PURPOSE: This study investigated cardiovascular and hemodynamic responses during the transition from rest to electrical stimulation-induced leg cycling exercise (ES-LCE) in individuals with chronic paraplegia (PARA). METHODS: Ten PARA (T(4)-T(9); ASIA A) participated in this study. Heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), and cardiac output (Q) were measured on a beat-to-beat basis at rest and during the first 60 s of ES-LCE. RESULTS: PARA exhibited two discrete MAP responses during ES-LCE. Those with high thoracic lesions (HIGH: T(4) -T(6), = 5) responded to ES-LCE with a significant rise in MAP (maxdelta 8.3 +/- 3.6 mm Hg), whereas MAP did not exhibit any sustained change from resting values during ES-LCE in those subjects with lower lesions (LOW: T -T, = 5). In HIGH PARA, the immediate increase in MAP corresponded to a decrease in HR (maxdelta 6.8 +/- 3.1 b x min(-1)), which returned toward resting levels by the end of 60 s. In contrast, for LOW PARA there was no change in HR from resting levels during transition to ES-LCE. In both subgroups, SV and Q were not significantly increased during ES-LCE. CONCLUSION: These results suggest that the on-transient responses of MAP during ES-LCE in HIGH PARA elicited reflex changes in HR via the arterial baroreflex, whereas in LOW PARA, an unchanged HR from rest was likely due to a constant MAP during ES-LCE.
PURPOSE: This study investigated cardiovascular and hemodynamic responses during the transition from rest to electrical stimulation-induced leg cycling exercise (ES-LCE) in individuals with chronic paraplegia (PARA). METHODS: Ten PARA (T(4)-T(9); ASIA A) participated in this study. Heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), and cardiac output (Q) were measured on a beat-to-beat basis at rest and during the first 60 s of ES-LCE. RESULTS: PARA exhibited two discrete MAP responses during ES-LCE. Those with high thoracic lesions (HIGH: T(4) -T(6), = 5) responded to ES-LCE with a significant rise in MAP (maxdelta 8.3 +/- 3.6 mm Hg), whereas MAP did not exhibit any sustained change from resting values during ES-LCE in those subjects with lower lesions (LOW: T -T, = 5). In HIGH PARA, the immediate increase in MAP corresponded to a decrease in HR (maxdelta 6.8 +/- 3.1 b x min(-1)), which returned toward resting levels by the end of 60 s. In contrast, for LOW PARA there was no change in HR from resting levels during transition to ES-LCE. In both subgroups, SV and Q were not significantly increased during ES-LCE. CONCLUSION: These results suggest that the on-transient responses of MAP during ES-LCE in HIGH PARA elicited reflex changes in HR via the arterial baroreflex, whereas in LOW PARA, an unchanged HR from rest was likely due to a constant MAP during ES-LCE.