Thoroughbred racehorses often undergo a reduction in training, or detraining, because of locomotor disorders or subsequent rehabilitation, psychological or behavioral issues, or other factors. Various types of detraining programs are used with racehorses, but only a few studies1–4 have evaluated the physiologic effects of reducing or ceasing training. It is important for planning the management of horses undergoing detraining to identify the effects and understand the changes that detraining induces in physiologic systems and subsequent racing performance.
The studies by Knight et al2 and Art and Lekeux5 revealed that the maximal rate of oxygen consumption (
o2max) of trained horses rapidly decreases and returns to pretraining values following 2 to 3 weeks of detraining. This is similar to the response of some human athletes in whom o2max declines within days of cessation of training.6,7 However, there are conflicting data to indicate that o2max in horses does not decrease until week 6 of a detraining period after 34 weeks of training8 or does not decrease even after 15 weeks of detraining following 6 months of training.1 Knight et al2 and Art and Lekeux5 studied mainly the effects of detraining after relatively shorter periods of training or submaximal training, compared with training conditions used by Butler et al1 and Tyler et al.8 The training status of horses before detraining may influence changes in cardiovascular function induced by detraining.9 Horses in the studies of Knight et al2 and Tyler et al8 were typically detrained in a yard with almost no physical activity, whereas detraining programs of horses in real-world settings vary according to the horses' physical status.
For the study reported here, our intent was to test whether use of detraining programs of different exercise intensities would result in differential changes in variables of interest (eg, oxygen transport, aerobic capacity, and indices of performance) at the end of detraining. We planned to assess the effects of detraining programs that are broadly applicable to certain types of common injuries sustained by racehorses. The experimental groups were designed to test for differences in the effects of detraining programs on horses that may run at a slower speed after a race because of muscle soreness (a cantering protocol), be walked as part of rehabilitation after tendinitis (a walking protocol), or remain in their stalls at all times because of bone fracture or other severe disease (a stall-rest protocol). The study was designed to provide data with which to better understand how detraining protocols involving different degrees of reduced activity affect racehorses, compared with the effects of detraining by means of stall rest alone.
The purpose of the study reported here was to determine whether Thoroughbred racehorses undergoing regular exercise at 1 of 2 intensities or stall rest during detraining would differentially maintain their cardiopulmonary and oxygen-transport capacities. We were also interested in assessing whether those changes in aerobic and circulatory capacities would differ from those determined in previous detraining studies. We hypothesized that the racehorses' aerobic and circulatory capacities would decrease in proportion to the reduction in exercise intensity during detraining. To test this hypothesis, Thoroughbreds were trained on a treadmill for 18 weeks, and aerobic capacity and oxygen-transport variables were quantified; then, the horses' aerobic capacities and oxygen-transport variables were again measured after a 12-week period of detraining during which they underwent different degrees of reduced exercise intensity.
Materials and Methods Horses
Twenty-seven Thoroughbreds (14 males, 2 geldings, and 11 females) were used in the study. At the onset of the study, the horses' mean ± SD age was 3.5 ± 0.9 years and body weight was 500 ± 32 kg. The horses had a carotid artery surgically moved from the carotid sheath to a subcutaneous location to facilitate arterial catheterization. After recovery from surgery, the horses were trained to run on a motorized treadmilla while wearing an open-flow mask.10 Horses were kept in 2-hectare pastures for approximately 8 hours/d and underwent no forced exercise for at least 6 months before treadmill experiments began. Protocols for the study were reviewed and approved by the Animal Welfare and Ethics Committee of the Japan Racing Association Equine Research Institute.
