Equine Muscular Physiology: Energy Metabolism and Fatigue

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Key Takeaways

• Equine skeletal muscle primarily utilizes fatty acids via oxidative phosphorylation at rest, sparing muscle glycogen for high-intensity exercise where it fuels anaerobic glycolysis; depletion of muscle glycogen is a direct correlate of fatigue in sprint and race disciplines.
• Glucose uptake across the sarcolemma, mediated by the GLUT4 transporter, is the rate-limiting step in muscle glucose utilization, and insulin resistance impairs this process, negatively impacting exercise recovery and overall metabolic health.
• Equine muscle exhibits a fiber-type spectrum from slow oxidative (Type I) to fast glycolytic (Type IIX), with hybrid phenotypes, and the proportion of these fibers dictates an individual's capacity for speed versus endurance.
• High mitochondrial volume in equine muscle supports significant aerobic capacity, which is further enhanced by training through increased mitochondrial density and oxidative enzyme activity, leading to improved fatty acid oxidation and glycogen sparing.
• Fatigue in horses is multifactorial, stemming from substrate depletion (glycogen, phosphocreatine), ionic shifts (hydrogen ions, inorganic phosphate), and thermoregulation, with no single biomarker reliably predicting fatigue across all disciplines.
• Lactate handling in equine muscle is efficient due to high buffer and transport capacity, which delays pH-mediated fatigue during anaerobic exercise, but this buffering capacity is not limitless and can be improved through specific training regimens.

This reference article examines the bioenergetic systems that power equine skeletal muscle and the physiological mechanisms that limit performance during exercise. It is written for veterinary students who have completed introductory physiology and are now integrating musculoskeletal and metabolic concepts into a clinical framework. The article addresses how horses generate ATP at rest and during exertion, how muscle fiber composition and substrate stores shape athletic capacity, and how fatigue emerges from the interaction of metabolic, ionic, and thermal disturbances. A companion article in this series covers cardiorespiratory adaptations and performance assessment.

At a Glance

Muscle Fiber Composition and Metabolic Phenotype

Equine skeletal muscle is characterized by adaptations that reflect both the evolutionary history of the horse as a grazing herbivore and centuries of selective breeding for athletic traits. These adaptations include a high muscle mass relative to body weight, an efficient muscle-tendon architecture, and a fiber-type composition with intrinsic shortening velocities greater than would be predicted for an animal of comparable size. The fiber-type spectrum spans slow oxidative type I fibers, fast oxidative type IIA fibers, and fast glycolytic type IIX fibers, with many fibers expressing hybrid phenotypes that allow graded metabolic and contractile properties. The proportion of these fibers varies by muscle, breed, and individual, and it is this variation that underpins differences in speed, stamina, and susceptibility to fatigue.

The metabolic character of a muscle is determined by its fiber composition and by the density of mitochondria and capillary supply. Equine skeletal muscle has a high mitochondrial volume, which permits a higher whole-animal aerobic capacity than would be expected from body size alone. This oxidative capacity is complemented by large intramuscular stores of energy substrates, particularly glycogen, and by high buffer and lactate transport capacities that preserve muscle function during anaerobic exercise. These features are not fixed, they respond to training in a fiber-type-specific manner, and the nature of the adaptive response depends on the intensity, duration, and type of exercise stimulus.

ATP Production Pathways

Muscle contraction depends on the continuous resynthesis of ATP. The immediate phosphagen system, comprising ATP and phosphocreatine, supports the first seconds of high-intensity work. Beyond this, ATP must come from anaerobic glycolysis or oxidative phosphorylation. The choice of pathway is governed by exercise intensity and duration, and by the availability of oxygen and substrate. At rest and during low-intensity exercise, oxidative phosphorylation of fatty acids and glucose predominates. As intensity rises, the contribution of anaerobic glycolysis increases, with a corresponding rise in lactate production and hydrogen ion accumulation.

Glycogen is the critical fuel for high-intensity exercise. The horse's large intramuscular glycogen stores are mobilized through glycogenolysis, and the rate of glycogen utilization is proportional to exercise intensity. Depletion of muscle glycogen is a well-recognized correlate of fatigue in racehorses and in horses performing repeated high-intensity efforts. The capacity to resynthesise glycogen after exercise depends on glucose uptake, which is mediated by the facilitative glucose transporter GLUT4. This transporter translocates from an intracellular pool to the cell surface in response to insulin and to contraction-induced signals, and it is the rate-limiting step in glucose utilization in skeletal muscle. Impaired GLUT4 translocation is a hallmark of insulin resistance, a condition that compromises metabolic flexibility and recovery in the equine athlete.

