Overtraining appears to be caused by too much high intensity training and/or too little regeneration (recovery) time often combined with other training and nontraining stressors. There are a multitude of symptoms of overtraining, the expression of which vary depending upon the athlete's physical and physiological makeup, type of exercise undertaken and other factors. The aetiology of overtraining may therefore be different in different people suggesting the need to be aware of a wide variety of parameters as markers of overtraining. At present there is no one single diagnostic test that can define overtraining. The recognition of overtraining requires the identification of stress indicators which do not return to baseline following a period of regeneration. Possible indicators include an imbalance of the neuroendocrine system, suppression of the immune system, indicators of muscle damage, depressed muscle glycogen reserves, deteriorating aerobic, ventilatory and cardiac efficiency, a depressed psychological profile, and poor performance in sport specific tests, e.g. time trials. Screening for changes in parameters indicative of overtraining needs to be a routine component of the training programme and must be incorporated into the programme in such a way that the short term fatigue associated with overload training is not confused with the chronic fatigue characteristic of overtraining. An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme. Screening for overtraining and performance improvements must occur at the culmination of regeneration periods.

Overtraining in athletes. An update.

Overtraining is an imbalance between training and recovery. Short term overtraining or ‘over-reaching’ is reversible within days to weeks. Fatigue accompanied by a number of physical and psychological symptoms in the athlete is an indication of ‘stateness’ or ‘overtraining syndrome’. Staleness is a dysfunction of the neuroendocrine system, localised at hypothalamic level. Staleness may occur when physical and emotional stress exceeds the individual coping capacity. However, the precise mechanism has yet to be established. Clinically the syndrome can be divided into the sympathetic and parasympathetic types, based upon the predominance of sympathetic or parasympathetic activity, respectively. The syndrome and its clinical manifestation can be explained as a stress response. At present, no sensitive and specific tests are available to prevent or diagnose overtraining. The diagnosis is based on the medical history and the clinical presentation. Complete recovery may take weeks to months.

Overtraining in elite athletes. Review and directions for the future.

In the natural habitat of our ancestors, physical activity was not a preventive intervention but a matter of survival. In this hostile environment with scarce food and ubiquitous dangers, human genes were selected to optimize aerobic metabolic pathways and conserve energy for potential future famines.1 Cardiac and vascular functions were continuously challenged by intermittent bouts of high-intensity physical activity and adapted to meet the metabolic demands of the working skeletal muscle under these conditions.

When speaking about molecular cardiovascular effects of exercise, we should keep in mind that most of the changes from baseline are probably a return to normal values. The statistical average of physical activity in Western societies is so much below the levels normal for our genetic background that sedentary lifestyle in combination with excess food intake has surpassed smoking as the No. 1 preventable cause of death in the United States.2

Physical activity has been shown to have beneficial effects on glucose metabolism, skeletal muscle function, ventilator muscle strength, bone stability, locomotor coordination, psychological well-being, and other organ functions. However, in the context of this review, we will focus entirely on important molecular effects on the cardiovascular system. The aim of this review is to provide a bird's-eye view on what is known and unknown about the physiological and biochemical mechanisms involved in mediating exercise-induced cardiovascular effects. The resulting map is surprisingly detailed in some areas (ie, endothelial function), whereas other areas, such as direct cardiac training effects in heart failure, are still incompletely understood.

For practical purposes, we have decided to use primarily an anatomic approach to present key data on exercise effects on cardiac and vascular function. For the cardiac effects, the left ventricle and the cardiac valves will be described separately; for the vascular effects, we will follow the arterial vascular …

Cardiovascular Effects of Exercise Training Molecular Mechanisms

When prolonged, excessive training stresses are applied concurrent with inadequate recovery, performance decrements and chronic maladaptations occur. Known as the overtraining syndrome (OTS), this complex condition afflicts a large percentage of athletes at least once during their careers. There is no objective biomarker for OTS and the underlying mechanism is unknown. However, it is not widely recognised that OTS and clinical depression [e.g. major depression (MD)] involve remarkably similar signs and symptoms, brain structures, neurotransmitters, endocrine pathways and immune responses. We propose that OTS and MD have similar aetiologies. Our examination of numerous shared characteristics offers insights into the mechanism of OTS and encourages testable experimental hypotheses. Novel recommendations are proposed for the treatment of overtrained athletes with antidepressant medications, and guidelines are provided for psychological counselling.

The unknown mechanism of the overtraining syndrome: clues from depression and psychoneuroimmunology.

Healthy humans regulate daily water balance remarkably well across their lifespan despite changes in biological development and exposure to stressors on hydration status. Acute or chronic body water deficits result when intakes are reduced or losses increase, but day-to-day hydration is generally well maintained so long as food and fluid are readily available. Total water intake includes drinking water, water in beverages, and water in food. Daily water needs determined from fluid balance, water turnover, or consumption studies provide similar values for a given set of conditions. A daily water intake of 3.7 L for adult men and 2.7 L for adult women meets the needs of the vast majority of persons. However, strenuous physical exercise and heat stress can greatly increase daily water needs, and the individual variability between athletes can be substantial.

Human water needs

Adrenal-sympathico function, blood carbohydrates and lipids, and water and electrolyte balance were studied in six highly trained male marathon runners prior to and after running a marathon (26.2 miles; 42.2 km) and on control days corresponding to the above times. Fluid intake was not sufficient to maintain body weight, the runners losing approximately 2.8 kg. Estimated plasma volume losses (161 ml, 4.4%) indicated that most of the fluid loss was extravascular. Tre rose an average 2.4 degrees C and a significant negative correlation between running time and rise in Tre was observed. Glucose, fatty acids, glycerol, hemoglobin, and plasma proteins were significantly elevated after the race. Small but statistically significant increments in lactate and pyruvate were also observed. Alterations in adrenal-sympathico function were indicated by increased levels of cortisol, epinephrine, and norepinephrine.

Acute blood biochemical alterations in response to marathon running.

The occurrence of possible prolonged alterations in plasma levels of cortisol, epinephrine, norepinephrine, selected energy metabolites, and water and electrolyte balance was assessed in six highly trained male marathon runners by measuring blood biochemical constituents on the 10th day before and for the three days following the running of a marathon. Post-race changes in hemoglobin, hematocrit, and protein levels indicated that a hemodilution had occurred, possibly as a result of elevated sodium levels. Epinephrine remained elevated until the second day. Cortisol was depressed on the first and third post-race days while variable levels were observed on the second day. No prolonged alterations were noted in norepinephrine, FFA, glycerol, triglycerides, glucose, lactate, and pyruvate.

Michael B. Maron

Papers

Acute blood biochemical alterations in response to marathon running.

Blood biochemical alterations during recovery from competitive marathon running.