Overtraining Syndrome

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Overtraining Syndrome Powered By Docstoc
 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
• 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
                     Classical Symptoms
•   Physiological
•   Psychological
•   Immunological
•   Biochemical

    Fry et al 1991
• Decreased performance (time, %RM)
• Inability to meet previous performance
• Recovery Prolonged
• Decreased muscular strength & work
• Loss of Coordination
• Chronic Fatigue
•   Feelings of Depression
•   General Apathy
•   Emotional instability
•   Difficulty concentrating
•   Fear of competition
• Increased susceptability to and severity
  of illnesses, colds and allergies
• Flu-like illness
• Minor scratches that heal slowly
• Bacterial infections
• Negative Nitrogen balance
• Depressed muscle glycogen
• 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
• 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
• 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
     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,
• Stores can become depleted – can drop
  2x during intense endurance exercise
• 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
• 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
           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
   The Cytokine Hypothesis
• Neutrophil accumulation      monocyte
•    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
• 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,
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
 • Questionnaires
 • Logs and RPE
 • Profile of mood states
• Steroid hormone responsible for many
  anabolic and androgenic qualities
• Acute bouts of heavy RT = increased **total
• 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
• 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
•   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
• 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
• Can vary over the course of a mesocycle
Free Testosterone and Cortisol
                        Subject A: FTES & A.M. CORT Levels

         10                                                    700
                  526                                          500

         6                               421
                                                         369 400
         4                                                   300
                                         3.1                   200
         2                                               2.3
                  1.6                                          100
         0                                                     0

                                FTES     CORT
Free Testosterone and Cortisol
                           Subject B: FTES & A.M. CORT Levels

          100                                                   700
           90                                                   600
           80                                                   500

                                            381                 400
           60       351                                   352
           40                                                 200
                                            34.3          37.9
           30                                                 100
           20                                                   0

                                   FTES     CORT
• 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
• 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
Problems with Hormonal
Lack of Ref Value – Individual differences
Knowledge of hormonal regulation
Need large sample volumes
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
• Found to be elevated in some along with
  elevations of myoglobin and lactate
• 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
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

                                                                     Subject A RBL
                                                                     Subject A PBL
              Week Week Week Week Week Week Week Week
               1    2    3    4    5    6    7    8
Resting and Peak Blood Lactate
                     Subject B: Resting and Peak Blood Lactate Levels

         12         11         11                 11.3         11.3      11.4



         6                                                5                                        RBL
                           3.8                                                  3.9                PBL
         4                                                              2.7
                                    2.3 2        2.2
                         1.6                                  1.8     1.8
              0 0                                                                     00   0 0 0
              Week 1 Week 2 Week 3 Week 4 Week 5 Week 6 Week 7 Week 8
         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
• 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
EPI                   unknown             acute

NE                    Unknown            acute

LACTATE                acute             acute

CPK                   Unknown           Normal training
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
•   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) 854-861. 2003.
•   Hooper, Sue et al.: Markers for Monitoring Overtraining and Recovery. Medicine and Science in Sports and Exercise 1995 106-112.
•   Kraemer, William J.:Strength Training Basics, Designing Work-outs to Meet Patient’s Goals. The Physician and Sports Medicine
•   Lehmann, M, Foster, C, Dickhuth, Hans-Herman, Uwe, A: Autonomic imbalance hypothesis and overtraining syndrome. Medicine and
    Science in Sports and Exercise, 1998 30(7) 1140-1145.
•   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: 520-526.
•   Petibois, Cyril et al.: Biochemical Aspects of Overtraining in Endurance Sports. Review Article. Sports Medicine 2002; 32(13): 867-878.
•   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), 1660-1666. 2002.
•   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): 80-97.
•   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: 502-509.
•   Smith, Lucille Lakier.: Overtraining, Excessive Exercise, and Altered Immunity. Review Article. Sports Medicine 2003; 33(5): 347-364.
•   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, 1995 10631070, 1995.
•   ACSM position paper: http://www.acsm.org/USOC_ACSMconsensus.htm pp 1-6.
•   Clarkson, PM, Nosaka, K. Muscle Finction after exercise-induced muscle damage and rapid adaptation. Medicine and Science in Sports and
    Exercise. 24(5); 512-20, 1992
•   Clarkson, PM, Tremblay, I. Exercise-induced muscle damage and rapid adaptation in humans. Journal of Applied Physiology. 65(1) 1-6,
•   Dressendorfer RH, Wade CE, Iverson D (987( Decereased Plasma testosterone in overtrained runners (abstract). Med Sci Sports exerc
•   Fry A.C. and Kraemer, W.J. Resistance exercise overtraining and overreaching neuroendocrine responses Review Article, Sports Medicine.
    1997 23 (2) 106-129
•   Fry A.C., Kraemer, W.J., Van Borselen, F, Lynch, J.M. Triplett, N.T., Koziris, L.P., Fleck, S.J: Catecholamine responses to short-term
    high-intensity resistance exercise overtraining. Journal of Applied Physiology 941-945.
•   Fry, R.W. et al.: Psychological and immunological correlates of acute overtraining. British Journal of Sports Medicine 1994; 28(4) 241-
•   Fry R.W, Morton Alan, Garcia Webb Peter and Keast, David: Monitoring exercise stress by changes in metabolic and hormonal responses
    over a 24-h period. European Journal of Applied Physiology 1991 63: 228-234.
•   Fry R.W., Morton, A, Keast, D. Overtraining in Athletes An Update: Review Article. Sports Medicine 12(1): 32-65, 1991.

•   Gleeson, Michael. Biochemical and immunological markers of overtraining: Review. Journal of sports Science and Medicine 2002 1, 31-