Bit & Bridle

Equine Subclinical Myopathy

Other Names

  • Subclinical Myositis
  • Subclinical Muscle Disease
  • Asymptomatic Myopathy
  • Occult Myopathy

What is Subclinical Myopathy in Horses?

Equine Subclinical Myopathy refers to muscle damage or dysfunction that occurs without the obvious clinical signs associated with more acute muscle disorders such as exertional rhabdomyolysis (tying-up). In subclinical disease, the horse does not present with the dramatic stiffness, pain, and reluctance to move typical of an acute episode — yet underlying muscle damage is occurring, and it can be detected through laboratory testing.

The condition is more common than many horse owners realise. Horses with subclinical myopathy may appear normal to outward inspection but show reduced performance, subtle gait asymmetries, or a tendency toward fatigue that is difficult to attribute to a specific cause. Identifying and managing subclinical myopathy is increasingly important in performance horse medicine, as it can quietly limit a horse’s capacity and career longevity.

The term covers a spectrum of underlying conditions — from nutritional deficiencies and inflammatory changes to genetic muscle disorders — and determining the specific cause is essential for effective management.

Causes of Subclinical Myopathy in Horses

Several distinct causes have been identified:

  • Nutritional deficiencies: Vitamin E and selenium are the most critical antioxidants for equine muscle health. Deficiency of either — or both — impairs the muscle’s ability to defend against oxidative damage during exercise, leading to chronic low-grade muscle cell death. Selenium-deficient soils across much of the UK and parts of South Africa mean many horses are at risk without supplementation.
  • Polysaccharide Storage Myopathy (PSSM): A genetic condition, particularly prevalent in draught breeds and Quarter Horses, in which abnormal glycogen accumulates in muscle cells. PSSM can present with subclinical muscle changes before progressing to clinical episodes of tying-up.
  • Recurrent Exertional Rhabdomyolysis (RER): In horses predisposed to RER (common in Thoroughbreds and Standardbreds), subclinical muscle stress can occur with every training session, even without overt clinical episodes.
  • Immune-mediated myositis: An autoimmune condition in which the immune system attacks muscle tissue, most commonly seen in Quarter Horses with a genetic predisposition. Can present initially as mild muscle wasting without frank pain.
  • Parasitic myopathy: Certain parasites, including Sarcocystis species and migrating strongyle larvae, can cause inflammatory damage to muscle tissue, sometimes without overt clinical signs.
  • Viral infections: Equine influenza, equine herpesvirus, and other systemic infections can trigger subclinical muscle inflammation, often reflected in elevated muscle enzymes for days after apparent clinical recovery.
  • Overtraining: Horses worked beyond their current fitness level without adequate recovery time can accumulate subclinical muscle damage.

Symptoms and Signs

By definition, subclinical myopathy does not produce overt symptoms. However, perceptive owners and riders may notice:

  • A subtle decline in performance — reduced stamina, reluctance to extend, earlier fatigue
  • Mild, non-specific stiffness, particularly after rest
  • Reduced impulsion or reluctance to engage the hindquarters
  • Muscle asymmetry, particularly in the hindquarters (one side visually less developed)
  • Slight behavioural changes: touchiness when groomed over the back or hindquarters
  • Poor coat condition, especially if nutritional deficiency is the underlying cause
  • Horses may be “a bit off” without any clear lameness on a flexion test

Often, subclinical myopathy is discovered incidentally when blood work is run for other reasons — the elevated muscle enzymes prompt further investigation.

Diagnosis

Diagnosis relies on a combination of:

  • Blood testing: Creatine kinase (CK) and aspartate aminotransferase (AST) are the primary muscle enzyme markers. Elevation of these enzymes at rest or after light exercise indicates muscle damage is occurring. Serial samples (at rest, 4 hours after exercise, 24 hours after exercise) are useful in characterising the pattern of damage.
  • Vitamin E and selenium levels: Blood selenium and serum vitamin E levels should be checked in any horse with suspected myopathy.
  • Genetic testing: PSSM1 and RER can be detected via genetic testing from hair follicle samples — this is now routine and affordable for suspected cases.
  • Muscle biopsy: In some cases, a small biopsy of the semimembranosus or semitendinosus muscle is sent for histopathological examination to characterise the type and extent of muscle damage.
  • Exercise tolerance tests: Structured exercise tests with serial enzyme sampling can reveal exercise-induced muscle damage not apparent at rest.

