Thomas M. Howard
Overtraining has been described and has been well known to athletes and trainers for decades. In 1923, Dr. Parmenter described overtraining as “a condition difficult to detect and still more difficult to describe. Evaluation should focus on training load, nutrition, sleep, rest, competition stress, and psychological state” (14).
There are multiple hypotheses on the cause of overtraining. There continues to be research on overtraining to further define the condition and pathophysiology and identify markers for diagnosis, treatment, and prevention.
Overtraining, if left unrecognized or untreated, can result in injury, poor performance, and early retirement.
Overtraining syndrome is a condition that arises along a continuum of fatigue.
The diagnosis of overtraining syndrome is one of exclusion and often requires an extensive workup of the athlete.
Treatment of overtraining syndrome is rest; however, it often requires a multidisciplinary approach involving the physician, trainers, nutritionist, and often, a sports psychologist.
Training: A series of stimuli or displacement of homeostasis to provide stimulation for adaptation. A progressive overload in an effort to improve performance.
Adaptation: A physiologic response to stress that results in an adjustment in function.
Recovery: Period of time following a training stimulus when adaptation occurs, resulting in supercompensation to allow better performance in the future (i.e., the training effect). Recovery includes hydration, nutritional replenishment, sleep/rest, stretching, relaxation, and emotional recovery.
Periodization: Planned sequencing of increased training loads and recovery periods within a training program.
Overreaching: A short-term decrement in performance after a period of overload (intensity or volume). This acute phase is thought to last 1-2 weeks. Some authors even consider overreaching to represent normal physiologic fatigue to overload training (2).
Overtraining syndrome: This syndrome is defined as prolonged decrease in sport-specific performance, usually > 2 weeks. It is manifested by premature fatigability, emotional and mood changes, lack of motivation, sleep disorders, pronounced vegetative somatic complaints, overuse injuries, and immune dysfunction (2,8,9). It is the result of prolonged heavy exercise over an extended period of time with inadequate recovery time between training sessions.
PHYSIOLOGIC CHANGES WITH TRAINING
Decreased salivary immunoglobulin A (IgA)
Increased white blood cells (WBCs), lymphocytes, natural killer cells, and polymorphonuclear cell (PMN) activity
Transient decrease in T helper/T suppressor (Th/Ts) ratio
Decreased serum glutamine
Increased testosterone proportional to exercise intensity and muscle mass stimulating glycogen regeneration and protein synthesis (anabolism).
Transient increase in cortisol relative to the duration and intensity of exercise. The stress response (catabolism).
The ratio of free testosterone to cortisol (FTCR) represents the balance of catabolism and anabolism. A 30% decrease in this ratio may suggest inadequate recovery or overreaching (5).
Norepinephrine increases before exercise (anticipation) and early in exercise, stimulating lipolysis.
Epinephrine increases proportional to exercise intensity.
Decreased sex hormone binding globulin (SHBG) production with intense exercise.
Suppression of pulsatile secretion of gonadotropin-releasing factor (GnRH), probably affected by stress and poor nutrition.
Growth hormone peak secretion at night and with exercise ˜50% [V with dot above]O2max, blunted response with intense exercise.
Overtraining affects 5%-15% of elite athletes at any one time and as much as two-thirds of runners during an athletic career. It may also be seen in amateur athletes.
More commonly seen in endurance events, such as swimming, cycling, or running. Overtraining in powerlifters is probably different.
Susceptible athletes include highly motivated, goal-oriented individuals; athletes who design exercise programs by themselves; and athletes that tend to be focused, conventional, and conservative.
Glycogen depletion: Chronic nutritional deficiency and extensive periods of heavy training lead to glycogen depletion in muscles, resulting in peripheral fatigue. Central fatigue is interrelated to changes in branched-chain amino acids (BCAAs); see central fatigue hypothesis (18).
Central fatigue hypothesis/BCAA hypothesis: Peripheral fatigue and nutrient depletion lead to the consumption of BCAAs with subsequent change in the BCAA to free tryptophan ratio in plasma. This favors transport of tryptophan into the central nervous system. Tryptophan is a precursor for serotonin 5-hydroxytryptamine, which causes central fatigue (1,6).
Autonomic imbalance: An increase in sympathetic activity from stress and overloaded target organs and increased catabolism leading to decreased sympathetic intrinsic activity. Chronically increased catecholamine levels causes downregulation of receptors and fatigue (12).