TY - CONF
T1 - Interaction of hypoxia and vascular occlusion on cardiorespiratory responses during exercise
AU - Keller-Ross, Manda L
PY - 2018/11/27
Y1 - 2018/11/27
N2 - 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% FiO2 and normoxia, 21% FiO2). 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 (VE) 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 VE, albeit via different mechanisms. While hypoxia increased tidal volume, vascular occlusion increased respiratory rate.
AB - 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% FiO2 and normoxia, 21% FiO2). 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 (VE) 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 VE, albeit via different mechanisms. While hypoxia increased tidal volume, vascular occlusion increased respiratory rate.
U2 - https://doi.org/10.1002/tsm2.60
DO - https://doi.org/10.1002/tsm2.60
M3 - Paper
ER -