Substrate Utilization and Glucose Homeostasis

Glucose homeostasis in the horse is regulated by the interplay of intestinal absorption, hepatic output, pancreatic insulin secretion, and peripheral uptake by muscle and adipose tissue. The enteroinsular axis, in which incretin hormones augment insulin secretion in response to oral glucose, is active in horses and influences postprandial insulin responses. The composition of the diet, particularly the starch and sugar content, modulates the magnitude of the incretin and insulin responses, and this has implications for the metabolic health of athletic and non-athletic horses alike.

In skeletal muscle, glucose uptake is the rate-limiting step in glucose utilization. The insulin-responsive GLUT4 isoform is the major mediator of insulin-stimulated glucose disposal, and its functional capability is impaired in muscle during insulin resistance in horses. The molecular mechanisms of altered glucose transport remain incompletely defined in all species, and the class III GLUT family members are particularly poorly understood. These gaps in knowledge limit the development of targeted therapeutic strategies for metabolic disorders in horses.

Training Adaptations and Metabolic Conditioning

Skeletal muscle in horses has considerable potential to adapt to training, and these adaptations have direct physiological consequences for stamina, strength, and speed. Endurance training increases mitochondrial density, oxidative enzyme activity, and capillary supply, enhancing the muscle's capacity to oxidise fatty acids and spare glycogen. Sprint training increases the activity of glycolytic enzymes and the buffering capacity of muscle, delaying the onset of pH-mediated fatigue. The specificity of these adaptations is captured by the question of what kind of stimulus produces what kind of muscular adaptation, and the published evidence supports distinct training approaches for racehorses, trotters, endurance horses, and sport horses.

The response to training is also influenced by circadian biology. Equine skeletal muscle contains a molecular clock, and the expression of exercise-relevant genes, including those involved in myogenesis, substrate metabolism, and mitochondrial biogenesis, varies across the 24-hour cycle. Regular exercise can alter the rhythmic expression of these genes, suggesting that the timing of training relative to the circadian cycle may influence the adaptive response. The practical implications of this for training schedule design are not yet fully defined.

Fatigue Mechanisms

Fatigue in the exercising horse is not a single phenomenon but a composite of metabolic, ionic, and thermal disturbances that converge to reduce force production. During high-intensity exercise, the accumulation of hydrogen ions and inorganic phosphate, the depletion of phosphocreatine, and the progressive fall in muscle glycogen all contribute to the decline in power output. During prolonged submaximal exercise, glycogen depletion, hyperthermia, and fluid and electrolyte loss are the dominant factors. The relative contribution of each mechanism depends on the discipline, the ambient conditions, and the individual horse.

Metabolomics offers a systems-level view of these disturbances by measuring the low-molecular-weight metabolites that are the downstream readouts of cellular signaling and metabolic flux. The application of metabolomics to equine exercise physiology has lagged behind human sport and exercise science, and the skeletal muscle metabolome of the horse remains incompletely characterized. A more complete understanding of the metabolomic changes that occur with exercise would improve the management and health of the athletic horse, but methodological barriers and the cost of high-throughput analysis currently limit its routine use.

Applied Assessment of Muscle Energy Status

Clinical evaluation of equine muscle energy metabolism begins with a structured history and examination, not with laboratory testing. The first decision point is whether the presenting problem reflects exercise intolerance, poor performance, or a suspected metabolic limitation. Each of these presentations narrows the differential and determines which diagnostic tools add value.

Exercise intolerance in a fit horse should prompt review of training history, recent workload changes, and diet composition before blood sampling. A horse that has been rested for several weeks will show reduced oxidative enzyme activity and altered substrate handling, so interpretation of any metabolic measurement must account for conditioning state. The equine skeletal muscle phenotype is highly plastic, and detraining produces measurable shifts in fiber characteriztics and metabolic capacity within weeks.

