Exercise Intolerance and Poor Performance in Horses

Stephanie J. Valberg • W. David Wilson

The popularity of performance horses has broadened our perspective on health beyond the conventional diagnosis of health or disease in a horse at rest.

Exercise Responses

As horses accelerate during exercise, motor units within active muscles fire in a coordinated fashion to produce the power necessary to drive the animal forward. Initially, slow-twitch type 1 muscle fibers are recruited, followed at increasing speed by recruitment of oxidative fast-twitch type 2A fibers and finally the fastest and most powerful muscle fibers, type 2X. The increased demand for adenosine triphosphate (ATP) to support muscle contractions during exercise can be met initially by small intracellular stores of creatine phosphate, but within seconds oxidative or glycolytic metabolism (or both) is activated. At submaximal speeds the major factors contributing to fatigue are motivation, total depletion of fuel reserves (glycogen), fluid and electrolyte losses, and hyperthermia.¹⁰¹ Nociceptive input from muscle receptors to the brain may be a primary motivator to discontinue exercise in many horses, as in people.¹⁰² Training increases the oxidative and endurance capacity of skeletal muscle by increasing the volume of mitochondria and the capillary density surrounding muscle fibers.¹⁰³ This delays the onset of fatigue by increasing the availability and metabolism of plasma free fatty acids and glucose, thus sparing muscle glycogen. Training also fine-tunes the motor unit recruitment pattern to provide the most efficient and coordinated pattern of movement.

When a horse accelerates toward a maximum speed, a peak in the total amount of oxygen consumed is realized (VO_2max). Additional energy to produce speeds beyond VfO_2max must be supplied by anaerobic glycolysis with lactic acidosis as a consequence. The term anaerobic threshold has been used to describe the speed at which this exponential rise in lactate begins to occur. This inflection point is usually at a velocity producing a blood lactate of 4 mM (VLA₄). Fatigue with maximum (fast) exercise occurs when muscle pH falls so low that glycolysis and excitation contraction coupling are inhibited and muscle ATP concentrations fall.^104,105 Muscle (ATP) begins to decrease after muscle lactate exceeds 40 to 80 mmol/kg of dry muscle and muscle pH falls below 6.8. Overall muscle glycogen stores are not a limiting factor with maximum exercise.¹⁰⁶ Training over time increases the mitochondrial volume and the ratio of type 2A to type 2X muscle fibers.^103,107 As a result, the onset of anaerobic metabolism is delayed until a higher speed is reached and horses are able to maintain a higher speed over a given distance.

The cardiovascular system plays a central role in the oxy­genation of blood by the lungs, the delivery of oxygen and other energy substrates to exercising muscles, and the removal of metabolic products from those muscles. Cardiac output increases with exercise in horses, largely as a function of an increase in heart rate.¹⁰⁸ As exercise begins, the heart rate quickly increases and then reaches a steady state within minutes at a submaximal speed. With increasing exercise intensity the heart rate shows a linear relationship with speed up to a maximum rate of 210 to 230 beats/min. The mean systemic arterial pressure does not change with submaximal exercise but rises with maximum exercise. Mean pulmonary arterial pressures increase with speed as the heart rate increases, reaching remarkably high levels that are four times resting values.¹⁰⁹ The oxygen-carrying capacity of the blood also rises with increasing speed through splenic contraction and a more than 50% increase in blood hemoglobin.¹¹⁰ The increase in blood viscosity that occurs with splenic contraction is believed to contribute to the increase in blood pressure with exercise.

