of each daybefore training. Subjects also completed the 65-question ver-sion of the POMS (25) once a week on the morning of the MT.Global mood state was determined by using the methoddescribed by Morgan et al. (26).

Additional measurements. Once per week a number ofadditional measurements were taken. Skinfold measure-ments were made to estimate percent body fat, and bodyweight was also measured. Subjects also recorded theirmorning resting heart rate every day for the duration of thestudy with the heart rate monitor (Polar Vantage NV).

Statistical analysis. One-way analysis of variance withrepeated measures was used with least significance differ-ence comparison performed to identify significant differencesbetween the individual means. The level of significance wasset at 0.05.

RESULTS

Subjects completed 2 wk of normal training (7 2h/wk), 2 wk of intensified training (14 5 h/wk), and afinal 2 wk of recovery training (3.5 2.5 h/wk) (Fig. 2).The laboratory tests were included during the calcula-tion of total hours of training completed in each period.The intensified training period predominantly con-sisted of high-intensity interval training, with signifi-cant increases in training inzones 3, 4,and5(450, 200,and 147%, respectively). The previous criteria for thedetection of overreaching set by Jeukendrup et al. (15)were used to determine whether the training protocolresulted in overreaching. The criteria to be met were 1)a reduction in performance in the laboratory tests and2) increased affirmative responses to questionnairesthat assessed impaired general health status, negativemood, psychological status, and feelings of fatigue.

All eight subjects completed the intensified trainingperiod and met the criteria for overreaching at theconclusion of the 2-wk intensified training phase. Someof the observed responses to intensified training in-cluded reduced performance in the form of reducedWmaxduring the MT, increased time taken to completethe TT, and a reduction in average work producedduring the IT. Maximal heart rate was reduced in allthree tests and responses to all questionnaires com-pleted were altered.

MT. After the 2 wk of intensified training, Wmax

significantly declined (Fig. 3A) and at completion of therecovery phase was unchanged from baseline values.After 1 wk of intensified training, Wmaxduring the MThad declined in six of the eight subjects. In the othertwo subjects, Wmax remained unchanged. On averageWmaxdeclined 3.3% duringweek 1 of intensified train-ing and 5.4% during week 2 of intensified training.Maximal V O2 (l/min) significantly declined (4.5%) af-ter the intensified training period; however, itwas unchanged after week 1 of intensified training.There were no changes in submaximal V O2 at 200 W(Table 2).

There was a 15 beats/min decline in maximal heartrate during the MT as a result of the intensified train-

ing (Fig. 3B); however, submaximal heart rate (at 200W) remained unchanged (Table 2). Maximal lactateconcentrations from the MT were lower in the intensi-fied training period; however, this did not reach statis-tical significance (Table 2). There were also no signifi-cant changes in resting or submaximal concentrationsof plasma lactate (Table 2). RPE scores reported at200 W were significantly increased during intensifiedtraining and after 2 wk of recovery were significantlylower than baseline scores (Table 2).

TT. Time taken to perform the TT significantly in-creased by 9.8% from 59.4 min during N to 65.3 min at

Fig. 3. Changes in maximum power output (A), maximum heart rate(B), and total scores of the 65-item version of the Profile of MoodStates questionnaire (POMS-65; C) during normal training, intensi-fied training, and recovery. bpm, beats/min. 1 Significantly differentfrom test 1, P 0.05. 2 Significantly different from test 2, P 0.05.3 Significantly different fromtest 3, P 0.05. 4 Significantly differentfrom test 4, P 0.05. 5 Significantly different from test 5, P 0.05.6 Significantly different from test 6, P 0.05.




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the end of thefirst week of intensified training (Fig. 4).Subjects on average took 4 min and 30 s longer tocomplete the given amount of work. Correspondingly,average power declined during intensified training andslightly but nonsignificantly increased after recoverytraining (Table 3). A decline in maximal heart rate and

average heart rate were noted in the TT after intensi-fied training (Table 3). Resting and maximal bloodlactate concentrations from the TT did not changesignificantly over the training period.

