To help resolve the mechanistic bases for haematological adaptations (~28% increase in red blood cell volume) of equids to high altitude (3800 m, barometric pressure Pb, 487 mm Hg) and exercise, plasma erythropoietin concentration ([EPO]) was measured at rest and following exercise in six, moderately fit equids (four Arabians, one Quarter Horse and one Shetland Pony; four females and two males; age 9.0 ± 4.5 years (mean ± SD)). [EPO] was measured on 2 days at 225 m (i.e. ~sea level; Pb, 743 mm Hg), over the course of a 10-day altitude exposure, and then again for 2 days after return to sea level. A standard track exercise test (submaximal, speed set-to-heart rate of 110 (trot), 150 (canter), 180 (gallop) bpm) was performed 2 days pre-high-altitude exposure and on three separate days at high altitude. In addition, a maximal incremental exercise test was performed on a high-speed motor-driven treadmill at sea level and 2 days following return to sea level from high altitude. Resting [EPO] increased from 28 ± 29 at sea level to 144 ± 46 mU ml− 1 (P < 0.05) on the first day at high altitude. By day 2 at high altitude, [EPO] had returned to baseline (31 ± 24 mU ml− 1, P>0.05 vs. pre-high altitude) and did not change over the remaining 8 days at high altitude nor over the 2 days after return to sea level. [EPO] was not significantly altered by acute exercise at sea level or at 3800 m. These results indicate that [EPO] increases rapidly (though transiently) in response to hypobaric hypoxia but not to acute exercise, and that exercise does not appear to potentiate the altitude response. Thus, if any [EPO]-derived haematological adaptations to high altitude are present, these appear to result from a transient ~4-fold elevation of [EPO] rather than any sustained increase in this signalling mechanism, at least in the equid.

This study tested the hypothesis that phenylbutazone would block the exercise-induced increase in cytokine markers of inflammation in blood. Blood samples were obtained from unfit Standardbred mares (age 10 ± 4 years, ~500 kg) before and after three different trials (standing control (CON), n = 9; exercise with phenylbutazone (EX-bute), n = 9; and exercise with water, n = 9). Comparisons were made for data collected in three trials, one where each horse underwent an incremental exercise test (graded exercise test (GXT)) where they were administered water as a placebo, a GXT following phenylbutazone administration (2 g given orally 2 h before the GXT) or standing parallel control where they stood quietly in stalls. During the GXT, horses ran on a treadmill (1 m s− 1 increases each min until fatigue, 6% grade). Blood samples were obtained 30 min before exercise, immediately after exercise and at 0.5, 1, 2, 4 and 24 h post-GXT or at matched time points during the parallel control trials. Samples were analysed using real-time PCR for measurement of mRNA expression of interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α) and interleukin (IL)-6 in samples collected during all three trials, and for IL-1 and IL-10 in samples collected for the CON and EX-bute trials. Data were analysed using ANOVA for repeated measures, and where appropriate, post hoc separation of means utilized the Student–Newman–Keuls test. The null hypothesis was rejected when P < 0.05. There were no changes (P>0.05) in IL-1, IL-6, IFN-γ or TNF-α during CON or following phenylbutazone administration. During the water trial, exercise resulted in significant increases in IFN-γ, IL-1 and TNF-α. It was concluded that high-intensity exercise results in a transient increase in the expression of inflammatory cytokines in blood that is blocked when phenylbutazone is administered to horses.

The objective of this experiment was to test the hypothesis that ageing and training alter plasma concentrations of the peptide hormone leptin. The rationale for the study is based on prior investigations performed at Rutgers University, where published reports documented that ageing disrupts the immune and endocrine responses to acute exercise. The training period for mature young (7.3 ± 0.6 years; n = 6) and old (22 ± 0.7 years; n = 6) (mean ± SE) Standardbred mares was the duration of the summer of 2009 at the Rutgers University Equine Exercise Physiology Laboratory. Mares exercise trained in groups of six in a free-stall motorized circular equine exercise machine for 30 min, three times per week. Each mare performed a graded exercise test before beginning the training, after 8 weeks and after 16 weeks of training. There was no difference in body mass due to age (P>0.10). Training caused an increased body mass in both old and young mares (P < 0.10). There was no effect of training on rump fat thickness; therefore, the increase in body mass was primarily due to an increase in fat-free mass (muscle mass). Old mares had significantly lower plasma leptin at all sample points. As a result of training, plasma leptin was reduced in both old and young mares (P < 0.10). In conclusion, age and training appear to alter the relationship between body composition and leptin.