After an initial abrupt rise, the respiratory rate increases linearly with the speed of trotting until, at a canter or gallop, respiration is linked to stride frequency on a 1 : 1 basis.^87,89 This leaves less time available for completing a respiratory cycle at faster speeds. To counter this, inspiratory and expiratory airflow velocities must increase to maintain or increase minute volume. As airflow rates increase, increased turbulence and an increased tendency for dynamic narrowing of the airways causes an increased resistance to flow and increases the work (energy cost) of breathing.^70,81 A finite maximum flow rate is eventually achieved, beyond which the expiratory muscles and the physical characteristics of the respiratory tract do not permit further increases in flow rate.⁸¹ In addition, a maximum stride frequency is reached, restricting the maximum respiratory rate to 140 to 150 breaths/min.^87,89 It has been suggested that beyond the finite maximum flow rate, the animal is forced to hypoventilate, which may result in arterial hypoxemia during maximal fast exercise.¹¹² The limitation placed on oxygen diffusion by blood hyperviscosity and the short transit time of blood through the pulmonary capillary bed at rapid heart rates also likely contribute to arterial hypoxemia.¹¹³ The arterial hypoxemia and incomplete saturation of hemoglobin that occur during strenuous exercise do not necessarily limit delivery of oxygen to the tissues, however, because the decline in blood oxygen tension is offset by the increase in the total blood hemoglobin oxygen content resulting from splenic contraction. This fact and the horse's ability to sustain at least a sixfold increase in cardiac output between rest and the point of maximum oxygen uptake (VO_2max)¹¹⁴ are the major factors that contribute to the enormous aerobic capacity of the horse.

In contrast to the muscular and cardiovascular systems, the respiratory system shows little adaptation to training. Whether the apparent inability of the equine respiratory system either to adjust to training¹¹⁵ or to compensate fully for the increased flow demands of heavy exercise limits athletic performance remains to be proven. However, it is likely that the maximally exercising horse is operating near the upper limit of ventilation and that even slight degrees of respiratory disease profoundly affect oxygen uptake and performance.¹¹⁶ Any condition that causes increased resistance to airflow, decreased minute volume, decreased diffusion of gases, ventilation-perfusion mismatch, shunt, or increased oxygen cost of breathing constitutes a respiratory cause of exercise intolerance.

Approach to Diagnosis of Exercise Intolerance and Poor Performance

Top athletes arise from both a genetic background that emphasizes athletic ability and environmental influences that capitalize on this inherent potential. A coordinated, energy­efficient gait, muscular power and endurance, a large capacity for oxygen transport, and several intangible factors such as the horse's mental toughness and competitive spirit and the rider's skill all contribute to successful performance. Poor performance most often results from inadequate training, a lack of genetic potential, or both, or from a congenital or acquired dysfunction of the locomotor, cardiovascular, or respiratory systems. The term exercise intolerance is often used to describe this inability to perform to an expected or previously attained intensity of exercise.

HISTORY. An accurate history is a fundamental part of the evaluation of exercise intolerance and should include the age, breed, and use of the horse and the training and feeding programs. The onset (time and rapidity) of the problem, previous perfor­mance history, activity level at which signs are observed, whether the horse performs well at first and then suffers tailing off of performance (no stamina), or whether performance is poor throughout the work period should be ascertained.

In particular, it is important from the history to distinguish between horses that have never been able to perform satisfac­torily and horses that suddenly or gradually show a reduction in the level of performance after a background of satisfactory performance. The first scenario suggests a lack of genetic potential, congenital abnormalities, or inadequate training. Some horses do not have the genetic background to perform the expected work (e.g., racing Quarter Horses rarely make good endurance horses, and Thoroughbreds from sprinting families rarely excel at distances of more than 1¼ miles).

CLINICAL EXAMINATION. Overt clinical diseases that cause exercise intolerance at moderate speeds usually can be diagnosed with a good history, physical examination, and selected ancillary diagnostic techniques. The diagnostic procedures and specific diseases that can be identified at rest are detailed in subsequent chapters in this book (particularly Chapters 30, 31, 37, 38, 41, and 42). Problems that are subclinical at rest provide a greater diagnostic challenge. When testing procedures at rest fail to identify the cause of exercise intolerance, various types of ancillary diagnostic procedures including exercise tests may be used to further define the problem. Because the respiratory, cardiovascular, musculoskeletal, and hematopoietic systems are all important for competitive performance and because diseases in these systems are the most likely causes of exercise intoler­ance, these systems should receive particular attention in the detailed clinical examination of the horse at rest.

