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Thoroughbred horses were exercised to fatigue on a treadmill at 62% and 100% of their VO2max. Hypoxemia occurred at the onset of exercise under both exercise conditions. This hypoxemia persisted to fatigue during the heavy exercise but progressively diminished as the exercise continued and had disappeared by the end of exercise at the lighter load. As a result of the hypoxemia the oxygen content of arterial blood during exercise at VO2max was 17% below its carrying capacity. However, under both experimental conditions the CaO2 still exceeded that of rest owing to an elevation in hemoglobin concentration. The temperature of blood at the point of fatigue was similar, 41.0 +/- 0.2 degrees C and 41.1 +/- 0.2 degrees C, for exercise at 62% and 100% VO2max, respectively. Muscle samples collected at rest and at the termination of exercise did not demonstrate major differences between the exercise conditions except for a higher [lactate] and lower pH following the heavy exercise. From these results it can be suggested that the combined effects of an elevated body temperature, changes in muscle pH, and oxygen delivery may all be factors contributing to limit exercise capacity in the horse.

To determine whether maximum oxygen uptake (VO2max) in the horse in influenced by type of exercise test, five different protocols were evaluated in eight untrained Thoroughbreds exercised on a treadmill. With all protocols, horses were given a 5 min warm-up on a 10 per cent treadmill slope. Three protocols were at a 10 per cent slope and included: 1) increasing the running speed by 1 to 2 m/sec every 60 secs from 4 m/sec to a maximum of 12 m/sec; 2) running at 12 m/sec until fatigue; and 3) running for 3 to 4 mins at speeds ranging from 6 to 12 m/sec with rest pauses between exercise bouts. The fourth protocol employed a 24 per cent slope where animals exercised for 5 mins at 2 m/sec followed by 3 mins at 5 m/sec, and 2 mins at 6 m/sec. The fifth test involved running at 11 m/sec while the slope of the surface was increased every 2 mins until the horses could not maintain the pace. A plateau in VO2 occurred in all protocols except when exercise was performed on a 24 per cent slope. Slow speed exercise at a steep grade (24 per cent) produced the highest VO2 (P < 0.05) even though there was no plateau in the VO2. A steady state for VO2 and VCO2 existed 90 secs after the onset of exercise with all protocols which involved 2 mins or more at each speed. The VO2 and VCO2 values at all speeds of the rapid incremental exercise test were not different to those found at steady state in the third exercise protocol.

Changes in blood gases, ions, lactate, pH, hemoglobin, blood temperature, total body metabolism, and muscle metabolites were measured before and during exercise (except muscle), at fatigue, and during recovery in normal and acetazolamide-treated horses to test the hypothesis that an acetazolamide-induced acidosis would compromise the metabolism of the horse exercising at maximal O2 uptake. Acetazolamide-treated horses had a 13-mmol/l base deficit at rest, higher arterial Po2 at rest and during exercise, higher arterial and mixed venous Pco2 during exercise, and a 48-s reduction in run time. Arterial pH was lower during exercise but not in recovery after acetazolamide. Blood temperature responses were unaffected by acetazolamide administration. O2 uptake was similar during exercise and recovery after acetazolamide treatment, whereas CO2 production was lower during exercise. Muscle [glycogen] and pH were lower at rest, whereas heart rate, muscle pH and [lactate], and plasma [lactate] and [K+] were lower and plasma [Cl-] higher following exercise after acetazolamide treatment. These data demonstrate that acetazolamide treatment aggravates the CO2 retention and acidosis occurring in the horse during heavy exercise. This could negatively affect muscle metabolism and exercise capacity.