IT. Average work over the complete IT was signifi-cantly reduced during intensified training and re-turned almost to baseline on completion of R training(Table 3). Average heart rate also declined (Table 3).Resting IT blood lactate concentrations were un-changed; however, maximal lactate concentrationswere significantly reduced (Table 3).

Time course of changes.The changes in performanceof the three exercise tests, expressed as a percentage ofinitial values, all show a similar time course of change

over the study period (Fig. 5). For both the TT and IT,the greatest reduction in performance occurs aroundthe middle of the intensified training period. Althoughthe decrease in performance toward the end of theintensified training period is still large, performancedoes not continually decrease. In all tests there is a

gradual decrease in performance until approximatelymidway through the intensified training period.

Biochemical and hormonal variables. Restingplasma ammonia and urea concentrations were un-changed throughout the testing period (Table 4). Rest-ing and maximal plasma epinephrine, norepinephrine,

and dopamine concentrations were also not differentduring the 6-wk training period (Table 4).

Substrate oxidation and cycling efficiency. Carbohy-drate and fat oxidation were unchanged over the 6-wkperiod. Fat oxidation had a tendency to be increasedduring the intensified training period; however, thiswas not statistically significant (Table 4). Submaximalefficiency, submaximal economy, and maximal economywere unaffected by the intensified training (Table 4).

Additional measures.Body weight and percent bodyfat significantly declined throughout the testing periodand were lowest after recovery training (Table 4). Dur-ing the intensified training period, resting heart rate

was not different than during normal training; how-ever, it was slightly, but significantly, than lower dur-ing recovery training (Table 4).

Questionnaire responses.Global mood state scores onthe POMS-65 were significantly increased from 90.4during normal training to 116.4 during the intensifiedtraining period (Fig. 3C). On completion of recoverytraining, scores returned to 91.5. From this question-naire, the subscales of tension, fatigue, and confusionwere also significantly elevated, whereas vigor signifi-cantly declined. No changes were evident in the de-pression or anger subscales. Altered mood states werealso identified by the POMS-22, with significantly ele-

vated total scores.Parts A and B of the DALDA were both increasedduring the intensified training period; however, onlypart B was significantly higher than during normaltraining (Fig. 6). The most common changes in sourcesof stress, as identified by part A of the DALDA, wererelated to sport training, sleep, and health. Part B ofthe DALDA showed the greatest changes during thethe intensified training period, with the majority ofsubjects showing changes on many of the items. Themost common alterations in responses were increasedproblems associated with the following areas: need for

Table 2. Selected changes in maximal test variables over the course of the study period

Maximal Test

N ITP R

P ValueWeek 1 Week 2 Week 3 Week 4 Week 5 Week 6

Maximal responsesV O2 max, ml/min 4,271187 4,372197 4,391196 4,078198* 4,110193* 4,380193 0.002V O2 max, ml kg1 min1 58.01.73 59.01.49 60.01.88* 55.51.50 56.51.90 60.61.60 0.002Maximal lactate, mmol/l 7.20.6 7.80.7 7.20.7 6.70.6 7.70.4 7.40.6 0.224

Submaximal responsesV O2 at 200 W ml/min 2,85272 2,76646 2,87339 2,82175 2,83467 2,74855 0.384HR at 20 0 W, b ea ts/min 1527 1468 1477 1456 1487 1488 0.063Lactate at 200 W, mmol/l 1.20.2 1.30.3 1.10.3 1.30.2 1.30.2 1.20.2 0.665RPE at 200 W 9.40.8 9.20.9 10.01.3 10.91.2* 9.41.1 8.50.8 0.011

Values are means SE. N, normal training; ITP, intensified training; R, recovery; V O2, oxygen consumption; HR, heart rate; RPE, ratingof perceived exertion. *Significantly different from N, P 0.05. Significantly different from R,P 0.05.

