Search PubMed⌕ Search

Biomedical subjects

L J McCutcheon

Publications and source records attributed to L J McCutcheon.

At least 19 recordsLinked to original sources

Training-induced alterations in glucose metabolism during moderate-intensity exercise.

In several species, physical conditioning (training) provokes a large shift in substrate utilisation during submaximal exercise. Few studies in horses have quantitatively examined these effects. Therefore, the effects of exercise training on plasma glucose kinetics during submaximal exercise were examined in 7 horses (5 Thoroughbred, 2 Standardbred; age 3-9 years) that had been paddock-rested for at least 6 months. Two days after determination of maximum aerobic capacity (VO2max), horses ran on a treadmill (4 degree incline) at 55% of VO2max (UT) for 60 min or until fatigue and then completed 6 weeks of moderate-intensity training on a treadmill (5 days/week). Following training and a second VO2max test, the horses completed exercise trials at the same absolute (ABS) and relative (REL) workload in random order, with at least 3 days between tests. After training, VO2max had increased (P<0.05) by 14.9% (mean +/- s.e. pretraining 118.4 +/- 7.4 ml/kg bwt/min; post-training 136.1 +/- 7.8 ml/kg bwt/min). Mean exercise duration was longer (P<0.05) in the ABS trial (57 +/- 1.9 min) than in the UT (46 +/- 3.9 min) and REL (49 +/- 4.6 min) trials. Plasma glucose concentration increased during exercise, and was lower (P<0.05) in ABS than in UT and REL at the end of exercise. Mean glucose rate of appearance (Ra) and disappearance (Rd) were 22 and 21% lower (P<0.05), respectively, in ABS than in UT, but mean glucose Ra and Rd did not differ between the UT and REL trials. Exercise-induced changes in glucagon, epinephrine and norepinephrine were blunted (P<0.05) in ABS, but not REL, when compared to UT. It is concluded that 6 weeks of moderate-intensity training results in a decrease in glucose flux during submaximal exercise at the same absolute, but not relative, workload. The training-induced decrease in glucose flux may, in part, be due to altered plasma concentrations of the major glucoregulatory hormones.

Adaptation, Physiological↗

Changes in skeletal muscle GLUT4 content and muscle membrane glucose transport following 6 weeks of exercise training.

This study examined changes in skeletal muscle GLUT4 content and glucose transport in isolated muscle membranes (GT) from horses before and 2 min after standardised submaximal exercise tests (SET) prior to and after completion of 6 weeks of training. Seven horses, age 3-9 years, body mass mean +/- s.e. 530 +/- 19 kg, and sedentary for at least 4 months, completed 6 weeks of training on a treadmill. An initial SET (UT) was performed on a 4 degree incline at a speed equivalent to 55% of pretraining VO2max and was repeated post-training at the same absolute workload (ABS). A third SET (REL) was performed at 55% of post-training VO2max. There was no significant pre- to postexercise change in GLUT4 content before or after training. Following training, total GLUT4 content was increased 2- or 3-fold in pre-exercise biopsies (pre UT: 0.30 +/- 0.05; pre ABS: 1.05 +/- 0.32; pre REL: 1.34 +/- 0.28 arbitrary units) (P<0.05) with similar increases in postexercise GLUT4 content (P<0.05) (post UT: 033 +/- 0.06; post ABS: 1.19 +/- 0.44; post REL: 1.43 +/- 0.31). GT increased 2.5- to 6-fold in postexercise muscle membrane vesicles in UT over a range of glucose concentrations. After training (ABS and REL), there was a 25-50% attenuation (P<0.05) in membrane GT in response to exercise in ABS and REL. These finding indicate that moderate intensity exercise training increased middle gluteal muscle GLUT4 content, but this change was not reflected in an increase in muscle membrane glucose transport activity in postexercise muscle samples.

Analysis of Variance↗

Detection of free radicals in ischemic and reperfused canine gracilis muscle flaps by use of spin-trapping electron paramagnetic resonance spectroscopy.