Physical Examination and Gait Assessment

The examination should quantify muscle mass symmetry, particularly over the epaxial muscles, gluteals, and semitendinosus. Asymmetry may indicate disuse, previous injury, or poor saddle fit instead of a primary metabolic problem. Gait evaluation at walk and trot on a straight line and circle identifies mechanical lameness that mimics metabolic fatigue. Muscle fasciculation, sweating patterns, and recovery heart rate after a standardized exercise test provide indirect information about metabolic strain.

A standardized exercise test is the most useful clinical tool for distinguishing metabolic limitation from cardiorespiratory or orthopedic disease. The test should be reproducible, incremental, and tailored to the horse's discipline. Heart rate, respiratory rate, and venous lactate concentration measured at set intervals create a profile that can be compared over time. A horse with impaired oxidative metabolism shows an early and steep rise in lactate at submaximal speeds, whereas a horse with normal muscle energetics maintains low lactate until near-maximal intensity.

Laboratory Assessment of Muscle Metabolism

Resting venous blood sampling provides limited information about muscle energy metabolism. Circulating glucose, insulin, and lactate concentrations reflect whole-body homeostasis instead of intramuscular events. However, resting hyperinsulinaemia or insulin resistance has direct implications for muscle glucose uptake, since GLUT4 translocation is the rate-limiting step in insulin-stimulated glucose disposal in skeletal muscle. Horses with insulin dysregulation may therefore have impaired capacity to replenish muscle glycogen after exercise, even when resting muscle mass and fiber composition appear normal.

The enteroinsular axis modulates postprandial insulin responses and influences glucose availability to muscle. A horse with exaggerated postprandial insulin secretion may show rebound hypoglycemia during prolonged work, contributing to premature fatigue. Oral glucose tolerance testing or measurement of fasting insulin and glucose can identify this pattern, but the results must be interpreted alongside the horse's body condition, diet, and recent exercise.

Muscle biopsy is the definitive method for assessing fiber composition, glycogen content, and oxidative capacity. Percutaneous biopsy of the middle gluteal muscle is the standard site. The sample should be frozen rapidly and processed for histochemistry or biochemical assay. Biopsy is indicated when a primary myopathy is suspected, when fiber-type distribution is relevant to the horse's discipline, or when glycogen storage disorders are in the differential. For most performance problems, however, the biopsy result does not change management, because the training program is adjusted regardless of the precise fiber percentages.

Metabolic Monitoring During Exercise

Serial venous lactate measurement during an incremental exercise test remains the most practical field assessment of muscle energy metabolism. The lactate threshold, defined as the speed at which blood lactate begins to accumulate exponentially, reflects the balance between aerobic production and clearance. A rightward shift in the lactate threshold after a training block indicates improved oxidative capacity. The same test repeated under identical conditions allows objective comparison.

Heart rate monitoring adds a second dimension. The heart rate at a given speed decreases with conditioning, and the relationship between heart rate and lactate provides information about the coupling of cardiovascular oxygen delivery to muscle oxygen utilization. A horse with a low lactate threshold and high heart rate at submaximal speeds has a different limitation than one with normal heart rate but early lactate accumulation.

Table 1 summarizes the monitoring parameters used during exercise testing and their interpretation.

Interpretation of Fatigue in the Clinical Setting

Fatigue in the exercising horse is multifactorial, and the clinician must determine which system fails first. Central fatigue, arising from altered neurotransmitter activity in the brain, is difficult to assess clinically and is often a diagnosis of exclusion. Peripheral fatigue involves depletion of intramuscular substrates, accumulation of metabolites, or failure of excitation-contraction coupling.

Glycogen depletion is the most common metabolic cause of fatigue in endurance exercise. Muscle glycogen content is finite, and once depleted, the horse cannot maintain high-intensity work regardless of cardiovascular capacity. The rate of glycogen utilization depends on exercise intensity, with higher intensities consuming glycogen more rapidly. Horses that fatigue at a predictable point in a race or ride, with recovery after carbohydrate feeding, likely have glycogen-limited performance.

Lactate accumulation and the associated fall in intramuscular pH impair cross-bridge cycling and enzyme function. This mechanism dominates in sprint and middle-distance events. The horse's buffering capacity, which is high in equine muscle, delays the onset of fatigue but does not prevent it. Training at or near the lactate threshold improves buffering capacity and shifts the fatigue point to higher speeds.