Fig. 4. Changes in time taken to complete TT during normal train-ing, intensified training, and recovery. 1 Significantly different fromtest 1, P 0.05. 2 Significantly different from test 2, P 0.05.3 Significantly different fromtest 3,P 0.05. 4 Significantly differentfrom test 4, P 0.05. 5 Significantly different from test 5, P 0.05.6 Significantly different from test 6, P 0.05.




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a rest, recovery, irritability, between-session recovery,general weakness, and training effort.

DISCUSSION

It is generally assumed that overtraining resultsfrom chronic exercise stress in the presence of aninadequate regeneration period. However, there are

nondistinct phases in the development of overtraining,which has been termed the overtraining continuum (9).The first phase along this continuum relates to thefatigue experienced after an isolated training session.Further intense training with insufficient recovery canlead to overreaching and increased complexity andseverity of symptoms (9). Finally, if high training loadsare continued with insufficient recovery from the over-

reached state, the overtraining syndrome may develop.Currently, there is no literature or information avail-able to discriminate between the early and late phasesof this continuum (9). To our knowledge, this is thefirststudy to attempt to identify the changes that occur inthe transition from acute fatigue to overreaching.

A number of examinations have measured perfor-

mance before and on completion of increased volumeand/or intensity training (5, 24, 33), whereas few haveexamined changes in performance during increasedtraining (15, 23). Lehmann et al. (19) reported a num-ber of performance changes before, during, and oncompletion of 4 wk of increased volume training inrunners. Subjects showed a decline in total runningdistance during incremental ergometric exercise after2 wk of training; however, performance was not signif-icantly reduced until after 4 wk of training was com-pleted. This may, in part, be explained by the gradedincrease in volume throughout the 4-wk period. Jeuk-endrup et al. (15) included examinations of TT perfor-mance before, at the midpoint, and after a 2-wk period

of intensified training in cyclists. Similar to the presentinvestigation, TT performance had declined signifi-cantly after 1 wk of training, although it declinedfurther after an additional week.

The present study incorporated an increased numberof performance assessments, including four TTs andfour ITs during the increased training period, in addi-tion to initial and recovery assessments. From theinformation on the time course of performancechanges, it appears that overreaching may be inducedafter a period of 7 days. Although TT performance wasdecreased during the first several days of increased

Fig. 5. Time course of changes of the exercise tests, expressed as apercentage of baseline, during normal training, intensified training,and recovery. F and dashed line, MT; and solid line, TT; anddotted line, IT.

Table 3. Selected changes in time trial and intermittent test variables over the course of the study period

N ITP R

PValueWeek 1 Week 2 Week 3 Week 4 Week 5 Week 6

Time trialMaximal HR,

beats/min 1793 1733* 1682* 1734* 1714* 1823 0.001Average HR,

beats/min 1623 1613 1562 1562 1564 1702 0.002Average

power, W 261.718.5 240.016.2* 239.517.1* 247.919.0 241.613.4 265.116.7 0.005Resting

lactate,mmol/l 1.320.23 1.290.24 0.930.12 1.290.27 1.090.11 1.430.35 0.292

Maximallactate,mmol/l 8.060.83 5.87.24 5.871.39 7.870.92 6.820.65 7.540.75 0.198

Intermittenttest

Averagework, kJ 181.310.1 171.210.3 169.810.6* 164.48.8* 169.18.9* 166.612.0* 172.99.7 177.88.7 0.001

Average HR,beats/min 1685 1664 1606* 1573* 1633* 1622 1714 1733 0.048

Restinglactate,

mmol/l 1.330.25 1.220.16 1.300.30 1.300.20 1.220.22 0.940.12 1.670.34 1.520.36 0.105Maximal

lactate,mmol/l 10.391.25 8.521.45 8.351.26* 8.451.35* 8.380.92 8.541.33 10.541.11 10.770.96 0.017

Values are means SE. *Significantly different from N, P 0.05. Significantly different from R, P 0.05.