OBJECTIVE: To determine whether free radicals are produced in ischemic and reperfused canine skeletal muscle, whether free radicals can be detected from effluent blood by use of spin-trapping electron paramagnetic resonance (EPR) spectroscopy, and whether free radical-induced skeletal muscle damage is detectable by use of light microscopy. ANIMALS: 6 healthy mixed-breed dogs. PROCEDURES: Dogs were anesthetized and both gracilis muscles were isolated, leaving only the major vascular pedicle intact. Ischemia was induced in 1 flap for 4 hours; the contralateral flap served as the control. Ischemic flaps were then reperfused for 15 minutes. alpha-Phenyl-N-tert-butylnitrone, a spin-trapping agent, was administered intravenously to each dog 1 hour prior to reperfusion. Following reperfusion, effluent blood samples from muscle flaps were obtained and processed for EPR spectroscopy. Muscle biopsy specimens were obtained for histologic evaluation, and dogs were euthanatized. RESULTS: Spin adducts were not detected in blood from control flaps. However, spin adducts were detected in all ischemic-reperfused muscle flaps. Principal signals identified were characteristic of oxygen- and carbon-centered radicals. Significantly more muscle damage was detected in ischemic-reperfused flaps, compared with control flaps. CONCLUSIONS AND CLINICAL RELEVANCE: Free radicals may be an important component of injury induced by ischemia and reperfusion of canine skeletal muscle. Spin-trap adducts of free radicals can be detected in effluent blood of canine muscle flaps by use of spin-trapping EPR spectroscopy. Spin-trapping EPR spectroscopy may be useful for the study of antioxidants and free radical scavengers in attenuating ischemia and reperfusion-mediated skeletal muscle damage.

Animals↗

Heat acclimation improves regulation of plasma volume and plasma Na(+) content during exercise in horses.

This study determined the plasma volume (PV) and ion responses to heat acclimation and exercise in six trained Thoroughbred horses during 21 days of exposure to heat and humidity (33 degrees C, 83% relative humidity) for 4 h/day. During the 2nd h on days 0, 3, 7, 14, and 21, horses performed a standardized treadmill test, running at 50% of peak O(2) uptake until pulmonary artery temperature reached 41.5 degrees C. Heat acclimation resulted in an increase in PV from 21.3 +/- 1.1 liters on day 0 to 24.3 +/- 1.0 liters on day 14, returning to 22.6 +/- 0.9 liters on day 21. The corresponding total plasma protein contents were 1,273 +/- 53, 1,455 +/- 81, and 1,377 +/- 57 g, respectively, and increases in total plasma Na(+) plus Cl(-) content were 5,145 +/- 126, 5,749 +/- 146, and 5,394 +/- 114 mmol, respectively. Thus changes in PV were accompanied by direct changes in plasma protein and osmolyte contents. With exercise on day 0, PV decreased by 7.1 +/- 0.7% at 5 min of exercise and remained decreased (-6.7 +/- 1.3%) at 5 min of recovery. By day 21, PV decreased significantly less than on day 0 (by 5.2 +/- 0.9% at 5 min of exercise), was decreased by only 2.0 +/- 1.6% at 5 min of recovery, and was fully restored at 15 min of recovery. Plasma Na(+) concentration increased 3 meq/l during the first 5 min of exercise and was normalized by 5 min of recovery on day 0 and by end exercise on day 21. It is concluded that improved ability to regulate PV during exercise in response to heat acclimatization is associated with an increased PV and an improved conservation of Na(+).

Acclimatization↗

Epinephrine inhibits exogenous glucose utilization in exercising horses.

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 +/- 1% maximum O(2) uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 micromol. kg(-1). min(-1); GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia ( approximately 8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was approximately 50% and approximately 33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was approximately 100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 +/- 44 mmol/kg dry muscle (dm)] than in F (218 +/- 28 mmol/kg dm) and G (201 +/- 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.

Adrenergic Agonists↗

Heat storage in horses during submaximal exercise before and after humid heat acclimation.

