Guinea pigs have been used in experimental models to evaluate allergic airway diseases such as asthma because they are rapidly sensitized Small Molecule Compound Library to aerolized ovalbumin without the need for intraperitoneal injections. These results in an airway response to challenge similar to that of asthmatic phenotypes, including a robust bronchoconstriction that is lacking in other rodents (Bice et al., 2000, Wenzel and Holgate, 2006 and Zosky and Sly, 2007). In addition, the pharmacological responses of guinea pig airways are very

similar to those of humans in comparison to any other animal model (Ressmeyer et al., 2006). Therefore, the aim of this study was to evaluate the effects of aerobic exercise on airway inflammation and remodeling in a model of chronic allergic airway inflammation in guinea pigs. This

study was approved by the review board for human and animal studies of the School of Medicine of the University of São Paulo (São Paulo, Brazil). All of the animals in the study received human care in compliance with the AZD8055 nmr Guide for the Care and Use of Laboratory Animals (NHI publication 85-23, revised 1985). Thirty male Hartley guinea pigs (250–280 g) were divided into four groups: Control (non-exercised and non-sensitized; C group; n = 7); Aerobic Exercise (non-sensitized and aerobically exercised; AE group; n = 7); Ovalbumin (OVA-sensitized and non-exercised; OVA group; n = 8) and OVA + AE (sensitized and aerobically exercised; OVA + AE group; n = 8). Animals were placed oxyclozanide in an acrylic box (30 cm × 15 cm × 20 cm) coupled to an ultrasonic nebulizer (Soniclear, SP, Brazil) and received seven sessions of OVA inhalation solution diluted in sterile saline (NaCl 0.9%). The Control and AE groups (non-sensitized) received the same number of inhalation sessions with sterile saline. All

inhalation sessions lasted 15 min or until the animal displayed respiratory distress (sneezing, coryza, cough or retraction of the thoracic wall) as previously described. OVA inhalation was performed for 8 weeks (3×/week) with increasing concentrations (from 1 to 20 mg/ml) to avoid OVA tolerance (Tiberio et al., 1997). Animals were initially adapted to the treadmill for 5 days (5 min, 8% inclination, 0.3 km/h). Next, a maximal exercise treadmill test was performed to establish the intensity of AE training (low intensity corresponded to 50% of the maximal speed). The maximal exercise treadmill test consisted of a 5-min warm-up (8% inclination, 0.3 km/h) followed by a gradual increase in treadmill speed (0.3 km/h every 3 min). The maximal exercise capacity was considered to be the maximal speed that animals were able to run after receiving 10 mechanical stimuli as previously described (Vieira et al., 2007). The speed of the AE was calculated as the average of the maximal speed achieved for each animal group in the maximal exercise treadmill test.