The present study tested the hypothesis that lactate concentration ([La− ]) would differ between sample sites and between assay techniques that used different analytical substrates. Six clinically normal adult (two Thoroughbreds, three Standardbreds and one Quarter Horse) mares weighing between 435 and 560 kg were used in the study. Each mare performed an incremental exercise test (graded exercise test, GXT) where it ran on a treadmill at a fixed 6% grade. The GXT started at 3 m s− 1 for 1 min with increased in speed by 1 m s− 1 every 60 s until the horses completed the final 10 m s− 1 step. Jugular vein, pulmonary arterial and carotid arterial blood samples (14 ml) were collected before exercise and during the last 10 s of each step of the GXT. [La− ] was measured in whole blood (WB, no manipulations), total blood (TB, where the red blood cells were lysed) and plasma. Data were used to calculate the velocity to produce [La− ] of 4 mmol l− 1 (VLA4) and 10 mmol l− 1 (VLA10). Statistical analysis utilized a three-way ANOVA and, where appropriate, the Holm–Sidak or the Student Neuman–Keuls method for post hoc comparisons. The null hypothesis was rejected when P < 0.05. There was an effect of exercise intensity on [La− ] for all three methods (P < 0.001) with all means during exercise significantly greater than the resting mean, and there were differences due to method (i.e. analytical substrate) (P < 0.001) and sample site (P = 0.043). Comparisons of least-squared means (LSM ± SE) within site revealed that there was a difference (P < 0.05) between jugular vein (5.41 ± 0.24) and carotid artery (6.24 ± 0.24) and between carotid and pulmonary artery (5.98 ± 0.24). There was no difference (P>0.05) between jugular vein and pulmonary artery. Within method, there was a difference (P < 0.05) between WB (6.54 ± 0.36) and TB (5.06 ± 0.36) and between TB and plasma (6.04 ± 0.64), but there was no difference (P>0.05) between WB (6.54 ± 0.36) and plasma (6.04 ± 0.64). Further analysis of the data demonstrated that the method and sample site influenced (P < 0.05) VLA4 and VLA10.

Twenty-seven mature Standardbred mares (9–27 years, ~522 kg) were used to test the hypothesis that training and short-term cessation of training would alter total plasma total carbon dioxide (tCO2) concentrations. Plasma tCO2 concentrations were measured in blood samples (20 ml) collected at rest from the same ten unfit mares that were used in two separate studies that were conducted 1 month apart. Comparisons between the samples obtained from the two trials were made to demonstrate the consistency of plasma tCO2 concentrations in the untrained population. Another set of resting blood samples was collected from an additional 17 mares that were being utilized in a training study that was under way during the same period. All the mares were housed in groups on dry lots, and were fed approximately 12 kg of mixed alfalfa-grass hay divided into two feedings per 24 h period. During the ‘detraining’ period, the 17 horses were housed in 5 × 5 m stalls, and were fed the same hay ration. Water and trace-mineral blocks were available ad libitum. Blood samples were collected from the mares prior to the last session of their 12 weeks of training at 60% HRmax (maximum heart rate), as well as on the third day following 2 days of detraining (simulated quarantine). Plasma tCO2 concentrations were measured in duplicate using a Beckman EL-ISE analyser. For data analysis, t-tests with the a priori level of statistical significance set at P < 0.05 were used. Resting plasma tCO2 concentrations were lower (P < 0.05) in the trained horses (31.4 ± 1.9 mMol l− 1) than in the untrained horses (34.4 ± 0.9 mMol l− 1). There were no effects (P>0.05) due to cessation of training. It was concluded that training causes a decrease in plasma tCO2 concentrations that is not reversed by limited cessation of training.