The effect of humid heat acclimation on thermoregulatory responses to humid and dry exercise-heat stress was studied in six exercise-trained Thoroughbred horses. Horses were heat acclimated by performing moderate-intensity exercise for 21 days in heat and humidity (HH) [34.2-35.7 degrees C; 84-86% relative humidity (RH); wet bulb globe temperature (WBGT) index approximately 32 degrees C]. Horses completed exercise tests at 50% of peak O(2) uptake until a pulmonary arterial temperature (T(pa)) of 41.5 degrees C was attained in cool dry (CD) (20-21.5 degrees C; 45-50% RH; WBGT approximately 16 degrees C), hot dry (HD 0) [32-34 degrees C room temperature (RT); 45-55% RH; WBGT approximately 25 degrees C], and HH conditions (HH 0), and during the second hour of HH on days 3, 7, 14, and 21, and in HD on the 18th day (HD 18) of heat acclimation. The ratios of required evaporative capacity to maximal evaporative capacity of the environment (E(req)/E(max)) for CD, HD, and HH were approximately 1.2, 1.6, and 2.5, respectively. Preexercise T(pa) and rectal temperature were approximately 0.5 degrees C lower (P < 0. 05) on days 7, 14, and 21 compared with day 0. With exercise in HH, there was no effect of heat acclimation on the rate of rise in T(pa) (and therefore exercise duration) nor the rate of heat storage. In contrast, exercise duration was longer, rate of rise in T(pa) was significantly slower, and rate of heat storage was decreased on HD 18 compared with HD 0. It was concluded that, during uncompensable heat stress in horses, heat acclimation provided modest heat strain advantages when E(req)/E(max) was approximately 1.6, but at higher E(req)/E(max) no advantages were observed.

Acclimatization↗

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.

Animals↗

Effects of warm-up intensity on kinetics of oxygen consumption and carbon dioxide production during high-intensity exercise in horses.

OBJECTIVE: To compare effects of low and high intensity warm-up exercise on oxygen consumption (VO2) and carbon dioxide production (VCO2) in horses. ANIMALS: 6 moderately conditioned adult Standard-breds. PROCEDURES: Horses ran for 2 minutes at 115% of maximum oxygen consumption (VO2max), 5 minutes after each of the following periods: no warm-up (NoWU); 10 minutes at 50% of VO2max (LoWU); or 7 minutes at 50% VO2max followed by 45-second intervals at 80, 90, and 100% VO2max (HiWU). Oxygen consumption and VCO2 were measured during exercise, and kinetics of VO2 and VCO2 were calculated. Accumulated O2 deficit was also calculated. RESULTS: For both warm-up trials, the time constant for the rapid exponential increase in VO2 was 30% lower than for NoWU. Similarly, the rate of increase in VCO2 was 23% faster in LoWU and HiWU than in NoWU. Peak values for VO2 achieved during the high-speed test were not significantly different among trials (LoWU, 150.2 +/- 3.2 ml/kg/min; HiWU, 151.2 +/- 4.2 ml/kg/min; NoWU, 145.1 +/- 4.1 ml/kg/min). However, accumulated O2 deficit (ml of O2 equivalents/kg) was significantly lower during LoWU (65.3 +/- 5.1) and HiWU (63.4 +/- 3.9) than during NoWU (82.1 +/- 7.3). CONCLUSIONS AND CLINICAL RELEVANCE: Both the low- and high-intensity warm-up, completed 5 minutes before the start of high-intensity exercise, accelerated the kinetics of VO2 and VCO2 and decreased accumulated O2 deficit during 2 minutes of intense exertion in horses that were moderately conditioned.

Animals↗

Skeletal muscle Na(+)-K(+)-ATPase and K+ homeostasis during exercise: effects of short-term training.