Training protocol
For 18 weeks, all horses exercised on a treadmill inclined at a 6% grade on 5 days each week and were pastured in 2-hectare pastures for approximately 6 h on each of the other 2 days. At the end of the 18-week training period, horses were detrained for 12 weeks in accordance with 1 of 3 protocols without access to pasture. Initially, the training program consisted of a warm-up (walking at 1.7 m/s for 1 minute and trotting at 3.5 m/s for 3 minutes), cantering for 3 minutes, and a cool-down (1.7 m/s for 3 minutes). The speed of cantering increased as the training progressed (weeks 1 to 3, 75% of the horse's maximal rate of oxygen consumption converted to standard temperature and pressure dry [o2max] of each horse for 3 minutes; weeks 4 to 6, 90% o2max for 3 minutes; weeks 7 to 10, 100% to 110% o2max for 3 minutes; and weeks 11 to 18, 90% o2max for 3 minutes on 3 d/wk and 110% to 115% o2max for 2 minutes on 2 d/wk). Exercise intensities of each horse during weeks 1 to 10, 11 to 18, and 19 to 30 were based on the results of standardized treadmill exercise protocol measurements performed at weeks 0 (prior to initiation of training), 10, and 18, respectively. The criteria for identifying o2max were no increase in oxygen consumption (o2) with increased speed, respiratory exchange ratio > 1.0, and exponentially increasing plasma lactate accumulation rate with increasing speed.11
Detraining protocols
Horses were randomly assigned to 1 of 3 groups for detraining with a cantering protocol, a walking protocol, or a stall-rest protocol. Horses undergoing the cantering protocol (canter group) exercised with a warm-up (walking at 1.7 m/s for 1 minute and trotting at 3.5 m/s for 3 minutes), cantering at 70% of the horse's o2max at the end of the training period (mean ± SD speed, 8.64 ± 0.68 m/s) for 3 minutes, and a cool-down (1.7 m/s for 3 minutes) on 5 days each week and were confined singly in 3 × 3-m stalls on the other 2 days each week. Horses undergoing the walking protocol (walk group) exercised in a walking machine at 1.7 m/s for 1 h/d on 5 days each week and were confined singly in 3 × 3-m stalls on the other 2 days each week. Each horse undergoing the stall-rest protocol (stall group) was confined individually in a 3 × 3-m yard that was approximately 20 m distant from its stall for 6 hours each day and was kept within its 3 × 3-m stall for the remainder of each day.
Standardized treadmill exercise protocol measurements
Standardized treadmill exercise protocol measurements were performed at weeks 0 (prior to initiation of training), 10, 18 (post-training data), and 30 (post-detraining data). After catheters and transducers were connected and tested, exercising of each horse commenced. The horse was warmed up by walking at 1.7 m/s for 2 minutes and trotting at 3.5 m/s for 5 minutes. The horse then locomoted up a 6% incline for 2 minutes each at 1.7, 4, 6, 8, 10, 12, and 13 m/s until it could not maintain its position at the front of the treadmill with humane encouragement. This was defined as exhaustion.
For each speed after warm-up, each horse ran on the treadmill for 100 seconds to allow oxygen-transport variables to reach steady state, then o2 was calculated during the final 20-second period. Arterial and mixed-venous blood samples (both 10 mL) were collected simultaneously during this time for measurement of blood gases and oxygen concentration, from which 
D and SV were calculated with the Fick principle.12 Heart rate was determined from ECG tracings obtained with bipolar electrodes that were amplifiedb and recorded on a personal computer with commercial hardwarec and softwared using a sample rate of 200 Hz. Following a run, the R-R intervals were analyzed over the final 20 seconds at each speed to calculate the mean heart rate at that sample time.
Oxygen consumption
To monitor oxygen consumption, each horse was fitted with a 25-cm-diameter open-flow mask through which a rheostat-controlled 3.8-kW blower drew air. Air flowed through 20-cm-diameter tubing and across a 25-cm-diameter pneumotachographe connected to a differential pressure transducerf; this was done to ensure that bias flows during measurements were identical to those used during calibrations. Bias flow was set to keep changes in expired oxygen and carbon dioxide concentrations < 1%. Oxygen and carbon dioxide concentrations were measured with an oxygen and carbon dioxide analyzer,g and calibrations to calculate rates of oxygen consumption and carbon dioxide production were performed with electronic mass-flowmetersh and the nitrogen-dilution and carbon dioxide-addition mass-balance technique.13 Gas analyzer and mass-flowmeter outputs were also recorded on the personal computer.
Blood sample collection
Before each horse was lead onto the treadmill, an 18-gauge, 6.4-cm catheteri was placed in its surgically relocated carotid artery, and an 8.5-F, 9-cm introducerj was placed in a jugular vein. A Swan-Ganz catheterk was passed via the jugular vein so that its tip was positioned in the pulmonary artery, confirmed by measuring pressure at its tip with a pressure transducer.l Mixed-venous blood samples (10 mL each) were collected from the tip of the Swan-Ganz catheter and arterial blood samples (10 mL each) were collected from the carotid catheter into syringes containing heparin at timed intervals and stored on ice until measured immediately following the experiment. Blood samples were analyzed with a blood gas analyzer,m and oxygen saturations were measured with a hemoximetern set to its equine algorithm. Following blood gas analysis and oximetry, blood samples were centrifuged at 1,870 × g for 10 minutes for measurement of plasma lactate concentration with a lactate analyzer.o
Temperature measurements
The Swan-Ganz catheter in the pulmonary artery was connected to a cardiac output computerp so that its thermistor registered pulmonary arterial temperature. Pulmonary arterial temperature was recorded at the time of each blood sample collection and used to correct the blood gas measurements.