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training, subjects could not be considered overreachedbecause mood state was unaltered. On the first day ofthe intensified training period subjects completed along-duration, high-intensity ride, and thus the initialdecline in performance most likely reflected fatiguefrom the previous training session. Therefore, al-though performance was significantly lower than base-line, subjects were acutely fatigued as opposed to over-reached. It is likely that complete recovery would haveoccurred within a few days. However, the continualexercise stress, without regeneration, results in failingadaptation and altered biochemical, physiological, and

psychological states (10), which identify the athletes asreaching a chronic as opposed to acute fatigue state.To determine whether a reduction in performance is

the result of acute fatigue from previous exercise, orfrom overreaching, the DALDA questionnaire may beeffective and practical. As described by Rushall (29), aperiod of baseline assessment should occur, with therecognition that scores may oscillate because of fatigue

from isolated training sessions. However, if scores re-main elevated for 4 consecutive days, a period of restshould occur. As can be seen from Fig. 6, scores fromthe questionnaire oscillate during normal training.However, scores are continually and consistently ele-vated above baseline for the minimum of 4 consecutivedays, approximately midway through the intensifiedtraining period. Thus, with the use of psychologicalquestionnaires, it is possible to discriminate acute fromchronic or excessive fatigue in the presence of uniformperformance decrements. Figure 6 suggests that in thisparticular investigation it took 37 days of intensified

training before overreaching developed.Continual intensive training after 7 days does not

result in further performance decrements; however,performance is still significantly below that of baselinevalues. It appears that subjects become somewhat tol-erant to the increased training, and this was expressedby a number of the subjects. A number of subjectsstated that they had reached a level of maximal fatigueand lethargy after thefirst week of training. Continuedtraining, therefore, did not result in a decline in per-formance because of the already high levels of fatigue.Interestingly, mood state continued to decline in thefinal week of intensified training. All exercise tests

employed in this study showed a similar time course ofchange (Fig. 5); however, the two performance tests(TT and IT) showed a similar magnitude of decline inperformance when expressed as change from baseline.It is important to consider the training status of theindividuals who participated in this study and to ap-preciate possible differences in responses betweenthese cyclists and elite or world-class athletes. It ispossible that the physiological, biochemical, and psy-chological responses observed in the present group ofmoderately trained cyclists may be similar to those ofmore highly trained cyclists. However, it is impossible

Fig. 6. Changes in Daily Analysis of Life Demands of Athletes(DALDA) part B a scores, indicating that symptoms are worsethan normal during normal training, intensified training, and re-covery.

Table 4. Selected changes in additional measures over the course of the study period

Additional Measures

N ITP R

PValueWeek 1 Week 2 Week 3 Week 4 Week 5 Week 6

Maximal plasma epinephrine,nmol/l 4.613.36 2.712.20 4.671.74 1.450.70 5.573.76 4.972.55 0.568

Maximal plasmanorepinephrine, nmol/l 24.8216.37 18.7212.71 34.1515.70 20.4811.52 33.449.90 31.8513.65 0.541

Maximal plasma dopamine,nmol/l 12.186.69 13.796.76 14.911.14 17.111.23 14.991.52 15.251.47 0.135

Maximal economy, J/L 4.70.1 4.70.1 4.60.1 4.70.1 4.70.1 4.60.1 0.361Economy at 200 W 4.20.1 4.30.1 4.20.1 4.30.1 4.20.1 4.40.1 0.456GE at 200 W 18.00.4 19.10.3 18.50.4 19.10.5 18.10.4 19.00.6 0.223CHO oxidation at 200 W,