Your vet will combine these findings with a full clinical examination and history to reach a diagnosis. In performance horses, consulting an equine sports medicine specialist is worthwhile.

Treatment

Treatment is tailored to the underlying cause:

  • Nutritional correction: For vitamin E and selenium deficiency, supplementation is the primary treatment. Natural vitamin E (d-alpha-tocopherol) is significantly more bioavailable than synthetic forms. Selenium supplementation must be carefully dosed — toxicity is possible with overdose. Work with your vet to establish appropriate levels based on blood testing.
  • Dietary management for PSSM: Affected horses are managed on a low-starch, low-sugar diet with increased fat (oil) as an energy source. This dramatically reduces muscle enzyme elevations and clinical episodes in most cases.
  • Exercise modification: Regular, consistent exercise (rather than intense sporadic work) is beneficial for most myopathic horses. Turnout should be maximised. Horses with active muscle damage benefit from a period of rest followed by a carefully graduated return to work.
  • Anti-inflammatory therapy: In immune-mediated myositis, corticosteroids may be prescribed to reduce the autoimmune attack on muscle tissue.
  • Parasite control: Address any parasite burden contributing to the condition with a strategic worming programme.

Prevention

  • Ensure all horses receive adequate vitamin E and selenium — have blood levels checked, particularly in horses in areas with selenium-deficient soils
  • Feed a balanced diet appropriate to the horse’s workload and breed
  • Implement a progressive, structured training programme — avoid sudden jumps in workload
  • Maximise turnout and consistent movement
  • Consider genetic testing for PSSM and RER in at-risk breeds before intensive training begins
  • Monitor horses after systemic illness — run CK/AST before returning to full work after a viral infection
  • Use a comprehensive, weight-adjusted worming programme based on faecal egg counts

Prognosis

Prognosis depends entirely on the cause. Horses with nutritional deficiency myopathy that is identified and corrected early typically recover fully. PSSM is a lifelong genetic condition, but with appropriate dietary management, most horses remain in comfortable work. Immune-mediated myositis can result in significant muscle wasting if not caught early, but responds well to treatment when identified promptly.

Horses in which subclinical myopathy has been causing chronic muscle damage may have some degree of permanent muscle fibre loss, but with appropriate management this need not be career-ending in most cases.

When to Call the Vet

Consult your vet if:

  • Your horse’s performance is declining without a clear explanation
  • You notice unexplained muscle asymmetry or wasting, particularly in the hindquarters
  • The horse is intermittently stiff after rest or exercise
  • A blood test has returned elevated CK or AST values
  • You are managing a breed known to be predisposed to PSSM or RER and want baseline testing
  • Your horse has recently recovered from a viral illness and you want to confirm muscle enzyme levels before returning to full work

Frequently Asked Questions

How is subclinical myopathy different from tying-up?

Tying-up (exertional rhabdomyolysis) is an acute, often dramatic episode of muscle damage associated with exercise — the horse becomes rigid, sweaty, and in obvious distress. Subclinical myopathy involves the same underlying mechanisms (muscle cell damage and elevated enzymes) but at a lower level that does not produce overt clinical signs. Many horses with subclinical myopathy are at risk of acute tying-up episodes if pushed beyond their current tolerance.

Can you tell if a horse has subclinical myopathy without blood tests?

Reliable diagnosis requires blood testing. Experienced riders and handlers may suspect something is wrong — reduced performance, subtle stiffness, behavioural changes — but these signs are non-specific and can have many causes. Blood enzyme testing is the minimum needed to confirm muscle involvement, with further investigation to identify the underlying cause.

Is selenium supplementation safe for all horses?

Selenium has a narrow therapeutic window — the gap between beneficial and toxic levels is small. Supplementation should always be based on blood testing rather than given routinely without knowing baseline levels. Selenium toxicity (selenosis) can cause hair loss, hoof problems, and neurological signs. Work with your vet to establish an appropriate dose for your horse’s specific needs and regularly recheck blood levels.

Can subclinical myopathy progress to more serious muscle disease?

Yes. If the underlying cause is not addressed, subclinical myopathy can progress to clinical disease — overt tying-up episodes, significant muscle wasting, or in the case of immune-mediated myositis, severe functional impairment. This is why investigating unexplained performance decline or elevated muscle enzymes promptly matters. Early intervention prevents progression in most cases.