HEMATOLOGIC ASSESSMENT. Hematologic tests have historically been popular in the evaluation of fitness and performance because they are easy to perform and because of 117 118 the important role of hemoglobin in oxygen transport. ^, Routine hematologic evaluation may be useful in monitoring the general health status and perhaps fitness of horses if the conditions of collection, particularly in relation to time of day and exercise, can be carefully controlled and if attention is paid to horses that become excited before or during sample collection.

Anemia can result in a decreased oxygen-carrying capacity during exercise. Veterinarians traditionally have regarded resting hematocrits below 35% as abnormal and likely to cause sub- optimal racing performance, but values lower than this have been found in normal Thoroughbred racehorses.¹¹⁹ Endurance horses and eventing horses usually have resting hematocrit values that are lower than those of racehorses.¹¹⁹ However, the fact that a significant proportion of equine red blood cells and hemoglobin is contained in the splenic reserve makes interpretation of resting values for these parameters difficult (inaccurate). There is no correlation between the resting level of hemoglobin and the total body hemoglobin or red cell mass.^110,119 Consequently, even though total body hemoglobin does increase in response to training and may correlate with performance, this cannot be determined from a resting blood sample. Measurement of the total hemoglobin or total red cell mass requires collection of a blood sample after strenuous exercise or after administration of epinephrine to mobilize the red cell reserve and the determination of plasma volume using a technique such as Evans blue dye dilution.¹¹⁰ These techniques have been used to document red cell hypervolemia in poorly performing, overtrained Standardbreds.¹¹⁰

Some veterinarians use the resting leukocyte count to monitor fitness, and particularly overtraining, in performance horses.¹¹⁹ Decreases in the neutrophil/lymphocyte (N/L) ratio have been used to indicate overtraining (training off or adrenal exhaustion). However, the N/L ratio varies in individual horses, depending on when it is determined in relation to the timing and type of exercise and on factors such as age, stress, and disease. Reliable evidence indicates that the N/L ratio is not a good predictor of adrenal status.¹²⁰ Indeed, adrenal function in horses with “adrenal exhaustion syndrome” remains to be accurately characterized based on reproducible function tests.

SERUM BIOCHEMICAL PROFILES. Biochemistry profiles are commonly used to monitor performance horses and to evaluate those with performance problems. These profiles are useful, but interpretation must take into account that when many measurements are performed, there is a high statistical prob­ability that one or two results will be outside the normal range (95% confidence).¹¹⁹ If only one or two results on a profile are slightly abnormal, the tests are best repeated on a second sample before the true significance of the result is ascribed. Biochemistry profiles are most useful in detecting horses with subclinical muscle problems (either primary exertional rhab­domyolysis or muscular strain secondary to skeletal problems), liver diseases, renal diseases, and gross disturbances in electrolyte and acid-base regulation. Biochemical profiles usually include aspartate aminotransferase (AST), creatine kinase (CK), LDH, alkaline phosphatase (AP), γ-glutamyltransferase (GGT), sorbitol dehydrogenase (SDH), blood urea nitrogen (BUN), creatinine, sodium (Na), potassium (K), chloride (Cl), bicarbonate, phosphate, calcium (Ca), magnesium (Mg), glucose, and other parameters that are of variable clinical relevance. Studies of horses during training have failed to show any correlation between resting or exercising values for these parameters and fitness.¹¹⁹ In endurance horses, evaluation of renal fractional excretions of electrolytes may provide better information regarding the horse's electrolyte balance than serum chemistry measurements alone.¹²¹

