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.