Inheritance of racing performance of Thoroughbred horses

Horse racing is a contest between horses, usually held for the purpose of betting. Thoroughbred horse racing is the most diffused form of horse racing throughout the world. Thoroughbred is one of the most versatile of horse breeds and has influenced the development of many other breeds. Thoroughbred horses served as a foundation stock for the development of the light horse breeds. The two types of horse racing are flat racing and jumping races/steeplechases. The measures of racing performance are broadly classified into three categories. They are time and its several variations, handicap or similar performance ratings and earnings. One common measure of the performance of racehorses evaluated genetically is racing time or final time. The heritability estimates differed according to method of estimation, age, sex, track and distance. Time measure generally had a heritability in the range of 0.1 to 0.2 with the higher values for shorter races. For handicap and earning measures the heritabilities reported were generally higher in the range of 0.3 to 0.4; hence these may be considered in genetic evaluation of racing performance of Thoroughbred horses. The average generation interval of Thoroughbred horses was 11.2 ± 4.5 and 9.7 ± 3.8 years for males and females respectively, which limits the genetic progress in racing horses. However, the major advantage is that the racing performance may be evaluated in both males and females and repeated observations can be obtained on the same animal in relatively short periods. These factors coupled with the reasonable heritability of some measures of racing performance, suggest that mass selection based on performance tests would be the selection procedure of choice to improve the racing performance of Thoroughbred horses. In general, the inbreeding at the rate that is usually practised in Thoroughbred population does not enable much gene fixing. However, practice of close inbreeding may be avoided, even though it still fascinates breeders at subconscious level.     

Prevalence of latent alpha-herpesviruses in Thoroughbred racing horses

The objective of this study was to detect and characterize latent equine herpes virus (EHV)-1 and -4 from the submandibular (SMLN) and bronchial lymph (BLN) nodes, as well as from the trigeminal ganglia (TG) of 70 racing Thoroughbred horses submitted for necropsy following sustaining serious musculoskeletal injuries while racing. A combination of nucleic acid precipitation and pre-amplification steps was used to increase analytical sensitivity. Tissues were deemed positive for latent EHV-1 and/or -4 infection when found PCR positive for the corresponding glycoprotein B (gB) gene in the absence of detectable late structural protein gene (gB gene) mRNA. The EHV-1 genotype was also determined using a discriminatory real-time PCR assay targeting the DNA polymerase gene (ORF 30). Eighteen (25.7%) and 58 (82.8%) horses were PCR positive for the gB gene of EHV-1 and -4, respectively, in at least one of the three tissues sampled. Twelve horses were dually infected with EHV-1 and -4, two carried a latent neurotropic strain of EHV-1, six carried a non-neurotropic genotype of EHV-1 and 10 were dually infected with neurotropic and non-neurotropic EHV-1. The distribution of latent EHV-1 and -4 infection varied in the samples, with the TG found to be most commonly infected. Overall, non-neurotropic strains were more frequently detected than neurotropic strains, supporting the general consensus that non-neurotropic strains are more prevalent in horse populations, and hence the uncommon occurrence of equine herpes myeloencephalopathy.     

Sudden death in training and racing Thoroughbred horses

We reviewed case records, necropsy reports, and histologic sections from 25 Thoroughbred racehorses that died suddenly at 3 Chicago racetracks. These were young horses ranging in age from 2 to 5 years. There were more females (n = 16) than males (n = 9), and the incidence of death increased slightly in the spring and summer. Twenty-one of the 25 horses died while racing or training. Only 8 of the 25 horses (32%) had lesions sufficient to account for the death. In 6 of those 8 cases, death was caused by massive thoracic or abdominal hemorrhage. The site or nature of the vascular defect in these cases could not be determined. One horse died of severe preexisting pulmonary disease, and one died of encephalitis and cardiac papillary muscle fibrosis. The cause of death was undetermined in 17 horses (68%). Nearly all horses had pulmonary edema, congestion, and/or hemorrhage. We postulate that these unexplained deaths were a result of exercise-induced acute cardiovascular failure.     

Estimation of genetic parameters of racing performance in Iranian Thoroughbred horses

The aim of this study was to estimate the genetic parameters of racing performance and investigate the fixed effects that influence the performance of Thoroughbred race horses. The data included the performance of two, three and four year old horses raced in flat races and consisted of 10,800 time records and 10,912 ranking value. Two criteria were used in order to analyze the performance: racing time and a normalized ranking value. The effects of age of horse at racing and post position were significant for all traits (P < 0.05). The effect of hippodrome also was significant for racing time (P < 0.001). The genetic parameters were estimated by the restricted maximum likelihood (REML) method using DFREML program. The heritability estimates for racing time at 1000, 1400 and + 1600 m were 0.13 (± 0.009), 0.11 (± 0.007) and 0.09 (± 0.009) and for ranking value were 0.15 (± 0.010), 0.17 (± 0.008), 0.13 (± 0.009) and 0.11 (± 0.013) for entire data set, 1000, 1400 and + 1600 m respectively. Estimates of repeatability of racing time for 1000, 1400 and + 1600 m were 0.26, 0.19 and 0.17; and for ranking value were 0.28, 0.32, 0.25 and 0.20 for entire data set, 1000, 1400 and + 1600 m respectively. The genetic correlation of two criteria was 0.68–0.79 depended on distances of races.     

