1. Carmen Bott November 18, 2003 HKIN 562 OVERTRAINING SYNDROME A Review of Contributing Factors and Markers of Regeneration Status among Anaerobic, Intermittent Sport Athletes

3. Overtraining Syndrome The process of training excessively and the fatigue state and associated symptoms that result Overtraining is the stimulus, OTS is the consequence An imbalance between stress of training and athletes tolerance of the stress

4. Overtraining Syndrome Occurs when actual physical performances are adversely affected and cannot be reversed without long- term rest and recovery Diagnosis is one of exclusion, not inclusion.

5. Classical Symptoms Physiological Psychological Immunological Biochemical Fry et al 1991

6. Physiological Decreased performance (time, %RM) Inability to meet previous performance Recovery Prolonged Decreased muscular strength & work capacity Loss of Coordination Chronic Fatigue

7. Psychological Feelings of Depression General Apathy Emotional instability Difficulty concentrating Fear of competition

8. Immunological Increased susceptability to and severity of illnesses, colds and allergies Flu-like illness Minor scratches that heal slowly Bacterial infections

9. Biochemical Negative Nitrogen balance Depressed muscle glycogen concentration Mineral depletion (zinc, cobalt, aluminum, selenium, copper) Elevated cortisol Low free testosterone

10. Forms of OTS Sympathetic Overtraining Sx Increased pulse rate at rest, decreased body mass, disturbed sleep, decreased pulse recovery, decreased appetitie, emotional instability Parasympathetic Overtraining Sx Progressive anaemia, low blood pressure, digestive disturbances, early fatigue, low resting pulse, fast return of heart rate to basal levels, decreased PBL, altered immune function, high fatigue ratings

11. Characteristics of Both Forms SOTS: stress response that proceeds exhaustion, may predominantly effect speed and power athletes and athletes who are younger. Also seems to be related to inappropriately intensive training sessions and too much psycho-emotional stress. POTS: associated with exhaustion of the neuroendocrine system, may predominantly affect endurance athletes

12. Diagnostic Complications Some symptoms may predispose other symptoms Some may disappear, while others appear in their place Different types of activity produces different symptoms No clear point where training fatigue finishes and overtraining begins

13. Who is Susceptible? Athletes at all levels of performance Highly motivated athletes Athletes with amateur coaches Sports where strength, speed and coordination are essential (Wolf 1961, found symptoms of OTS 73 of 95 cases) Athletes trying to make the jump to the next level Athletes with little training experience

14. Some symptoms disappear Increasing state of fatigue Continued intensive training Increasing complexity & severity of Sx Acute fatigue Overload stimulus Over- reaching OTS A Continuum of OT Sx (Fry et al)

15. Pathogenesis

17. The Glutamine Hypothesis AA found within the human body; produced in skeletal muscle Glutamine homeostasis placed under stress when tissues are stressed catabolically (surgery, trauma, burns, acidosis) Stores can become depleted – can drop 2x during intense endurance exercise

18. Exercise-induced Immunosuppression Acute bout of exercise produces similar responses to infection – increase in number of leukocytes Between 3 and 72 hrs post exercise, viruses and bacteria may threaten the immune system and increase risk of infection Insufficient recovery = cumulative effect

19. Tissue Trauma Occurs when: training is strenuous and exhaustive, an athlete increases exercise volume & or intensity, abruptly + not enough recovery Markers of tissue damage include creatine kinase, serum urea, myoglobin, 3-methyl-histidine and C-reactive protein.

20. Tissue Trauma Overload injuries due to repetitive microtrauma present a more gradual onset of symptoms compared to acute injuries Repetitive forces encountered on landing and push-off must be considered. Fatigued muscles, resulting from adapting to higher training loads, may react in the same manner as weak muscles & become strained

21. High Impact Forces Muscles that contract quickly to absorb force are likely the source of microtrauma Ground reaction forces (absent in cycling) Eccentric contractions result in greater muscle fiber injury Concentric hypoxia = muscle ischemia?? No, b/c circulating monocytes are not activated and CTK not elevated

22. The Cytokine Hypothesis Exercise-induced microtrauma to the musculoskeletal system and the inflammatory response is the precursor episode(s) to OTS Local inflammation leads to chronic inflammation when recovery is insufficient

23. Neutrophil accumulation monocyte accumulation Upregulation of cytokines Released from monocytes; they direct local inflammatory responses and activate immune cells and direct influx of WBCs The Cytokine Hypothesis

24. Pro-inflammatory Cytokines The release from monocytes causes systemic inflammation and a paradigm of sickness behaviour and subsequent activation of the SNS and the HPAA. Released in large quantities, therefore they can act on several organ systems

