R J Rose’s research while affiliated with The University of Sydney and other places

Twenty-three Thoroughbred racehorses that were presented for a standard incremental exercise test also performed a test at an intensity equivalent to 115% V̇O2max in an effort to evaluate their anaerobic capacity by measuring the maximal accumulated oxygen deficit (MAOD). Submaximal V̇O2 values for speeds 3 to 10 m/s and V̇O2max were determined for horses exercising on a treadmill inclined at a 10% slope. An individual regression equation of speed and V̇O2 was used to calculate the speed for each horse to exercise at 115% V̇O2max and the energy demand for exercise at this intensity. The horses underwent a warm-up period consisting of 5 min at 50% V̇O2max followed by walking for 5 min at 1.5 m/s. The treadmill was then acclerated as rapidly as possible until a speed of 115% V̇O2max was attained. During the test, expired gas samples were collected at 0, 15, 30, 45, 60 s and every 30 s until fatigue. MAOD was calculated by subtracting the measured oxygen uptake from the calculated oxygen demand. A 5 min post exercise blood sample was collected for measurement of plasma [lactate]. The MAOD values ranged from 36 to 94 mlO2 equivalents/kg and the V̇O2max values ranged from 128 to 170 ml/kg/min. The mean ± s.e. MAOD values were 59 ± 3 mlO2 equivalents/kg and mean V̇O2max was 146 ± 2 ml/kg/min. Mean plasma [lactate] was 23.0 ± 1.2 mmol/l. MAOD was weakly correlated with V̇O2max (r = 0.514, P < 0.05), but was not correlated with run time, plasma lactate or treadmill work. The test of MAOD was suitable for use during clinical exercise testing.

Administration of oral fluids prior to exercise may provide a fluid ‘buffer’ supporting cardiorespiratory and thermoregulatory function during prolonged exercise. Six Standardbred horses, previously acclimatised to a treadmill and a respiratory gas collection mask, were used in a crossover study and were given ∼17.5 litres hypotonic commercial electrolyte mixture via a nasogastric tube, 90 min before exercise. Total fluid was equivalent to 4% bwt, administered in 3 equal doses, 20 min apart, the last 50 min before exercise resulting in a mean ± s.e. pre-exercise plasma total protein (TPP) of 57.6 ± 0.6 g/l, compared with 63.5 ± 0.5 g/l (P < 0.01) when no fluid was given. One week later, each horse received the alternate treatment. The exercise test consisted of 90 min at 30% V̇O2max with measurements taken throughout exercise. Exercise increased temperature, haematocrit, TPP, [glucose], [lactate] and pH and decreased plasma [K] and [Cl], respiratory exchange ratio and PaCO2. There was no effect of exercise duration on heart rate, cardiac output, stroke volume, V̇O2 V̇CO2, [HCO3] or PaO2. Fluid administration resulted in lower TPP, plasma [Cl], [HCO3] and [Na] during exercise. Although fluid administration before exercise did not improve cardiorespiratory and thermoregulatory function, the fluid treated group had a higher plasma volume which may be advantageous to horses exercising in hot and humid environments.

This study investigated the effects of increased fat consumption on aerobic and anaerobic performance. Eight Thoroughbred horses that had undergone a 9 week, 6 days/week conditioning programme were randomly divided into 2 groups, Group F (5 horses) and Group C (3 horses). For 2 weeks before the study all horses consumed a standard diet (2% fat) fed as 2 equal portions. Horses then undertook an incremental treadmill exercise test (+10% slope); 3 min at 4 m/s, 2 min at 6 m/s and 1 min at 8 m/s. Speed was then increased by 1 m/s every 60 s until fatigue. Maximal accumulated oxygen deficit (MAOD) was determined 72 h later. Horses in Group F were then fed a diet containing 12% of the digestible energy in the form of fat (390 ml corn oil), a diet that was isocaloric with the control diet. Horses in Group C continued to receive the standard diet. All horses continued training (3600 m/day, at speeds up to 10 m/s, 6 days/week). After 4 weeks, the exercise tests were repeated. Prior to fat supplementation, V̄O2max was mean ± s.e. 145 ± 5.3 and 148.0 ± 6.0 ml/kg/min, time to fatigue during the MAOD test was mean ± s.e. 84.2 ± 18.4 and 85.0 ± 14.8 s, mean ± s.e. peak plasma [lactate] was 24.8 ± 3.1 and 23.5 ± 1.7 5 mmol/l and MAOD was 56.5 ± 5.3 and 68.1 ± 4.7 mlO2eq/kg for Groups F and C respectively. The V̄O2max and run time to fatigue in the incremental exercise test did not change in either group following fat supplementation. Run time (mean ± s.e. 97.2 ± 17.8 s), MAOD (65.5 ± 6.2 mlO2eq/kg) and peak plasma [lactate] (29.5 ± 2.6 mmol/l) increased during the MAOD test in Group F but remained unchanged in Group C. Resting muscle [glycogen] depletion during the MAOD test was not altered by the dietary manipulation. Provision of an increased proportion of the diet in the form of fat increased high intensity exercise capacity and the MAOD during intense treadmill exercise.

