Exercise intolerance in retrievers - Veterinary Medicine
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Exercise intolerance in retrievers
When a dog from one of the popular retriever breeds is brought to you because it collapsed while exercising or seems to tire easily, you need to sift through the many potential underlying causes. It could be anything from an out-of-shape weekend athlete to a dog with an inherited metabolic myopathy. Here are some of the conditions to consider.


CXMD should be suspected when typical clinical signs are seen in a young male retriever puppy. Serum CK activities are markedly increased as early as 1 week of age and peak at 6 to 8 weeks, just before overt clinical signs appear. After this time, CK activities plateau at about 100 times normal values, with more dramatic increases following exercise.45,52 Electromyography reveals pseudomyotonic discharges in most muscles by 10 weeks of age. Muscle biopsies reveal marked myofiber size variation, necrosis, and regeneration with multifocal myofiber mineralization. Immunocytochemical studies document the absence of the sarcolemmal protein dystrophin.51 The causative mutation for CXMD in the golden retriever has been identified, and a DNA test is commercially available (Health Gene, Toronto Ontario: http://www.healthgene.com/vet/) for diagnosis in affected golden retrievers and to determine genetic status in carrier females. Most affected dogs become nonambulatory or develop aspiration pneumonia and are euthanized. A few dogs with less severe weakness stabilize by 6 months of age and can live functional lives as sedentary pets.45,52

Centronuclear myopathy. A muscle disorder that is inherited as an autosomal recessive trait has been reported in male and female Labrador retrievers.51,52,55 At birth, affected puppies are indistinguishable from their normal littermates, but muscular weakness, awkward gait, and decreased exercise tolerance become apparent by 2 to 6 months of age and progressively worsen.55 As the disease progresses, severely affected pups develop a low head carriage, ventroflexion of the neck, and a gait characterized by short, stilted strides.51,55,56 The hind legs are often advanced simultaneously in a synchronous, bunny-hopping fashion. Clinical signs are exacerbated by stress, excitement, and cold temperatures.51

Affected dogs exhibit pronounced atrophy of the proximal limb muscles and the muscles of mastication but no pain on muscle palpation.51,52,55 Postural reactions and proprioceptive function are normal as assessed by knuckling and hopping. Tendon reflexes (especially patellar reflexes) are reduced or absent, even in mildly affected dogs, by 1 month of age.51,55 In most dogs, the signs stabilize between 8 months and 1 year of age, so dogs that are still ambulatory at that age may remain functional as pets.52,55 Megaesophagus leading to aspiration pneumonia has been seen in a few affected dogs.55

Diagnosis should be suspected based on clinical signs, signalment, and laboratory findings. Serum CK activities are within normal limits or only mildly increased, and other routine hematologic and biochemical analyses are normal.51,52,55 Electromyography reveals spontaneous activity in the affected muscles. Histologic examination of muscle is a reliable tool for diagnosis, revealing marked variation in muscle fiber diameter with angular atrophy of both fiber types, and in some cases, a Type 1 myofiber predominance, resulting in a previous name for this condition—Type II myofiber deficiency.51,55 As the disease progresses and affected dogs mature, many myofibers display centrally placed nuclei. This feature, as well as similarities between this condition and the human muscle disorder centronuclear myopathy, prompted a change in the name of this condition to centronuclear myopathy (CNM).56 In 2003, a mutation in the gene encoding protein tyrosine phosphatase-like, member A (PTPLA) was identified as the causative genetic mutation for CNM in Labrador retrievers, and a DNA test is now commercially available (Alfort School of Veterinary Medicine, France: http://labradorcnm.com/).56 This mutation-based test can be used to diagnose a clinically affected puppy or to screen potential breeding animals for carrier status.

X-linked myotubular myopathy. In 2008, we described a 5-month-old male Labrador retriever with rapidly progressive weakness and muscle atrophy that was clinically more severely affected than most pups with CNM.57 Muscle biopsies determined that the pup had a distinct myopathy with central mitochondrial accumulations. Multiple male littermates and half-siblings were similarly affected.57 Since that time, numerous male puppies from three different litters in western Canada have been evaluated and determined to have this same myopathy (Snead EC, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada: Unpublished data, 2009). Affected puppies first exhibit weakness and hind limb atrophy at 5 to 7 weeks of age, and this progresses to the point that they are nonambulatory or recumbent by 6 months of age.57,58 Patellar reflexes are decreased or absent, and laryngeal weakness and dysphagia occur terminally. Serum CK activity is normal or only slightly increased.57 Immunoblot analysis has revealed that myotubularin is absent in muscle extracts from affected dogs, and the mutation causing this rare X-linked myotubular myopathy has recently been identified.58


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