Time to exhaustion
Run time to exhaustion after the horse reached 10 m/s (texhaustion) during the standardized treadmill exercise protocol was measured with a stopwatch. Timing started when the horse began running at 10 m/s and stopped when the horse could no longer maintain its position at the front of the treadmill.
Statistical analysis
Data are reported as median, range, mean, and SD. Two-way repeated-measures ANOVA was used to analyze differences in variables among the 3 protocol groups or differences between post-training and post-detraining data. A Tukey procedure was used for post hoc pairwise comparisons. Statistical analyses were performed with commercial software,q and significance was defined as a value of P ≤ 0.05.
Results
Group characteristics after 18 weeks of training
For the stall group, body weight was higher (P = 0.035) and Cao2 and Ca-
o2 were lower (P = 0.04 and P = 0.05, respectively) than values for the walk group after training. However, no other variables differed among the 3 protocol groups (Table 1).
Oxygen-transport and performance-related variables at the end of 18 weeks of training in 3 groups of 9 horses that subsequently underwent 12-week detraining programs involving cantering (canter group), walking (walk group), or stall rest (stall group).
| Â | Detraining protocol group | Â | |||||
|---|---|---|---|---|---|---|---|
| Â | Canter | Walk | Stall | Â | |||
| Variable | Mean (SD) | Median (range) | Mean (SD) | Median (range) | Mean (SD) | Median (range) | P value |
| Body weight (kg) | 490.7 (34.2)ab | 484 (448–558) | 483.1 (31.3)a | 472 (445–527) | 521.6 (27.5)b | 522 (482–559) | 0.04 |
| Age (y) | 3.56 (0.88)a | 3 (3–5) | 3.33 (0.71)a | 3 (3–4) | 3.56 (1.01)a | 3 (3–6) | 0.94 |
| texhaustion (seconds) | 288 (81)a | 284 (160–360) | 275 (70)a | 258 (160–405) | 266 (46)a | 275 (170–385) | 0.79 |
| o2max (L O2 [STPD]/s) | 1.54 (0.17)a | 1.59 (1.24–1.74) | 1.53 (0.17)a | 1.59 (1.27–1.74) | 1.61 (0.14)a | 1.62 (1.44–1.91) | 0.58 |
| o2max/kg (mL O2 [STPD]/[s·kg]) | 3.14 (0.33)a | 3.08 (2.57–3.66) | 3.17 (0.29)a | 3.27 (2.72–3.50) | 3.10 (0.35)a | 3.03 (2.66–3.56) | 0.85 |
| Vo2max (m/s) | 11.5 (0.9)a | 11.6 (10.3–12.6) | 11.4 (0.9)a | 11.5 (10.3–13.0) | 11.2 (0.8)a | 11.3 (10.0–12.6) | 0.77 |
| VLA4 (m/s) | 8.37 (0.65)a | 8.27 (7.59–9.56) | 7.72 (1.07)a | 7.80 (5.42–9.25) | 8.20 (1.57)a | 8.41 (4.96–9.77) | 0.43 |
| Dmax (L blood/s) | 6.79 (0.55)a | 6.74 (5.82–7.48) | 6.60 (0.82)a | 6.38 (5.43–7.63) | 7.08 (0.52)a | 7.17 (6.38–7.92) | 0.30 |
| Dmax/kg (mL blood/[s·kg]) | 13.9 (0.9)a | 13.8 (12.6–15.3) | 13.7 (1.1)a | 13.6 (11.7–15.0) | 13.7 (1.1)a | 13.8 (12.1–15.1) | 0.87 |
| SVmax (L blood) | 2.04 (0.17)a | 2.04 (1.77–2.34) | 1.96 (0.17)a | 1.93 (1.66–2.19) | 2.13 (0.21)a | 2.04 (1.90–2.43) | 0.17 |
| SVmax/kg (mL blood/kg) | 4.15 (0.20)a | 4.24 (3.78–4.80) | 4.06 (0.23)a | 4.09 (3.55–4.31) | 4.14 (0.43)a | 4.14 (3.48–4.58) | 0.81 |
| HRmax (beats/min) | 215 (11)a | 215 (204–235) | 218 (8)a | 219 (204–229) | 221 (9)a | 223 (209–236) | 0.40 |
| VHRmax (m/s) | 11.8 (0.8)a | 11.9 (10.8–13.7) | 11.5 (0.8)a | 11.6 (10.1–13.7) | 12.2 (1.1)a | 12.0 (11.0–12.5) | 0.39 |
