Introduction Venous distention via sub-systolic occlusion of the lower limbs may augment ventilation via stimulation of group III/IV afferent neurons. Purpose The purpose of this study was to examine the ventilatory response to graded lower extremity venous occlusion during exercise in healthy adults. Methods Nineteen adults (9 men, 25±5 yr) completed two visits. Visit 1: a maximal cycle ergometry exercise test. Visit 2 included a 30% peak workload cycle exercise with randomized inflations of bilateral thigh pressure tourniquets to 20, 40, 60, 80, 100 mmHg for 2 min each, separated by 2 min of deflation. Three min of cycling occurred prior to cuffing (CTL). Expired minute ventilation (VE), whole body gas exchange, rating of perceived exertion and dyspnea were measured during each session. Results VE increased significantly from the control condition (exercise only, control, CTL) to each occlusion pressure (p<0.05) with the greatest increase at 100 mmHg (CTL to 100 mmHg: 31.5±6.6 to 40.1±10.7 L/min). Respiratory rate (RR) increased as well (CTL to 100 mmHg: 24.8±6.0 to 30.9±11.5 breaths/min, p<0.05, condition effect) with no change in tidal volume (p>0.05). Tidal volume to inspiratory time (VT/TI) increased significantly from the CTL condition to each occlusion pressure (CTL to 100 mmHg: 1.5±0.3 to 1.8±0.4 L/min, p<0.05, all pressures). Dyspnea and RPE increased with all occlusion pressures from CTL exercise (p<0.05, all pressures). Conclusion Our findings suggest that mild-to-moderate venous occlusion of the lower extremity evokes a tachypneic breathing pattern which, in turn, augments VE and perceived breathing effort during exercise.
Background:The interaction of group III/IV afferents and chemoreflex during exercise is critical in healthy adults during high altitude exercise or in clinical populations who experience hypoxia. Purpose: Investigate the cardiorespiratory response to simultaneous vascular occlusion (to activate group III/IV afferents) and hypoxia (to activate chemoreflex) during cycling exercise. Methods: 18 adults (9 women, 25 ± 5 years) attended two sessions. Session 1: maximal cycle ergometry test. Session 2: two 26-minute bouts (randomized between hypoxia, 12.5% FiO 2 and normoxia, 21% FiO 2 ). Participants cycled at 30% of peak workload for 3 minutes (control, CTL) followed by alternating 2 minute periods of bilateral vascular occlusion of the proximal thigh at pressures of 20, 40, 60, 80, 100 mm Hg in a randomized sequence. Results: Ventilation (V E ) increased from CTL to 100 mm Hg during hypoxia (39 ± 9 to 51 ± 16 L/min) and normoxia (31 ± 7 to 39 ± 9 L/min, P < 0.01). Respiratory rate increased with vascular occlusion (P < 0.05) but not hypoxia (P = 0.10). Tidal volume was greater during hypoxia (P < 0.05), with no influence of vascular occlusion (P = 0.40). Mean arterial pressure and heart rate increased more with hypoxia compared with normoxia (P < 0.05). Conclusions: Our findings suggest that vascular occlusion and hypoxia both increase V E , albeit via different mechanisms. While hypoxia increased tidal volume, vascular occlusion increased respiratory rate. K E Y W O R D Scirculatory occlusion, group III and IV muscle afferents, hypoxia, ventilation and blood pressure | 65 KELLER-ROSS Et aL.
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