The autonomic cardiovascular respiratory (ACR) response to hypoglycemia has been reported in a static and fragmentary fashion and with limited use of cardiovascular variability spectral analysis. To characterize a dynamic and integrative ACR response to hypoglycemia we assessed, in 13 healthy subjects under control, peak hypoglycemia induced by administering 0.2 U/kg of insulin, and recovery conditions, instantaneous 5-min time-courses of: time series of RR intervals (RR), systolic (SP), diastolic (DP) and pulse (PP) pressures, tidal volume (VT) and respiratory frequency (RF) obtained from ECG, arterial pressure (AP) and respiratory (Res) signals; their low-frequency powers (LFRR, LFSP, LFDP, LFPP), their respective central frequencies (CFLFRR, CFLFSP, CFLFDP, CFLFPP), and high-frequency powers (HFRR, HFRes), computed by a time-frequency distribution; baroreflex (BRS) and respiratory sinus arrhythmia (RSAS) sensitivities computed by alpha index and their coherences (cBRS, cRSAS) by a cross-time-frequency distribution. For statistical analysis, 1-min epoch means (EM) of dynamics were obtained. With respect to control, peak hypoglycemia (48±6 mg/100 ml) provoked 1. decreases (p<0.03) in: five EM of HFRR, LFRR, BRS and RSAS dynamics, three EM of CFLFPP and cBRS, two EM of CFLFRR and CFLFSP; 2. increases (p<0.02) in: five EM of SP, DP, PP, VT and RF, three EM of HFRes, two EM of LFSP and LFDP, one EM of LFPP; 3. no change in CFLFDP, RR and cRSAS. Hypoglycemia modifies the basal fluctuating time-courses of ACR measures, specifically eliciting: sympathetic measures powers increase (except LFRR) associated with central frequencies reductions; SP, DP and PP increments, indicating stroke volume elevation; BRS and cBRS decreases allowing AP to rise; vagal activity index and RSAS reductions determining greater RR regularity; and increased pulmonary ventilation. These effects integrate a dynamic mechanism of sympathetic, cardiovascular and respiratory activation, whose consequence is increased cardiac output with greater oxygen content to ameliorate the harmful effects of neuroglycopenia.