g/min 3.120.09 2.750.21 2.60.22 2.60.21 2.840.16 2.430.19 0.303Fat oxidation at 200 W, g/min 0.340.04 0.350.09 0.460.07 0.440.07 0.340.06 0.410.05 0.081Resting HR, beats/min 521 471 541 531 511 491 0.004POMS-22 0.30.7 0.30.7 2.00.8 2.81.3* 0.20.2 1.00.6 0.019Plasma urea, mmol/l 2.20.2 2.30.1 2.60.2 2.80.2 2.40.1 2.40.2 0.057Plasma ammonia, mol/l 38.67.5 60.214.4 45.115.3 60.814.4 40.514.9 48.112.9 0.067Body weight, kg 73.72.5 74.02.5 73.22.4* 73.32.3 72.72.2* 72.22.3* 0.001Body fat, % 14.61.1 14.31.1 13.81.2* 13.21.0* 13.11.1* 13.31.2* 0.001

Values are means SE. GE, gross efficiency; CHO, carbohydrate; POMS-22, short form of the Profile of Mood States questionnaire;DALDA, Daily Analysis of Life Demands of Athletes.




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to speculate on the time course of changes and thevolume of training necessary to induce similar alter-ations in performance in elite cyclists.

At the end of thefirst week of the intensified trainingperiod, it took the subjects 9.8% longer to complete thesimulated TT. Given that the daily variation of thistest is 3% (16), the major decline in performance canbe attributed to the effects of the intensified training

protocol. Similarly, Jeukendrup et al. (15) reported a5% increase in time taken to complete a TT. Thisincrease in time taken to complete an 8.5-km TT (15) issomewhat lower than the 9.8% found in this investiga-tion. The TT performed by the subjects in the presentstudy was of longer duration (to approximate a 40-kmTT), which may explain the different results from thoseof the earlier study (15).

Lehmann et al. (19) reported an 8% decline in totalrunning distance during incremental ergometric exer-cise in eight middle- and long distance runners whoperformed 3 wk of increased volume training, from 85to 174 km/wk. A 29% reduction in time to fatigue wasfound in a group offive elite soldiers after 10 days ofincreased-intensity running training (8). A similar de-cline in time to fatigue on a cycle ergometer (27%) wasreported by Urhausen et al. (33) after an undefinedindividual increase in intensive training. From theinformation derived from the present study and thosementioned above, it appears that the longer the dura-tion of the exercise bout the larger the impact of over-reaching on performance.

Changes in mood state as assessed by the DALDAand POMS occurred alongside the performance reduc-tions. Continued elevateda scores, indicating symp-toms are worse than normal can be a useful tool indetermining early overreaching. The subscales of the

POMS may be useful to identify psychological aspectsthat may be disturbed in individual athletes. Changesin mood state are highlighted in the overtraining liter-ature, and the POMS has been found to show signifi-cant changes during overreaching and overtraining inother studies as well as the present investigation (7,13, 27).

Presently, the mechanisms behind the reduction inperformance are relatively unknown. Glycogen deple-tion has been previously suggested as a cause of theunderperformance characteristic of overtraining (5).Intensive training may result in a decline in glycogenstores and an increased reliance of fat metabolism.However, the results of this study suggest that sub-

strate metabolism was unchanged after intensifiedtraining. Other evidence to suggest that subjects in thepresent study were not glycogen depleted includes un-changed resting, submaximal, and maximal blood lac-tate concentrations.

It has also been suggested that some of the perfor-mance changes that occur with overtraining and over-reaching may be due to reduced efficiency (1). Inade-quate recovery of cellular homeostasis can lead tofatigue of motor units and thus additional, less efficientmotor units may need to be recruited in a bid tomaintain performance (9). To our knowledge, this is

the first study to systematically investigate eithergross efficiency or economy after a period of intensifiedtraining. No changes in either of these variables werenoted in this investigation, and thus there is presentlyno evidence to suggest that changes in gross efficiencyor economy can explain the performance deteriorationthat occurs with overreaching or overtraining. Othersuggested mechanisms have included changes in met-

abolic enzyme concentrations and chronic dehydration(31). However, it would be expected that chronic dehy-dration would result in an increase in submaximalheart rate to maintain cardiac output. This was notevident in this study or other overtraining investiga-tions (15, 19, 30, 33).