| Cao2 (mL O2 [STPD]/dL) | 26.2 (1.4)ab | 26.0 (24.2–28.6) | 26.2 (1.2)a | 26.3 (24.5–27.9) | 24.7 (1.4)b | 24.2 (23.1–26.7) | 0.04 |
| Co2 (mL O2 [STPD]/dL) | 3.3 (1.0)a | 2.9 (1.8–4.7) | 2.8 (0.7)a | 2.8 (1.7–3.8) | 2.7 (1.0)a | 2.7 (1.6–4.7) | 0.31 |
| Ca--o2 (mL O2 [STPD]/dL) | 22.9 (1.2)ab | 22.9 (20.9–24.6) | 23.4 (1.1)a | 23.3 (21.6–25.2) | 22.0 (1.2)b | 21.7 (20.4–24.0) | 0.05 |
| Hemoglobin (g/dL) | 22.5 (1.4)a | 22.6 (20.1–24.5) | 22.5 (1.0)a | 22.5 (20.9–23.6) | 21.7 (0.8)a | 21.7 (20.7–22.9) | 0.18 |
| Sao2 (%) | 86.6 (4.6)a | 84.9 (82.3–94.8) | 86.2 (4.6)a | 85.1 (79.8–93.5) | 85.9 (4.3)a | 84.5 (79.9–92.5) | 0.96 |
| So2 (%) | 11.3 (3.9)a | 9.7 (6.3–18.3) | 10.4 (4.6)a | 9.7 (5.7–20.9) | 9.4 (3.2)a | 9.7 (5.8–16.0) | 0.61 |
| Pao2 (mm Hg) | 77.7 (6.2)a | 79.1 (66.7–86.4) | 77.2 (6.9)a | 74.3 (67.9–89.6) | 78.9 (7.6)a | 80.0 (66.4–88.2) | 0.88 |
| Po2 (mm Hg) | 19.3 (3.1)a | 17.5 (14.6–22.6) | 17.5 (3.1)a | 16.9 (12.1–21.3) | 18.5 (3.0)a | 17.2 (15.3–23.0) | 0.49 |
For 18 weeks, all horses were exercised on a treadmill inclined at a 6% grade 5 days each week and were pastured in 2-hectare pastures for approximately 6 hours on each of the other 2 days. At the end of the 18-week training period, horses were detrained in accordance with 1 of 3 protocols without access to pasture for 12 weeks. Initially, the training program consisted of a warm-up (walking at 1.7 m/s for 1 minute and trotting at 3.5 m/s for 3 minutes), cantering for 3 minutes, and a cool-down (1.7 m/s for 3 minutes). The speed of cantering increased as the training progressed (weeks 1 to 3, 75% o2max of each horse for 3 minutes; weeks 4 to 6, 90% o2max for 3 minutes; weeks 7 to 10, 100% to 110% o2max for 3 minutes; and weeks 11 to 18, 90% o2max for 3 minutes on 3 d/wk and 110% to 115% o2max for 2 minutes on 2 d/wk). Exercise intensities of each horse during weeks 1 to 10, 11 to 18, and 19 to 30 were based on the results of standardized treadmill exercise protocol measurements obtained at weeks 0 (prior to initiation of training), 10, and 18, respectively. The criteria for identifying o2max were no increase in o2 with increased speed, respiratory exchange ratio > 1.0, and exponentially increasing plasma lactate accumulation rate with increasing speed.
STPD = Standard temperature and pressure dry.
For a given variable, mean values with different superscript letters differ (P ≤ 0.05) significantly; mean values with the same superscript letter do not differ (P > 0.05) significantly.
Group characteristics after 12 weeks of detraining
At the end of the detraining period, body weights of horses in the canter and walk groups had increased from their post-training values (Table 2). The mean weight increase in the canter group was 9.3 kg (1.9% [P = 0.03]), and the mean weight increase in the walk group was 9.7 kg (2.0% [P = 0.05]). Although the heavier horses in the stall group gained a similar amount of weight (mean weight increase, 8.1 kg [1.6%]), weight at the end of the detraining period was not different (P = 0.08) from the post-training value.