EVALUATION OF THE RESPIRATORYTRACT. Standard param­eters of a routine examination, including rectal temperature, respiratory rate, respiratory character, mucous membrane color, and capillary refill time, should be carefully evaluated at rest. The presence of nasal discharge, cough, edema, jugular disten­tion or pulsation, or other signs suggesting local or systemic disease should be noted. The larynx, muscular process of the arytenoid cartilages, retropharyngeal area, and trachea should be palpated for size and symmetry. The heart and lungs should be carefully auscultated and percussed at rest, and ausculta­tion of the lungs should be repeated as the horse is induced to breathe more deeply by application of a rebreathing bag. When stridor is part of the history, the upper respiratory tract should receive particular attention in the diagnostic evaluation. Not only must the character of the noise be determined, but the extent of work the patient can tolerate before exhibiting diminished performance must be established, because this helps in the interpretation of abnormalities seen on the endoscopic examination (see the Abnormal Respiratory Noise [Stridor] section earlier). Often the onset and intensity of the stridor coincide with a decrease in work capacity that is typical of certain obstructive airway diseases. Endoscopy, including treadmill endoscopy if facilities permit or over-the-ground videoendos­copy, and radiography form an important part of the diagnostic evaluation of horses with upper airway abnormalities¹²² (see the Respiratory Distress [Dyspnea] and Abnormal Respiratory Noise [Stridor] sections earlier). The most common abnormali­ties of the upper airway that cause poor performance include dorsal displacement of the soft palate, dynamic pharyngeal collapse, dynamic collapse of the left arytenoid cartilage in association with ILH, epiglottic entrapment, pharyngitis, and collapse of the alar folds.^97,99 Diminished performance in horses with mild or subclinical viral infection is probably mediated at least partly by abnormalities in the respiratory tract.¹²³ If no abnormalities are detected at rest, functional disturbances of airflow may occur during maximum exercise, and these disorders can best be identified by examining the upper airway using videoendoscopy on a treadmill during exercise or using over-the-ground videoendoscopy units. Slow-motion playback must be used because many abnormalities occur rapidly with each respiratory cycle. In particular, dorsal displacement of the soft palate and the extent of dynamic laryngeal obstruction with ILH can be more fully evaluated with videoendoscopy during exercise.^{97,99,122,124} Over-the-ground videoendoscopy has the distinct advantage of allowing the horses to be examined under the exact conditions in which the problem occurs. The presence of inspiratory or expiratory obstruction can be further evaluated during treadmill exercise by introducing transducers via the nostrils to measure airway pressures at the level of the pharynx and trachea.^99,122 During a treadmill exercise test, samples for blood gas analysis can be drawn from extension tubing connected to an 18-gauge, 2-inch catheter inserted into the transverse facial artery.

Further diagnostic evaluation of the lower airways is indicated in horses with an abnormal respiratory rate or character, cough, nasal discharge, abnormal lung sounds, prolonged recovery after application of a rebreathing bag, or with a history of EIPH, cough, or respiratory distress with exercise. Horses in which excess mucus or exudate can be demonstrated in the trachea during endoscopy performed after exercise are also candidates for further evaluation. Applicable tests include a complete blood count, tracheal wash or BAL, endoscopy, radiography, and ultrasound examination (see the Cough and Abnormal Respiratory Noise [Stridor] sections earlier). Tracheal wash samples collected after exercise are more likely to identify lower airway disease than those collected before exercise.¹²⁵ Respiratory viral infection, EIPH, bronchiolitis, hyperreactive airways, and RAO are all conditions that may not be apparent at rest but that constitute significant causes of exercise intolerance.