The effect of high-intensity exercise on the respiratory capacity of skeletal muscle was studied in horses which ran five 600-m bouts on a track with 2 min of rest between exercise bouts, or once to fatigue on a treadmill at an intensity that elicited the maximal oxygen uptake. Venous blood and biopsy samples of the middle gluteal muscle were collected at rest, after each exercise bout, and 30 and 60 min post-exercise. Blood samples were analyzed for lactate concentration and pH and muscle samples for metabolites, pH, and respiratory capacity. Venous blood and muscle pH declined to 6.91 +/- 0.02 and 6.57 +/- 0.02, respectively, after the fifth track run and to 6.98 +/- 0.02 and 6.71 +/- 0.07, respectively, after treadmill running. Muscle metabolite changes were consistent with the metabolic response to high-intensity exercise. Muscle respiratory capacity declined greater than 20% (P less than 0.05) after a single exercise bout and was 45% of the control value after the fifth track run. Tissue respiration was depressed 60 min post-exercise but was normal 24 h later. These observations suggest that high-intensity exercise impairs the respiratory capacity of the working muscle. Although this occurred in parallel with reductions in pH, other factors could be responsible for this response.

Maintenance of muscular contraction during exercise requires large amounts of chemical energy. Although various sources of energy are available, adenosine triphosphate (ATP) is the universal intracellular vehicle of chemical energy within skeletal muscle. This article will focus on the various mechanisms of the production and breakdown of ATP.

Several biochemical components of the white portion of the gastrocnemius (WGM), plantaris (PM), and soleus (SM) muscles of the rat and middle gluteal (MGM) muscle of the horse were compared based on wet and dry weight, protein, and total creatine concentrations ([TCr]). The water content was similar for the rat hindlimb muscles, however, the concentrations of protein, ATP, phosphocreatine (PCr), creatine, and glycogen ranked as SM less than PM less than WGM for all reference bases except total creatine. In contrast, concentrations of ATP, creatine, and PCr were similar in all muscles studied when expressed as ratios of [TCr]. Horse MGM had the lowest percent of water and protein per gram wet or dry weight but highest glycogen concentration of the muscles studied, irrespective of the reference base used to express concentrations. Coefficients of variation were lowest when muscle constituents were related to [TCr]. It is concluded that expressing muscle constituents relative to total creatine results in the smallest variation and is a good method for making comparisons between muscles of similar fiber composition. However, essential information concerning different types of muscle may be lost when this reference base is used.

A case of granulomatous enteritis in a three-year-old thoroughbred horse is described. Onset of clinical signs succeeded pyrexia of unknown aetiology. The horse was emaciated, depressed and inappetent but diarrhoea was not a feature of the condition. There was hypoproteinaemia, anaemia, leucopaenia and abnormal small-intestinal carbohydrate absorption. Rectal biopsy revealed granulomatous changes in the rectal mucosa. As a result of these findings, euthanasia was performed and an autopsy was carried out. Histopathology showed marked villous atrophy in the small intestine with a diffuse mononuclear cellular infiltration involving mainly the submucosa and lamina propria. There were occasional granulomatous foci. The mononuclear cells consisted mainly of lymphocytes and histiocytes. No aetiological agent was isolated.

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Experiments were undertaken to determine whether respiratory masks worn by horses exercising strenuously on a treadmill may interfere with normal gas exchange. Four collection systems, two flow-through systems and two incorporating one-way valve systems with subject-generated airflow were studied. Six horses performed standard treadmill exercise tests consisting of a 2-min warm up followed by galloping 1 min each at 8,9, and 10 m/s. Each horse exercised six times while wearing each of the four respiratory masks. Each flow-through system was used twice with flow rates of 2,360 and 3,840 l/min for one system, and 3,840 and 6,300 l/min for the other. Arterial blood gas tensions were measured during exercise at each speed for each system and were compared with values measured when the horses performed the same test without wearing a mask. Hypercapnia developed during exercise with each of the respiratory masks except with the 6,300-l/min flow-through system. All horses became hypoxemic during every exercise test, but it was most severe when systems incorporating one-way valves were used. This, plus the degree of hypercapnia observed and a suboptimal heart rate-O2 uptake relationship, indicated that such systems severely impede ventilation and suggest that experiments performed while utilizing them do not represent the normal exercise condition.

