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00005768-199807000-0002000005768_1998_30_1146_snyder_overtraining_7report< 56_0_3_8 >Medicine & Science in Sports & Exercise© Williams & Wilkins 1998. All Rights Reserved.Volume 30(7)July 1998pp 1146-1150Overtraining and glycogen depletion hypothesis[Applied Sciences: Symposium: Training/Overtraining: The First Ulm Symposium]SNYDER, ANN C.Section Editor(s): Foster, Carl; Lehmann, Manfred ChairsDepartment of Human Kinetics, University of Wisconsin-Milwaukee, Milwaukee, WI 53201Submitted for publication October 1997.Accepted for publication November 1997.The author extends her appreciation to Harm Kuipers, Carl Foster, Bo Cheng, Asker Jeukendrup, Mattius Hesselink, Rodrique Servais, and Erik Fransen, all of whom were colleagues during the investigations reported in this paper.Address for correspondence: Ann C. Snyder, Ph.D., Department of Human Kinetics, University of Wisconsin-Milwaukee, P.O. Box 413, Milwaukee, WI 53201. E-mail:acs@uwm.edu.Ann C. Snyder was a Fulbright Scholar at the University of Maastricht during some of the reported investigations.ABSTRACTOvertraining and glycogen depletion hypothesis. Med. Sci. Sports Exerc., Vol. 30, No. 7, pp. 1146-1150, 1998. Low muscle glycogen levels due to consecutive days of extensive exercise have been shown to cause fatigue and thus decrements in performance. Low muscle glycogen levels could also lead to oxidation of the branched chain amino acids and central fatigue. Therefore, the questions become, can low muscle glycogen not only lead to peripheral and central fatigue but also to overtraining, and if so, can overtraining be avoided by consuming sufficient quantities of carbohydrates? Research on swimmers has shown that those who were nonresponsive to an increase in their training load had low levels of muscle glycogen and consumed insufficient energy and carbohydrates. However, cyclists who increased their training load for 2 wk but also increased carbohydrate intake to maintain muscle glycogen levels still met the criteria of over-reaching (short-term overtraining) and might have met the criteria for overtraining had the subjects been followed for a longer period of time. Thus, some other mechanism than reduced muscle glycogen levels must be responsible for the development and occurrence of overtraining.Athletic training generally involves much high intensity exercise to enhance athletic performance. Overtraining syndrome occurs when exercise training and recovery become imbalanced, and instead of enhanced performance resulting from exercise training, decrements in exercise performance occur. Two distinct types of overtraining are currently known (13). With long-term overtraining, many weeks if not months are needed for recovery, and for many athletes this could mean the loss of a competitive season. With the less severe form of overtraining, overreaching (or "short-term" overtraining), recovery generally occurs within days (up to approximately 14 d).As moderate to high intensity exercise uses carbohydrates as the primary energy source, consecutive days of long duration running (3 d, 10 miles·d−1) have been shown to result in decreased levels of muscle glycogen when dietary carbohydrate intake remained constant (3). Delayed muscle glycogen resynthesis also occurs (4). Decrements in exercise performance have been shown when muscle glycogen levels become depleted (11) as fatigue occurs. Similarly, cyclists in the Tour de France cycling series have dropped from the series when muscle glycogen levels were not replaced during the daily races and/or during the recovery time of the day (2). Thus, low muscle glycogen levels can result in muscular fatigue. Along with reduced energy store levels, low muscle glycogen levels can reduce the levels of the branched chain amino acids (through their oxidation to glucose) and lead to central fatigue and possibly overtraining (14). Therefore, if a regimen of high intensity exercise is continued for a number of days, can over-reaching and/or overtraining occur as a result of reduced muscle glycogen levels caused by heavy training? If so, can over-reaching and/or overtraining be avoided by consuming sufficient carbohydrates to maintain muscle glycogen levels during periods of heavy training?Costill et al. (4) serendipitously examined the first question while studying the effects of a 10-d period of approximately twice the normal training on male collegiate swimmers. The main purpose of this investigation was to determine if the sudden increase in training stress would result in decrements in muscular power and aerobic endurance exercise performance. Of the 12 subjects who increased their training load from approximately 4,000 m·d−1 to 9,000 m·d−1, 4 subjects had difficulty completing the training load (nonresponders) and were compared as a subgroup against the other 8 subjects (responders). Following the increased period