OVERTRAINING SYNDROME A Review of Contributing Factors and Markers of Regeneration Status among Anaerobic, Intermittent Sport Athletes Carmen Bott November 18, 2003 HKIN 562 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 athlete’s tolerance of the stress 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. Classical Symptoms • Physiological • Psychological • Immunological • Biochemical Fry et al 1991 Physiological • Decreased performance (time, %RM) • Inability to meet previous performance • Recovery Prolonged • Decreased muscular strength & work capacity • Loss of Coordination • Chronic Fatigue Psychological • Feelings of Depression • General Apathy • Emotional instability • Difficulty concentrating • Fear of competition Immunological • Increased susceptability to and severity of illnesses, colds and allergies • Flu-like illness • Minor scratches that heal slowly • Bacterial infections Biochemical • Negative Nitrogen balance • Depressed muscle glycogen concentration • Mineral depletion (zinc, cobalt, aluminum, selenium, copper) • Elevated cortisol • Low free testosterone 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 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 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 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 A Continuum of OT Sx (Fry et al) Some symptoms disappear Increasing state of fatigue Continued intensive training Increasing complexity & severity of Sx Acute Overload Over- fatigue stimulus reaching OTS Pathogenesis 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 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 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. 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 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 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 The Cytokine Hypothesis • Neutrophil accumulation monocyte accumulation • Upregulation of cytokines • Released from monocytes; they direct local inflammatory responses and activate immune cells and direct influx of WBCs 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 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 Review of Markers Detection of Impending OTS: • Endocrine Markers • Testosterone, cortisol and ftes:cort • Catecholamines • Plasma Markers • Creatine Phosphokinase (CPK) • Peak Blood Lactate • Glutamine • Cytokines 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 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 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 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 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 Free Testosterone and Cortisol Subject A: FTES & A.M. CORT Levels 10 700 600 8 526 500 pmol/L nmol/L 6 421 369 400 4 300 3.1 200 2 2.3 1.6 100 0 0 1 week FTES CORT Free Testosterone and Cortisol Subject B: FTES & A.M. CORT Levels 100 700 90 600 80 500 pmol/L nmol/L 70 381 400 60 351 352 300 50 40 200 34.3 37.9 30 100 25.4 20 0 1 Week FTES CORT 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 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. Problems with Hormonal Markers 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 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 Peak Plasma Lactate • Intermediate product in the breakdown of glycogen • Decreased PBL response indicates parasympathetic OT (standardized maximal test) • Corresponds with glycogen level depletion Resting and Peak Blood Lactate Subject A: Resting and Peak Blood Lactate Levels 14 13.1 11.3 11.8 11.3 12 9.9 10 9.2 7.9 7.8 Subject A RBL mmol/L 8 Subject A RBL 6 Subject A PBL 4 2 0 Week Week Week Week Week Week Week Week 1 2 3 4 5 6 7 8 Week Resting and Peak Blood Lactate Subject B: Resting and Peak Blood Lactate Levels 12 11 11 11.3 11.3 11.4 10.9 10 8 RBL mmol/L 6 5 RBL 3.8 3.9 PBL 4 2.7 2.3 2 2.2 2.2 1.6 1.8 1.8 2 0 0 00 0 0 0 0 Week 1 Week 2 Week 3 Week 4 Week 5 Week 6 Week 7 Week 8 Week 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 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 Endurance athletes at rest and after 2-3 weeks of heavy intensified training Marker Normal Heavy Training Training Plasma 431 471 Cortisol (nM) Plasma 686 646 Glutamine (цM) Plasma 137 564 CPK (U/l) Source: Gleeson, Review 2002 Resistance Exercise Overreaching and Overtraining Volume Intensity TEST rest & acute no change CORTISOL rest and no change or acute slight decrease FTES:CORT rest and No change acute EPI unknown acute NE Unknown acute LACTATE acute acute CPK Unknown Normal training values Fry and Kraemer 124 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 References • Halson, S. 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