A peripheral vasodilating agent, isoxsuprine hydrochloride, administered as an oral paste, was evaluated to determine its efficacy for the treatment of navicular disease. In a clinical trial, 13 horses with navicular disease were treated at a dose rate of 0.6 mg/kg body weight (bwt) twice daily for periods of six to 14 weeks. Twelve of the horses became completely sound while being treated, although two required a 50 per cent increase in dose. Nine of the horses have remained sound two to 10 months after ceasing therapy. In a controlled randomised double blind clinical trial, 16 horses with navicular disease were assigned to treatment with either a placebo paste or isoxsuprine paste for three weeks and then re-examined. All the horses treated with isoxsuprine showed improvement in gait, with seven of eight horses becoming sound, whereas only two horses treated with a placebo paste showed slight improvement. This difference in response was highly significant (P less than 0.001). To evaluate any physiological and biochemical effects of isoxsuprine, it was administered to five Standardbred geldings at dose rates of 0.6 mg/kg bwt and 1.2 mg/kg bwt. Complete blood counts, routine plasma biochemical parameters, cardinal signs and blood pressure measurements were performed up to 24 h after a single dose. No significant change in any of these parameters was found. To assess the peripheral vasodilatory action of isoxsuprine, infra-red thermography of the lower limb was performed before and up to 8 h after administration to horses. This revealed a significant increase in distal limb temperature which occurred from 90 to 480 mins after isoxsuprine administration. The maximum mean increase in distal limb temperature was 3.1 degrees C and this occurred 4 h after administration of the drug.

The effects of repeated arthrocentesis and injection of local anesthetic agents, lidocaine HCl or mepivacaine HCl on the equine middle carpal joint were investigated. Synovial fluid samples were evaluated before, and 12, 24 and 48 hours following, treatment. The greatest changes from pretreatment values occurred in synovial fluid cellularity. Repeated arthrocentesis caused a moderate increase in cell counts, while injection of local anesthetics caused a greater increase. Alterations in mucin clot quality, hyaluronic acid content, fluid viscosity, total protein and immunoglobulin G were generally of no significance. The most sensitive sampling time to detect changes caused by a given treatment was 24 hours following treatment while the 12 hour sampling period appeared to be the best at detecting differences between treatments. Repeated arthrocentesis has a definite effect on synovial fluid composition but the effects appear to decrease with repeated centesis. Lidocaine HCl and mepivacaine HCl are irritating to the synovial environment. Clear differences between responses to the drugs could not be identified.

Plasma biochemical values were measured in 14 horses, before a 160 km endurance ride, immediately after 85 km, immediately after 160 km, after 30 min recovery period and the day after the ride. For statistical analysis, a group of 7 horses that completed the ride at a mean speed of 234 metres per min (m/min) (Fast Group) was compared with 7 horses that completed the ride at a mean speed of 144 m/min (Slow Group). Estimations were made of sodium, potassium, chloride, bicarbonate, glucose, creatinine, urea, bilirubin, iron, total protein, albumin, calcium, phosphate, cholesterol, alkaline phosphate, gammaglutamyl transferase, lactate dehydrogenase, alpha hydroxybutyrate dehydrogenase, asparate amino transferase, alanine amino transferase, cortisol and insulin. Disturbances in biochemical values associated with endurance exercise reflected dehydration, hepatic dysfunction, reduced renal function and muscle damage. The faster the speed of exercise, the greater was the stress as reflected by cortisol values. The Fast Group of horses also demonstrated lower glucose and higher CK and LD values than the Slow Group of horses. However, biochemical values the day after the ride were similar to values before the ride.

