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Referências sobre sympathetic overtraining syndrome

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beta2-Adrenergic receptor downregulation and performance decrements during high-intensity resistance exercise overtraining.

Fry AC, Schilling BK, Weiss LW, Chiu LZ.

Human Performance Laboratories, The University of Memphis, Department of Health and Sport Sciences, Memphis, Tennessee, USA. afry@memphis.edu

Previous research on overtraining due to excessive use of maximal resistance exercise loads [100% 1 repetition maximum (1 RM)] indicates that peripheral muscle maladaptation contributes to overtraining-induced performance decrements. This study examined the cellular and molecular responses of skeletal muscle to performance decrements due to high-relative-intensity (%1 RM) resistance exercise overtraining. Weight-trained men were divided into overtrained (OT, n = 8) and control (Con, n = 8) groups. The OT group performed 10 x 1 at 100% 1 RM daily for 2 wk, whereas the Con group performed normal training 2 days/wk. Muscle biopsies from the vastus lateralis muscle, voluntary static and dynamic muscle performances, and nocturnal urinary epinephrine were assessed before (pre) and after (post) overtraining. Overtraining occurred as indicated by a decrease in 1-RM strength for the OT group (mean +/- SE; OT pre = 159.3 +/- 10.1 kg, OT post = 151.4 +/- 9.9 kg, Con pre = 146.0 +/- 12.9 kg, Con post = 144.9 +/- 13.3 kg), as well as a 36.3% decrease in mean power at 100% 1-RM loads. Normal training could be resumed only after 2-8 wk of training cessation. Muscle beta(2)-adrenergic receptor (beta(2)-AR; fmol/mg protein) density significantly decreased by 37.0% for the OT group and was unchanged for the Con group (-1.8%). Nocturnal urinary epinephrine for the OT group increased by 49%, although this was not significant (effect size = 0.42). The ratio of nocturnal urinary epinephrine to beta(2)-AR density suggested a decreased beta(2)-AR sensitivity for the OT group (2.4-fold increase). Overtraining occurred based on decreased muscular force and power. Desensitization of the beta(2)-AR system suggests that this may be an important contributor to performance decrements due to excessive use of maximal resistance exercise loads.

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PMID: 16888042 [PubMed - indexed for MEDLINE]


 
2: Med Sci Sports Exerc. 1994 Sep;26(9):1165-73.
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Performance decrements with high-intensity resistance exercise overtraining.

Fry AC, Kraemer WJ, van Borselen F, Lynch JM, Marsit JL, Roy EP, Triplett NT, Knuttgen HG.

Center for Sports Medicine, Pennsylvania State University, University Park 16802.

The purpose of this investigation was to study a high-intensity resistance exercise overtraining protocol resulting in muscular strength decrements. Seventeen weight-trained males were divided into an overtraining group (OT; N = 11; mean +/- SE, age = 22.0 +/- 0.9 yr,) that exercised on a squat machine daily for 2 wk with 100% of 1 repetition maximum (RM) relative intensity, and a control group (CON; N = 6; age = 23.7 +/- 2.4 yr) that exercised 1 d.wk-1 with low intensity (50% 1 RM). Test batteries were conducted at the beginning (test 1), after 1 wk (test 2), and after 2 wk (test 3) of the study. One RM performance significantly decreased from test 1 to test 3 (P < 0.05) for the OT group (mean = -12.2 +/- 3.8 kg), but not the CON group (mean = -1.1 +/- 0.8 kg). Isokinetic and stimulated isometric muscle force significantly decreased for the OT group compared with the CON group by test 3. The primary site of maladaptation appeared to be in the periphery as indicated by changes in stimulated force, circulating CK activity, and exercise-induced lactate responses. This protocol produced a significant decrease in 1 RM performance, thus providing a model for the study of short-term, high-intensity resistance exercise overtraining.

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PMID: 7808252 [PubMed - indexed for MEDLINE]


 
3: J Appl Physiol. 1998 Dec;85(6):2352-9.
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Pituitary-adrenal-gonadal responses to high-intensity resistance exercise overtraining.