When the Metabolic Diagnosis Changes Management

The metabolic assessment changes management in specific circumstances. A horse with documented insulin dysregulation and poor glycogen replenishment benefits from dietary modification and timed carbohydrate provision after exercise. A horse with a low lactate threshold and normal cardiorespiratory function requires a different training stimulus, with more aerobic base work at intensities below the threshold. A horse with normal metabolic parameters and persistent poor performance needs investigation of other systems, including the upper airway, cardiac function, and musculoskeletal structures.

The choice of diagnostic approach also depends on available equipment. Field lactate meters provide immediate results but require calibration and careful sample handling. Laboratory analyzers are more accurate but introduce a delay between sampling and result. Muscle biopsy requires specialised processing and interpretation, and the procedure is not available in all practices. The clinician should select the least invasive test that answers the specific question, and should not pursue metabolic testing when the history and examination point clearly to another cause.

Documenting Metabolic Findings

Documentation should record the test protocol, environmental conditions, and all measured values in a format that allows direct comparison on repeat testing. Speed, distance, heart rate, and lactate should be recorded at each step. The horse's body weight, tack, rider, and footing should be noted, because each influences the metabolic demand. Photographs of the horse before and after exercise, and of any muscle asymmetry, provide useful longitudinal reference.

The interpretation should state the likely metabolic limitation, the evidence supporting it, and the specific training or dietary changes recommended. A follow-up exercise test should be scheduled after a defined training period, typically 6 to 8 weeks, to assess response. The same protocol must be used, because changing the test invalidates the comparison.

Circadian and Temporal Considerations

Recent evidence indicates that exercise-relevant genes in equine skeletal muscle show circadian rhythmicity, and that regular exercise modifies these expression patterns. This has practical implications for training schedules. A horse trained at the same time each day may show different metabolic responses than one trained at irregular times. The clinical significance of these findings is still emerging, but the clinician should consider timing of training and testing when interpreting metabolic data. Repeated testing should be performed at the same time of day to reduce this source of variability.

Recognized Complications and Early Detection

Metabolic fatigue in the equine athlete is usually self-limiting, but several complications require prompt recognition. Exertional rhabdomyolysis represents the most clinically significant failure mode. Early indicators include shortened stride, reluctance to maintain pace, muscle fasciculation over the gluteal and epaxial musculature, and dark or reduced urine output. Detection depends on serial assessment during and immediately after exercise, with palpation of muscle firmness and monitoring of urine color guiding the decision to stop work. Serum creatine kinase and aspartate aminotransferase activities confirm the diagnosis but rise over hours, so they confirm instead of enable early detection.

Heat stress and electrolyte depletion frequently coexist with metabolic fatigue. Horses that stop sweating, develop a rectal temperature above 40.5°C, or show synchronous diaphragmatic flutter have progressed beyond simple substrate depletion. The discriminating feature is that these horses do not recover with rest alone and require active cooling and fluid therapy. Synchronous diaphragmatic flutter, a thumping contraction of the diaphragm, indicates hypocalcemia and often accompanies heavy sweating with electrolyte loss.

Glycogen depletion syndromes present differently. A horse that finishes a bout of work but remains stiff, reluctant to eat, and slow to recover over 24 to 48 hours has likely exhausted intramuscular glycogen stores. Equine skeletal muscle adaptations and genomics describe large intramuscular glycogen stores as a defining feature of the horse, and their depletion explains the prolonged recovery seen after repeated high-intensity efforts. Early detection relies on tracking recovery time across successive workouts instead of on any single examination.

Common Clinical Errors and Corrective Actions

The most frequent error in assessing metabolic fatigue is attributing poor performance exclusively to cardiorespiratory limitation while ignoring muscle energy status. Muscle biopsy and metabolomic profiling are underused in equine practice, and the equine metabolomics literature notes that the field lags behind human sports medicine. The corrective action is to include muscle assessment in the workup of any horse with unexplained performance decline, particularly when gait evaluation is unremarkable.

A second error is misreading behavioral resistance as a training or temperament problem. A horse that refuses to maintain pace, resists the bit, or shortens stride may be protecting fatigued muscle instead of disobeying. The discriminating check is to compare performance early in the session with performance after a brief walk break. Genuine fatigue improves transiently with low-intensity recovery, whereas behavioral resistance typically does not.