Oxygen-transport and performance-related variables in the horses in Table 1 after a 12-week period of detraining (following 18 weeks of training) according to 1 of 3 protocols (canter, walk, and stall groups).
| Â | Detraining protocol group | |||||
|---|---|---|---|---|---|---|
| Â | Canter | Walk | Stall | |||
| Variable | Mean (SD) | Median (range) | Mean (SD) | Median (range) | Mean (SD) | Median (range) |
| Body weight (kg) | 500.0 (42.9)*a | 494 (457–586) | 492.8 (29.2)*a | 481 (460–541) | 529.7 (27.1)a | 518 (499–576) |
| texhaustion (seconds) | 269 (62)a | 270 (176–285) | 201 (50)*b | 192 (120–378) | 182 (69)*b | 172 (92–324) |
| o2max (L O2 [STPD]/s) | 1.44 (0.09)a | 1.43 (1.30–1.59) | 1.37 (0.13)*a | 1.37 (1.09–1.54) | 1.41 (0.12)*a | 1.37 (1.26–1.61) |
| o2max/kg (mL O2 [STPD]/[s·kg]) | 2.90 (0.31)*a | 2.93 (2.38–3.05) | 2.77 (0.27)*a | 2.73 (2.29–3.35) | 2.67 (0.26)*a | 2.64 (2.23–3.24) |
| Vo2max (m/s) | 11.4 (0.8)a | 11.6 (10.3–10.9) | 10.5 (0.6)*ab | 10.3 (9.9–12.7) | 10.1 (0.4)*b | 10.1 (9.4–12.2) |
| VLA4 (m/s) | 8.46 (0.45)a | 8.49 (7.82–8.41) | 6.54 (0.81)*b | 6.52 (5.40–9.34) | 6.66 (0.66)*b | 6.42 (5.60–8.67) |
| Dmax (L blood/s) | 6.08 (0.16)*a | 6.11 (5.80–6.26) | 6.02 (0.71)a | 6.26 (4.63–6.71) | 6.16 (0.48)*a | 6.06 (5.62–7.20) |
| Dmax/kg (mL blood/[s·kg]) | 12.2 (1.0)*a | 12.3 (10.4–13.1) | 12.3 (1.6)*a | 12.4 (9.7–14.2) | 11.6 (0.9)*a | 11.7 (9.9–14.0) |
| SVmax (L blood) | 1.89 (0.12)*a | 1.89 (1.73–2.10) | 1.83 (0.18)a | 1.89 (1.43–2.00) | 1.85 (0.15)*a | 1.80 (1.68–2.07) |
| SVmax/kg (mL blood/kg) | 3.79 (0.28)*a | 3.82 (3.42–3.97) | 3.73 (0.44)*a | 3.73 (2.99–4.28) | 3.49 (0.30)*a | 3.39 (3.09–4.36) |
| HRmax (beats/min) | 210 (6)a | 211 (201–218) | 205 (6)*a | 202 (198–217) | 208 (12)*a | 211 (191–219) |
| VHRmax (m/s) | 11.8 (1.1)a | 11.9 (10.5–13.2) | 10.6 (0.7)*ab | 10.4 (9.9–13.0) | 10.5 (1.0)*b | 10.6 (8.6–13.0) |
| Cao2 (mL O2 [STPD]/dL) | 27.5 (1.8)*ab | 27.6 (25.4–30.4) | 26.4 (2.0)a | 26.3 (23.5–30.3) | 26.9 (1.5)*b | 26.4 (25.3–29.7) |
| Co2 (mL O2 [STPD]/dL) | 4.0 (1.0)a | 4.3 (2.0–5.4) | 3.6 (1.5)a | 3.1 (1.8–6.8) | 3.9 (1.4)*a | 3.1 (2.3–5.7) |
| Ca-o2 (mL O2 [STPD]/dL) | 23.5 (1.5)a | 23.4 (21.7–26.3) | 22.8 (1.7)a | 23.2 (20.5–25.6) | 23.0 (1.4)a | 22.6 (21.7–26.2) |
| Hemoglobin (g/dL) | 22.8 (1.4)a | 22.6 (20.6–24.8) | 22.2 (1.7)a | 21.5 (20.0–25.0) | 22.1 (1.1)a | 22.3 (20.7–24.1) |
| Sao2 (%) | 90.7 (5.1)*a | 90.6 (79.0–96.2) | 88.7 (3.6)*a | 88.8 (82.6–93.9) | 91.1 (4.4)*a | 91.1 (86.0–96.9) |
| So2 (%) | 13.1 (3.3)a | 13.5 (6.6–17.8) | 12.4 (4.7)a | 11.2 (5.8–22.6) | 13.0 (4.0)*a | 10.8 (8.1–18.2) |
| Pao2 (mm Hg) | 77.8 (7.3)a | 78.4 (65.9–86.4) | 81.6 (6.6)a | 78.9 (74.9–93.3) | 84.5 (11.4)a | 85.2 (69.7–101.4) |
| Po2 (mm Hg) | 19.0 (2.4)a | 19.6 (14.4–22.2) | 19.7 (3.5)*a | 20.6 (14.8–24.6) | 19.1 (2.1)a | 19.3 (15.1–22.7) |
Compared with post-training values, o2max/kg decreased by 7.2% (P = 0.04), 12.4% (P = 0.001), and 13.2% (P = 0.003) in the canter, walk, and stall groups, respectively. The post-detraining o2max/kg values did not differ among the 3 protocol groups (P = 0.21; Table 2). The speed at which o2max was reached (Vo2max) in the canter group did not change after detraining (P = 0.70), whereas those of the walk and stall groups decreased by 7.1% (P = 0.03) and 9.6% (P = 0.002), respectively.