25. Exercise Prescription Variables During anabolic phase, training stimulus is most effective Supercompensation depends on magnitude of stimulus Principles: Individualization, Specificity, Progressive Overload Training Variables: exercise choice & sequence, # sets and reps, rest periods, tempos

26. Review of Markers

27. Detection of Impending OTS: Endocrine Markers Testosterone, cortisol and ftes:cort Catecholamines Plasma Markers Creatine Phosphokinase (CPK) Peak Blood Lactate Glutamine Cytokines

28. Detection of Impending OTS: Biochemical Markers Muscle glycogen stores Physiological Markers Heart Rate – resting, maximal, variability Psychological & Info processing Markers Questionnaires Logs and RPE Profile of mood states

29. Testosterone Steroid hormone responsible for many anabolic and androgenic qualities Acute bouts of heavy RT = increased **total levels Affected by chronic RT = increased Increased RT volume = decreased resting levels, which may impact protein synthesis in skeletal muscle tissue and neural regulation of muscle activity

30. Cortisol Also a steroid hormone Increases gluconeogenic activity in the liver, decreasing glucose uptake and increasing glycogen synthesis in muscle tissue and mobilizing AA Important during recovery b/c protein- catabolic effect on skeletal muscle

31. Cortisol Reflects long-term training stress (> 1mo) Elevated levels found in overtrained athletes Increase RT Vol & Intensity, cort levels HI RT + HI EE = cort levels MAXIMAL RT overtraining has no change **therefore data on endurance athletes cannot be compared to anaerobic athletes

32. FTES: CORT Indicator of anabolic-catabolic status of the individual Correlation exists between an increase in strength and increase in ratio Decreaes of 30% indicate insufficient regeneration in sprint and strength sports Responses can vary from different exercise prescriptions Can vary over the course of a mesocycle

33. Free Testosterone and Cortisol

35. Catecholamines Regulate metabolic and cardiocirculatory reactions and adaptations to physical and psychological stress. Exercise induced responses are due to SNS input and correlated with exercise intensity Shorter high intensity exercise results in greater catecholamine secretion and shows a higher Epi:NE ratio

36. Catecholamines Due to NE spillover from SNS synapses Also, high psych stress during physical exercise is followed by obvious increases in Epi and NE. With endurnace training, a decrease in glycogen availablility increases catecholamine levels, yet resting levels decreased.

37. Lack of Ref Value – Individual differences Knowledge of hormonal regulation Need large sample volumes Expensive Diurnal variations Influence of external factors Different plasma half lives Monthly hormonal fluctuation - females Problems with Hormonal Markers

38. Plasma Creatine Kinase A well-documented index of muscle damge in athletes Found to be elevated in some along with elevations of myoglobin and lactate dehydrogenase Well-trained athletes may not exhibit increased levels (reg ecc training) Females – estrogen may have a membrane stabilizing effect

39. Peak Plasma Lactate Intermediate product in the breakdown of glycogen Decreased PBL response indicates parasympathetic OT (standardized maximal test) Corresponds with glycogen level depletion

41. Resting and Peak Blood Lactate

43. Plasma Glutamine Decrease could be due to an increased demand by tissues, decreased production or altered transport kinetics Baseline levels are higher in elite athletes Acute OT = depressed levels of plasma glutamine (no studies on O-R) after prolonged exercise but not after short-term exercise

44. Glutamine 5 days of overload training resulted in decreased levels and permanently low levels found during periods of prolonged training and in OT athletes Linked to chronic states of fatigue Plasma levels increase temporarily after injestion of a meal containing protein

45. MarkerNormal Training Heavy Training Plasma Cortisol (nM) 431471 Plasma Glutamine (цM) 686646 Plasma CPK (U/l) 137564 Endurance athletes at rest and after 2-3 weeks of heavy intensified training Source: Gleeson, Review 2002

46. Volume Intensity TEST rest & acute no change CORTISOL rest and acute no change or slight decrease FTES:CORT rest and acute No change EPI unknown acute NE Unknown acute LACTATE acute CPK UnknownNormal training values Resistance Exercise Overreaching and Overtraining Fry and Kraemer 124

47. Suggested Battery of Tests to Detect Impending OTS Performance testing Profile of Mood State Questionnaire Log of responses to training (fatigue, soreness) PBL and Plasma cortisol response Plasma CPK activity Nocturnal urinary NE and Epi secretion Routine haemotology (Hb, Fe, Leukocyte #) Feedback to coach

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