Fry AC, Kraemer WJ, Ramsey LT.

Human Performance Laboratories, University of Memphis, Memphis, Tennessee 38152, USA.

Weight-trained men [OT; n = 11; age = 22.0 +/- 0.9 (SE) yr] resistance trained daily at 100% one-repetition maximum (1-RM) intensity for 2 wk, resulting in 1-RM strength decrements and in an overtrained state. A control group (Con; n = 6; age = 23.7 +/- 2.4 yr) trained 1 day/wk at a low relative intensity (50% 1 RM). After 2 wk, the OT group exhibited slightly increased exercise-induced testosterone (preexercise = 26.5 +/- 1.3 nmol/l, postexercise = 29.1 +/- 5.9 nmol/l) and testosterone-to-cortisol ratio (preexercise = 0. 049 +/- 0.007 nmol/l, postexercise = 0.061 +/- 0.006 nmol/l) and decreased exercise-induced cortisol (preexercise = 656.1 +/- 98.1 nmol/l, postexercise = 503.1 +/- 39.7 nmol/l). Serum concentrations for growth hormone and plasma peptide F [preproenkephalin (107-140)] were similar for both groups throughout the overtraining period. This hormonal profile is distinctly different from what has been previously reported for other types of overtraining, indicating that high-relative-intensity resistance exercise overtraining may not be successfully monitered via circulating testosterone and cortisol. Unlike overtraining conditions with endurance athletes, altered resting concentrations of pituitary, adrenal, or gonadal hormones were not evident, and exercise-induced concentrations were only modestly affected.

PMID: 9843563 [PubMed - indexed for MEDLINE]

 
4: J Appl Physiol. 1994 Aug;77(2):941-6.
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Catecholamine responses to short-term high-intensity resistance exercise overtraining.

Fry AC, Kraemer WJ, Van Borselen F, Lynch JM, Triplett NT, Koziris LP, Fleck SJ.

Center for Sports Medicine, Pennsylvania State University, University Park 16802.

Seventeen weight-trained males were divided into an overtraining group [OT; n = 11; age = 22.0 +/- 0.9 (SE) yr] that weight trained their legs daily for 2 wk with 100% 1 repetition maximum relative intensity on a squat machine and a control group (n = 6; age = 23.7 +/- 2.4 yr) that exercised 1 day/wk with low relative intensity (50% 1 repetition maximum). Test batteries including strength assessments and resting and exercise-induced concentrations of epinephrine and norepinephrine were conducted at the beginning, middle, and end (tests 1-3, respectively) of the study. Strength capabilities decreased by test 3 for the OT group (P < 0.05). Resting catecholamine concentrations did not change for either group during the study, whereas exercise-induced concentrations of both epinephrine (test 1 = 3,407.9 +/- 666.6 pmol/l, test 2 = 7,563.7 +/- 1,210.6 pmol/l, test 3 = 6,931.6 +/- 919.3 pmol/l) and norepinephrine (test 1 = 42.9 +/- 7.4 nmol/l, test 2 = 70.0 +/- 8.8 nmol/l, test 3 = 85.2 +/- 14.5 nmol/l) significantly increased by tests 2 and 3 for only the OT group. Correlation coefficients suggested decreased responsitivity of skeletal muscle to sympathetic nervous system activity. It appears that altered exercise-induced sympathetic nervous system activity accompanies high relative intensity resistance exercise overtraining and may be among the initial responses to the onset of the previously theoretical sympathetic overtraining syndrome.

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PMID: 8002551 [PubMed - indexed for MEDLINE]


 
5: Eur J Appl Physiol. 2004 Mar;91(2-3):140-6. Epub 2003 Oct 2.
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Hormonal responses in athletes: the use of a two bout exercise protocol to detect subtle differences in (over)training status.

Meeusen R, Piacentini MF, Busschaert B, Buyse L, De Schutter G, Stray-Gundersen J.

