Fipronil contamination impairs cardiorespiratory control of rainbow trout during aerobic exercise

Fipronil is a widely detected phenylpyrazole insecticide in aquatic ecosystems that acts as a GABA receptor antagonist in arthropods, but its effects on vertebrate cardiorespiratory physiology are not well understood. In this study, we investigated whether environmentally relevant concentrations of fipronil (0.5 μg l^-1, 96 h) impair the cardiovascular and ventilatory responses of rainbow trout (Oncorhynchus mykiss) during aerobic exercise. Using dorsal aortic and buccal cannulations, we continuously recorded heart rate (f_H), mean arterial pressure (MAP), ventilatory rate (f_V) and amplitude (V_AMP) before and after pharmacological blockades (autonomic blockades using atropine and propranolol, and a GABAergic blockade to simulate the effects of fipronil with bicuculline). Exposure to fipronil induced significant tachycardia (∼35%), without affecting MAP or f_V. It also increased intrinsic heart rate, even after double autonomic blockade, suggesting direct effects on cardiomyocytes. During exercise, contaminated fish exhibited impaired ventilatory amplitude and autonomic imbalance characterized by vagal withdrawal and sympathetic overdrive. Interestingly, the GABA antagonist bicuculline reproduced the tachycardic pattern observed in contaminated fish, suggesting that fipronil acts through GABAergic disruption of the neural centers involved in cardiac control. These sublethal impairments in autonomic regulation likely reduce the aerobic capacity and ecological resilience of fish in contaminated habitats. ENVIRONMENTAL IMPACT STATEMENT: This study demonstrates that acute exposure to the globally prevalent insecticide fipronil, at an environmentally relevant concentration, causes significant sublethal dysfunction in the neurophysiological control of cardiorespiratory systems in rainbow trout. By disrupting GABAergic signaling, fipronil compromises the integrated cardiovascular and ventilatory responses essential for sustaining aerobic exercise. These findings reveal a critical pathway through which pesticide pollution can impair physiological performance, thereby reducing the fitness and adaptive resilience of fish populations facing concurrent anthropogenic stressors such as climate change and habitat degradation. The results underscore the need to consider subtle, neurotoxic mechanisms in environmental risk assessments for aquatic ecosystems.