Heart rate during exercise with leg vascular occlusion in spinal cord-injured humans

Feed-forward and feedback mechanisms are both important for control of the heart rate response to muscular exercise, but their origin and relative importance remain inadequately understood. To evaluate whether humoral mechanisms are of importance, the heart rate response to electrically induced cycling was studied in participants with spinal cord injury (SCI) and compared with that elicited during volitional cycling in able-bodied persons (C). During voluntary exercise at an oxygen uptake of ∼1 l/min, heart rate increased from 66 ± 4 to 86 ± 4 (SE) beats/min in seven C, and during electrically induced exercise at a similar oxygen uptake in SCI it increased from 73 ± 3 to 110 ± 8 beats/min. In contrast, blood pressure increased only in C (from 88 ± 3 to 99 ± 4 mmHg), confirming that, during exercise, blood pressure control is dominated by peripheral neural feedback mechanisms. With vascular occlusion of the legs, the exercise-induced increase in heart rate was reduced or even eliminated in the electrically stimulated SCI. For C, heart rate tended to be lower than during exercise with free circulation to the legs. Release of the cuff elevated heart rate only in SCI. These data suggest that humoral feedback is of importance for the heart rate response to exercise and especially so when influence from the central nervous system and peripheral neural feedback from the working muscles are impaired or eliminated during electrically induced exercise in individuals with SCI. </jats:p

Cerebral Blood Flow Velocity during High Volume Plasmapheresis in Fulminant Hepatic Failure

High volume plasmapheresis has previousy been found to improve neurological statuses in patients with fulminant hepatic failure. We investigated the relationship between the neurological status and cerebral blood flow velocity (Vmean) during high volume plasmapheresis in 18 consecutive patients (ten females and eight males) with fulminant hepatic failure, with a mean age of 43 (range 9 to 57) years. The mean arterial pressure (MAP) and intracranial pressure (ICP) were also recorded. A total of 16% of body weight was exchanged with fresh frozen plasma per day. Thirty-six plasma exchanges were performed with a median of 2 (range 1 to 8) per patient. Eleven of the patients survived (61%), nine after liver transplantation. Following the first high volume plasmapheresis, the coma score improved from 6 (1-8) to 2 (0-8) (p &lt; 0.05), Vmean increased from 40 (14-152) to 62 (16-186) cm S−1 (p &lt; 0.05), and MAP from 72 (35-118) to 94 (47-138) mmHg (p &lt; 0.05). The intracranial pressure (ICP) was monitored and remained unchanged in nine patients whereas the cerebral perfusion pressure (MAP minus ICP) increased in the surviving group from 55 (40-74) to 80 (50-91) mmHg (p = 0.07) in contrast to no changes in the non survival group. In conclusion this study suggests that the neurological status, may improve during high volume plasmapheresis as MAP and Vmean increase the cerebral oxygen delivery. </jats:p

Differential responses to sympathetic stimulation in the cerebral and brachial circulations during rhythmic handgrip exercise in humans

The sympathetic neural regulation of the cerebral circulation remains controversial. The purpose of the present study was to determine how exercise modulates the simultaneous responsiveness of the cerebral and brachial circulations to 'endogenous' sympathetic activation (cold pressor test). In nine healthy subjects, heart rate (HR) and mean arterial blood pressure (MAP) were continuously measured during cold pressor tests (4 degrees C water) conducted at rest and during randomized bouts of rhythmic handgrip of 10, 25 and 40% of maximal voluntary contraction. Doppler ultrasound was used to examine brachial artery blood flow (FBF) and middle cerebral artery (MCA) mean blood velocity (V-mean), and indices of vascular conductance were calculated for the brachial artery (forearm vascular conductance, FVC) and MCA (cerebral vascular conductance index, CVCi). End-tidal P-co2 (P-ET,P-CO2) was evaluated on a breath-by-breath basis. Handgrip evoked increases in HR, FBF, FVC and MCA V-mean (P &lt;0.05 versus rest), while MAP and CVCi were unchanged and P-ET,P-CO2 fell slightly (P &lt;0.05 versus rest). Increases in MAP and HR during the cold pressor test were similar at rest and during all handgrip trials. Forearm vascular conductance was markedly reduced with the cold pressor test at rest (-45 +/- 8%), but this vasoconstrictor effect was progressively attenuated with increasing exercise intensity (FVC -17 +/- 3% during exercise at 40% of maximal voluntary contraction; P &lt;0.05). In contrast, the small reduction in CVCi with cold pressor test was similar at rest and during handgrip (approximately -5%). Our data indicate that while the marked vasoconstrictor responses to sympathetic activation in the skeletal muscle vasculature are blunted by handgrip exercise, the modest cerebrovascular responses to a cold pressor test remain unchanged

Prefrontal and motor cortex EEG responses and their relationship to ventilatory thresholds during exhaustive incremental exercise

Purpose: The purpose of this study was to measure the EEG response in the prefrontal cortex (PFC) and motor cortex (MC) during incremental exercise and align these responses with ventilatory parameters. Methods: The EEG activity at the motor (MC) and frontal cortices was measured during an incremental exercise test (IET) in 11 cyclists (peak oxygen uptake (V˙O2peak) 4.1 ± 0.74 (SD) L min−1). EEG power spectral densities were calculated for alpha slow (αS) (8–10 Hz), alpha fast, (αF) (10–13 Hz), Beta (β) (13–30 Hz), and Gamma (γ) (30–40 Hz). EEG data were calculated as % change from eyes open (EO) baseline and a repeated measures analysis of variance (ANOVA) was performed on regions of interest (ROI), time and bandwidth. Results: All EEG activity increased from 50 % V˙O2peak to ventilatory threshold (VT) (P = 0.045) and respiratory compensation point (RCP) (P = 0.019) and decreased from RCP to end of exercise (END) (P = 0.04). Significant differences between regions were found at the VLPFC and MC for both αS and αF. αS and αF increased from 50 % V˙O2peak to RCP (14.9 ± 10.2 to 23.8 ± 15.5 and 18.9 ± 10.6 to 26.12 ± 12.7, respectively) and then decreased to END (23.8 ± 15.5 to 14.4 ± 10.3 and 26.1 ± 12.7, to 17.7 ± 8.8, respectively) (P < 0.01) and concomitantly only decreased significantly in MC in αF from VT to END (P < 0.05). Conclusion: There is a decline in the EEG response to exercise in the PFC following the RCP, whilst alpha activity in the MC is preferentially maintained; therefore, changes within the PFC appear to play a role in exercise termination