Effect of sucralfate on total carbon dioxide concentration in horses subjected to a simulated race test

The purpose of this study was to test the hypothesis that sucralfate, a gastric ulcer medication, would alter plasma concentrations of total carbon dioxide (tCO2), lactate (LA), sodium (Na+), potassium (K+), chloride (Cl-) and total protein (TP), as well as calculated plasma strong ion difference (SID) and packed cell volume (PCV) in horses subjected to a simulated race test (SRT). Six unfit Standardbred mares (approximately 520 kg, 9-18 years) were used in a randomized crossover design with the investigators blinded to the treatment given. The horses were assigned to either a control (40-50 mL apple sauce administered orally (PO)) or a sucralfate (20 mg/kg bodyweight dissolved in 40-50 mL apple sauce administered PO) group. Each horse completed a series of SRTs during which blood samples were taken via jugular venipuncture at five sampling intervals (prior to receiving treatment, prior to SRT, immediately following exercise, and at 60 and 90 min post-SRT). During the SRTs, each horse ran on a treadmill fixed on a 6% grade for 2 min at a warm-up speed (4 m/s) and then for 2 min at a velocity predetermined to produce VO2max. Each horse then walked at 4 m/s for 2 min to complete the SRT. Plasma tCO2, electrolytes, LA, and blood PCV and TP were analysed at all intervals. No differences (P>0.05) were detected between control and sucralfate for any of the measured variables. There were differences (P<0.05) in tCO2, SID, PCV, TP, LA and electrolyte concentrations relative to sampling time. However, these differences were attributable to the physiological pressures associated with acute exercise and were not an effect of the medication. It was concluded that sucralfate did not alter plasma tCO2 concentration in this study.     

Study of laryngopharyngeal pathology in Thoroughbred horses in southern California

Reasons for performing study: There is increasing anecdotal evidence among horse owners, trainers and equine clinicians of a high prevalence of subepiglottic ulcers, suggested to have a negative effect on racing performance. Objectives: To provide a prevalence study and pathological characterisation of laryngopharyngeal lesions with emphasis in the subepiglottic area and, in particular, subepiglottic ulcers. Methods: The study was carried out on 91 Thoroughbred racehorses received for post mortem examination from 4 major Southern California racetracks. The most common reason for submission was catastrophic musculoskeletal injury, but others include sudden death, laminitis, colic, colitis, neurological disorders, pleuropneumonia and arytenoid chondropathy. Laryngopharyngeal specimens were collected and examined grossly; selected cases were also examined histopathologically. Results: Thirteen horses (14.3%) had at least one type of laryngopharyngeal abnormality, 7 horses (7.7%) had lesions in the subepiglottic soft tissues, including 4 subepiglottic ulcers, 2 soft palate ‘kissing lesions' and one 'subepiglottic scar’. Eight horses (8.8%) had lesions elsewhere in the laryngopharynx, including mucosal ulcerations, arytenoid chondropathy, epiglottic entrapment and partial absence of arytenoid cartilage. Conclusions and potential relevance: Lesions in the subepiglottic area were among the most prevalent in this study, suggesting that an important percentage of laryngopharyngeal abnormalities may be missed during routine endoscopy of the standing horse, which often does not include the examination of subepiglottic tissues. Pathologically, subepiglottic ulcers were chronic‐active with viable hyperplastic epithelial margins, suggesting that proper healing and re‐epithelialisation should occur with appropriate treatment. In most cases, the lesions observed do not necessarily indicate a clinical problem and more extensive prevalence studies and correlation between abnormalities found and performance are needed to assess the clinical relevance of subepiglottic soft tissue lesions accurately.     

Profiling the careers of Thoroughbred horses racing in Australia between 2000 and 2010

Reasons for performing study: Research investigating trends in racehorse careers require a benchmark for accurate comparison. Currently little whole population data exists for horses racing in Australia. Objectives: To determine the range and variation in career length and number of career starts for horses racing in Australia. To document and provide evidence regarding the current differences between the sexes for career length and careers starts. Methods: Racing data were collected for Thoroughbreds over a 10‐year period. Career length, number of career starts and spells per year were evaluated. Statistical analyses were performed using the statistical package R. Results: A total of 2,782,774 performance records yielded career information for 164,046 horses. Median career length and number of career starts for the population were 14.7 months and 10 starts, respectively. Significant differences (P<0.001) were present between the sexes for all career outcomes. Between 2000 and 2010, the percentage of Thoroughbreds racing in Australia with careers longer than 12, 24, 36 and 48 months was 56.65, 32.35, 16.66 and 7.74, respectively. Conclusions and potential relevance: Clear differences in career outcomes exist between intact males, females and geldings racing in Australia. Future research should be conscious of these differences when analysing population data.     

