Longlasting nociceptive stimulation is known to cause atrophy of adjacent muscles. The aim of this study was to determine further the possible mechanisms of this pathological phenomenon. Unilateral fracture of the paw was performed under pentobarbital anaesthesia in several experimental groups (n = 8-11) of female and male rats. Dry muscle weights of the soleus (SOL), extensor digitorum longus (EDL), gastrocnemius (GA) and tibialis anterior (TA) were determined 7 days following the bone fracture and compared to the weight of contralateral control muscles. To demonstrate the reflex origin of this atrophy, deafferentation of the paw by dorsal root section (L4_5) was performed before or after unilateral fracture of hindlimb metatarsal bones. In female rats, the fracture resulted in a significant loss of muscle weight in all the four muscles examined. When the hindlimb was deafferented prior to the fracture, no muscle atrophy developed, and neither did deafferentation itself cause any appreciable change in muscle weight except in male rats. This supports the concept that this type of atrophy is reflex in origin. Deafferentation, when performed after the fracture, did not prevent the weight loss in extensor muscles (SOL, GA), while the flexors (EDL, TA) did not in general lose any weight. The results in male rats had a similar trend as in female rats, although the weight loss was significantly smaller. Our results showed that the mechanism of reflex muscle atrophy following metatarsal bone fracture involves a component which is dependent on afferent information from the injured paw. Differences in the degree of affection of different muscle types (extensors vs flexors, slow vs fast muscles) and of female and male rats suggest that the muscle atrophy is the result of a complex process that probably also involves hormonal mechanisms.
After anterior cruciate ligament (ACL) injury, a decrease in muscle strength associated with muscle atrophy is frequently observed. The temporal and spatial effects of reconstructive surgery on muscle atrophy have not been examined in detail. This study aimed to 1) reveal the short and mid-term effects of reconstructive surgery on muscle atrophy, and 2) investigate the differences in the degree of atrophy after ACL reconstruction in the hindlimb muscles. ACL transection with or without reconstructive surgery was performed unilaterally on the knees of rats. Untreated rats were used as controls. At one or four weeks post-surgery, the relative muscle wet weights (wet weight/body weight) of the hindlimb muscles were calculated to assess atrophy. At one week post-surgery, muscle atrophy was induced by ACL transection and further aggravated by reconstructive surgery. Reconstructive surgery facilitated recovery from muscle atrophy in some muscles compared with those without reconstructive surgery (ACL transection alone) at four weeks post-surgery. Muscle atrophy after ACL reconstruction was greater in the rectus femoris and plantar flexors than in the semitendinosus and plantar extensors at one week post-surgery. These results indicate that reconstructive surgery exacerbates muscle atrophy in the first week post-surgery, while facilitating recovery between the first and fourth week post-surgery. After reconstructive surgery, muscle atrophy was observed not only in the quadriceps and hamstrings, but also in the lower leg muscles, suggesting the need for muscle strengthening interventions for the lower leg muscles as well as the quadriceps and hamstrings.