The larynx and its muscles are important for ventilation, coughing, sneezing, swallowing, Valsalva's maneuver and phonation. Due to their functional demands, the intrinsic laryngeal muscles have a unique phenotype: very small and fast fibers with high mitochondrial content. How aging affects their function is largely unknown. In this study, we tested the hypothesis that an intrinsic laryngeal muscle (thyroarytenoid muscle, a vocal fold adductor) would become weaker, slower and fatigable with age. Muscles from Fischer 344-Brown Norway F1 hybrid rats (6-, 18 and 30 months of age) were used for in vitro contractile function and histology. Thyroarytenoid muscles generated significantly lower twitch and tetanic forces at 30-mo vs. 6- and 18-mo. Maximal shortening velocity (V_max) decreased 20% at 30-mo (vs. 6-mo) and velocity of unloaded shortening (V₀) was slower at 18- and 30-mo by 29 and 27% vs. 6-mo. There was no histochemical evidence of altered myosin ATPase activity at 18- or 30-mo of age. Fatigue resistance was significantly decreased at 18- and 30-mo. We also found abundant mitochondrial clusters and ragged red fibers in the muscles of 30-mo old rats, and there was an age-related increase in glycogen-positive fibers. We conclude that rat thyroarytenoid muscles become weaker, slower and more fatigable with age. These functional changes are not due to alterations in myosin ATPase activity, but a switch in the expression of myosin isoforms remains a possibility. Finally, the alterations in mitochondrial and glycogen content indicate a shift in the metabolic characteristics of these muscles with age.