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While there is no single therapy available that will
halt cachexia or sarcopenia, a multimodal approach, including pharmacologic and nutritional intervention in addition to exercise programs, may minimize muscle loss due to these syndromes. And in the case of cachexia, addressing the underlying disease is imperative for minimizing loss of LBM.
Several novel pharmacologic therapies are currently undergoing trials for use in both cachectic and sarcopenic humans and may serve as a starting point for therapeutic opportunities that may benefit veterinary patients in the future but are beyond the scope of this review.
In humans, both resistance and aerobic exercise have been shown to be effective in minimizing muscle loss and improving muscle function, as well as attenuating inflammatory markers, reducing fatigue, and improving quality of life in geriatric and cachectic patients suffering from loss of LBM.8 These actions are thought to be
due to anabolic effects of exercise including stimulation of IGF-1, inhibition of inflammatory mediators and myostatin, as well as increased antioxidant capacity through enhancement of free radical scavenging enzymes and other mechanisms. While instituting such programs poses unique challenges in veterinary patients, it is possible and likely would be enjoyed by the majority of canine patients. Simple plans could include increasing normal daily activities of a geriatric canine patient (short walks, hikes, and playing catch) and may improve their agility and attenuate muscle loss. Cats can often be encouraged to exercise through play activities such
as replicating the hunt experience, utilizing stairs and laser pointers. Many geriatric dogs and cats suffer from degenerative joint disease (DJD), which may impact their level of activity; this can be effectively managed through nutritional interventions (therapeutic joint diets, omega-3 (n-3) fatty acid supplementation) as well as judicious pharmacologic pain management. Addressing DJD often greatly enhances self-initiated exercise in geriatric dogs and cats and may assist in improving quality of life, mobility, and muscle mass/function with little cost or risk to the family. It is critical that the veterinary team address such conditions when instituting plans to increase a geriatric patient’s activity.
Nutrition holds great potential for combating many of the mechanisms involved in both cachexia and sarcopenia. Inflammation is believed to play a fundamental role
in development of age- and disease-related muscle
loss as outlined above. Long-chain n-3 fatty acids have demonstrated anti-inflammatory effects in both humans and dogs and cats and therefore may assist in attenuating the inflammatory component that is
so fundamental in both of these syndromes. On the veterinary side, n-3 fatty acids have also been shown to
An Urban Experience
improve appetite and reduce muscle loss in dogs with heart failure.9
Antioxidants and mitochondrial cofactors may also
be beneficial as part of multimodal therapy for muscle wasting syndromes, due to the pivotal role that oxidative stress plays in their pathogenesis. While efficacy
of antioxidants appears promising for patients with cachexia, optimal dosage, route of administration or the most effective combinations have not been established, and studies in veterinary patients at this point in time are lacking.
In veterinary patients suffering from muscle loss it is also critical that caloric and protein requirements are met daily. This is an issue plaguing CKD patients. While renal therapeutic foods have historically been characterized as unpalatable, recent studies found that 94% of cats and 97% of dogs with CKD successfully transitioned
to Prescription Diet k/d.10,11 Nonetheless, hyporexia (decreased food intake) is quite common in the CKD patient. In the case of insufficient caloric intake muscle will ultimately be catabolized to provide a necessary source of energy. Patients eating insufficient calories are often also not meeting their protein requirements, further perpetuating muscle loss. While studies focused on supplementing protein or specific amino acids in humans have shown mixed benefits, it is generally agreed that meeting the patient’s basic need for nitrogen and the essential amino acids is imperative. Since insufficient caloric and protein intake further exacerbates muscle wasting in cachectic pets it must be prevented when possible through meticulous use of antiemetics, appetite stimulants, proper feeding orders, and when necessary and appropriate, enteral nutritional interventions such as esophagostomy tube placement. A thorough nutritional assessment as part of every patient visit greatly reduces the risk of malnutrition in both healthy and diseased senior pets.
Figure 1: Overlapping Mechanisms of Cachexia and Sarcopenia

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