Department of Human Physiology and Sportsmedicine, Free University of Brussels, Pleinlaan 2, 1050, Brussels, Belgium. rmeeusen@vub.ac.be

In overtrained athletes, several signs and symptoms have been associated with the imbalance between training and recovery. However, reliable diagnostic markers for distinguishing between well-trained, overreached (OR) and overtrained (OT) athletes are lacking. A hallmark feature of overtraining syndrome (OTS) is the inability to sustain intense exercise and recover for the next training or competition session. We therefore devised a test protocol utilizing two bouts of maximal work. With this test protocol we tried to establish a difference in hormonal responses between the training status of T and OR athletes. Seven well-trained cyclists participated in this study and were tested before and after a training camp. We also present the data of one OT motocross athlete who was clinically diagnosed as overtrained. All athletes performed two maximal exercise tests separated by 4 h. Blood was analyzed for cortisol, adrenocorticotrophic hormone (ACTH), growth hormone and prolactin (PRL). Performance decreased by 6% between the first and the second exercise test in the OR group and by 11% in the OT subject. Moreover, during the second exercise test there were more marked differences between the T and OR athletes; in particular, the OT subject did not show an increase in some of the hormonal responses. PRL increased only by 14% in the OT subject's second test and there was a 7% decrease in ACTH. The two exercise approach enables us to detect subtle performance decrements that will not be identified by one exercise trigger. The hormonal responses to the second exercise test were different between the T and OR athletes (the increase in the T group was higher than in the OR that was higher than in the OT). The results of the case presentation of an overtrained athlete provide evidence of an altered and dysfunctional hypothalamic-pituitary axis response to two bouts of maximal exercise. These findings can be used to develop markers for diagnosis of OTS and to begin to address the pathologic mechanism operative in the syndrome, as well as providing an outcome measure to evaluate possible therapeutic regimes.

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PMID: 14523562 [PubMed - indexed for MEDLINE]


 
6: J Appl Physiol. 2006 Jun;100(6):1876-82. Epub 2006 Jan 26.
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Temporal response of desmin and dystrophin proteins to progressive resistance exercise in human skeletal muscle.

Woolstenhulme MT, Conlee RK, Drummond MJ, Stites AW, Parcell AC.

Human Performance Research Center, 120-E Richards Bldg., Brigham Young University, Provo, UT 84602, USA.

We have investigated the adaptations of the cytoskeletal proteins desmin and dystrophin in relationship to known muscular adaptations of resistance exercise. We measured desmin, dystrophin, and actin protein contents, myosin heavy chain (MHC) isoform distribution, muscle strength, and muscle cross-sectional area (CSA) during 8 wk of progressive resistance training or after a single bout of unaccustomed resistance exercise. Muscle biopsies were taken from the vastus lateralis of 12 untrained men. For the single-bout group (n=6) biopsies were taken 1 wk before the single bout of exercise (week 0) and 1, 2, 4, and 8 wk after this single bout of exercise. For the training group (n=6), biopsies were taken 1 wk before the beginning of the program (week 0) and at weeks 1, 2, 4, and 8 of the progressive resistance training program. Desmin, dystrophin, and actin protein levels were determined with immunoblotting, and MHC isoform distribution was determined using SDS-PAGE at each time point for each group. In the training group, desmin was significantly increased compared with week 0 beginning at week 4 (182% of week 0; P<0.0001) and remained elevated through week 8 (172% of week 0; P<0.0001). Desmin did not change at any time point for the single-bout group. Actin and dystrophin protein contents were not changed in either group at any time point. The percentage of MHC type IIa increased and MHC type IIx decreased at week 8 in the training group with no changes occurring in the single-bout group. Strength was significantly increased by week 2 (knee extension) and week 4 (leg press), and it further increased at week 8 for both these exercises in the training group only. Muscle CSA was significantly increased at week 4 for type II fibers in the training group only (5,719+/-382 and 6,582+/-640 microm2, weeks 0 and 4, respectively; P<0.05). Finally, a significant negative correlation was observed between the desmin-to-actin ratio and the percentage of MHC IIx (R=-0.31; P<0.05, all time points from both groups). These data demonstrate a time course for muscular adaptation to resistance training in which desmin increases shortly after strength gains and in conjunction with hypertrophy, but before changes in MHC isoforms, whereas dystrophin remains unchanged.

