Research Blog

Overtraining: its effects on performance and psychological state

Soccer superstar Landon Donovan, a case study in overtraining

Soccer superstar Landon Donovan (right) has been the face of American soccer for the last 10 years. He recently stunned  soccer fans by taking a break from the beautiful game citing mental and physical exhaustion. Landon Donovan's public lack of motivation and mental and physical fatigue are surely signs of overtraining syndrome. Fortunately, after several months of rest he was able to return to the pitch. Here we discuss overtraining's effect on the athletes'  performance, cognition and mood. In addition, scientists have recently isolated a molecule that may be responsible for overtraining syndrome.

Overtraining syndrome is prevalent throughout athletics, regardless of sport. Studies have shown that over half of professional soccer players will experience overtraining syndrome during a season, 60% of distance runners will experience overtraining syndrome at some point in their career and a third of athletes at a six week basketball camp experienced overtraining syndrome. Overtraining occurs in both high volume training regimens, like swimming programs, and high intensity training regimens, like weightlifting.  Overtraining refers to the act of training above the body's capacity for recovery which results in overtraining syndrome. As with any disease or disorder, the first question to ask is what are the signs and symptoms of overtraining syndrome?

Signs and Symptoms of Overtraining Syndrome:
Decreased physical performance
General fatigue, feeling lethargic
Change in appetite
Irritable, restless, excitable, anxious
Loss of bodyweight
Loss of motivation
Lack of mental concentration
Feelings of depression

What is interesting about these symptoms is that researchers currently believe that overtraining can take one of two routes depending on the style of training: overtraining syndrome through the sympathetic nervous system or the overtraining syndrome via the parasympathetic nervous system. Both are divisions in the body's autonomic nervous system. The sympathetic nervous system is responsible for fight-or-flight response: elevating heart rate, releasing adrenaline and blood vessel constriction at the digestive organs among other functions. The parasympathetic nervous system is primarily active while at rest and essentially slows down the heart rate and activates the digestive and other housekeeping organs. It is believed that high volume aerobic training can bring on parasympathetic overtraining symptoms such as fatigue.  High intensity training leads to sympathetic overtraining symptoms such as excitability, anxiety and insomnia. Whether through high intensity or high volume training, understanding how to prevent overtraining syndrome is naturally beneficial to athletes and their coaches.

Maintaining a balance between training at a sufficient intensity or volume to generate increased performance without leading to overtraining syndrome often requires that coach and athlete work together to individualize a training program. Undertraining  and acute overload do not produce the desired performance improvement. To produce an optimal improvement in athletic performance the athlete must train by overreaching: stressing the body through muscle overload, but with proper rest for recovery. Training above the body's capacity for recovery, overtraining, is detrimental to performance and leads to overtraining syndrome. The figure below, adapted from a great review on the subject (The Unknown Mechanism of the Overtraining Syndrome, 2002. Armstrong and VanHeest), demonstrates the effects that increasing training intensity or volume has on the body and performance.

ExerciseMed has discussed immunity weakness following prolonged exercise, called the open window theory, and chronic fatigue brought on by glycogen depletion. Apparently, neither of these physiological deficiencies are responsible for overtraining syndrome. Clues on the root of overtraining syndrome can be found in its similarity to other psychological disorders. The way the body reacts to overtraining follows the pattern laid out by general adaptation syndrome: alarm, resistance and exhaustion. Each stage is founded upon hormone imbalances. Mood imbalance is another factor. A ten-year study found that college swimmers' scores on a profile of mood states test rose in a dose-dependent manner with training volume over the course of the competitive swimming season, only returning to baseline at the conclusion of the season (Psychological monitoring of overtraining and staleness, 1987. Morgan, et al.).  Perhaps the most striking lead to the physiological nature of overtraining syndrome comes from its similarity to major depression.

Many of the characteristics of overtraining symptom overlap with major depression. In fact, 80% of the overtrained swimmers in Morgan's study were found to be clinically depressed; that is, depressed according to diagnosis with their signs and symptoms. Besides the signs and symptoms, biochemical markers are similar as well. Blood cortisol levels are decreased in both overtraining syndrome and major depression. Epinephrine levels are also altered in both. The adrenal dysfunction (responsible for epinephrine) and cortisol reduction implicate two separate neuroendocrine axis: the sympathetic-adrenal medullary and the hypothalamic-pituitary-adrenocortical axis. Neurotransmitter serotonin and its predecessor tryptophan are altered by both disorders, either in production or reception. Furthermore, anti-depressants have successfully been used to treat both the physical and psychological components of overtraining syndrome in elite athletes.

Recently, much excitement has been generated in the neurology and physiology communities over exercise-induced neurogenesis and brain plasticity. While exercise increases neurogenesis, overtraining and major depression alike result in reduced brain plasticity and neural retraction in animal models. One potential candidate for causing this exercise effect is AMPK agonist 5-Aminoimidazole-4-carboxyamide-1-Beta-D-ribofuranoside (AICAR). Interestingly, 7 days of treatment with AICAR on mouse models produced neurogenesis and enhanced memory, but 14 days of treatment diminished this effect (Muscle fatigue and cognition:what is the link? 2012. Kobilo and van Praag). However, because AICAR cannot cross the blood brain barrier it likely acts through another, as of now, unknown signaling molecule.