The objective of this study was to determine the effects of 10 consecutive days of moderate intensity training on 1) the concentration of middle gluteal muscle Na(+)-K(+)-ATPase as determined by vanadate-facilitated 3H[ouabain binding; and 2) plasma potassium regulation before, during and after exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max). Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. There additional horses undertook no training or exercise tests and served as controls for determination of middle gluteal muscle Na(+)-K(+)-ATPase concentration. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For each high intensity exercise protocol, horses completed a 10 min warm-up at 50% VO2max, followed by exercise at 100% of pre-training VO2max (6 degrees incline, mean speed 9.8 m/s) until fatigue. Training resulted in a 13.8% increase in resting plasma volume (pre: 20.9 +/- 0.8 l; post: 23.8 +/- 0.9 l; P = 0.03), and an 8.9% increase in VO2max (pre: 142 +/- 4 ml/kg/min; post: 155 +/- 4 ml/kg/min; P = 0.004) during HI. Peak values for plasma potassium concentration and content during exercise decreased by 13% (P = 0.02) and 7% (P = 0.0002), respectively, after training whereas training had no effect on increases in packed cell volume, plasma total solids, and erythrocyte K+ concentration and content during exercise. Following training, there was also a significant (23%) increase in Na(+)-K(+)-ATPase concentration in biopsies of middle gluteal muscle, as measured by vanadate-facilitated 3H[ouabain binding. We conclude that 10 days of moderate intensity exercise results in increases in skeletal muscle Na(+)-K(+)-ATPase and attenuation in the elevation in plasma K+ during high intensity exercise at the same absolute workload. The increase in middle gluteal muscle Na(+)-K(+)-ATPase concentration is consistent with decreases in K+ efflux from working muscle during exercise.

Animals↗

Muscular and metabolic responses to moderate-intensity short-term training.

The objectives of this study were to determine the effects of 10 consecutive days of moderate-intensity training on 1) the muscular metabolic response to exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max); and 2) mitochondrial enzyme markers (citrate synthase, CS; succinate dehydrogenase, SDH; 3-hydroxy-acyl-CoA dehydrogenase, HAD) of oxidative capacity in middle gluteal muscle. Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For the HI, horses completed a 10 min warm-up, followed by exercise at 100% of pre-training VO2max (mean speed 9.8 m/s) until fatigue. Training resulted in an 8.9% increases in VO2max (Pre: 142 +/- 4 ml/kg bwt/min; Post: 155 +/- 4 ml/kg bwt/min) and a 24% increase in run time to fatigue during HI. Whereas VO2 during HI was not altered by training, peak values for VCO2 and R were significantly lower following training. Compared to HI1, there was a 45% reduction in the net rate of muscle glycogenolysis during HI2. Peak (end exercise) values for plasma and muscle lactate concentrations decreased by 22 and 23%, respectively, after training. Training also attenuated the exercise-associated increase in plasma norepinephrine, but there was no effect on plasma epinephrine concentrations. Maximal activities of CS, SDH, and HAD were unaltered by training. We conclude that 10 days of moderate-intensity exercise results in decreases in muscle glycogenolysis and anaerobic metabolism during high-intensity exercise at the same absolute workload. Furthermore, development of measurable increases in mitochondrial oxidative potential may not be required for expression of these metabolic adaptations in early training.

3-Hydroxyacyl CoA Dehydrogenases↗

Equine sweating responses to submaximal exercise during 21 days of heat acclimation.

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32-34 degrees C, 80-85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6 degrees incline) at a speed eliciting 50% of maximal O(2) uptake until a pulmonary artery temperature of 41.5 degrees C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na(+), K(+), and Cl(-)) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5 degrees C (range 19.09 +/- 1.41 min on day 0 to 20.92 +/- 1.98 min on day 3). Peak SR during exercise (ml. m(-2). min(-1)) increased on day 7 (57.5 +/- 5. 0) but was not different on day 21 (48.0 +/- 4.7) compared with day 0 (52.0 +/- 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na(+) concentration for a given SR during exercise and recovery; this contributed to an approximately 26% decrease in calculated total sweat ion losses (3,112 +/- 114 mmol on day 0 vs. 2,295 +/- 107 mmol on day 21). By day 21, there was a decrease in sweating threshold ( approximately 1 degrees C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na(+) concentration and SR during recovery.

