['Sympathetic activation induced by sleep-disordered breathing may contribute to cardiovascular morbidity. However, the apnea-hypopnea index (AHI) excludes respiratory effort-related arousals (RERAs) associated with inspiratory flow limitation without oxygen desaturation. We sought to determine whether RERAs are associated with sympathetic activation.', 'Twenty-five adults (12 males, 13 females) with AHI\u2009<\u200910/h and RERA index >5/h were included in this study. Power spectral density analysis was performed on two non-contiguous 10-min segments containing inspiratory flow limitation and arrhythmia-free electrocardiogram during N2 sleep. One segment contained RERA; the other did not, NO-RERA. Spectral power was described in a low-frequency domain (LF; 0.04-0.15\xa0Hz), primarily sympathetic modulation, and a high frequency domain (HF; 0.15-0.4\xa0Hz), parasympathetic modulation.', 'Analyses of LF and HF powers were made using normalized and absolute values. LF power was greater during RERA compared to NO-RERA (50.3 vs. 30.1\xa0%, p\u2009<\u20090.001) whereas HF power was greater during NO-RERA compared to RERA (69.9 vs. 49.7\xa0%, p\u2009<\u20090.001). The LF/HF ratio was greater during RERA than NO-RERA (1.01 vs. 0.43, p\u2009<\u20090.001). Gender differences emerged using absolute values of power: The percentage increase in LF power during RERA relative to NO-RERA was significantly greater for females than males, 247.6 vs. 31.9\xa0%, respectively (p\u2009<\u20090.02).'] Do respiratory effort-related arousals contribute to sympathetic modulation of heart rate variability?