Sudden death in racing Thoroughbred horses: an international multicentre study of post mortem findings

Reasons for performing study: To improve the understanding of exercise related sudden death in Thoroughbred racehorses. Objectives: To describe the post mortem findings in cases of sudden death associated with exercise in 268 Thoroughbred racehorses. Methods: Gross and histological post mortem findings of 268 cases of sudden death were collated and reviewed. Cases originated from 6 racing jurisdictions around the world. Sudden death was defined as acute collapse and death in a closely observed and previously apparently healthy Thoroughbred racehorse, during, or within one hour after, exercise. Cause of death as determined by the attending pathologist was categorised as definitive, presumptive or unexplained and compared between the different populations. Cardiopulmonary lesions recorded at post mortem examination were compared between different populations. Results: Pathologists recorded a definitive cause of death in 53% (143/268) of cases. Major definitive causes of sudden death included cardiac failure, apparent pulmonary failure, pulmonary haemorrhage, haemorrhage associated with pelvic fractures or with idiopathic blood vessel rupture, and spinal cord injury. A presumptive cause of death was made in 25% (67/268) of cases and death remained unexplained in 22% (58/268) of cases. There were several statistically significant inter‐population differences in the cause of death and in reporting of cardiopulmonary lesions. Conclusions: Sudden death can be attributed to a variety of causes. Causes of sudden death and the lesions found in cases of exercise‐related sudden death are similar in different racing jurisdictions. However, the lesions are often not specific for the cause of death and determination of the cause of death is therefore affected by interpretation by the individual pathologist.     

Serum IgE concentration and exercise-induced pulmonary hemorrhage in racing quarter horses

Using an ELISA test with specific equine antisera, resting and post-exercise serumIgE concentrations were determined in 20 horses exhibiting varying degrees of exercise- induced pulmonary hemorrhage (EIPH), and in 10 horses identified endoscopically as non-bleeders.

Significantly higher serum IgE concentrations (P<0.01) were present in horses which bled profusely than in those which bled mildly or not at all. Reductions in serum IgE concentrations were evident following exercise in most horses and, even though these reductions were not statistically significant, this suggested the possibility that circulating IgE had become bound to basophils or to bronchial mast cells as a result of the exercise.     

Equine serum lipids: serum lipoprotein profiles of Morgan and Thoroughbred horses.

The serum of lipoproteins of 10 Morgan and 8 Thoroughbred horses were examined by 2 methods of polyacrylamide gel electrophoresis. A significant breed difference in the beta-lipoprotein to alpha-lipoprotein ratio was seen in gradient slab electrophoresis. A breed difference in the number of peaks, but no difference in beta-lipoprotein to alpha-lipoprotein ratio, was found in disc gel electrophoresis. These results have been correlated to indicate differences in charge of alpha-lipoprotein components and in size of beta-lipoprotein components between these 2 breeds of horses.     

Effect of nasogastric administration of sodium bicarbonate on carbon 13 isotopic enrichment of carbon dioxide in serum of horses

OBJECTIVE: To determine the effect of administration of commercially available sodium bicarbonate (NaHCO3) on carbon 13 (13C) isotopic enrichment of carbon dioxide (CO2) in serum of horses. ANIMALS: 7 healthy Thoroughbreds. PROCEDURES: Sodium bicarbonate (450 g) was administered via nasogastric intubation to horses. Horses had been fed a diet obtained from the same source and had access to water from the same source for 3 months before the study. Blood samples were collected immediately before and at 2, 4, 6, and 24 hours after administration of NaHCO3. The concentration of total CO2 in serum was measured by use of a commercial analyzer. The 13C enrichment of bicarbonate in serum was estimated by measurement of 13C enrichment of CO2 released by acidification of the serum. The 13C enrichment of commercially available NaHCO3 was also determined and compared with that of CO2 in serum of horses before administration of NaHCO3. RESULTS: Commercially available NaHCO3 had a 13C enrichment significantly different from that of carbon dioxide in serum of horses before treatment. Administration of NaHCO3 increased the concentration of total CO2 from pretreatment values. The 13C enrichment of CO2 in serum was only transiently and minimally affected after administration of NaHCO3. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of NaHCO3 was not detected by measuring 13C enrichment of CO2 in serum of horses.     

Effect of oral L-carnitine on its concentration in the plasma of yearling Thoroughbred horses

After an oral dose of 10 g of L-carnitine the plasma concentrations of free and total carnitine increased in five yearling thoroughbred horses, reaching a peak two to four hours after administration, but in two horses there was no increase. In the five which responded, the mean (+/- sd) peak increase in total carnitine concentration was 15.1 +/- 6.9 mumol/litre from a predose mean of 18.8 +/- 3.4 mumol/litre, and the mean peak increase in free carnitine concentration was 13.5 +/- 3.1 mumol/litre from a pre-dose mean concentration of 12.5 +/- 2.2 mumol/litre. These changes were similar to those observed previously in a group of adult thoroughbred horses given 10 g of L-carnitine. There was no consistent pattern of change in the concentration of acetylcarnitine in the seven yearling horses.