Ten mature Standardbred mares (9–13 years, ~522 kg) were used to test the hypothesis that pelleted dietary supplementation would alter total plasma bicarbonate (tCO2) concentrations. All the mares used in this study were unconditioned, but were familiarized to the laboratory setting and running on a treadmill. Each of the ten mares was semi-randomly assigned one of four dietary treatments. The four treatments (oats as control and three pelleted feed supplements: Drive, Omolene and Strategy) were administered in a crossover fashion throughout a 4-week testing period. These products were chosen based on the frequency of their use by Standardbred/Thoroughbred owners and trainers in New Jersey. The horses underwent a simulated race test (SRT) on a treadmill (6% grade) at the end of each administration period. During the SRT, horses ran for 2 min at 4 m s− 1, 2 min at the speed previously shown to correspond to VO2max and 2 min at 4 m s− 1. Blood was collected before supplement treatment ( − 4 h), 10 min prior to exercise and at 0, 60 and 90 min post-exercise. Plasma concentrations of bicarbonate, sodium, potassium and chloride were measured using a Beckman ELISE analyser. The major finding of this study indicates that the plasma [tCO2], chloride and sodium concentrations were not altered by the dietary supplements studied (P>0.05). There were differences (P < 0.05) in plasma [tCO2] across sampling intervals ( − 4 h, − 10 min, +0 min, +60 min and +90 min) that were attributable to acute exercise (mean ± SE: 34.4 ± 0.9, 33.2 ± 1.1, 20.2 ± 0.8, 31.5 ± 0.8, 30.3 ± 1.6 mmol l− 1). There was a slight effect of treatment (P < − 0.05) on potassium levels. However, exercise was the main factor that caused substantial changes (P < 0.05) in the plasma tCO2, potassium, haematocrit and total protein concentrations. It was concluded that the pelleted diet supplements examined do not alter plasma [tCO2] in horses.

Previous studies of the effect of age on maximal aerobic capacity (maximal rate of oxygen consumption, VO2max) in horses have only grouped horses (young, middle-aged and old) for statistical analysis. Those experiments were not designed to determine a break point due to age. The purpose of this study was to utilize data collected over the last 15 years to test the nature of the association between age and VO2max, and secondarily, to determine whether there is a ‘breakpoint’ in the age-related decline in aerobic capacity. Data were acquired from 50 unfit Standardbred mares ranging in age from 4 to 29 years, and were used in a retrospective regression analysis in order to characterize the age-related decline in VO2max. All VO2max values were measured using the same incremental graded exercise test protocol. The data were analyzed using a curvilinear regression analysis predicting VO2max from age, and the break point was determined using univariate simple contrasts. There was a significant decline in VO2max with age (R2 = 0.554; P < 0.001). The data analysis demonstrated a notable downturn in cardiopulmonary function between the ages of 18 and 20 years (P < 0.001). Such results indicate similar responses to age between humans and horses. These results have implications for improving training methods in active older horses.

The purpose of this study was to test the hypothesis that the gastric ulcer medications, ranitidine and omeprazole, would alter plasma concentrations of total carbon dioxide (tCO2), lactate (LA), Na+, K+, 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). Twelve unfit Standardbred mares (~520 kg, 9–18 years) were used in a randomized crossover design with the investigators blind to the treatment given. Each mare received a treatment three times daily (TID) at 06.30, 12.30 and 18.30 hours. The treatments administered orally were omeprazole (4 mg kg− 1 was given in the morning with apple sauce given at the later, two dosing times to encourage good behaviour), ranitidine (6 mg kg− 1 crushed and mixed in 20 ml apple sauce) and control (20 ml apple sauce TID). Each horse completed a series of SRTs with blood samples taken via jugular venipuncture at five 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− 1) and then for 2 min at a velocity predetermined to produce VO2max. Each horse then walked at 4 m s− 1 for 2 min to complete the SRT. Plasma tCO2, electrolytes, LA and TP concentrations and PCV–TP were measured in duplicate at all intervals. No differences (P>0.05) were detected between control, ranitidine or omeprazole 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 not an effect of the medication. It was concluded that ranitidine or omeprazole did not alter plasma tCO2 concentration.

This study tested two hypotheses. First, that moderate exercise would alter maternal and foetal heart rate (HR) in the horse. Second, that pregnancy would alter the HR, plasma cortisol and plasma lactate response to moderate exercise in mares. Six unfit, pregnant Standardbred mares (6–19 years) underwent two incremental graded exercise tests (GXT). The first GXT was performed at approximately 9 months of gestation, which represents c. 80% of the total pregnancy time, and the second GXT at approximately 6 months post-parturition. During the GXT, mares ran on a treadmill up a fixed 6% incline completing three 1 min steps at velocities of 4, 6 and 7 m s− 1. Maternal HR was obtained via both electrocardiograph (ECG) and the ventricular waveform obtained from a micromanometer catheter. Data were recorded at rest, at 4, 6 and 7 m s− 1 of the GXT and at 0, 1, 2, 3, 4 and 5 min post-GXT. Foetal HR rate was measured via ECG before, immediately after and at 1, 2, 3, 4 and 5 min post-GXT. Radioimmunoassay (RIA) kits were used to measure plasma cortisol concentration in samples collected before the GXT, immediately after exercise and after 5 min of recovery. Plasma lactate concentrations (LA) were measured at rest, at 4, 6 and 7 m s− 1 and at 5 min post-GXT. Plasma cortisol concentrations were measured using RIA and the samples collected at rest, immediately after and at 5 min post-GXT. Exercise caused no change (P>0.05) in foetal HR. Maternal HR, plasma LA and plasma cortisol concentration were greater (P < 0.05) during the post-parturient GXT compared with the pre-parturition GXT. Body weight (mean ± SE) was lower after parturition (570 ± 20 vs. 505 ± 22 kg; P < 0.05). Consequentially, there were differences (P < 0.05) in work rate (watts) at each step of the GXT (1557 ± 53 vs. 1381 ± 60; 2339 ± 80 vs. 2071 ± 90; and 2571 ± 121 vs. 2416 ± 105 W). These data suggest that mares benefit from greater cardiovascular efficiency during pregnancy. Additionally, the lack of a change in foetal HR suggests that the unborn foal is not stressed during moderate maternal exercise.