The mechanism(s) for the reduced maximal perfor-mance appears to be related to the generation of fa-tigue before the maximal engagement of the cardiore-spiratory and/or metabolic systems. The underlyingcause(s), of fatigue is not clear. However, from thisstudy it appears that subjects demonstrate an in-creased perception of exertion, identified by signifi-cantly higher submaximal RPE scores.

During the intensified training period, maximalheart rate was decreased in all three performancetests. Jeukendrup et al. (15), Lehmann et al. (19), andUrhausen at al. (33) all reported reduced maximalheart rates after increased training. This may possiblybe the result of a reduced power output observed dur-ing maximal exercise. At this stage, however, it is notclear whether the decreased maximal heart rate andpossibly a decreased cardiac output are the cause orthe consequence of premature fatigue. There have beensuggestions that disturbances in the autonomic ner-vous system are responsible for the altered heart rateduring overtraining (20). Decreased sympathetic influ-

ence and/or increased parasympathetic influence, de-creased -adrenoreceptor number or density, increasedstroke volume, and plasma volume expansion are allpossible mechanisms for the reduction in maximalheart rate (34). However, strong evidence for any ofthese mechanisms is lacking.

Lehmann et al. (19) reported a tendency towardincreased stroke volume after an increase in trainingvolume in middle- and long-distance runners. This wasin conjunction with a decreased maximal heart rate. Arecent study by Hedelin et al. (12) reported increasedplasma volume and reduced maximal heart rates aftera 50% increase in training volume in elite canoeists.Although performance was not assessed after recovery

and therefore it could not be determined whether theathletes were fatigued or overreached, there was norelationship between the changes in maximal heartrate and changes in blood volume.

Decreases in maximal heart rate may also be theresult of a downregulation of the sympathetic nervoussystem or changes in parasympathic/sympathetic tone.A number of investigations have examined changes inplasma and urinary catecholamine production duringperiods of intensified training that resulted in over-reaching or overtraining (12, 19, 32). Lehmann et al.(19) reported decreased nocturnal urinary norepineph-




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rine and epinephrine excretion and increased submaxi-mal plasma norepinephrine concentration after an in-crease in training volume. Submaximal and maximalheart rates significantly declined along with thechanges in catecholamines. However, the findings ofunchanged catecholamine concentrations and signifi-cantly decreased maximal heart rates, as evidencedduring the present study, have also been reported (12,

32). Unchanged resting, submaximal, and maximalfree epinephrine and norepinephrine concentrationswere described by Urhausen et al. (32) in under-performing cyclists and triathletes over a 15-mo pe-riod. Although catecholamine concentration remainedstable, maximal heart rate was significantly reduced.Finally, Hedelin et al. (12) also reported decreasedmaximal heart rates, yet no changes in resting cate-cholamine production were observed. Thus there doesnot appear to be a consistent relationship betweenchanges in heart rate and changes in catecholamineconcentration. However, downregulation of -adreno-receptors, or a decrease in receptor number, may occur

as a result of the prolonged exposure to catecholaminesthat can occur as a result of intensified training and/orpsychological stress (20, 34). This may be one unex-plored alteration that could explain the reduction inmaximal heart rate observed in overtrained athletes.

The lack of change in maximal lactate concentrationat the end of MT is in contrast to other investigations(15, 19, 21). Although maximal lactate concentrationsfell from 7.2 to 6.7 mmol/l, this was not statisticallysignificant. The reduction in maximal lactate concen-tration observed in the overtraining literature has pre-viously been suggested to result from reduced glycogenstores (5). However, both carbohydrate and fat oxida-tion were unchanged during the intensified training

period, and resting lactate concentration was also un-altered.

