Overtraining, a cause of impaired
Fact or Fiction?
By Sune Persson, DVM, Ph.D., Professor em.
Swedish University of Agricultural Sciences
Department of Large Animal Clinical Sciences
P.O. Box 7018, SE-750 07 Uppsala, Sweden
Prolonged fast work training produces an increase of the total red cell volume (RCV) in the horse. Provided the normal variations due to breed, sex, age, and body size are considered RCV is related to state of training, racing performance, and various markers for exercise tolerance e.g. heart rate (HR), blood lactate (LA), and oxygen uptake (VO²) responses to track and treadmill exercise.
In Sweden, however, Standardbred trotters with impaired racing performance referred for clinical exercise tolerance testing frequently have an abnormally increased total red cell volume i.e. significantly exceeding the reference values for the respective sex and age groups of normally performing trotters (RCHV- red cell hypervolaemia). In some cases, RCHV appears to be associated with clinical entities such as heart disease, chronic obstructive pulmonary disease, and exercise induced pulmonary haemorrhage. In most horses with RCHV, however, thorough clinical examination at rest does not lead to a diagnosis of disease and these horses have been suggested to be 'overtrained', i.e. they have developed a chronic stress syndrome due to prolonged excessive fast work training and racing and exhibit diminished racing performance. Thus, in retrospect, they have fewer annual placings in races, earn less prize money, and perform slower racing speed than in the previous, usually successful, racing career. In Sweden, an attempt to evaluate current racing form objectively has been made by transformation of racing records reported annually by the Swedish Racing Association to normalize the distribution of number of starts, placings, earnings, and best racing times and calculate an individual performance index (IPI) based on these data. This index may be regarded as a normally distributed phenotypic measure of racing performance of an individual horse in relation to contemporaries of corresponding age and sex in any particular year. IPI, too, drops markedly during the year of diagnosis of RCHV.
In Sweden, trotters usually make their racing debut at the age of two years and are allowed to compete until the age of 12 years. The handicap system is based on accumulated prize money and the races open to horses with large accumulated purses imply gradually tougher competition. In order to remain competitive the horses have to be trained more intensely and are eventually approaching their inherent limit for adaptational capacity. Empirically, intensive early fast work training may result in an initial superior, but, also shorter successful racing career. As an average, these horses may approach their genetically determined limit to adaptation to training and racing after three to four years of racing. Continued intensified training may then result in a state of chronic stress as indicated by a low resting blood level of cortisol and a decreased response to ACTH stimulation indicating adrenocortical exhaustion found in these horses. This results in ceased further improvement of or even declined racing form and development of a secondary RCHV probably due to a relative tissue hypoxia during maximal exercise. These horses frequently show signs of psychic stress being harnessed before a race as indicated by a high resting heart rate, muscle tremor, and sweating and they are excited and pulling hard at the reins during the race.
Thus, in spite of being faster in races even in the year of diagnosis, the RCHV horses do not differ with respect to earnings and placings from the average Standardbred racehorse population (RH) during the years following diagnosis. One important reason for this apparent paradox is that their accumulated purses earned in the previous successful racing careers means that they have to race against tougher concurrent elite competitors. As a consequence of this a steep decline in the number of starts in races occurs following the year of diagnosis and very few RCHV horses are still racing thee years later. This is not entirely due to the fact that mares usually retire from racing at an earlier age than stallions and geldings in order to be used as broodmares. RCHV develops more frequently in male horses than in mares probably due to the stimulating effect of the male sex hormone (testosterone) on the red blood cell production in the bone marrow. This is also evident from the sex distribution in a group of 116 RCHV horses in which mares comprised 13% as against 39% in the cintemporary RH population.
The cause and development of RCHV and the causal association with impaired racing performance are still enigmatic, however. In horses RCHV should be expected to be secondary to insufficient oxygen supply or utilization as primary polycytemia (neoplastic) is virtually unknown in domestic animals. Chronic lung and possibly heart disease have been observed in association with RCHV in race horses, but development of RCHV when evidence of disease impairing oxygen delivery to the tissues is lacking it may be reasonable to assume that a peripheral circulatory disorder causing inadequate oxygen supply to the active muscle fibres during strenuous exercise may induce an increased compensatory, red blood cell production. This hypothesis has yet to be proven, although it is interesting to note that the muscle fibre capillary density is lower in RCHV horses than in RH and, further, to compare this condition with a chronic stress syndrome in man causing ineffective regulation of the peripheral distribution of the blood flow and inadequate oxygen supply to the active muscle groups (vasoregulatory asthenia) during heavy exercise. This syndrome is not uncommon in intensely trained human athletes, although these do not develop RCHV.
Although it doesn't seems likely that RCHV is the cause of the impairment of the racing performance, but, rather, a concomitant marker for a state of overtraining, it does have effects on lung functions. Thus, the increased red cell volume implies that these cells constitute a larger fraction of the blood (hematocrit) increasing the blood viscosity and, consequently, the flow resistance through the central and peripheral capillary beds. This results in greatly increased pulmonic and systemic blood pressures during maximal exercise when the red call reservoir in the spleen is completely mobilized. The pulmonary blood pressure frequently exceeds the tenacity of the capillary wall leading to lung bleeding which appears to occur more frequently in RCHV horses.
There is also evidence of a pulmonary mismatch between ventilation and circulation, reflected in a gradually increasing difference in the ventilation/perfusion ratio (VA/Q) during incremental exercise between RCHV horses and RH leading to lower oxygen content in the arterial blood in the RCHV horses during exercise. This is compensated for, however, by the larger circulating red cell volume and oxygen delivery leading to lack of difference in oxygen uptake between RH and RCHV horses. The significant mismatch in VA/Q together with the presence of blood in the trachea in 83% in a study of a group of RCHV horses after exercise support the hypothesis that stress failure of the capillary and alveolar walls results in exercised induced pulmonary bleeding and in low grade pulmonary oedema.
Standardbred racing may be compared to mid-distance running in the human athlete, i.e. the horses need both a high aerobic and a high anaerobic metabolic capacity to compete successfully. Thus, they need to recruit the fast twitch anaerobic IIB fibres to be able to increase speed in the finish of a race. This means that high speed training and racing will make these fibres gradually more oxidative as indicated by the increased mitchondrial density of these muscle fibres in RCHV horses probably at the expense of their speed of contraction. Thus, these horses, in spite of a high endurance capacity, may no longer be fit for Standardbred racing.
RCHV horses usually have a history of intensified fast work training in an attempt to meet the increasing competitive demands on the race track. Consequently, a change of training schedule with reduced or discontinued fast work training and racing against less tough competition on smaller tracks are usually recommended which may result in a partial, transient improvement of racing performance observed after diagnosis of RCHV.
Although a change in the training regimen of these horses, primarily by reduction of the fast work training, may partly improve the racing performance transiently, RCHV, indicating overtraining, appears to be a significant predictor of prolonged relative impairment of the racing capacity in Standardbred trotters and may denote the end of their previous often successful racing careers.