Four standardbred horses with subcutaneously relocated carotid arteries were given a seven week training programme of treadmill exercise at a gradient of 19 per cent in order to assess if there were any effects of exercise and training on haematology, arterial blood gas and acid base measurements, plasma biochemistry and heart rate. The exercise consisted of one minute walking at 110 metres/minute followed by five minutes trotting at 200 metres/minute, twice daily in the first week. The period of trotting exercise was increased by one minute per week so that by the seventh week the horses were being given 12 minutes trotting twice daily. Before training commenced venous blood samples, for complete blood counts and plasma biochemistry, and arterial samples, for blood gas, acid base and lactate measurements, were taken at rest, after five minutes and 15 minutes of treadmill exercise (200 metres/minute) and 30 minutes and 60 minutes after completing the exercise. Heart rate was measured by telemetric electrocardiogram at similar intervals. This exercise test and blood collection were repeated after one, three, five and seven weeks of training. The only significant changes were a decrease in exercise lactate with training, increases in exercise and recovery total protein. The haematological response to treadmill exercise included an increase in certain red cell parametes and a leucocytosis which was caused by both a neutrophilia and a lymphocytosis. These effects had largely disappeared by 30 minutes after exercise and all values had returned to resting values by one hour after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Eleven horses were studied throughout a 12 week training schedule. Serial blood samples were taken for haematological analysis and an extensive biochemical profile, including the following parameters: sodium, potassium, chloride, bicarbonate, glucose, creatinine, urea, bilirubin, iron, total protein, albumin, alkaline phosphatase, aspartate aminotransferase, creatine kinase, gamma glutamyl transferase, calcium phosphate and cholesterol. There were few significant changes detected and it was concluded that routine haematological and biochemical screening has no useful role in assessing the fitness of horses under these conditions.

Muscle biopsy samples were collected from the left middle gluteal muscle of the horses participating in day 2 (speed and endurance test) of a three day event. Six Thoroughbred horses were biopsied the day before and within 30 minutes of completion of the speed and endurance test. Serial muscle sections were reacted histochemically for myosin adenosine triphosphatase activity after acid pre-incubation to demonstrate Type I, IIA and IIB fibers and the glycogen content in the individual fibers was assessed using the periodic acid Schiff (PAS) reaction. Total glycogen in muscle was measured fluorometrically after hydrolysis to glucose. A significant decrease (P less than 0.001) in total muscle glycogen of 306.0 +/- 34.6 mmoles glucose units/kg (dry weight) (mean +/- SE) occurred when samples collected before exercise were compared to those collected following exercise. A significant decrease (P less than 0.05) in the percentage of Type I fibers having medium PAS staining intensity occurred when pre and post-exercise samples were compared. Significant decreases (P less than 0.01 and P less than 0.001 respectively) in the percentage of Type IIA and IIB fibers classified as having high PAS staining intensity occurred when post-exercise samples were compared with those pre-exercise. There were significant increases (P less than 0.01 and P less than 0.001 respectively) in the percentage of Type IIA and IIB fibers classified as having medium PAS staining intensity when the samples collected after the exercise were compared with those before the exercise.

This article provides an overview of the characteristics of skeletal muscle, with an emphasis on equine skeletal muscle. A discussion of many of the adaptive processes that can occur in this tissue in response to altered states of physical activity is also included.

For determination of 3 muscle fiber types in equine skeletal muscle, a comparison of 2 preincubation buffers, each followed by myosin adenosine triphosphatase staining, was made. Serial sections of the muscle samples (n = 75) were preincubated in an acid buffer (pH 4.6) or a formaldehyde-glycine buffer (pH 7.25) and then were stained for myosin adenosine triphosphatase. Differentiation of muscle fibers into type I, IIA, and IIB was identical with both techniques; however, in the samples prepared at pH 4.6, type I fibers were black; type IIA, light gray; and type IIB, dark gray. In the samples prepared at pH 7.25, types I, IIA, and IIB fibers were white, light gray, and dark gray respectively. The formaldehyde-glycine preincubation buffer (at pH 7.25) gave more consistent results, was easier to prepare, and retained cytoarchitecture better, compared with the samples prepared at pH 4.6.