EVALUATION OF THE CARDIOVASCULAR SYSTEM. A full evaluation of the mucous membranes, capillary refill time, pulse rate, pulse character and rhythm, heart rate and rhythm, and auscultatory findings is an important part of the evaluation of the performance horse. Failure to maintain cardiac output because of an inability to regulate either heart rate or stroke volume is the mechanism through which cardiac diseases induce exercise intolerance. Many cardiac dysrhythmias and valvular dysfunctions are apparent on auscultation of the resting horse. However, the contribution of mild abnormalities to exercise intolerance may require exercise testing. In addition, some arrhythmias and valvular or myocardial dysfunctions can be detected only during or shortly after exercise. Thus resting and exercising electrocardiography and echocardiography before and immediately after exercise are indicated.^99,122 The heart rate can be monitored during exercise using either telemetric electrocardiography or commercial heart rate monitors. Electrocardiograms (ECGs) provide the additional benefit of evaluating both heart rate and rhythm. Supraventricular tachyarrhythmias, the most important of which is atrial fibril­lation (AF) in horses, can lead to heart rates exceeding 240 beats/min at submaximal exercise.¹²⁶ Under these circumstances, cardiac output may be limited by the decreased time available for diastolic perfusion of the myocardium; the absence of atrial contraction; and the reduced time for passive ventricular filling, leading to reduced stroke volume. Many horses with AF maintain efficient circulation at rest and during light exercise but are intolerant to strenuous exercise because they are unable to increase cardiac output sufficiently at rapid heart rates.¹²⁷ Some horses show transient paroxysmal AF during exercise but not at rest.¹²⁷ These are often easiest to observe in ECG tracings obtained within 60 seconds after an exercise test. Conversion to sinus rhythm, either spontaneously with quinidine sulfate or with electroconversion,¹²⁸ usually leads to a return to normal performance in horses with AF.^129,130 The ability to maintain cardiac output can be compromised by other cardiac arrhythmias such as ventricular tachycardia and ventricular premature depolarization.^99,131 The frequency of premature depolarization can increase with exercise, and the timing of resultant abnormal extra systoles can reduce cardiac output even at submaximal heart rates.¹³¹ Intraatrial block, second- degree atrioventricular (AV) block, and intraventricular block have also been documented in exercise-intolerant, poorly 132133

performing horses.^132,133 Horses with cardiac arrhythmias may show abnormal elevations in lactate concentration in response to exercise, indicating a lowered anaerobic threshold, which 111

contributes to exercise intolerance.¹¹¹

Electrocardiography is believed by some veterinarians to be of value in identifying myocarditis. 1 wave abnormalities (positive and peaked T waves, in contrast to the normal diphasic T waves) in multiple leads on resting ECG traces have been found in a high percentage of horses with a history of fading during the final portion of a race.¹³² T waves are highly labile, affected by training status, and the mechanism by which abnormal T waves are generated is uncertain. However, T wave changes have been identified in some horses with myo- 119133134

carditis confirmed at necropsy. ’ ’ Myocarditis may be more definitively documented by evaluating cardiac troponin I.¹³⁵ A positive correlation has been demonstrated between heart size and racing performance.¹³³ Electrocardiography has been used to assess performance potential by heart score measurement. The heart score represents the mean QRS duration in leads 1, 2, and 3 expressed in milliseconds and has been strongly correlated with heart weight and prize money won by racehorses.^119,133 The physiologic basis for heart score remains in dispute, and expertise is required to standardize leads and measure QRS complexes.

An echocardiogram provides essential information in many cases in which clinical evidence of valvular or myocardial dysfunction is present. The pericardium, the size of the heart chambers, the presence of congenital defects, the function of valvular leaflets, and myocardial contractility all can be assessed (see Chapter 30). Decreased myocardial contractility, regurgitant leaks caused by valvular incompetence, left-to-right shunts, and increases in afterload such as occur in aortic stenosis result in systolic dysfunction and a drop in cardiac output.¹³⁶ A pulsed, continuous, or color flow Doppler technique may be necessary to determine the size and significance of any disturbances to flow. Cardiac conditions such as effusive pericarditis and myocardial fibrosis and peripheral vascular conditions that inhibit venous return may interfere with ventricular filling during diastole, resulting in decreased end-diastolic volume, stroke volume, and cardiac output.¹³⁶ Measurement of fractional shortening before and immediately after treadmill exercise, when pulse rates are above 100 beats/min, permits documentation of resting and exercise-induced myocardial dysfunction.⁹⁹ Contrast angiographic studies may be indicated if congenital or acquired cardiac outflow problems are suspected. Nuclear angiocardiography is also useful for evaluating myocardial contractility, cardiac chamber enlargement, outflow prob­lems, and other abnormalities. Hemodynamic studies, which measure pulmonary capillary wedge pressure, pulmonary driving pressure, and pressure in the right side of the heart and pulmonary artery, have proven useful in detecting early cardiac and pulmonary failure in poorly performing trotting horses. These studies involve the introduction of flow directional balloon-tipped catheters through the jugular vein into awake horses.¹³⁷

