Physical exercise performance in temperate and warm environments is decreased by an impaired arterial baroreflex.

The present study aimed to investigate whether running performance in different environments is dependent on intact arterial baroreceptor reflexes. We also assessed the exercise-induced cardiovascular and thermoregulatory responses in animals lacking arterial baroafferent signals. To accomplish these goals, male Wistar rats were subjected to sinoaortic denervation (SAD) or sham surgery (SHAM) and had a catheter implanted into the ascending aorta to record arterial pressure and a telemetry sensor implanted in the abdominal cavity to record core temperature. After recovering from these surgeries, the animals were subjected to constant- or incremental-speed exercises performed until the voluntary interruption of effort under temperate (25° C) and warm (35° C) conditions. During the constant-speed exercises, the running time until the rats were fatigued was shorter in SAD rats in both environments. Although the core temperature was not significantly different between the groups, tail skin temperature was higher in SAD rats under temperate conditions. The denervated rats also displayed exaggerated increases in blood pressure and double product compared with the SHAM rats; in particular, in the warm environment, these exaggerated cardiovascular responses in the SAD rats persisted until they were fatigued. These SAD-mediated changes occurred in parallel with increased variability in the very low and low components of the systolic arterial pressure power spectrum. The running performance was also affected by SAD during the incremental-speed exercises, with the maximal speed attained being decreased by approximately 20% in both environments. Furthermore, at the maximal power output tolerated during the incremental exercises, the mean arterial pressure, heart rate and double product were exaggerated in the SAD relative to SHAM rats. In conclusion, the chronic absence of the arterial baroafferents accelerates exercise fatigue in temperate and warm environments. Our findings also suggest that an augmented cardiovascular strain accounted for the early interruption of exercise in the SAD rats.

Excitatory amino acid receptors in the dorsomedial hypothalamus are involved in the cardiovascular and behavioural chemoreflex responses.

The present study investigated the role of the dorsomedial hypothalamus (DMH) on cardiovascular and behavioural responses of chemoreflex activation in conscious rats. The arterial chemoreflex was activated by potassium cyanide (KCN, 40 µg, i.v.) before and after bilateral microinjection of lidocaine (2%) or kynurenic acid (2.7 nmol) into the DMH. Locomotor activity was measured to assess the chemoreflex behavioural response. Bilateral microinjection of lidocaine into the DMH produced a significant reduction in the pressor response induced by chemoreflex activation (+51 ± 4 versus +34 ± 5 mmHg, n = 5, P < 0.05). A similar reduction in the pressor chemoreflex response was also observed after microinjection of kynurenic acid into the DMH (+50 ± 3 versus +22 ± 5 mmHg, n = 6, P < 0.05). Strikingly, the behaviour/locomotor activity induced by chemoreflex activation was virtually abolished after blockade of excitatory amino acid receptors in the DMH with kynurenic acid (44 ± 6 versus 5 ± 4 cm, n = 6, P < 0.05). There was no correlation between the reduction in pressor and behavioural chemoreflex responses (r = -0.186, P > 0.05). The bradycardic response of the chemoreflex was not altered by lidocaine or kynurenic acid microinjected into the DMH. These results strongly suggest that the excitatory amino acid receptors in the DMH are essential for full expression of the behavioural response of the chemoreflex and participate, at least in part, in the integration of the pressor response of the chemoreflex in conscious rats.