The effect of intranasal administration of oxygen at a flow rate of 10 litres per minute for 10 minutes, was studied in a total of 19 foals (thoroughbred and pony) aged between 0.5 and 12 hours. Arterial blood samples were collected before and after oxygen administration for the determination of paO2, paCO2, pHa and base excess. The foals were divided into three groups: five spontaneously delivered thoroughbred and pony foals (group 1), seven term induced thoroughbred foals (group 2) and seven induced premature pony foals (group 3). To examine the effect of duration of oxygen administration on blood gas values, three foals aged five to seven days received intranasal oxygen for 40 minutes and serial arterial blood samples were collected. Significant increases in paO2 values were found in group 1 and group 2 foals in response to intranasal oxygen. When the groups were compared, groups 1 and 2 had significantly higher paO2 values than group 3 foals, whether breathing air or oxygen. The duration of administration of intranasal oxygen had no significant effect on blood gas values.

The effects of training on skeletal muscle composition were studied in four Standardbred geldings given a seven week submaximal treadmill training programme. Before the start of training, muscle biopsies were collected from the left middle gluteal muscle for the determination of muscle fibre types, oxidative capacity and capillary numbers using histochemical techniques. The concentrations of citrate synthase, 3-hydroxyacyl-CoA dehydrogenase (HAD), lactate dehydrogenase and total muscle glycogen were measured using fluorometric methods. Muscle biopsy samples were repeated after one, three, five and seven weeks of training and the same measurements performed. No significant changes were found in muscle fibre types or capillary numbers as a result of training, although there was an increase in the oxidative capacity of the Type IIB fibres after seven weeks training. After seven weeks of training there were also increases in the concentrations of citrate synthase and HAD and a decrease in lactate dehydrogenase. Before commencement of training the horses underwent a standardised submaximal exercise test and muscle glycogen concentrations were measured before and immediately after the exercise. This procedure was repeated after one, three, five and seven weeks of training. A progressive decrease in the rate of glycogen utilisation occurred throughout the period of training, which by seven weeks was 36 per cent lower than that before training.

We have attempted to present an overview of some of the methods used for identifying and studying the fibers and motor units of skeletal muscle, and to give a short discourse on the particular strengths and weaknesses of these methods. It was not our intention to reach a final conclusion of there being only one way to identify muscle fibers or that the subject is closed to additional research. Quite the contrary, we intended to demonstrate that in the past two decades there has been an explosion of knowledge in this field. In the introduction, we suggested that the era of a simple classification scheme for categorizing fibers has passed. We also posed a number of questions. It seems that an appropriate conclusion would be to return to these questions with some answers. Our first question was "what is the purpose of fiber typing?" To us, its intent is to provide as much information as possible about fibers, accentuating their similarities and differences, such that the designated groupings are most meaningful. This has become increasingly difficult as the complex nature of skeletal muscle fibers has been unravelled and the diversity of those fibers previously thought to be similar is exposed. However, fiber typing schemes provide valuable information concerning the nature of the fibers and are important in attempting to describe the nature of muscle. Therefore, fiber typing is a necessary step in describing the complex characteristics of skeletal muscle. We also asked "is more information needed?" Clearly more information is needed to develop a complete understanding of the biochemical and functional aspects of muscle and how it adapts to a variety of experimental or naturally occurring perturbations. Thus, as time passes and more information is amassed, a constant revision of the schemes for identifying fibers can be expected. This is a positive sign of a viable field. A third question was "is it worth trying to keep up or can one be expected to keep up with the seemingly rapid changes in the identification schemes used for fiber typing?" This seems like an absurd question, and yet, it has been posed to us by university professors who are "comfortable with" and continue to use the old system(s) of muscle and fiber identification and who do not want to "see things change." This question, when asked in any field, implies an unwillingness to make the effort to stay abreast with advancements occurring in that field.(ABSTRACT TRUNCATED AT 400 WORDS)