Changes in morning heart rate, body weight, andpercent body fat have previously been suggested asmarkers of overtraining. However, many studies havefailed to show changes in these variables as a result ofintensified training (8, 15 19, 33). Individual variationmay partly explain the lack of changes in resting heartrate from baseline.

Conclusion. Decreased performance was observedalmost immediately after the onset of increased train-ing, which is likely the result of acute fatigue from theinitial training sessions. Successive training stimuliresulted in further fatigue, reductions in performance,and increased mood disturbance in the group of sub-jects studied. After 7 days of intensified training, astate of overreaching developed. Maximum heart ratewas dramatically reduced and perception of exertionwas increased. Changes in substrate utilization andcycling efficiency and economy were unrelated to per-formance changes associated with overreaching andthus cannot explain the increased fatigue and de-creased performance.

We thank Chris Dewaele and Luc Vanmelckebeke for assistancein analyzing plasma catecholamines.

REFERENCES

1. Bahr R, Opstad PK, Medbo JI, and Sejersted OM. Strenu-ous prolonged exercise elevates resting metabolic rate andcauses reduced mechanical efficiency. Acta Physiol Scand 141:555563, 1991.

2. Barron JL, Noakes TD, Levy W, Smith C, and Millar RP.Hypothalamic dysfunction in overtrained athletes. J Clin Endo-crinol Metab 60: 803806, 1985.

3. Borg G. Perceived exertion: a note on history and methods.Med Sci Sports Exerc5: 9093, 1973.

4. Cheng B, Kuipers H, Snyder AC, Keizer HA, JeukendrupA, and Hesselink M. A new approach for the determination ofventilatory and lactate thresholds. Int J Sports Med 13: 518228, 1992.

5. Costill DL, Flynn MG, Kirwan JP, Houmard JA, MitchellJB, Thomas R, and Park SH. Effects of repeated days ofintensified training on muscle glycogen and swimming perfor-mance. Med Sci Sports Exerc 20: 249254, 1988.

6. Frayn KN.Calculation of substrate oxidation rates in vivo fromgaseous exchange. J Appl Physiol 55: 628634, 1983.

7. Fry RW, Grove JR, Morton AR, Zeroni PM, Gaudieri S,and Keast D. Psychological and immunological correlates ofacute overtraining. Br J Sports Med 28: 241246, 1994.

8. Fry RW, Morton AR, Garcia-Webb P, Crawford GP, and

Keast D.Biological responses to overload training in endurancesports. Eur J Appl Physiol 64: 335344, 1992.

9. Fry RW, Morton AR, and Keast D. Overtraining in athletes.An update. Sports Med 12: 3265, 1991.

10. Fry RW, Morton AR, and Keast D. Periodisation and theprevention of overtraining. Can J Sport Sci 17: 241248, 1992.

11. Gaesser GA and Brooks GA. Muscular efficiency duringsteady-rate exercise: effects of speed and work rate. J ApplPhysiol38: 11321138, 1975.

12. Hedelin R, Kentta G, Wiklund U, Bjerle P, and Henriks-son-Larsen K. Short-term overtraining: effects on performance,circulatory responses, and heart rate variability. Med Sci SportsExerc32: 14801484, 2000.

13. Hooper S, MacKinnon LT, and Hanrahan S. Mood states asan indication of staleness and recovery. Int J Sport Psychol 28:112, 1997.

14. Hooper SL, Mackinnon LT, Howard A, Gordon RD, andBachmann AW. Markers for monitoring overtraining and re-covery. Med Sci Sports Exerc 27: 106112, 1995.

15. Jeukendrup AE, Hesselink MK, Snyder AC, Kuipers H,and Keizer HA. Physiological changes in male competitivecyclists after two weeks of intensified training. Int J Sports Med13: 534541, 1992.

16. Jeukendrup A, Saris WHM, Brouns F, and Kester ADM. Anew validated endurance performance test.Med Sci Sports Exerc28: 266270, 1996.