Acclimatization↗

Effects of prior exercise on muscle metabolism during sprint exercise in horses.

The effect of warm-up exercise on energy metabolism and muscle glycogenolysis during sprint exercise (Spr) was examined in six fit Standardbred horses exercised at 115% of maximal O(2) consumption (VO(2 max)) until fatigued, 5 min after each of three protocols: 1) no warm-up (NWU); 2) 10 min at 50% of VO(2 max) [low-intensity warm-up (LWU)]; and 3) 7 min at 50% VO(2 max) followed by 45-s intervals at 80, 90, and 100% VO(2 max) [high-intensity warm-up (HWU)]. Warm-up increased (P < 0.0001) muscle temperature (T(m)) at the onset of Spr in LWU (38.3 +/- 0.2 degrees C) and HWU (40.0 +/- 0. 3 degrees C) compared with NWU (36.6 +/- 0.2 degrees C), and the rate of rise in T(m) during Spr was greater in NWU than in LWU and HWU (P < 0.01). Peak VO(2) was higher and O(2) deficit lower (P < 0. 05) when Spr was preceded by warm-up. Rates of muscle glycogenolysis were lower (P < 0.05) in LWU, and rates of blood and muscle lactate accumulation and anaerobic ATP provision during Spr were lower in LWU and HWU compared with NWU. Mean runtime (s) in LWU (173 +/- 10 s) was greater than HWU (142 +/- 11 s) and NWU (124 +/- 4 s) (P < 0. 01). Warm-up was associated with augmentation of aerobic energy contribution to total energy expenditure, decreased glycogenolysis, and longer run time to fatigue during subsequent sprint exercise, with no additional benefit from HWU vs. LWU.

Adenosine Triphosphate↗

Comparison of three methods for estimation of exercise-related ion losses in sweat of horses.

OBJECTIVE: To quantify total fluid loss in sweat of Thoroughbreds during >3 hours of low-intensity exercise in controlled conditions and to calculate and compare estimated ion losses in sweat, according to 3 methods. ANIMALS: 6 exercise-trained Thoroughbreds. PROCEDURE: Fluid and ion losses in sweat were measured in 6 horses exercising at 40% of the speed that elicited maximum oxygen consumption for 45 km. Horses were given a 15-minute rest period at the end of three 15-km exercise phases. Horses completed 2 exercise trials. Ion losses in sweat were calculated, using measurements of local sweating rate and sweat ion composition (SWT), change in net exchangeable cation content (CAT), and change in extracellular ion content (PLAS) derived from plasma total solids and ion concentrations. RESULTS: Measurement of SWT revealed a mean (+/- SEM) fluid loss in sweat during 45 km of exercise of 27.5 +/- 1.6 L. Total ion loss in sweat was approximately 241 g or 7.8 mol with higher sodium losses in the second and third phases of exercise compared with the first phase. Losses of sodium and potassium calculated by SWT or CAT were not significantly different from each other, whereas losses of these ions as determined by PLAS were significantly lower. CONCLUSIONS AND CLINICAL RELEVANCE: Calculation of ion losses from a mean whole body sweating rate extrapolated from either local sweating rate and sweat ion composition or from change in net exchangeable cation content provide similar results, whereas ion losses determined by changes in extracellular ion content derived from plasma total solids and ion concentration results in underestimation of actual losses.

Animals↗

Sweating. Fluid and ion losses and replacement.