The Dmax/kg and SVmax/kg decreased in all groups after 12 weeks of detraining (Table 2). For the canter, walk, and stall groups, the mean change in Dmax/kg from the post-training value was −11.6% (P = 0.003), −9.9 % (P = 0.03), and −14.1% (P = 0.001), respectively; the mean change in SVmax/kg from the post-training value was −8.5% (P = 0.01), −8.3% (P = 0.02), and −14.4% (P < 0.001), respectively. The post-detraining values did not differ among the 3 protocol groups.
The texhaustion was shorter for the walk and stall groups in the standardized treadmill exercise protocol after 12 weeks of detraining compared with texhaustion after 18 weeks of training. For the walk and stall groups, the mean change in texhaustion was −26.3% (P < 0.001) and −33.1% (P < 0.001), respectively (Table 2). The texhaustion for horses in the canter group did not change (P = 0.26) as a result of detraining.
Compared with post-training values, the mean VHRmax in the canter group did not change after detraining (P = 0.87), whereas after detraining mean VHRmax in the walk and stall groups decreased by 8.0% (P = 0.01) and 13.4% (P < 0.001), respectively (Table 2). The mean HRmax measured during the standardized treadmill exercise protocol decreased for both the walk and stall groups by 6.1% (P = 0.001 and P = 0.004, respectively).
After 12 weeks of detraining, the VLA4 in the canter group was unchanged (P = 0.65), compared with the post-training value (Table 2). However, mean VLA4 in the walk and stall groups decreased by −14.5% (P = 0.003) and −17.1% (P = 0.009), respectively.
The mean Ca-o2 and hemoglobin concentration did not change after detraining for any of the protocol groups (Table 2). The Cao2 increased in the canter and stall groups (P = 0.03 and P = 0.002, respectively) and Co2 increased in the stall group (P = 0.009), compared with post-training values. In all protocol groups, detraining resulted in increased mean Sao2 (P = 0.001 to P = 0.02); however, values did not differ among protocol groups. The mean So2 in the stall group increased (P = 0.002) after detraining, but post-detraining So2 did not differ among protocol groups. The Po2 in the walk group increased (P = 0.02) after detraining but was not different from that of the canter group or the stall group (P = 0.058).
Discussion
The present study was undertaken to evaluate whether changes in aerobic capacities and associated exercise performance variables would differ in previously trained horses that underwent a period of detraining during which they maintained different intensities of activity. Results indicated that different intensities of activity during detraining resulted in different effects on cardiopulmonary and oxygen-transport capacities in racehorses.