of training, the nonresponder swimmers had significantly reduced muscle glycogen levels. The nonresponder swimmers consumed less calories (3,631 kcal·d−1) than did those who handled the training load (4,682 kcal·d−1). As the total energy expenditure of the athletes was estimated at approximately 4,500 kcal, the subjects who did not handle the increased workload consumed approximately 1,000 kcal less daily than their energy needs. The nonresponders also consumed less carbohydrate (5.3 g·kg−1·d−1) than did the responders (8.2 g·kg−1·d−1). Although 5 g·kg−1·d−1 has previously been shown to maintain muscle glycogen levels during rowing training (16), the nonresponders consumed only 43% of their calories as carbohydrates (4), far below the recommended 70% carbohydrate intake and at the very low end of the 45-60% that athletes generally consume (15). Muscular power, sprint swimming ability (approximately 11 s), and swimming endurance ability (approximately 270 s) were not affected by the increased training load or the reduced muscle glycogen levels of the nonresponder athletes. Costill et al. (4) concluded from these results that the muscle glycogen levels of the nonresponders were high enough to not impair the swimming test results but were inadequate for the energy required during training and thus resulted in chronic fatigue. The chronic fatigue, if continued for a long enough period of time, could become over-reaching and/or overtraining.As the responder group of swimmers in Costill et al. (4) had sufficient dietary intake of carbohydrates to maintain muscle glycogen levels throughout the period of increased training, the question then becomes: Can overtraining be avoided with sufficient carbohydrate intake? To answer this question, we performed a number of studies in the laboratory of Harm Kuipers at the University of Maastricht (10,17,18). The primary investigation utilized eight male competitive cyclists who had been cycling in races for at least 2 yr. The subjects were followed during three time periods: normal (moderate) training (7 d, NORM), overtraining (15 d, OVER) and recovery (6 d, REC). During the OVER period, the cyclists performed mainly high intensity interval training (66% of time at >90% V˙O2max) with some endurance training (24% of time at 70% V˙O2max) and some moderate intensity interval training (10% of time at 80% V˙O2max). Daily, the subjects completed a questionnaire dealing with their subjective evaluation on how they felt (10) and the rating of perceived exertion during the exercise bout (1). To ensure sufficient carbohydrate intake and enhance muscle glycogen resynthesis, the subjects consumed 160 g of carbohydrate in a liquid (Extran, Nutricia Inc., Zoetermeer, the Netherlands; 100% maltodextrin) during the first 2 h after the daily exercise bout as per Ivy et al. (7,8). An incremental exercise test to volitional fatigue performed on a bicycle ergometer was used as the performance measure. As no single measure has been found to determine the occurrence of over-reaching and/or overtraining, we used five different criteria similar to those recommended by Lehmann et al. (13). The five criteria used were as follows: 1) greater than 10-W reduction in maximal workload during incremental test, 2) maximal heart rate reduced by greater than 5 beats·min−1, 3) plasma cortisol levels reduced by more than 60 nmol·L−1, 4) the ratio of maximal lactate to rating of perceived exertion reduced more than 20 points, and 5) an increase of at least five affirmative responses on the daily questionnaire. If a subject obtained any three of the five criteria, they were classified as over-reached.All eight subjects met the criteria of over-reaching. The subjects consumed sufficient carbohydrates and energy during the OVER training period (Fig. 1) to maintain normal muscle glycogen levels during that period (Fig. 2). Carbohydrate intake accounted for 64.0 ± 2.5% of the energy consumed during the NORM period and 67.4 ± 2.1% during the OVER period.Figure 1-Carbohydrate and energy consumption during the NORM and OVER training periods. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Figure 2-Resting muscle glycogen levels during the NORM and OVER training periods. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Maximal workload (Wmax) was decreased 3% during the OVER training period. Likewise, oxygen uptake and heart rate were similar during the NORM and OVER training periods for the lower workloads (i.e., 100, 150, 200, 250, and 300 W), but at 350 W and Wmax workloads, they were significantly reduced during OVER when compared with NORM. Conversely, plasma lactate for all workloads was greater during NORM than OVER (Fig. 3). As expected, RPE values followed a trend of becoming greater as exercise intensity increased and were not different at any given workload for the three training periods (Fig. 4). Finally, the ratio of plasma lactate to rating of perceived exertion (HLa: RPE) was decreased from the NORM to the OVER training time period and increased some following the REC period for all workloads but was not yet back to the NORM value (Fig. 5). For the maximal workload, HLa:RPE was significantly reduced during the OVER period when compared with that of the NORM (Fig. 6).Figure 3-Plasma lactate levels for the incremental exercise during the NORM, OVER, and REC training periods. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Figure 4-Ratings of perceived exertion (RPE) for the incremental exercise during the NORM, OVER, and REC training periods. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Figure 5-The ratio of plasma lactate to rating of perceived exertion (HLa:RPE) for the incremental exercise during the NORM, OVER, and REC training periods. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Figure 6-The ratio of maximal lactate to rating of perceived exertion (HLa:RPE) during the NORM, OVER, and REC training periods. *Significantly different from NORM. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Two additional nonperformance measures were analyzed: plasma cortisol levels and affective questionnaire responses. Plasma cortisol levels were significantly reduced during the OVER training period when compared with the NORM training period and remained reduced during the REC period (Fig. 7). During the NORM training period, the subjects answered very few of the questionnaire questions affirmatively; however, during the 2 wk of the OVER period (OVER1 and OVER2), the number of positively answered questions increased significantly (Fig. 8). The questions that were answered most positively during the heavy training period were: Are you more quickly fatigued? Are your muscles more stiff or painful? Do you have the feeling of not being completely recovered? Is it harder for you to complete the training?Figure 7-Resting plasma cortisol levels during the NORM, OVER, and REC training periods. *Significantly different from NORM. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Figure 8-Affirmative questionnaire responses during the NORM, OVER wk 1 (OVER1), OVER wk 2 (OVER2), and REC training periods. *Significantly different from NORM. Adapted from Snyder, A. C., H. Kuipers, B. Cheng, R. Servais, and E. Fransen. Overtraining following intensified training with normal muscle glycogen. Med. Sci. Sports Exerc. 27:1063-1070, 1995.Possibly the most sensitive and easy to measure criterion variable is the HLa:RPE ratio. We initially observed that this ratio might be an indicator of an athlete's degree of over-reaching/overtraining when working with speed skaters (5). The presumption is that with intensive training as the concentration of blood lactate (expressed in mM) is reduced and the rating of perceived exertion (on the 10-point scale) stays the same, the ratio of the two (multiplied by 100) will be reduced to probably less than 100 (i.e., blood lactate concentration is less than rating of perceived exertion). Using the same exercise training protocol on two different groups of subjects, the HLa:RPE was significantly reduced during the maximal workload in both studies (17,18). Similar results were obtained by Jeukendrup and Hesselink (9), who initially compared a lactate profile curve (up to 4 mM lactate) of an athlete not responding to training with that during the preseason and observed a right shifting of the values, but no other remarkable differences; therefore, the athlete was determined to be in good physical condition. When maximal lactate was later obtained, much lower values were observed, and the athlete was deemed overtrained (9). Others (4,6,12) have observed lower submaximal and maximal lactate levels following periods of heavy training, but no one else has combined blood lactate and RPE to examine the ratio that in essence corrects for the right shifting that normally occurs with exercise training (6).From the results of the literature reviewed, it would seem that even though low muscle glycogen levels may be associated with exercise-induced fatigue (peripheral and central), some other mechanism must be responsible for the occurrence of over-reaching/overtraining, as over-reaching, and quite possibly overtraining, occurred in the presence of normal muscle glycogen levels. Although we did not follow scientifically the subjects from the investigations we performed, communication with the subjects indicated that minimally a month was required for most of them to recover from the training regimen. 