The principal aim of this study was to examine whether alterations in sweat composition occurred during training. Ten Thoroughbred horses were trained 6 days per week for 9 weeks on a treadmill (+10% slope), 5 at moderate intensity, (80–100% V̇O2max) and 5 at low intensity, (40–45 % V̇O2max). On Day 1 of training and at the end of weeks 1, 2, 5 and 9, the horses performed a standardised exercise test (SET). Sweat was collected onto an absorbent pad lined with plastic and held against the skin with rubber straps. Samples were obtained from the neck and girth areas during exercise and for 10 minutes post exercise. Sweat composition during exercise (in mmol/l) was [Na+] = 143.5, [Cl−] = 181.5, [K+] = 37.5, [Ca++] = 5.1, [Mg++] = 4.2, [urea] = 5.1 and [protein] = 6.4 g/l. Training resulted in a decrease in [Ca++] of 1.6 ± 0.8 mmol/l (P < 0.05) after the first week of training. The type of training had no effect on sweat composition. Sweat produced in the post exercise period had higher [Na+], [Cl−] and [urea] than that produced during exercise. Training does not substantially alter the composition of equine sweat in response to an intense SET.

We sought a physiological marker of overtraining in horses, using commonly practised field and laboratory tests to allow early prediction and treatment of the syndrome. Thirteen Standardbred horses were trained as follows: phase 1 (endurance, 7 weeks), phase 2 (high intensity, 9 weeks) and phase 3 (overload, 18 weeks). In phase 3 the horses were divided into 2 groups: overload training (OLT) and control (C). The OLT group exercised at greater intensities, frequencies and durations than the C group. Overtraining occurred after 31 weeks and was defined as a significant decrease in treadmill run time to fatigue (RT) in response to a standardised exercise test (SET). Variables measured included: feed intake, bodyweight (BWT), resting haematology and plasma biochemistry and treadmill SETs to measure RT. The OLT group had a decrease in BWT after week 28 (P<.05) without a reduction in feed intake and a reduction in RT during the SET after 31 weeks. Signs persisted after 2 weeks of a reduced training load confirming overtraining. Haematology and biochemistry failed to detect any markers of overtraining. Although no physiological markers of overtraining were identified, empirical observations revealed that the behaviour of horses in the OLT group was different from those in the C group during the period of overtraining. This study reflects that a model of overtraining has been developed based on measurement of a reduction in performance; however, there were no consistent changes in haematology or serum biochemical values in association with the decrement in performance capacity.

We examined 106 Thoroughbred (TB) and 51 Standardbred (SB) racehorses that were presented because of poor performance. All horses were in training and had raced within 2 weeks of presentation. Horses were acclimatised (2–4 runs) and tested on a treadmill set at a 10% slope. The exercise test consisted of 3 min at 4 m/s, 2 min at 6 m/s, then 1 min steps at 8, 10, 11, 12 and 13 m/s or until the horse could not maintain pace with the treadmill. At the end of each speed, arterial blood and expired gas samples were collected and heart rate recorded. Measurements during the test included: arterial blood gas tensions, plasma lactate concentration [LA], V̇O2, V̇CO2, O2 pulse (V̇O2/HR), heart rate, maximum stride length (SLmax), post exercise haematocrit (PCVPE), total red cell volume (CV) and total run time. The TB ran longer than SB (522 vs. 477 s) and had higher values for CV, PCVPE, V̇O2max, V̇O2-200, maximum O2 pulse, V200, VHRmax, post exercise [LA] ([LAPE]) and SLmax. There were no breed differences for VLA4 and PaO2 at 10 m/s. In the TB, significant correlations (Spearman's rank order) (P<0.01) were found for treadmill run time with: PCVPE, V̇O2max, V̇O2–200, peak O2 pulse, PaO2 at 10 m/s, PaCO2 at 10 m/s, V200, VLA4, [LAPE], VHRmax, maximum blood temperature and SLmax. In the SB significant but lower correlations (P<0.05) were found for treadmill run time with: PCVPE, V̇O2max, V200, VLA4, [LAPE], VHRmax, maximum blood temperature and SLmax. While these results may not be applicable to normal racehorses, the indices which correlated best with treadmill run time were generally those indicating a high capacity for oxygen transport.