This study tested the hypothesis that orange peel (O) and decaffeinated black tea (T) extracts would alter markers of exercise performance as well as exercise-induced mRNA expression for the inflammatory cytokines IL-6, TNF-alpha and IFN-gamma. Nine healthy, unfit Standardbred mares (age: 10±4years, ∼450kg) were assigned to three treatment groups in a randomized crossover design where each horse was administered one of the following; placebo (O; 21 water), black tea extract in water (T; 21) or orange peel extract in water (W; 21), via a nasogastric tube. One hour later the horses completed an incremental graded exercise test (GXT) on a treadmill at a fixed 6% grade with measurements and blood samples obtained at rest, at the end of each 1min step of the GXT and at 2 and 5min post-GXT. An additional set of blood samples for Polymerase Chain Reaction (PCR) measurements of mRNA was obtained before exercise and at 5 and 30min and 1, 2, 4 and 24h post-GXT. The GXTs were conducted between 0700 and 1200h not less than 7days apart. There were no differences (P>0.05) in VO2max, respiratory exchange ratio, run time, velocity at VO2max, core body temperature, haematocrit, creatine kinase (CK), plasma lactate concentrations, HR, right ventricular pressure (RVP) or pulmonary artery pressure (PAP) across treatments. A major finding was that orange peel extract significantly reduced post-exercise VO2 recovery time (W = 112±7, O = 86±6, and T = 120±11s). There was a significant difference in plasma total protein concentration (TP) in the O runs compared with water and T. TNF-alpha mRNA expression was lower in the T runs compared with water and O trials. IFN-gamma mRNA expression levels appeared to be lower in both the T and O extract runs compared with the water trials. The mRNA expression of IL-6 was unaltered across treatment groups. These data suggest that orange peel and black tea extracts may modulate the cytokine responses to intense exercise. Orange peel extract reduced post-exercise recovery time and may potentially enhance the ability of horses to perform subsequent bouts of high-intensity exercise.

This study used a randomized crossover design, with investigators blind to the treatment given, to test the hypothesis that seven commercially available electrolyte supplements would alter plasma concentrations of Na+, K+, Cl−, lactate, total protein (TP) and total carbon dioxide (tCO2) as well as plasma strong ion difference (SID) and haematocrit (HCT). Ten unfit Standardbred mares (∼450 kg, 4–9 years) completed a series of simulated race exercise tests (SRT) during which venous blood was collected at five sampling intervals (prior to receiving electrolyte treatment, prior to the SRT, immediately following exercise and at 60 and 90 min post-SRT). Plasma electrolyte and tCO2 concentrations were measured in duplicate using a Beckman EL-ISE electrolyte analyser. No difference (P>0.05) between treatments was detected at any of the five sampling intervals for plasma [Na+], [K+], [Cl−] or [tCO2]. Similarly, no significant difference was detected between treatments across each of the five sampling intervals for plasma SID, HCT or TP concentration. There were differences (P<0.05) in plasma [Na+], [K+] and [tCO2] (as well as plasma SID, HCT, and TP concentration) in the immediately post-SRT samples that were attributable to the physiological pressures associated with acute exercise. No differences (P>0.05) were detected between treatments across the pre-electrolyte and pre-SRT sampling intervals for plasma lactate concentration. There was, however, a significant time by treatment interaction during the 0, 60 and 90 min post-SRT sampling intervals for this parameter. The electrolyte supplements featured in this investigation did not affect either plasma tCO2 concentration or SID; however, this result does not rule out the potential for other supplements, especially those containing alkalinizing ingredients, to exert an effect that could push a horse towards threshold values.