It is difficult to compare results of the present study with those of previous detraining studies because different investigators used horses of different ages that were trained at different intensities for different periods followed by detraining periods of different durations. Previous investigations of detraining in horses have studied 6 to 13 horses with only 4 to 7 horses in each treatment group.1–4,8 In the present study, 27 horses (9 horses/protocol group) were assessed. To our knowledge, this is the largest study of detraining conducted to date; furthermore, the horses underwent more extensive training prior to detraining than horses in all but one of the previous detraining studies.8
We originally hypothesized that after detraining, horses in the canter group would better maintain their o2max/kg with a smaller change from their post-training value, compared with findings in the other 2 protocol groups. Although the decrease in o2max/kg in the canter group was only 60% and 50% of the decreases in the walk and stall groups, respectively, it did not differ from the other groups, presumably because of high variability among the horses (ranges of o2max/kg in the canter, walk, and stall groups were 2.38 to 3.05 mL O2 [standard temperature pressure dry]/[s·kg], 2.29 to 3.35 mL O2 [standard temperature pressure dry]/[s·kg], and 2.23 to 3.24 mL O2 [standard temperature pressure dry]/[s·kg], respectively). The statistical power of 0.46 was less than the desired value of 0.8, so the lack of difference must be interpreted cautiously. In terms of circulatory convective delivery of oxygen, decreases in o2max/kg observed in all protocol groups after 12 weeks of detraining were attributable to reduced Dmax/kg rather than changes in blood capacitance for oxygen, because Ca--o2 did not decrease (Table 2). These results suggest that horses may need to be exercised at intensities greater than moderate (at least periodically) to retain their Dmax/kg and o2max/kg. The observed decrease in SVmax/kg may have resulted from reduced total blood and plasma volumes.14 It has been reported that 2 to 4 weeks of inactivity in endurance-trained humans reduces blood volume by 9% during exercise.15
In contrast to previous studies in horses1,5 and humans16 in which HRmax either remained unchanged or increased with detraining, HRmax in the canter group of the present study remained unchanged but HRmax in the walk and stall groups decreased following detraining (Table 2). It is unclear why horses in the present study should have a response opposite to that of humans, although reduced HRmax could clearly contribute to reduction in Dmax/kg and o2max/kg after detraining because the reduced Dmax/kg and SVmax/kg could have contributed to the observed increase in Sao2 by increasing time for equilibration of oxygen across the alveolar-capillary membrane.
After 12 weeks of detraining, Ca-o2 of the horses at exhaustion did not decrease even in the stall group (Table 2), which is consistent with findings of previous equine studies.1,2 A study9 of cessation of training in highly trained humans found that 3 weeks of inactivity did not reduce maximal Ca-o2; however, maximal Ca-o2 decreased by 7% after 12 weeks of detraining. The Cao2 in the canter and stall groups increased after detraining, presumably a result of increased Sao2, and helped to maintain Cao2. Changes in hemoglobin concentration and Sao2 and So2 determine Cao2 and Cvo2 because Cao2 and Cvo2 are the products of hemoglobin concentration and Sao2 and So2, respectively.17 Hemoglobin concentration did not change after detraining in any protocol group, and although Sao2 increased in all protocol groups and Sv-o2 increased slightly (as did Cv-o2) in the stall group, these changes did not alter Cao2. The hemoglobin concentration in horses has been reported to increase slightly18 or not change with training,19 although in our experience this depends greatly on the intensity and duration of training. After 3 weeks of detraining in 1 study,5 hemoglobin concentration at rest decreased, but hemoglobin concentration at exhaustion did not, perhaps because of splenic release of erythrocytes that increases the total number of circulating erythrocytes by as much as 50%.20
Reduced Co2 due to lower So2 and Po2 might potentially enhance Ca-o2 and, in terms of circulatory delivery of oxygen, deliver more oxygen to myocytes because of higher oxygen extraction, suggesting that reduced Co2 due to lower So2 and Po2 might increase Vo2max. However, considerable evidence from humans, rats, and goats suggests that limitation of peripheral tissue diffusion plays an important role in determining oxygen delivery at Vo2max,21–23 and data from horses breathing hyperoxic gas supports this hypothesis as well.24,25 The peripheral diffusion limitation hypothesis predicts that if the peripheral diffusing capacity for oxygen remains constant (ie, no change in capillary density or mitochondrial volume density), lower Po2 is required to generate sufficient pressure to deliver the reduced oxygen flux when o2max decreases.21,24,25 Because Pvo2 increased and Vo2max decreased following detraining in the present study, this implies that peripheral diffusing capacity for oxygen decreased during detraining so that a higher pressure was required to achieve a lower oxygen flux. Reduced capillary density and mitochondrial volume density in the skeletal muscle as a result of detraining could explain why peripheral diffusing capacity for oxygen appeared to be lower in the detrained horses.26
Tyler et al27 reported that in Standardbreds, texhaustion decreased by 26% after 6 weeks of detraining and texhaustion and Vo2max were correlated (R = 0.83). Highly trained human athletes' performances decrease rapidly when the training stimulus disappears or is insufficient to retain training-induced adaptations.6,28 However, despite the post-detraining reduction in o2max/kg in the canter group in the present study, those horses maintained texhaustion, an index of performance, and also maintained VLA4, Vo2max, and VHRmax. These findings suggest that some aspects of adaptation to the trained state are not regulated uniformly and may change at different rates during periods of training or detraining. The mechanism by which values of some training-induced performance variables were maintained more than the values of some oxygen-transport variables is intriguing. Better understanding of these relationships may be beneficial for designing detraining protocols for racehorses that minimize effects on performance and expedite the horse's return to racing performance following a period of detraining.