17. Kreider R, Fry AC, and OToole M. Overtraining in sport:terms, definitions, and prevalence. In: Overtraining in Sport,edited by Kreider R, Fry AC, and OToole M. Champaign, IL:Human Kinetics, 1998, p. viiix.

18. Kreider RB, Fry AC, and OToole ML. Overtraining in Sport.

Champaign, IL: Human Kinetics, 1998, p. xi, 403.19. Lehmann M, Dickhuth HH, Gendrisch G, Lazar W, ThumM, Kaminski R, Aramendi JF, Peterke E, Wieland W, andKeul J. Training-overtraining. A prospective, experimentalstudy with experienced middle- and long-distance runners. IntJ Sports Med12: 444452, 1991.

20. Lehmann M, Foster C, Dickhuth HH, and Gastmann U.Autonomic imbalance hypothesis and overtraining syndrome.Med Sci Sports Exerc30: 11401145, 1998.

21. Lehmann M, Gastmann U, Petersen KG, Bachl N, Seidel A,Khalaf AN, Fischer S, and Keul J. Training-overtraining:performance, and hormone levels, after a defined increase intraining volume vs. intensity in experienced middle- and long-distance runners. Br J Sports Med 26: 233242, 1992.




11/11

22. Lehmann M, Jakob E, Gastmann U, Steinacker JM, andKeul J. Unaccustomed high mileage compared with intensitytraining-related neuromuscular excitability in distance runners.Eur J Appl Physiol70: 457461, 1995.

23. Lehmann MJ, Lormes W, Opitz-Gress A, Steinacker JM,Netzer N, Foster C, and Gastmann U. Training and over-training: an overview and experimental results in endurancesports. J Sports Med Phys Fitness 37: 717, 1997.

24. Mackinnon LT, Hooper SL, Jones S, Gordon RD, andBachmann AW. Hormonal, immunological, and hematologicalresponses to intensified training in elite swimmers. Med SciSports Exerc29: 16371645, 1997.

25. McNair DM, Lorr M, and Droppleman LF. Profile of MoodStates Manual. San Diego, CA: Educational and Industrial Test-ing Services, 1971.

26. Morgan WP, Brown DR, Raglin JS, OConnor PJ, andEllickson KA. Psychological monitoring of overtraining andstaleness.Br J Sports Med 21: 107114, 1987.

27. Morgan WP, Costill DL, Flynn MG, Raglin JS, andOConnor PJ. Mood disturbance following increased training inswimmers. Med Sci Sports Exerc 20: 408414, 1988.

28. Moseley L and Jeukendrup A. The reliability of cycling effi-ciency.Med Sci Sports Exerc 33: 621627, 2001.

29. Rushall BS. A tool for measuring stress tolerance in eliteathletes. J Appl Sport Psychol 2: 5166, 1990.

30. Snyder AC, Kuipers H, Cheng B, Servais R, and FransenE.Overtraining following intensified training with normal mus-cle glycogen. Med Sci Sports Exerc 27: 10631070, 1995.

31. Stone MH, Keith RE, Kearney JT, Fleck SJ, Wilson GD,and Triplett NT. Overtraining: a review of the signs, symptomsand possible causes. J Appl Sport Sci Res 5: 3550, 1991.

32. Urhausen A, Gabriel HH, and Kindermann W. Impairedpituitary hormonal response to exhaustive exercise in over-trained endurance athletes. Med Sci Sports Exerc 30: 407414,1998.

33. Urhausen A, Gabriel HH, Weiler B, and Kindermann W.Ergometric and psychological findings during overtraining: along-term follow-up study in endurance athletes. Int J SportsMed19: 114120, 1998.

34. Zavorsky GS. Evidence and possible mechanisms of alteredmaximum heart rate with endurance training and tapering.Sports Med29: 1326, 2000.



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Time Course of Performance Changes and Fatigue Markers During Intensifed Training in Trained Cyclists