Muscle biopsy samples were collected from the middle gluteal muscle of seven horses undergoing a nine-month endurance training programme. Samples were collected before the programme began and again after three, six and nine months of training. A fifth sample was collected three months after training ceased. Serial muscle sections were reacted histochemically for myosin adenosine triphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) pre-incubation, and muscle fibres identified as type I, IIA, IIB or IIC. The oxidative capacity of individual fibres was assessed, using the reduced nicotinamide dinucleotide tetrazolium reductase stain, and the number of intermyofibrillar capillaries adjacent to each fibre was counted after staining, using the alpha-amylase periodic acid Schiff technique. Biochemical analyses involved the fluorometric measurement of the enzymes citrate synthase, 3-hydroxy acyl CoA dehydrogenase and lactate dehydrogenase as markers of end terminal oxidative, beta oxidative and glycolytic potential, respectively. There was an increase in the percentage of type IIB fibres having high nicotinamide dinucleotide tetrazolium reductase staining after three months training. This increase persisted throughout the period of training and during the period without training. There was an increase in the number of capillaries adjacent to type IIB fibres after six and nine months training. These had returned to near pre-training numbers after three months without training. There were increases in the activities of citrate synthase and 3-hydroxy acyl CoA dehydrogenase after three months training. The activities of both enzymes continued to rise throughout training and the highest activities were attained after nine months.(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined the effects of acute high-intensity exercise on the rate and capacity of Ca2+ uptake and Ca2+-stimulated adenosinetriphosphatase (ATPase) activity of the sarcoplasmic reticulum and the reversibility of these effects. Thoroughbred horses were run at maximal O2 uptake on a high-speed treadmill until fatigued. Muscle temperatures and biopsy samples were collected at rest, immediately after exercise, and 30 and 60 min after exercise. Blood samples were collected at rest and 5 min after exercise. Muscle and blood (lactate concentration) were three- and fivefold greater than pre-exercise values. Muscle temperature and pH immediately after post-exercise were 43 degrees C and 6.55, respectively, but approached rest values by 60 min after exercise. The initial rate and maximal capacity of Ca2+ uptake of muscle homogenates and isolated sarcoplasmic reticulum were significantly depressed immediately after exercise. This depression was paralleled by decreased activity of the Ca2+-stimulated ATPase. However, both Ca2+ uptake (rate and capacity) and Ca2+4-ATPase activity had returned to normal by 60 min after exercise. These findings demonstrate that changes in sarcoplasmic reticulum function after high-intensity exercise may be induced but not sustained by local changes in muscle pH and/or temperature.

Five standardbred geldings received intravenous clenbuterol hydrochloride and saline in a crossover experiment to evaluate the effects of clenbuterol on certain cardiorespiratory parameters during and after treadmill exercise. The exercise test consisted of four steps. Step 1 at a speed of 76 m per minute, step 2 at 129 m per minute, step 3 at 190 m per minute and step 4 at 236 m per minute. The duration of each step was two minutes, except step 4 which was four minutes. The treadmill was set at a grade of 19 per cent. Before exercise, 30 minutes after clenbuterol or saline administration, arterial and mixed venous blood gases, mean arterial pressure, mean pulmonary artery pressure, telemetric electrocardiogram and respiratory rate were measured. The measurements were repeated immediately before completion of step 2, step 4 and after one minute, 10 minutes and 30 minutes of recovery from exercise. After clenbuterol administration there was a transient fall in mean arterial pressure, which had returned to control values by 90 seconds. There was no change in mean pulmonary artery pressure. During exercise the heart rate was significantly higher at the end of steps 1 and 4 and after 10 minutes recovery when horses given clenbuterol were compared with those given saline. No adverse effects on the electrocardiogram were demonstrated. Effects of clenbuterol on blood gases included an increase in PaO2 and decrease in PaCO2 one minute after exercise, when compared to saline. It was concluded from the parameters examined that there was no evidence that clenbuterol had any significant untoward effect on the circulatory system of exercising horses.