Understanding overtraining syndrome is fruitless without understanding how to treat it. It is important to realize that outside stressors play a role in overtraining syndrome. The best defense is to keep outside stress to a minimum. If this is not possible due to occupational or family obligations, it may be a good idea to reduce training volume or intensity during periods of high outside stress. Keep the body healthy: stay hydrated, maintain caloric balance, and keep up on sleep. Whether an athlete or the athlete's coach or doctor, be aware of the psychological state of the athlete through conversation or mood questionnaires. Finally, treat overtraining syndrome with rest. The longer the overtraining syndrome has occurred, the longer the rest treatment needed.

Researchers are just beginning to understand the complexities of overtraining syndrome, this young exercise physiology frontier will yield new discoveries through cross-disiplinary research.

Exercise Intensity for Optimal Fat Oxidation

Overweight boy tries to shed some pounds by running.

For those exercising to shed pounds (like this boy to the right) finding the optimal exercise intensity for burning fat may aid in weight loss. It appears that the although the exercise intensity that peak fat oxidation rate occurs is similar in males and females, but is influenced by training and obesity.

During exercise the body has three primary sources of energy to choose from: carbohydrates, fats and proteins. Carbohydrates are broken down faster and require less oxygen consumption per calorie than fats or proteins. For this reason, carbohydrates stored in the muscle or liver are the body's primary source of energy during intense exercise lasting 1 to 20 minutes in duration. During exercise shorter than a minute, the body utilizes phosphocreatine in the muscle. Phosphocreatine transfers its high energy phosphate group to ADP forming ATP, the muscles direct source of energy. Because glycogen in the muscle and liver is rapidly depleted during intense exercise, the body must begin using fats for ATP production during exercise lasting longer than 20 minutes in duration. Because the rate of energy substrate utilization and oxygen consumption are not the principal limiting factors during less intense exercise, the body uses fats for energy in an effort to conserve its stores of precious glycogen. Fats are used for energy production as free fatty acids in a process called beta oxidation. Proteins generally play a more minor role during exercise because they are not readily broken down for energy.

Understanding the optimal exercise intensity for maximum fat utilization is useful for patients trying to lose excess fat. The exercise intensity must balance between achieving a high enough exercise intensity so that significant calories are used, but not such a high exercise intensity that carbohydrates become the preferred source of energy. Several research groups have looked into the optimal exercise intensity to maximize fat oxidation. Apparently it differs for the exercise performed and the demographics of the subjects. This suggests that the optimal exercise intensity for fat oxidation should be tailored to the individual.

A study in 2008 found that the absolute peak fat oxidation was similar in males and females when scaled to fat-free mass, but lower in overweight individuals (Peak fat oxidation rate during walking in sedentary overweight men and women, 2008. Bogdanis, et al.). In this study the exercise activity was walking and the subjects were sedentary overweight men and women. Exercise intensity was measured as a percent of maximal heart rate and oxygen consumption (%VO2max). VO2max is the velocity at which maximum oxygen is consumed and therefore represents the maximum aerobic energy output.  The energy substrates can be determined based on the ratio of oxygen consumed and carbon dioxide expired. This is called the respiratory quotient and is represented as O2 consumed divided by CO2 expired. The figure below shows how the contribution of fats and carbohydrates varies with exercise intensity (measured with %VO2max).

Percent Fat and carbohydrate (CHO) contribution to the energy expenditure at each stage of the treadmill test for men and women, and peak fat oxidation rates (as %fat), plotted against the relative exercise intensity (%VO2max). Values are mean± SE.

The peak fat oxidation rate in the overweight men and women was similar, about 40% of VO2max. This corresponded to about 59% of maximal heart rate.  A large amount of variation in the results suggests that exercise intensity ideally would be individually tailored. The absolute peak fat oxidation, when scaled to body mass, was lower than similar studies looking at subjects who are not overweight. The figure below demonstrates the distribution of exercise intensities that peak fat oxidation occurred displayed in box plots.

Optimal exercise intensity for fat oxidation.  Box plots of relative exercise intensity that elicited peak fat oxidation (PFO) rate in men and women, expressed as a percentage of maximal heart rate (%HRmax) and maximal oxygen uptake (%VO2max).

Why overweight persons have a lower fat oxidation capacity is not known. It is possible that it is a factor that leads to obesity; after all, a reduced capacity to utilize fat would theoretically make it harder to burn fat off. However, it could also stem from being overweight from a currently unknown pathway. 

A more recent study found that exercise training increases the exercise intensity slightly for peak fat oxidation rate (Effects of supervised exercise training at the intensity of maximal fat oxidation in overweight young women, 2012.  Tan, et al.). This study used running, rather than walking, to measure exercise intensity. The subjects were young, overweight, Chinese women. The experimental group completed a 8-week training program. The training program was 5 days a week and consisted of a 10 minute warm-up (stretching and jogging), 40 minutes running at the peak fat oxidation velocity as determined for each individual, followed by a 10 minute cool down (walking and stretching). The maximal fat oxidation occurred at 34.1% of VO2max prior to training and 36.9% of VO2max after the 8-week training period. Both exercise intensities are lower than the aforementioned study with walking as the exercise type. Fat mass was significantly reduced; subjects lost an average of 13% of their fat mass. No significant change was observed in the controls who did not participate in the training program. 

Both these studies suggest that understanding the exercise intensity at which maximal fat oxidation occurs may be able to make exercise more effective at reducing body fat. Although the exercise intensity at which maximal fat oxidation occurs varies considerably in the general population, having a general idea of where it occurs could aid individuals in burning fat during exercise. As these two studies show, and other studies lend support, the exercise intensity, as measured by percent of VO2max and percent of maximum heart rate, vary across exercise character.

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