Summary The pattern of variation in heart rate on a beat‐to‐beat basis contains information concerning sympathetic (SNS) and parasympathetic (PNS) contributions to autonomic nervous system (ANS) modulation of heart rate (HR). In the present study, heart period (RR interval) time series data were collected at rest and during 3 different treadmill exercise protocols from 6 Thoroughbred horses. Frequency and spectral power were determined in 3 frequency bands: very low (VLF) 0–≤ 0.01, low (LO) >0.01–≤ 0.07 and high (HI) >0.07–≤ 0.5 cycles/beat. Indicators of sympathetic (SNSI = LO/HI) and parasympathetic (PNSI = HI/TOTAL) activity were calculated. Power in all bands fell progressively with increasing exercise intensity from rest to trot. At the gallop VLF and LO power continued to fall but HI power rose. SNSI rose from rest to walk, then fell with increasing effort and was lowest at the gallop. PNSI fell from rest to walk, then rose and was highest at the gallop. Normalised HI power exceeded combined VLF and LO power at all gaits, with the ratio HI to LO power being lowest at the walk and highest at the gallop. ANS indicators showed considerable inter‐horse variation, and varied less consistently than raw power with increasing physical effort. In the horses studied, the relationship between power and HR changed at exercise intensities associated with heart rates above approximately 120–130 beats/min. At this level, humoral and other non‐neural mechanisms may become more important than autonomic modulation in influencing heart rate and heart rate variability (HRV). HRV at intense effort may be influenced by respiratory‐gait entrainment, energetics of locomotion and work of breathing. HRV analysis in the frequency domain would appear to be of potential value as a noninvasive means of assessing autonomic modulation of heart rate at low exercise intensities, only. The technique may be a sensitive method for assessing exercise response to experimental manipulations and disease states.
The guidelines for interpretation and clinical relevance of premature depolarisations observed during and immediately after treadmill exercise tests in poor performing Thoroughbred racehorses deserves further evaluation.
Summary Reasons for performing study: The proposed biological mechanisms for exercise‐induced pulmonary haemorrhage (EIPH) are many and varied. Better knowledge of risk factors should lead to achievable measures to reduce the incidence. Objectives: To identify risk factors associated with epistaxis following racing in UK Thoroughbreds, to gain possible insights into the pathogenesis of the condition and to investigate the association between epistaxis and race finishing position. Methods: The association of epistaxis occurring on UK racecourses between 1996 and 1998 with a wide range of race‐, horse‐ and start‐level variables was examined in multivariable mixed effect logistic regression analyses. Four multivariable analyses were conducted, one for all race types considered collectively and one each for flat, hurdle and steeplechase race types considered separately. Results: Risk of epistaxis was significantly increased for hurdle and steeplechase race types compared to both flat and National Hunt flat races. In 3 of the 4 final models, there was a significant biological trend for increasing risk of epistaxis with increasing ground hardness (‘going’) and accumulated years spent racing. However, in flat races epistaxis was such a rare outcome (0.33 cases per 1000 starts) that this subset analysis had insufficient power to measure the detectable effect of ‘going’ as statistically significant. Horses with epistaxis were significantly more likely to have a poorer finishing position than those without blood at the nostrils. Conclusions: Findings were consistent with the theory that locomotory impact‐induced trauma contributes to exercise‐induced epistaxis. Further validation of this hypothesis through application of similar methods to endoscopically visible EIPH and through biomechanical studies is warranted. Potential relevance: Knowledge of significant risk factors should allow formulation of practical measures, such as track watering, to reduce the risks of EIPH and epistaxis in racehorses.
To define the metabolic response to maximal exercise in the thoroughbred horse under field conditions, muscle biopsies and venous blood samples were taken from five horses after a single 800-m gallop and from four horses after a single 2,000-m gallop. Muscle and blood samples were also collected during 60 min of recovery. After exercise muscle ATP contents were decreased by 30 +/- 7 (SD) and 47 +/- 3% after the 800- and 2,000-m gallops, respectively. As indicators of purine catabolism, ammonia and uric acid increased in plasma, the accumulation being greater after the 2,000-m gallop. Blood ammonia peaked immediately after exercise and uric acid after 40-60 min of recovery. Muscle glycogen utilization over the 800- and 2,000-m gallops averaged 2.68 +/- 0.90 and 1.06 +/- 0.12 mmol glucosyl units.kg dry muscle-1.s-1, respectively, and the total used amounted to 27.3 +/- 6.6 and 32.5 +/- 8.8% of the initial store. Muscle lactate accumulation averaged 123.5 +/- 49.7 and 167.3 +/- 20.7 mmol/kg dry muscle, respectively, and declined during recovery with half times of 22.9 +/- 4.2 and 18.9 +/- 6.6 min. Blood lactate peaked 5-10 min after exercise. Exercise resulted in only a small increase in muscle glycerol content, but this continued to rise during recovery reaching 9-12 mmol/kg dry muscle after 20 min. During this time the increase in muscle glycerol content exactly matched the decline in glycerol 3-phosphate.
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