The effects of training intensity and duration on blood lactate concentrations during submaximal and after maximal treadmill exercise were investigated in 2 groups of 5 Thoroughbred horses. Horses were trained on a treadmill in either a ‘fast’ or ‘slow’ group. In the ‘fast’ group, all exercise after an initial warm-up was at speeds which resulted in blood lactate concentrations in the range 4–8 mmol/l. In the ‘slow’ group, all training exercise was at half the speed but equal distance. Incremental speed treadmill tests were repeated after 1, 2, 3, 5, 7 and 9 weeks training. Treadmill speeds and oxygen uptake at blood lactate of 4 mmol/l (VLa4 and V̇O2-4) and blood lactate concentration at 9 m/s (La9) were measured. Blood was also collected at 2 or 5 min intervals after a run to fatigue at 115% of maximum oxygen uptake (V̇O2max). Peak and 10 min post exercise lactate concentrations were measured, and disappearance rate (mmol/l/min) calculated. Runs to fatigue were repeated after 5 and 9 weeks of training. Data were analysed by repeated measures ANCOVA. Mean ± s.e.m. VLa4 increased from 7.0 ± 0.5 to 9.2 ± 0.2 m/s (P<0.001) and La9 decreased from 8.0 ± 1.0 to 3.9 ± 0.3 mmol/l (P<0.001) over the 9 weeks training. The pooled V̇O2-4 increased from mean ± s.e.m. 96 ± 6.6 to 122 ± 5.6 ml/min/kg (P<0.01) after training. An increase in the pooled %V̇O2max-4 from 79 ± 3.4% to 84 ± 2.4% after 9 weeks training was not statistically significant. There were no significant effects of training intensity on changes in VLa4, La9, or V̇O2-4 and no significant effects of training on lactate concentrations after exercise to fatigue at 115% V̇O2max. The training induced decrease in blood lactate concentration during submaximal exercise is not dependent on intensity of exercise during training.

Muscle glycogen resynthesis rates were studied in 6 Standardbred geldings that were exercised on a treadmill inclined at 10% slope to deplete muscle glycogen prior to treatments. Each horse completed 15 min at 50% V̇O2max, 15 min at 70% V̇O2max, 5 min at 90% V̇O2max then rested for 30 min. This was followed by 6, 1 min sprints at 100% V̇O2max with 5 min rest periods between sprints. Muscle biopsies were taken from the middle gluteal muscle at a depth of 8 cm using the same locations in each horse. Samples were taken before, at the end of exercise and 3, 6, 9, 12 and 24 h after treatment. Blood samples were collected before exercise, immediately after exercise, then every 60 min for 8 h after treatment. Thirty min after exercise each horse was treated with either 6 g/kg dextrose i.v. as a 20% solution in an isotonic electrolyte solution at a mean (± s.e.) infusion rate of 1.67 ± 0.05 1/h, or with a solution of equivalent volume of polyionic isotonic fluid (control) at the same infusion rate. Mean pre-exercise and post infusion peak plasma glucose concentrations were 4.9 ± 0.1 and 28.6 ± 2.8 mmol/l and 4.7 ± 0.2 and 6.0 ± 0.5 mmol/l, for treatment and control respectively. Mean pre-exercise and peak insulin concentrations were 0.007 ± 0.002 and 0.123 ± 0.022 μu/l and 0.006 ± 0.001 and 0.012 ± 0.002 μu/l, for treatment and control respectively. There were significant effects of both time and treatment for glucose and insulin (P<0.05). Mean rates of glycogen resynthesis for the first 12 h were 14.6 ± 2.6 mmol/kg/h and 2.6 ± 3.1 mmol/kg/h respectively for treatment and control and 7.0 ± 1.6 mmol/kg/h and 3.8 ± 1.2 mmol/kg/h for the first 24 h after treatments. The administration of large doses of dextrose i.v. after exercise increases the rate of muscle glycogen resynthesis.

We tested the hypothesis that training would result in more rapid increase in V̇O2 and V̇CO2 following the onset of submaximal exercise. Six Standardbred horses were used and trained at submaximal intensities for 5 weeks. Horses were trained 6 days per week on an inclined treadmill (10% slope) at intensities between 40 and 70% V̇CO2max. At the onset of training horses ran 2600 m/day which progressively increased to 4500 m/day by week 5. Testing was carried out before training and after weeks 3 and 5 of training. The test involved exercise at 2 speeds, 4 m/s and 8 m/s, both for 3 min with one h recovery between the 2 speeds. All horses performed at both speeds but the initial speed was randomly allocated. An open flow gas collection system was used to measure V̇O2 and V̇CO2 every 15 s for the first min of exercise and every 30 s thereafter. After 5 weeks training, mean body weight and V̇O2max (mean ± s.e.) of the group had altered from 433 ± 5 kg to 430 ± 8 kg (P > 0.05) and from 104 ± 5 ml/kg/bwt/min to 116 ± 6 ml/kg/bwt/min (P < 0.05), respectively. There were no significant training effects on the rate of change of V̇O2 or V̇CO2 at either of the test speeds. By 45 s, the V̇O2 and V̇CO2 values had reached 85 to 95% of mean steady state values at both intensities of exercise. In general, steady state V̇O2 and V̇CO2 values were evident by 60 s of exercise. We conclude that horses have rapid increases in gas exchange at the start of exercise and these are not influenced by low intensity training.