A third error involves overinterpreting a single blood sample. Lactate and glucose concentrations fluctuate rapidly with sampling site, handling, and time since exercise. Serial sampling with consistent technique, or reliance on heart rate recovery as a proxy, produces more reliable clinical decisions than isolated values.

Limitations of Current Evidence

The evidence base for equine muscle metabolism carries important gaps. Much of the training literature derives from Thoroughbreds, Standardbreds, and endurance horses, with limited data on sport horses and draught breeds. Scientific background for skeletal muscle conditioning acknowledges that scientific conditioning methods have not been fully integrated into equine practice, and expert opinion still differs on optimal training intensity and duration for specific disciplines.

The molecular understanding of glucose transport in equine muscle remains incomplete. Facilitative glucose transporters in equine insulin-sensitive tissue states that the pathways mediating GLUT4 translocation are not fully elucidated in any species, and the molecular mechanisms of altered glucose transport in insulin resistance remain elusive. Clinicians should therefore interpret metabolic testing with appropriate caution and avoid overstating the diagnostic certainty of any single biomarker.

Circadian variation adds another layer of complexity. Exercise influences circadian gene expression in equine skeletal muscle demonstrates that exercise alters the rhythmic expression of metabolic genes, but the clinical implications for training scheduling are not yet defined. Expert opinion differs on whether training at consistent times of day improves metabolic efficiency, and current evidence does not support a firm recommendation.

Referral and Escalation Criteria

Referral for specialist evaluation is warranted when a horse shows recurrent episodes of exertional rhabdomyolysis, persistent elevation of muscle enzymes beyond 48 hours, or progressive muscle atrophy despite appropriate management. Specialist centers offer muscle biopsy with histopathology, histochemistry for fiber typing, and metabolomic analysis that is not routinely available in practice. Metabolomics in equine sport and exercise identifies skeletal muscle metabolomics as a promising but underutilised diagnostic avenue.

Laboratory involvement is appropriate when baseline metabolic testing reveals persistent hyperinsulinaemia or insulin resistance, because glucose homeostasis and the enteroinsular axis links these findings to equine metabolic syndrome and laminitis risk. Such horses require dietary modification and longitudinal monitoring instead of a single intervention.

Regulatory reporting obligations vary by jurisdiction and competition context. Veterinarians should consult AVMA practice resources for professional guidance and WOAH terrestrial animal health standards where international movement or competition rules apply. Medication used to manage metabolic conditions must comply with the relevant racing or equestrian authority, and current formulary references should be consulted before prescribing.

Troubleshooting Guide

Frequently Asked Questions

How Should I Interpret Muscle Enzyme Activities When My Practice Laboratory Cannot Perform a Full Metabolic Panel?

When a full metabolic panel is unavailable, interpret resting serum creatine kinase and aspartate aminotransferase activities in conjunction with signalment, history, and gait assessment. Mild elevations may reflect recent exercise, sampling artefact, or subclinical muscle turnover, whereas marked elevations warrant further investigation. If biopsy or advanced metabolomic profiling is not accessible, serial sampling after a standardized exercise test provides a practical substitute. A rising trend across repeated samples carries more diagnostic weight than a single abnormal value. The MSD Veterinary Manual offers guidance on interpreting muscle enzyme results in context. Document the sampling interval relative to exercise, because timing materially affects interpretation.

What Is the Minimum Equipment Needed to Monitor Metabolic Fatigue in the Field?

A heart rate monitor, a calibrated stopwatch, and a stethoscope form the core field kit. Respiratory rate and effort, mucous membrane color, and capillary refill time provide indirect evidence of metabolic strain when blood sampling is impractical. Gait quality and behavioral indicators, such as reluctance to maintain pace or loss of collection, remain the most accessible fatigue markers. For glycogen status, serial body condition scoring and muscle palpation are crude but repeatable. When laboratory access is limited, prioritize consistent documentation of exercise duration, speed, and recovery heart rate over sophisticated assays. The AVMA practice resources describe standard approaches to field-based patient assessment that apply to equine athletes.

How Do My Monitoring Decisions Change for a Young Horse in Early Training Compared with a Fit Adult?