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PMID: 16439510 [PubMed - indexed for MEDLINE]


 
7: Sports Med. 1995 Oct;20(4):251-76.
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Blood hormones as markers of training stress and overtraining.

Urhausen A, Gabriel H, Kindermann W.

Institute of Sports and Preventive Medicine, University of Saarland, Saarbrücken, Germany.

An imbalance between the overall strain experienced during exercise training and the athlete's tolerance of such effort may induce overreaching or overtraining syndrome. Overtraining syndrome is characterised by diminished sport-specific physical performance, accelerated fatiguability and subjective symptoms of stress. Overtraining is feared by athletes yet there is a lack of objective parameters suitable for its diagnosis and prevention. In addition to the determination of substrates (e.g. lactate, ammonia and urea) and enzymes (e.g. creatine kinase), the possibilities for monitoring of training by measuring hormonal levels in blood are currently being investigated. Endogenous hormones are essential for physiological reactions and adaptations during physical work and influence the recovery phase after exercise by modulating anabolic and catabolic processes. Testosterone and cortisol are playing a significant role in metabolism of protein as well as carbohydrate metabolism. Both are competitive agonists at the receptor level of muscular cells. The testosterone/cortisol ratio is used as an indication of the anabolic/catabolic balance. This ratio decreases in relation to the intensity and duration of physical exercise, as well as during periods of intense training or repetitive competition, and can be reversed by regenerative measures. Correlations have been noted with the training-induced changes of strength. However, it seems more likely that the testosterone/cortisol ratio indicates the actual physiological strain in training, rather than overtraining syndrome. The sympatho-adrenergic system might be involved in the pathogenesis of overtraining. Overtraining appears as a disturbed autonomic regulation, which in its parasympathicotonic form shows a diminished maximal secretion of catecholamines, combined with an impaired full mobilisation of anaerobic lactic reserves. This is supposed to lead to decreased maximal blood lactate levels and maximal performance. Free plasma adrenaline (epinephrine) and noradrenaline (norepinephrine) may provide additional information for the monitoring of endurance training. While prolonged aerobic exercise conducted at intensities below the individual anaerobic threshold lead to a moderate rise of sympathetic activity, workloads exceeding this threshold are characterised by a disproportionate increase in the levels of catecholamines. In addition, psychological stress during competitive events is characterised by a higher catecholamines to lactate ratio in comparison with training exercise sessions. Thus, the frequency of training sessions with higher anaerobic lactic demands or of competition, should be carefully limited in order to prevent overtraining syndrome. In the state of overtraining syndrome and overreaching, respectively, an intraindividually decreased maximum rise of pituitary hormones (corticotrophin, growth hormone), cortisol and insulin has been found after a standardised exhaustive exercise test performed with an intensity of 10% above the individual anaerobic threshold.(ABSTRACT TRUNCATED AT 400 WORDS)

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PMID: 8584849 [PubMed - indexed for MEDLINE]


 
8: Sports Med. 1997 Feb;23(2):106-29.
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Resistance exercise overtraining and overreaching. Neuroendocrine responses.

Fry AC, Kraemer WJ.

Department of Human Movement Sciences and Education, University of Memphis, Tennessee, USA. fry.andrew@cc.memphis.edu

Overtraining is defined as an increase in training volume and/or intensity of exercise resulting in performance decrements. Recovery from this condition often requires many weeks or months. A shorter or less severe variation of overtraining is referred to as overreaching, which is easily recovered from in just a few days. Many structured training programmes utilise phases of overreaching to provide variety of the training stimulus. Much of the scientific literature on overtraining is based on aerobic activities, despite the fact that resistance exercise is a large component of many exercise programmes. Chronic resistance exercise can result in differential responses to overtraining depending on whether either training volume or training intensity is excessive. The neuroendocrine system is a complex physiological entity that can influence many other systems. Neuroendocrine responses to high volume resistance exercise overtraining appear to be somewhat similar to overtraining for aerobic activities. On the other hand, excessive resistance training intensity produces a distinctly different neuroendocrine profile. As a result, some of the neuroendocrine characteristics often suggested as markers of overtraining may not be applicable to some overtraining scenarios. Further research will permit elucidation of the interactions between the neuroendocrine system and other physiological systems in the aetiology of performance decrements from overtraining.

