In crustaceans, hemocytes rapidly aggregate and bind bacteria that breach the exoskeleton. These aggregates can become lodged in gill microvasculature and impair O2 uptake, decreasing aerobic metabolism. In shrimp, tail-flipping is a predator escape response fueled by anaerobic energy stores. When depleted by activity, these stores are replenished aerobically. We hypothesized that exposure to bacteria would impair recovery from muscle fatigue in Atlantic brown shrimp Farfantepenaeus aztecus. Shrimp were injected with saline or a sublethal dose (2.5 x 105 g-1) of bacterium Vibrio campbellii. At 4 or 24 h after injection, shrimp were repeatedly induced to tail-flip to fatigue (initial tail-flips). After 20 min recovery in well-aerated water, shrimp were induced to tail-flip to fatigue again. Recovery from fatigue was expressed as the number of tail-flips in the second bout of activity as a percentage of initial tail-flips. Contrary to expectation, bacterial exposure had no significant effect on recovery from fatigue. However, in the 4 h but not the 24 h group, shrimp exposed to bacteria performed significantly more initial tail-flips than saline-injected controls (mean 50.86 ± 3.62 SEM and 35.25 ± 3.62 tail-flips, respectively; p = 0.005). We speculate that shrimp exposed to bacteria upregulate arginine kinase, an enzyme essential to the creation of anaerobic energy stores, driving an increase in initial tail-flip activity. These results suggest that predatory escape behavior in shrimp as measured here is resilient to fluctuations in aerobic metabolism (NSF DBI-1359079, IOS-1147008).