A young horse in early training has lower mitochondrial volume and smaller intramuscular glycogen stores, so fatigue develops at lower absolute workloads. Monitoring should emphasize gradual workload progression and frequent recovery assessment, because the adaptive response to training is still developing. The fit adult tolerates higher intensity and longer duration, but its larger glycogen reserve means depletion events are more severe when they occur. For the young horse, prioritize gait quality and enthusiasm as fatigue indicators. For the fit adult, monitor heart rate recovery and respiratory effort more closely. Skeletal muscle adaptations and muscle genomics of performance horses describes how training alters fiber composition and metabolic capacity across the performance career.

What Should I Record in the Medical Record for an Equine Athlete Presenting with Unexplained Fatigue?

Record the exact exercise history for the preceding 72 hours, including intensity, duration, surface, and ambient conditions. Document feed and water intake, particularly the timing of the last meal relative to exercise, because glycogen restoration depends on post-exercise feeding. Note any recent changes in training program, shoeing, or tack that could alter gait efficiency. Record resting heart rate, respiratory rate, and rectal temperature, then perform a standardized exercise test if the horse is sound. Serial measurements of heart rate recovery at fixed time points provide objective data for trend analysis. The metabolomics review in equine sport and exercise highlights how metabolite profiles can complement clinical records, though this technology is not yet routine in practice.

How Should I Explain Metabolic Fatigue to an Owner Who Expects a Simple Diagnosis?

Frame fatigue as a normal physiological response to energy demand instead of a disease. Explain that muscle relies on stored glycogen and that depletion, not structural damage, explains most performance loss. Use the analogy of a fuel tank that refills only with rest and appropriate nutrition. Clarify that blood tests may be normal because fatigue is a metabolic state, not an inflammatory condition. Emphasize that training increases the muscle's capacity to store and use fuel, which is why conditioning programs produce visible improvement. Advise that persistent fatigue despite adequate rest warrants re-evaluation, because the differential includes subclinical lameness, poor dentition, or early metabolic disease. The scientific background for skeletal muscle conditioning provides a framework for explaining how training changes muscle physiology in terms owners can understand.

When Should I Refer an Equine Athlete with Fatigue to a Specialist Center?

Refer when fatigue is accompanied by abnormal gait, muscle atrophy, pigmenturia, or failure to improve after two weeks of reduced training. Also refer when serial muscle enzyme activities rise progressively despite rest, or when the horse shows signs of systemic illness such as fever, tachycardia, or tachypnoea at rest. A specialist center offers muscle biopsy with histochemistry, quantitative glycogen analysis, and advanced imaging that may identify subclinical myopathy or metabolic disorder. Regional referral criteria vary, so consult WOAH terrestrial animal health standards for guidance on transport and welfare during referral. Early referral is preferable when the history suggests a progressive process instead of simple training fatigue.

Related Clinical & Scientific Guides

• Canine Respiratory System: Anatomy and Physiology
• Comparative Anatomy of the Mammalian Kidney
• Feline Cardiopulmonary Physiology: Heart-Lung Interactions

References and Further Reading

• Skeletal muscle adaptations and muscle genomics of performance horses.. 2016.
• A scientific background for skeletal muscle conditioning in equine practice.. 2007.
• Metabolomics in equine sport and exercise.. 2021.
• Glucose homeostasis and the enteroinsular axis in the horse: a possible role in equine metabolic syndrome.. 2014.
• Exercise influences circadian gene expression in equine skeletal muscle.. 2014.
• Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology.. 2014.
• NCBI Bookshelf: Veterinary and Comparative Biomedical Sciences. NCBI Bookshelf.
• MSD Veterinary Manual, Professional Edition. MSD Veterinary Manual.
• American Veterinary Medical Association Practice Resources. American Veterinary Medical Association.

Related Articles

• Equine Muscular System: Major Muscle Groups and Function
• Equine Digestive Physiology: Cecum and Colon Fermentation
• Equine Digestive System: Anatomy and Physiology of the Hindgut
• Equine Hoof Physiology: Growth, Keratinization, and Shock Absorption
• Equine Exercise Physiology: Cardiorespiratory Adaptations and Performance Assessment

This article is educational professional reference material for veterinary audiences. It is not a substitute for veterinary diagnosis, individual clinical judgment, current product labeling, or applicable regulatory requirements.