In the horse, sweat is produced by apocrine glands which are present over most haired and nonhaired skin. Although sweat secretion is initiated under a number of circumstances, the central drive for sweating in response to a thermal stimulus is the primary mechanism for its production. Sweating is an essential and primary mechanism for heat dissipation during exercise or exposure to hot ambient conditions. The rate of sweat production will reflect the interaction of numerous factors, including exercise intensity, ambient conditions, state of hydration, and the training or heat acclimation status of the individual horse. Thus, the sweating rates produced in response to an exercise-induced thermal load can be further increased by high ambient temperature or humidity which reduces evaporative efficiency, thereby contributing to the rate of rise in core body temperature. Equine sweat is an isotonic to slightly hypertonic secretion with sodium, chloride, and potassium contributing the major ionic components. The ionic composition of equine sweat is largely rate dependent and therefore is affected by factors such as ambient conditions and exercise intensity which result in elevations in sodium concentration in response to increases in sweating rate. Large sweat fluid losses associated with prolonged exercise will incur significant ion deficits, leading to alterations in skeletal muscle ion content and the potential for muscular dysfunction. With respect to exercise performance, however, the more important consequence of sweat fluid losses is the impairment of temperature regulation that accompanies severe dehydration. Although it is advantageous to restore a proportion of the fluid and ion losses incurred during prolonged exercise, few strategies will fully and safely replace the electrolyte losses incurred. Nevertheless, daily electrolyte supplementation of a good-quality diet will provide an effective method of replacing sweat ion losses during training and competition under most ambient conditions.

Animals↗

Thermoregulatory adaptations associated with training and heat acclimation.

The large metabolic heat load generated as a consequence of muscular work requires activation of thermoregulatory mechanisms in order to prevent an excessive and potentially dangerous rise in body temperature during exercise. Although the horse has highly efficient heat dissipatory mechanisms, there are a number of circumstances in which the thermoregulatory system may be overwhelmed, resulting in the development of critical hyperthermia. The risk for development of life-threatening hyperthermia is greatest when (1) the horse is inadequately conditioned for the required level of physical performance; (2) exercise is undertaken in hot and particularly, in hot and humid ambient conditions; and (3) there is an impairment to thermoregulatory mechanisms (e.g., severe dehydration, anhidrosis). Both exercise training under cool to moderate ambient conditions and a period of repeated exposure to, and exercise in, hot ambient conditions (heat acclimation) will result in a number of physiologic adaptations conferring improved thermoregulatory ability. These adaptations include an expanded plasma volume, greater stability of cardiovascular function during exercise, and an improved efficiency of evaporative heat loss as a result of alterations in the sweating response. Collectively, these adjustments serve to attenuate the rise in core body temperature in response to a given intensity of exercise. The magnitude of the physiologic adaptations occurring during exercise training and heat acclimation is a reflection of the thermal load imposed on the horse. Therefore, when compared with a period of training in cool conditions, the larger thermal stimulus associated with repeated exercise in hot ambient conditions will invoke proportionally greater thermoregulatory adaptations. Although it is not possible to eliminate the effects of adverse environmental conditions on exercise performance, it is clear that a thorough exercise training program together with a subsequent period of acclimatization will serve to ameliorate the impact of the environment. Based on our current understanding of the nature and extent of thermoregulatory adaptations in the horse, the following conclusions can be made: 1. A 2- to 3-month period of exercise training geared toward the specific athletic endeavor to be undertaken will result in substantial improvements in thermoregulatory capacity and is an absolute requirement for horses required to compete in hot ambient conditions. 2. Although physical training in a cool environment improves physiologic responses to exercise at high ambient temperatures, a 2-week period of moderate exercise training in these more adverse conditions is necessary for optimization of thermoregulatory function and physical performance. 3. Heat acclimation does not reduce the need for close monitoring of horses during training and competition in the heat. This is particularly true in hot, humid ambient conditions, where the biophysical limitations to sweat evaporation can result in development of severe hyperthermia, regardless of the state of training or heat acclimation.

Acclimatization↗

Hydration effects on physiological strain of horses during exercise-heat stress.