EVALUATION OF THE SKELETAL SYSTEM. A lameness examination including appropriate flexion tests and other stress tests should be completed to help rule out musculoskeletal problems. If lameness is observed, appropriate diagnostic nerve blocks, radiographs, scintigraphy, rectal examination of the bony pelvis and aortoiliofemoral arterial pulses, or ultrasound examinations are indicated to help localize the lameness and determine its cause, significance, and prognosis. Some lameness problems that are evident only at high speed may best be evaluated using treadmill exercise. For example, aortoiliofemoral thrombosis reduces peripheral perfusion but often causes only progressive hindlimb lameness with exercise. Foot balance should be carefully assessed at rest and, if possible, during exercise, because gait changes and subtle lameness related to foot imbalance can adversely affect performance. Dynamic evaluation of hoof balance can be accomplished by examining videotapes recorded from behind the horse while it is exercising on a high-speed treadmill or by trotting the horse over force plates embedded in a firm level surface.¹³⁸

Subtle lameness can increase the metabolic cost of locomo­tion by inducing changes in gait and coordination, which accelerate the onset of fatigue. In the same fashion, some horses may have an inefficient gait that reduces their performance capacity. Video imaging systems and gait analysis may play an increasingly important role in identifying these individuals in the future.

EVALUATION OF THE MUSCULAR SYSTEM. Primary skeletal muscular limitations on performance may occur as the result of painful conditions such as exertional rhabdomyolysis or weakness due to defects in energy generation or loss of muscle mass. In resting samples, high serum AST may indicate chronic rhabdomyolysis. Measurement of serum CK 4 to 6 hours after an exercise test is most useful in detecting horses with chronic or subclinical forms of exertional rhabdomyolysis. Serum muscle enzyme concentrations measured in blood samples collected immediately after exercise are often normal, but in horses with chronic exertional rhabdomyolysis significant abnormal elevations may be seen when CK peaks at 4 to 6 hours after completion of exercise. In the past it has been recommended that the exercise test be conducted at a speed and duration of exercise similar to that expected of the horse in competition. However, it has been shown that a 15- to 30-minute test at a slow trot more frequently produces abnormal elevations in serum CK (more than twofold to threefold) in susceptible horses.¹³⁹ Standardbreds and Thoroughbreds with histories of recent episodes of recurrent exertional rhabdomyolysis and horses with type 1 polysaccharide storage myopathy (PSSM) often show a greater than twofold increase over normal resting 139

values in response to an exercise test.¹³⁹ Horses with type 2 PSSM may show exercise intolerance after 10 to 15 minutes under saddle, reluctance to pick up and maintain a canter, or inability to collect and maintain self-carriage under saddle without abnormal elevations in serum CK. Subtle loss of muscle mass and performance decline can occur with deficiencies in vitamin E, warranting assessment of serum alpha-tocopherol concentrations.

