New findings r What is the topic for this review?During the exercise recovery period, the combination of centrally mediated decreases in sympathetic nerve activity with a reduced signal transduction from sympathetic nerve activation into vasoconstriction, as well as local vasodilator mechanisms, contributes to the fall in arterial blood pressure seen after exercise. r What advances does it highlight? Important findings from recent studies include the recognition that skeletal muscle afferents may play a primary role in postexercise resetting of the baroreflex via discrete receptor changes within the nucleus tractus solitarii and that sustained postexercise vasodilatation of the previously active skeletal muscle is primarily the result of histamine H 1 and H 2 receptor activation.A single bout of aerobic exercise produces a postexercise hypotension associated with a sustained postexercise vasodilatation of the previously exercised muscle. Work over the last few years has determined key pathways for the obligatory components of postexercise hypotension and sustained postexercise vasodilatation and points the way to possible benefits that may result from these robust responses. During the exercise recovery period, the combination of centrally mediated decreases in sympathetic nerve activity with a reduced signal transduction from sympathetic nerve activation into vasoconstriction, as well as local vasodilator mechanisms, contributes to the fall in arterial blood pressure seen after exercise. Important findings from recent studies include the recognition that skeletal muscle afferents may play a primary role in postexercise resetting of the baroreflex via discrete receptor changes within the nucleus tractus solitarii and that sustained postexercise vasodilatation of the previously active skeletal muscle is primarily the result of histamine H 1 and H 2 receptor activation. Future research directions include further exploration of the potential benefits of these changes in the longer term adaptations associated with exercise training, as well as investigation of how the recovery from exercise may provide windows of opportunity for targeted interventions in patients with hypertension and diabetes.

Altered systemic hemodynamics following exercise can compromise cerebral perfusion and result in syncope. As the Wingate anaerobic test often induces pre-syncope, we hypothesized that a modified Wingate test could form the basis of a novel model for the study of post-exercise syncope and a test-bed for potential countermeasures. Along these lines, breathing through an impedance threshold device has been shown to increase tolerance to hypovolemia, and could prove beneficial in the setting of post-exercise syncope. Therefore, we hypothesized that a modified Wingate test followed by head-up tilt would produce post-exercise syncope, and that breathing through an impedance threshold device (countermeasure) would prevent post-exercise syncope in healthy individuals. Nineteen recreationally active men and women underwent a 60° head-up tilt during recovery from the Wingate test while arterial pressure, heart rate, end-tidal CO2, and cerebral tissue oxygenation were measured on a control and countermeasure day. The duration of tolerable tilt was increased by a median time of 3 min 48 sec with countermeasure compared to control (P < 0.05) and completion of the tilt test increased from 42% to 67% with countermeasure. During the tilt, mean arterial pressure was greater (108.0 ± 4.1 vs.100.4 ± 2.4 mmHg; P < 0.05) with countermeasure compared to control. These data suggest that the Wingate syncope test produces a high incidence of pre-syncope which is sensitive to countermeasures such as inspiratory impedance.

Following exercise, a decrease in central blood volume can compromise cerebral perfusion and result in syncope. Breathing through an impedance threshold device (ITD) has been shown to restore central blood volume under several hypovolemic conditions. Therefore, we hypothesized that ITD breathing would prevent post‐exercise syncope following a 1‐min Wingate test. We studied 19 recreationally active men and women, subjecting them to a 60° head‐up tilt during recovery from the Wingate test. Measurements included arterial pressure, heart rate, end‐tidal PCO2, and cerebral tissue oxygenation index on a control and breathing intervention (ITD) day. Mean arterial pressure was greater during the last 30 sec of head‐up tilt on the ITD day compared to the control day (97.1 ± 2.1 vs 91.9 ± 1.8 mm Hg; P < 0.05). Cerebral tissue oxygenation tended to be greater during the last 30 sec of head‐up tilt on the ITD day compared to the control day (71.8 ± 0.6 vs 70.7 ± 0.8 mm Hg; P = 0.07). The length of head‐up tilt was compared between study days for each subject. When contrasting this difference, the ITD lengthened the median tilt time by 7 min 20 sec (P = 0.20). These data suggest that the ITD may be beneficial in preventing post‐exercise syncope induced by a Wingate exercise model.

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