Biopsy samples were obtained from the middle gluteal muscle of 10 Thoroughbred horses undergoing a commercial race-training program. Samples were obtained before the program began and again after 6 and 12 weeks of training. All horses had raced at least once by the 12th week of training. Serial sections of muscle were examined histochemically for myosin adenosinetriphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) preincubation, and then muscle fibers were identified as types I, IIA, IIB, or IIC. The oxidative capacity of individual fibers was assessed, using the reduced nicotinamide dinucleotide tetrazolium-reductase stain, and the number of intermyofibrillar capillaries adjacent to each fiber were counted after staining, using the alpha-amylase-periodic acid-Schiff technique. Biochemical analyses involved the fluorometric measurement of 3 enzymes--citrate synthase, 3-hydroxy-acyl coenzyme A dehydrogenase, and lactate dehydrogenase--as markers of end terminal oxidative, beta-oxidative, and glycolytic potentials, respectively. Changes in fiber-type percentages did not occur in response to training. There was a significant (P less than 0.01) increase in the percentage of type IIB fibers, having high nicotinamide dinucleotide-tetrazolium reductase staining after 12 weeks of training. Alterations in the number of capillaries adjacent to each fiber type did not occur during the training period. There were increases in the activities of both citrate synthase and 3-hydroxy-acyl coenzyme A dehydrogenase after 6 weeks (P less than 0.05) and 12 weeks (P less than 0.001) of training. Alterations in the activity of lactate dehydrogenase did not occur in response to training.

Muscle biopsy samples were collected from the left middle gluteal muscle of horses participating in competitive barrier trials. Twelve horses were biopsied the day before and within 30 minutes of completion of an 800 m barrier trial. A further six horses were sampled the day before, and within 30 minutes of, completion of a 1200 m barrier trial. Serial muscle sections were examined histochemically for myosin adenosine triphosphatase activity after acid preincubation, to demonstrate type I, IIA and IIB fibres. The glycogen content in the individual fibres was assessed using the periodic acid Schiff (PAS) reaction. Total glycogen in muscle was measured fluorimetrically after hydrolysis to glucose. Significant decreases in total muscle glycogen levels of 167.1 +/- 22.2 and 158.1 +/- 23.2 mmoles glucose units kg-1 (dry weight) (mean +/- standard error) occurred from pre- to post trial samples for horses in both 800 and 1200 m trials respectively. There were no significant differences between the decreases in total muscle glycogen from horses in either 800 m or 1200 m trials. In both 800 m and 1200 m trials there was a significant decrease in the percentage of type IIA and IIB fibres classified as having high PAS staining intensity, and a significant increase in the percentage of fibres classified as having medium staining intensity when samples taken after the trial were compared to those taken before the trial.

With some, but not all, types and intensities of exercise, lactate accumulates in the blood and in the muscles engaged in the exercise. A great deal of attention has been directed towards attempting to understand the dynamics of lactate production and removal at the onset of exercise, during exercise, and during the recovery process following exercise. It has been hoped that an unravelling of these events would provide a key to understanding cellular metabolism and its regulation during exercise. The purpose of this introductory paper to a symposium on lactate is to present a brief overview of some of the conditions that influence the rate and magnitude of lactate accumulation during exercise. It is pointed out that many conditions influence the rate and magnitude of the accumulation of lactate in blood and muscles. Included are diet, state of physical fitness, and the type and duration of the exercise. We have cautioned against trying to evaluate the state of oxygen delivery to muscle and the state of tissue oxygenation from the appearance of lactate in blood. We have pointed out the positive aspects of lactate production based on how it augments the cellular supply of ATP, thereby allowing for high intensity exercise, and also the negative aspects that develop as a result the reduction in pH which adversely influences many cellular processes essential for muscular activity.

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.

This article reviews what are considered the basic concepts of gas transport, blood gases, and acid-base physiology is most mammalian species. Techniques for the appropriate collection of blood samples for blood gas and acid-base determinations in the newborn foal are described. Guidelines for interpretation of these values in the normal foal and those animals undergoing respiratory and metabolic derangements are provided.