Muscle biopsy is a relatively simple procedure that can prove useful for characterizing the nature of an identified exertional myopathy. However, the procedure is not widely used in the diagnostic assessment of poor performance because the evaluation of samples requires considerable histochemical expertise. Percutaneous techniques using a 6-mm-diameter needle (Bergstrom biopsy needle, Mortenson, Copenhagen, Denmark) and local anesthetic are routinely used. The middle gluteal muscle is most often sampled because it is relatively accessible and active at all intensities of exercise. ^,, In adult horses a biopsy is collected at a depth of 2½ to 3 inches from a site 8 inches from the tuber coxae along a straight line connecting the point of the tuber coxae with the base of the tail. Open surgical biopsies are most easily obtained from the semimembranosus or semitendinosus muscle at a site approxi­mately 3 inches below the tuber ischii. After the skin has been shaved and aseptically prepared, lidocaine is injected under the skin. A 2-inch-long incision is made through the skin and fascia, and two parallel incisions, 1 inch long and ½ inch apart, are made vertically in the muscle. The muscle is grasped in one place, to prevent handling artifacts, and the biopsy is first transected proximally, freed to a depth of ¼ inch, and then transected distally. The disadvantage of open surgical biopsies is that a recovery period of 1 week is often required, whereas horses can immediately begin to exercise when a needle biopsy is used. Muscle samples should be sent to a laboratory, where they will be frozen in isopentane that has first been chilled in liquid nitrogen. Commonly used histologic and histochemical stains include adenosine triphosphatase (ATPase) after alkaline and acid preincubations, nicotinamide dinucleotide diaphorase (NADH), periodic acid-Schiff (PAS), and hematoxylin and eosin.

An estimate of the state of training can be made by determin­ing the percentage of type 1, type 2A, and type 2X muscle fibers, as well as the oxidative capacity of skeletal muscle in these small muscle samples. In general, horses suited for short­distance, fast exercise have a greater proportion of fast-twitch fibers in the middle gluteal muscles than horses suited for longer distance events, which have a higher proportion of slow-twitch type 1 fibers.¹⁴⁰ However, there are many successful athletes that do not follow this pattern. The proportion of type 1 relative to type 2 fibers is thought to be genetically based and cannot be manipulated to a great extent by training, whereas age and training increase the proportion of oxidative fast-twitch type 2A fibers relative to type 2X fibers.^103,107,139 Histochemical assessment of NADH staining or quantitative measurement of enzymes such as citrate synthase in biopsy samples frozen rapidly in liquid nitrogen may provide a guide to the state of aerobic fitness.¹³⁶ The use of muscle biopsies in horses with poor performance has also aided in the identifica­tion of oxidative enzyme defects in Arabian horses and glycogen storage disorders in Quarter Horses that can markedly affect 140 141

performance.¹⁴⁰,¹⁴¹

Standardized Exercise Testing

Exercise intolerance is ultimately a neuromuscular phenomenon resulting from extreme metabolic stress at the level of the muscle fibers.¹⁰⁴ Under many circumstances premature muscle fatigue occurs secondary to disorders that affect oxygen transport (cardiopulmonary systems) or mechanical efficiency (lameness) (Box 5.20). Standardized treadmill exercise tests are often required to assess the function of these systems at high speeds to determine the primary cause of poor performance and to measure the metabolic response of skeletal muscle relative to work intensity. In a substantial number of cases, poor perfor­mance results from related or unrelated disorders in more than one body system, such as dynamic airway obstruction and cardiac dysrhythmia in the same horse.⁹⁹

TREADMILL TESTS. Horses often need to be acclimated to a treadmill before representative exercise testing can be per­formed. Standardbred horses are typically exercised while wearing their usual racing tack, whereas horses of other breeds are typically exercised in a halter or bridle with a lead rope attached to each side. Most horses exercise comfortably on a treadmill after two to four training sessions at speeds that include all gaits to be tested. Breaking into a canter is an important skill to train horses to perform on the treadmill. During one of the training sessions, endoscopy of the upper airway can be performed to evaluate upper airway function during maximal speeds. Two types of standardized exercise tests can be used: a high-speed test, in which horses are acceler­ated to maximal speed for their normal racing distance, or an incremental test, in which speed is increased every 1 or 2 minutes until fatigue is reached. The incremental exercise test is used most commonly because it includes both submaximal and maximal intensities and is readily reproducible. Many exercise tests are performed with the treadmill set at a 6% to

10% slope to minimize the possibility of injury at top speeds and to ensure that maximum exercise intensity is reached.