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[CrossRef] [Full Text] [Medline Link] [Context Link] OVERTRAINING; OVER-REACHING; MUSCLE GLYCOGEN; CARBOHYDRATE SUPPLEMENTATION; BLOOD LACTATE; RPE; CORTISOLovid.com:/bib/ovftdb/00005768-199807000-0002000003647_1985_54_343_borg_perceived_|00005768-199807000-00020#xpointer(id(R1-20))|11065213||ovftdb|SL0000364719855434311065213P28[CrossRef]10.1007%2FBF02337176ovid.com:/bib/ovftdb/00005768-199807000-0002000003647_1985_54_343_borg_perceived_|00005768-199807000-00020#xpointer(id(R1-20))|11065405||ovftdb|SL0000364719855434311065405P28[Medline Link]4065121ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1989_10_s32_brouns_controlled_|00005768-199807000-00020#xpointer(id(R2-20))|11065213||ovftdb|SL00004355198910s3211065213P29[CrossRef]10.1055%2Fs-2007-1024952ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1989_10_s32_brouns_controlled_|00005768-199807000-00020#xpointer(id(R2-20))|11065405||ovftdb|SL00004355198910s3211065405P29[Medline Link]2663741ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1988_9_198_foster_normalization_|00005768-199807000-00020#xpointer(id(R6-20))|11065213||ovftdb|SL000043551988919811065213P33[CrossRef]10.1055%2Fs-2007-1025005ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1988_9_198_foster_normalization_|00005768-199807000-00020#xpointer(id(R6-20))|11065405||ovftdb|SL000043551988919811065405P33[Medline Link]3410624ovid.com:/bib/ovftdb/00005768-199807000-0002000002412_1994_28_239_jeukendrup_overtraining_|00005768-199807000-00020#xpointer(id(R9-20))|11065213||ovftdb|SL0000241219942823911065213P36[CrossRef]10.1136%2Fbjsm.28.4.239ovid.com:/bib/ovftdb/00005768-199807000-0002000002412_1994_28_239_jeukendrup_overtraining_|00005768-199807000-00020#xpointer(id(R9-20))|11065405||ovftdb|SL0000241219942823911065405P36[Medline Link]7894954ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1992_13_534_jeukendrup_physiological_|00005768-199807000-00020#xpointer(id(R10-20))|11065213||ovftdb|SL0000435519921353411065213P37[CrossRef]10.1055%2Fs-2007-1021312ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1992_13_534_jeukendrup_physiological_|00005768-199807000-00020#xpointer(id(R10-20))|11065405||ovftdb|SL0000435519921353411065405P37[Medline Link]1459749ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1991_12_444_lehmann_overtraining_|00005768-199807000-00020#xpointer(id(R12-20))|11065213||ovftdb|SL0000435519911244411065213P39[CrossRef]10.1055%2Fs-2007-1024711ovid.com:/bib/ovftdb/00005768-199807000-0002000004355_1991_12_444_lehmann_overtraining_|00005768-199807000-00020#xpointer(id(R12-20))|11065405||ovftdb|SL0000435519911244411065405P39[Medline Link]1752709ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1993_25_854_lehmann_overtraining_|00005768-199807000-00020#xpointer(id(R13-20))|11065213||ovftdb|00005768-199307000-00015SL0000576819932585411065213P40[CrossRef]10.1249%2F00005768-199307000-00015ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1993_25_854_lehmann_overtraining_|00005768-199807000-00020#xpointer(id(R13-20))|11065404||ovftdb|00005768-199307000-00015SL0000576819932585411065404P40[Full Text]00005768-199307000-00015ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1993_25_854_lehmann_overtraining_|00005768-199807000-00020#xpointer(id(R13-20))|11065405||ovftdb|00005768-199307000-00015SL0000576819932585411065405P40[Medline Link]8350709ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1995_27_1063_snyder_overtraining_|00005768-199807000-00020#xpointer(id(R18-20))|11065213||ovftdb|00005768-199507000-00016SL00005768199527106311065213P45[CrossRef]10.1249%2F00005768-199507000-00016ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1995_27_1063_snyder_overtraining_|00005768-199807000-00020#xpointer(id(R18-20))|11065404||ovftdb|00005768-199507000-00016SL00005768199527106311065404P45[Full Text]00005768-199507000-00016ovid.com:/bib/ovftdb/00005768-199807000-0002000005768_1995_27_1063_snyder_overtraining_|00005768-199807000-00020#xpointer(id(R18-20))|11065405||ovftdb|00005768-199507000-00016SL00005768199527106311065405P45[Medline Link]7564974Overtraining and glycogen depletion hypothesisSNYDER, ANN C.Applied Sciences: Symposium: Training/Overtraining: The First Ulm Symposium730InternalMedicine & Science in Sports & Exercise2000322317FEB 2000Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?SMITH, LLhttp://journals.lww.com/acsm-msse/Fulltext/2000/02000/Cytokine_hypothesis_of_overtraining__a.11.aspx2060http://pdfs.journals.lww.com/acsm-msse/2000/02000/Cytokine_hypothesis_of_overtraining__a.00011.pdfInternalMedicine & Science in Sports & Exercise10.1249/MSS.0b013e318191259c20094151155-1163MAY 2009Development and Characterization of an Overtraining Animal ModelHOHL, R; FERRARESSO, RL; DE OLIVEIRA, RB; LUCCO, R; BRENZIKOFER, R; DE MACEDO, DVhttp://journals.lww.com/acsm-msse/Fulltext/2009/05000/Development_and_Characterization_of_an.23.aspx351http://pdfs.journals.lww.com/acsm-msse/2009/05000/Development_and_Characterization_of_an.00023.pdfhttp://dx.doi.org/10.1249%2fMSS.0b013e318191259cInternalThe Journal of Strength & Conditioning Research2004181185-193FEB 2004Tissue Trauma: the Underlying Cause of Overtraining Syndrome?SMITH, LLhttp://journals.lww.com/nsca-jscr/Fulltext/2004/02000/TISSUE_TRAUMA__THE_UNDERLYING_CAUSE_OF.28.aspx246disable