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

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

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

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)

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

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

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

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.

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

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

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

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

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

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. G.I. Lancaster, A. Jeukendrup, and M. Gleeson. Immunological Respnses to overreaching in cyclists. Medicine and Science in Sports and exercise. 35 (5) Hooper, Sue et al.: Markers for Monitoring Overtraining and Recovery. Medicine and Science in Sports and Exercise Kraemer, William J.:Strength Training Basics, Designing Work-outs to Meet Patients Goals. The Physician and Sports Medicine 2003;31(8): Lehmann, M, Foster, C, Dickhuth, Hans-Herman, Uwe, A: Autonomic imbalance hypothesis and overtraining syndrome. Medicine and Science in Sports and Exercise, (7) Lieber, Richard an Friden, Jan.: Muscle Damage is not a function of muscle force but of active muscle strain. Journal of Applied Physiology 1993; 74: Petibois, Cyril et al.: Biochemical Aspects of Overtraining in Endurance Sports. Review Article. Sports Medicine 2002; 32(13): Pichot, V., T.Busso, F. Roche, M. Garet, F. Costes, D. Duverney, J.R. Lacour and J.C. Barthelemy. Autonomic adaptations to intensive and overload training periods: a laboratory study. Medicine and Science in Sports and Exercise. Vol 34(10), Rowbottom, David, Keat, David and Morton, Alan. The emerging role of glutamine as an indicator of exercise stress and overtraining a review. Sports Medicine 1996; 21 (2): Rowbottom, Keast, Goodman and Morton: The haematological, biochemical and immunological profile of athletes suffering from the overtraining syndrome. European Journal of Applied Physiology 1995; 70: Smith, Lucille Lakier.: Overtraining, Excessive Exercise, and Altered Immunity. Review Article. Sports Medicine 2003; 33(5): Snyder, Ann C., H Kuipers, Bo Cheng, Rodrique Servais and Erik Fransen. Overtraining following intensified training with normal muscle glycogen. Medicine and Science in Sports and exercise, , ACSM position paper: pp 1-6.

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