Carmen BottNovember 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 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
Some symptoms disappear
Increasing state of fatigue
Continued intensive training
Increasing complexity & severity of Sx
Acutefatigue
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
Subject A: FTES & A.M. CORT Levels
1.6
3.12.3
526
421369
0
2
4
6
8
10
1
week
pmol
/L
0
100
200
300
400
500
600
700
nmol
/L
FTES CORT
Free Testosterone and Cortisol
Subject B: FTES & A.M. CORT Levels
25.434.3 37.9
351 381 352
2030405060708090
100
1
Week
pmol
/L
0
100
200
300
400
500
600
700
nmol
/L
FTES CORT
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
Subject A: Resting and Peak Blood Lactate Levels
11.3 11.813.1
7.9
9.9
7.89.2
11.3
0
2
4
6
8
10
12
14
Week1
Week2
Week3
Week4
Week5
Week6
Week7
Week8
Week
mm
ol/L
Subject A RBL
Subject A RBL
Subject A PBL
Resting and Peak Blood Lactate
Subject B: Resting and Peak Blood Lactate Levels
0
1.62.3 2.2
5
1.8
3.9
00
3.8
2 2.2 1.82.7
0 0
11 11 10.9 11.3 11.3 11.4
0 00
2
4
6
8
10
12
Week 1 Week 2 Week 3 Week 4 Week 5 Week 6 Week 7 Week 8
Week
mm
ol/L
RBL
RBL
PBL
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
Marker Normal Training
Heavy Training
Plasma
Cortisol (nM)
431 471
Plasma Glutamine (цM)
686 646
Plasma
CPK (U/l)
137 564
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 acute
CPK Unknown Normal 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) 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 2003;31(8):39-45.• • 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.• •
References
• 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, 1988.
• • Dressendorfer RH, Wade CE, Iverson D (987( Decereased Plasma testosterone in overtrained runners (abstract). Med Sci Sports exerc
19:S10.• • 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-
245.• • 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, 31-41.