Butler et al1 found no decrease in o2max following a 15-week detraining period in horses that walked for 20 minutes daily. However, there was an apparent reduction in o2max of 11%, but that change was not significant, possibly because they used only 4 horses in the study and it lacked sufficient statistical power. Therefore, we hypothesized that walking for 1 hour each day for 12 weeks would minimally defend aerobic capacity in horses. The energy cost of transport for equids is independent of speed29 and can be calculated.30 After training, exercise intensity and total daily locomotor energy expenditure of the walk group were estimated to be 9.0% of o2max and 16.1 J/kg, respectively. In contrast, the exercise intensity and total daily locomotion energy expenditure for the canter group after training were 70% of o2max and 10.7 J/kg, respectively. Although total energy expenditure of the canter group was only two-thirds that of the walk group, the canter group maintained several performance-related factors including Vo2max, VHRmax, VLA4, and texhaustion. Presumably, the walk group failed to maintain these factors because of its lower exercise intensity during detraining.31,32 Although the stall group had lower VHRmax than the canter group, the walk group VHRmax did not differ from that of the other 2 protocol groups, suggesting that even just walking during detraining might help to maintain some factors related to training-induced aerobic capacity. Rehabilitation programs for humans with essential hypertension or coronary disease frequently involve walking as a treatment, and walking has been reported to reduce submaximal o2 and heart rate.33 Walking may provide similar benefits to Thoroughbreds during detraining, although how those benefits would impact a horse's ability to return to high aerobic power is unknown.
Results of the present study indicated that horses exercised at 70% o2max during detraining (canter group) following an 18-week high-intensity training program could maintain texhaustion, VHRmax, and VLA4, but not o2max/kg, SVmax/kg, or Dmax/kg in response to intense submaximal exercise. During detraining, walking for 1 hour each day might help to maintain VHRmax and Vo2max, compared with the effects of stall rest; however, in the present study, most of the values of oxygen-transport variables for the walk group were similar to those of the stall group. Regardless of detraining protocol, Cao2 was not reduced in horses after 12 weeks of detraining.
Acknowledgments
Supported by the Japan Racing Association.
Presented in abstract form at the 9th International Conference on Equine Exercise Physiology, Chester, United Kingdom, June 2014.
ABBREVIATIONS
| Cao2 | Arterial oxygen concentration |
| Ca-o2 | Arterial-mixed-venous oxygen concentration difference |
| Co2 | Mixed-venous oxygen concentration |
| HRmax | Maximal heart rate |
| Po2 | Mixed-venous oxygen partial pressure |
| Cardiac output |
| max | Maximal cardiac output |
| max/kg | Maximal mass-specific cardiac output |
| Sao2 | Arterial oxygen saturation |
| SV | Cardiac stroke volume |
| SVmax | Maximal cardiac stroke volume |
| SVmax/kg | Maximal mass-specific cardiac stroke volume |
| So2 | Mixed-venous oxygen saturation |
| texhaustion | Run time to exhaustion after reaching 10 m/s during a standardized treadmill exercise protocol |
| VHRmax | Speed eliciting maximal heart rate |
| VLA4 | Speed at which plasma lactate concentration reaches 4mM after 2 minutes during a standardized treadmill exercise protocol |
| o2max | Maximal rate of oxygen consumption |
| o2max/kg | Maximal mass-specific rate of oxygen consumption |
| Vo2max | Speed eliciting maximal rate of oxygen consumption |
Footnotes
Mustang 2200, Kagra, Fahrwangen, Switzerland.
SM-29, Fukuda Denshi, Tokyo, Japan.
DATAQ DI-720, DATAQ, Akron, Ohio.
Windaq Pro+, DATAQ, Akron, Ohio.
LFE-150B, Vise Medical, Chiba, Japan.
TF-5, Vise Medical, Chiba, Japan.
MG-360, Vise Medical, Chiba, Japan.
CR-300, Kofloc, Kyoto, Japan.
Surflow, Terumo, Tokyo, Japan.
MO95H-8.5, Baxter International, Deerfield, Ill.
SP5107U, Becton, Dickinson and Company, Franklin Lakes, NJ.
Statham P23d, Gould Instruments, Valley View, Ohio.
ABL-555, Radiometer, Copenhagen, Denmark.
OSM-3, Radiometer, Copenhagen, Denmark.
YSI 2300 STAT Plus, Yellow Springs Instruments, Yellow Springs, Ohio.
COM-2, Baxter International, Deerfield, Ill.
JMP 6.0.3, SAS Institute Inc, Cary, NC.
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