This study examined the effects of hyperhydration, exercise-induced dehydration, and oral fluid replacement on physiological strain of horses during exercise-heat stress. On three occasions, six horses completed a 90-min exercise protocol (50% maximal O2 uptake, 34.5 degrees C, 48% relative humidity) divided into two 45-min periods (exercise I and exercise II) with a 15-min recovery between exercise bouts. In random order, horses received no fluid (NF), 10 liters of water (W), or a carbohydrate-electrolyte solution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (Q), stroke volume (SV), core body temperature, sweating rate (SR), or sweating sensitivity during exercise I. In contrast, after exercise II, exercise-induced dehydration in NF (decrease in body mass: NF, 5.6 +/- 0.8%; W, 1.1 +/- 0.4%; CE, 1.0 +/- 0.2%) resulted in greater heat storage, with core body temperature approximately 1. 0 degrees C higher compared with W and CE. In exercise II, the greater thermal strain in NF was associated with significant (P < 0. 05) decreases in Q (10 +/- 2%), SV (9 +/- 3%), SR, and sweating sensitivity. We concluded that 1) preexercise hyperhydration provided no thermoregulatory advantage; 2) maintenance of euhydration by oral fluid replacement ( approximately 85% of sweat fluid loss) during exercise in the heat was reflected in higher Q, SV, and SR with decreased heat storage; and 3) W or an isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

Animals↗

Rate and composition of sweat fluid losses are unaltered by hypohydration during prolonged exercise in horses.

Rate and ionic composition of sweat fluid losses and partitioning of evaporative heat loss into respiratory and cutaneous components were determined in six horses during three 15-km phases of exercise at approximately 40% of maximal O2 uptake. Pattern of change in sweat rate (SR) and composition was similar during each phase. SR increased rapidly for the first 20 min of exercise but remained at approximately 24-28 ml . m-2 . min-1 during the remainder of each phase. Similarly, the concentrations of Na and Cl in sweat increased until 30 min of exercise but were unchanged thereafter. Sweat osmolality and concentrations of Na and Cl were positively correlated with SR. Sweat K concentration decreased during exercise but was not correlated with SR. Fluid losses were 33.8 +/- 1.5 liters, resulting in decreases of approximately 21% in plasma volume and approximately 11% in total body water. The approximately 6% hypohydration was not associated with an alteration in SR, sweat composition, or heat storage. Respiratory and cutaneous evaporative heat loss represented approximately 23 and 70%, respectively, of the total heat dissipated, and the partitioning of heat loss was similar in each exercise phase. We conclude that SR and the relative proportions of respiratory and cutaneous evaporative heat loss are unchanged in horses during prolonged low-intensity exercise despite moderate hypohydration.

Animals↗

Use of dew-point hygrometry, direct sweat collection, and measurement of body water losses to determine sweating rates in exercising horses.

OBJECTIVE: To compare dew-point hygrometry, direct sweat collection, and measurement of body water loss as methods for determination of sweating rate (SR) in exercising horses. ANIMALS: 6 exercise-trained Thoroughbreds. PROCEDURE: SR was measured in 6 horses exercising at 40% of the speed that elicited maximum oxygen consumption for 45 km, with a 15-minute rest at the end of each 15-km phase. Each horse completed 2 exercise trials. Dew-point hygrometry, as a method of local SR determination, was validated in vitro by measurement of rate of evaporative water loss. During exercise, local SR was determined every 10 minutes by the following 2 methods: (1) dew-point hygrometry on the neck and lateral area of the thorax, and (2) on the basis of the volume of sweat collected from a sealed plastic pouch attached to the lateral area of the thorax. Mean whole body SR was calculated from total body water loss incurred during exercise. RESULTS: Evaporation rate measured by use of dew-point hygrometry was significantly correlated (r2 = 0.92) with the actual rate of evaporative water loss. There was a similar pattern of change in SR measured by dew-point hygrometry on the neck and lateral area of the thorax during exercise, with a significantly higher SR on the neck. The SR measured on the thorax by direct sweat collection and by dew-point hygrometry were of similar magnitude. Mean whole body SR calculated from total body water loss was not significantly different from mean whole body SR estimated from direct sweat collection or dew-point hygrometry measurements on the thorax. CONCLUSIONS: Dew-point hygrometry and direct sweat collection are useful methods for determination of local SR in horses during prolonged, steady-state exercise in moderate ambient conditions. Both methods of local SR determination provide an accurate estimated of whole body SR.

Animals↗