Conducting primary research studies on the causes of overtraining is difficult because it’s unethical to induce overtraining syndrome, which can damage a person’s performance for months. Kreher and Schwartz (2012) reviewed previously published overtraining research and summarized seven hypotheses (see Figure 5) for mechanisms that cause overtraining syndrome.
HYPOTHESIS #1: AUTONOMIC NERVOUS SYSTEM IMBALANCE
This represents an imbalance between the parasympathetic and sympathetic nervous systems, which directly impacts HRV. In overtrained athletes, decreased HRV on waking may disrupt normal modulation of the autonomic nervous system. Balance between sympathetic and parasympathetic forces may be restored after a week of rest (Pichot et al. 2002).
HYPOTHESIS #2: OXIDATIVE STRESS
Excessive oxidative stress leads to muscle damage and muscle fatigue. Oxidative stress is a disruption in the balance between the production of reactive oxygen species (like free radicals) and antioxidant defenses in the cells that neutralize free-radical buildup. Skeletal muscle is the body’s largest consumer of oxygen and is vulnerable to oxidative stress. Oxidative stress can cause damage to mitochondrial proteins, cell membranes and even DNA (Sayer et al. 2013).
HYPOTHESIS #3: GLYCOGEN DEPLETION
Low levels of muscle glycogen may impair performance if a person’s diet is inadequate for the amount of exercise they are performing. Kreher and Schwartz (2012) say some research suggests that glycogen depletion can alter the synthesis of central neurotransmitters involved in fatigue.
HYPOTHESIS #4: CENTRAL FATIGUE
Overtraining often disrupts mood, sleep and behavior. The central fatigue hypothesis proposes that the central nervous system is not providing adequate drive to recruited working muscles. Kreher and Schwartz (2012) say central fatigue results from numerous physiological changes, including increases in brain levels of tryptophan (an essential amino acid involved in protein biosynthesis), decreased branched-chain amino acid (BCAA) concentrations, and increased synthesis of serotonin (a neurotransmitter) in the brain.
HYPOTHESIS #5: GLUTAMINE DEPLETION
Glutamine is important for immune function. Glutamine also plays a role in DNA synthesis, acid-base balance, and gluconeogenesis—making new glucose or energy for exercise. Low plasma glutamine concentrations have been reported in overtrained individuals (Halson & Jeukendrup 2004).
HYPOTHESIS #6: INCREASED INFLAMMATION
The increased inflammation or cytokine hypothesis suggests that overtraining syndrome is a physiological adaptation or maladaptation to excess stress initiated by an imbalance between training and recovery (Smith 2000). Those who train at a very intense level for long periods of time without adequate rest may enter a state of chronic inflammation with high levels of cytokines. This chronic inflammation has been highly correlated with overtraining syndrome (Smith 2000).
HYPOTHESIS #7: DYSREGULATION OF THE HYPOTHALAMUS
Kreher and Schwartz (2012) summarize several studies indicating that cortisol, testosterone and other hormones regulated by the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axes may be altered when clients (especially endurance exercise clients) are overtraining.
For more information about ways to prevent overtraining, plus a much wider discussion of the topic and a full reference list, please see “Heart Rate Variability & Overtraining” in the online IDEA Library or in the January 2015 print issue of IDEA Fitness Journal. If you cannot access the full article and would like to, please contact the IDEA Inspired Service Team at (800) 999-4332, ext. 7.
Halson, S.L., & Jeukendrup, A.E. 2004. Does overtraining exist? An analysis of overreaching and overtraining research. Sports Medicine, 34 (14), 967-81.
Kreher, J.B., & Schwartz, J.B. 2012. Overtraining syndrome: A practical guide. Sports Health, 4 (2), 128-38.
Pichot, V., et al. 2002. Autonomic adaptations to intensive and overload training periods: A laboratory study. Medicine & Science in Sports & Exercise, 34 (10), 1660-66.
Sayer, A.A., et al. 2013. New horizons in the pathogenesis, diagnosis and management of sarcopenia. Age and Ageing, 42 (2), 145-50.
Smith, L.L. 2000. Cytokine hypothesis of over- training: A physiological adaptation to excessive stress? Medicine & Science in Sports & Exercise, 32 (2), 317-31.
Regular exercise helps inflammation as an effective protector and treatment against chronic diseases associated with low-grade inflammation.