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PMID: 9068095 [PubMed - indexed for MEDLINE]


 
9: J Appl Physiol. 2007 Jan;102(1):94-102. Epub 2006 Sep 7.
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Anticipatory responses of catecholamines on muscle force production.

French DN, Kraemer WJ, Volek JS, Spiering BA, Judelson DA, Hoffman JR, Maresh CM.

Human Performance Laboratory, Department of Kinesiology, Unit 1110, University of Connecticut, Storrs, CT 06269-1110, USA.

Few data exist on the temporal relationship between catecholamines and muscle force production in vivo. The purpose of this study was to examine the influence of preexercise arousal on sympathoadrenal neurohormones on muscular force expression during resistance exercise. Ten resistance-trained men completed two experimental conditions separated by 7 days: 1) acute heavy resistance exercise protocol (AHREP; 6 x 10 repetitions parallel squats, 80% 1 repetition maximum) and 2) control (Cont; rest). Peak force (F(peak)) was recorded during a maximal isometric squat preceding each set and mean force (F(mean)) was measured during each set. Serial venous blood samples were collected before the AHREP and immediately preceding each set. Blood collection times were matched during Cont. Preexercise epinephrine (Epi), norepinephrine (NE), and dopamine (DA) increased (P <or= 0.05) above Cont by 270, 255, and 164%, respectively. During exercise, Epi, NE, and DA continued to increase by 512, 271, and 38%, respectively, above preexercise values. F(peak) and F(mean) decreased by approximately 20-25% over the course of the AHREP. Post hoc data analysis revealed that five subjects (F(maintainers)) showed no decline (P >or= 0.05) in muscular performance (F(peak), F(mean)) during AHREP and that five subjects (F(reducers)) had significant reductions in F(peak) and F(mean). Integrated area under the curve for Epi, NE, and F(peak) were greater (P < 0.02) for F(maintainers) than F(reducers). In conclusion, an anticipatory rise in catecholamines existed, which may be essential for optimal force production at the onset of exercise.

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PMID: 16959907 [PubMed - indexed for MEDLINE]


 
10: Eur J Appl Physiol Occup Physiol. 1997;76(2):187-91.
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Monitoring high-intensity endurance training using neuromuscular excitability to recognize overtraining.

Lehmann M, Baur S, Netzer N, Gastmann U.

Department of Sports Medicine, Medical Hospital, University of Ulm, Germany.

The minimal rectangular current pulse that produces a single contraction of reference muscles at different pulse durations has been recommended as a marker of the neuromuscular excitability (NME) of skeletal muscles. NME is improved in well-trained, non-fatigued endurance athletes and deteriorates after prolonged heavy exercise and high-volume overtraining. The hypothesis was tested that a deterioration in NME also indicates an early stage in the overtraining process during high-intensity endurance training. Six subjects participated for 40-60 min per day in a 6-week, 6-days-per-week, intensive, steady-state and interval training program using a cycle ergometer. Training was stopped each day on volitional exhaustion. On day 7 of each week training was of low intensity for about 30-40 min. Submaximum and maximum power output were significantly increased after 3 weeks, but there was no further improvement, rather a deterioration after week 6 compared to week 3. Even after 2 weeks of regeneration no supercompensation was evident, rather a decrease in maximum power output. NME was slightly improved after 3 weeks, but deteriorated after 6 weeks, and was again normalized after 2 weeks of regeneration. The discrepancy between normalization of NME and still-deteriorated performance ability after 2 weeks of regeneration reflects additional significant, and probably central mechanisms that explain persistent performance incompetence. Deterioration in NME may indicate an early stage in the overtraining process during high-volume as well as high-intensity endurance overtraining, but normalization does not necessarily indicate sufficient regeneration.

PMID: 9272779 [PubMed - indexed for MEDLINE]