Several measurements are possible during treadmill exercise testing. In its simplest form, the heart rate can be monitored after 1 minute at each intensity of exercise using a heart rate monitor, although recording of an ECG during exercise provides additional information about exercise-associated dysrhythmias.⁹⁹ Blood samples can also be drawn from a jugular catheter during the final 15 seconds at each speed. A linear relationship between heart rate and speed is expected, with a plateau forming at the maximum heart rate. The maximum heart rate does not change with training, but the speed at which the maximum heart rate is reached should increase with training. As an alternative, a linear regression can be used to determine the horse's speed at a heart rate of 200 beats/min (V₂₀₀). V₂₀₀ is close to the anaerobic threshold, may predict aerobic capacity, increases with increasing fitness, and has a high individual predictability that allows for early and valid detection of clinical disorders that limit performance.,, The speed at which horses reach a maximum heart rate has been proposed as a better measure than V₂₀₀ because it is an absolute rather than a relative measure; however, measurement of maximum heart rate requires a more strenuous exercise test. Parameters such as the velocity at which the whole blood lactate value reaches 4 mmol/L (V_la4) and the heart rate at which blood lactate reaches 4 mmol/L (HR_LA4) can be calculated to evaluate the anaerobic threshold.^111,142 The rate of lactate accumulation may also provide valuable information.

Lactate concentrations can be determined in either whole blood or plasma. Recent studies suggest whole blood lactate may provide a more accurate reflection of lactate accumulation than plasma lactate¹⁴³ because red blood cells actively take up lactate and buffer it, and the type and number of red blood cell lactate transporters differ markedly among horses.

The value of V₂₀₀, V_la4, HR_la4, and other parameters is that they provide standards against which improvement or deterioration in fitness can be assessed, and individual horses can be objectively compared.^111,119,142 Hematocrit can also be easily determined from blood samples obtained at each speed to provide a rough estimate of the number of circulating red blood cells. Blood samples drawn before and 4 hours after exercise for measurement of CK activity can be used to screen for subclinical exertional rhabdomyolysis.

Further evaluation of the oxygen transport system can be obtained in laboratories where the sophisticated open-flow gas-collection system necessary to measure oxygen consumption (VO₂) is available. During the incremental exercise test, a plateau in oxygen consumption eventually is reached, representing maximum oxygen uptake. VO₂ can be used at submaximal speeds to calculate the oxygen cost of locomotion, and Vθ_2max, a key indicator of aerobic capacity, can be determined. The cardio­pulmonary system can be further evaluated during exercise by measuring arterial blood gases from the transverse facial artery using an 18-gauge indwelling catheter.¹⁴² An accurate measure of the total red blood cell volume in a horse can be determined using an Evans blue dye dilution technique immediately after maximal exercise.

FIELD TESTS. Standardization of field exercise tests is difficult because weather, track conditions, and other factors influence the amount of work performed. The simplest form of exercise test involves timing a horse exercising maximally over a fixed distance and evaluating heart rate recovery rates at specific time points after exercise. Additional information can be obtained by measuring heart rate during exercise using a heart rate monitor or telemetric ECG.¹¹⁹ As fitness improves, the heart rate for a given speed of exercise should be lower. Incremental field exercise tests have been used most successfully in Standardbred horses in which the heart rate and blood lactates were measured after several heats at predetermined increases in pace. At speeds above 450 m/min, lactate begins to accumulate in the blood during exercise; the precise kinetics of accumulation depends on the horse's fitness and exercise capacity. V_LA4 has been used in field exercise tests to monitor responses to training. Fitness responses include a lower heart rate and lactate concentration for the same exercise speed. The value of these measurements is only as good as the standardization of the testing procedures used.