The effect of ageing in spinal cord injured humans on the blood pressure and heart rate responses during fatiguing isometric exercise

2002 ◽  
Vol 86 (6) ◽  
pp. 479-486 ◽  
Author(s):  
Scott Petrofsky ◽  
Michael Laymon
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Isometric Exercise ◽  
Spinal Cord Injured

Diurnal Blood Pressure Variation in Quadriplegic Chronic Spinal Cord Injury Patients

1991 ◽  
Vol 80 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Henry Krum ◽  
William J. Louis ◽  
Douglas J. Brown ◽  
Graham P. Jackman ◽  
Laurence G. Howes
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Ambulatory Monitoring ◽  
Pressure Variation ◽  
Night Time ◽  
Cord Injury ◽  
Blood Pressure Variation ◽  
Neurologically Intact

1. Measurement of blood pressure and heart rate over a 24 h period was peformed in 10 quadriplegic spinal cord injury patients and 10 immobilized, neurologically intact orthopaedic subjects by using the Spacelabs 90207 automated ambulatory monitoring system. 2. Systolic and diastolic blood pressure fell significantly at night in orthopaedic subjects but not in quadriplegic patients, and night-time blood pressures were similar in both groups. 3. Cumulative summation of differences from a reference value (cusum analysis) confirmed a markedly diminished diurnal blood pressure variation in the quadriplegic patients. 4. These findings could not be accounted for on the basis of blood pressure variations during chronic postural change. 5. Heart rate fell significantly at night in both groups. 6. The findings suggest that the increase in blood pressure during waking hours in neurologically intact subjects is a consequence of a diurnal variation in sympathetic activity (absent in quadriplegic patients with sympathetic decentralization) which is independent of changes in physical activity.

Effects of spinal cord transection on sympathetic discharge in decerebrate-unanesthetized cats

1989 ◽  
Vol 257 (6) ◽  
pp. R1506-R1511 ◽  
Author(s):  
L. C. Weaver ◽  
R. D. Stein
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spectral Analysis ◽  
Spinal Cord Transection ◽  
Renal Nerves ◽  
Frequency Range ◽  
Renal Nerve ◽  
Sympathetic Discharge ◽  
Nerve Discharge

Previous experiments in our laboratory have shown that discharge of splenic, mesenteric, and splanchnic nerves is well maintained after spinal cord transection in chloralose-anesthetized cats (8, 9, 11). The primary purpose of this investigation was to determine if maintained sympathetic discharge could be observed after spinal transection in the absence of chloralose anesthesia. In cats anesthetized with alphaxalone-alphadolone, changes in splanchnic discharge, blood pressure, and heart rate caused by decerebration and removal of the forebrain were observed. This procedure decreased blood pressure, increased heart rate, and had no immediate effect on sympathetic discharge or its rhythm (assessed by power density spectral analysis). One hour after decerebration and termination of anesthesia, splanchnic discharge had increased by approximately 36%. Next, effects of spinal cord transection on discharge of splanchnic, mesenteric, and renal nerves were observed in the decerebrate-unanesthetized cats. Splanchnic discharge decreased by 50%, mesenteric nerve discharge was unchanged, and renal nerve discharge decreased by 97%. Therefore, splanchnic nerve discharge was not as well maintained in decerebrate-unanesthetized cats as it had been in chloralose-anesthetized animals, and the remaining splanchnic discharge appeared to affect mesenteric nerves preferentially. Finally, spectral analysis of the splanchnic discharge demonstrated that before cord transection, most of the signal was in the 0- to 6-Hz frequency range, whereas after transection the proportion of signal in this frequency range was significantly reduced and the proportion in higher frequencies (7-25 Hz) was significantly increased. This loss of low-frequency rhythmicity is consistent with findings in our previous studies in chloralose-anesthetized cats.

Forearm endurance training attenuates sympathetic nerve response to isometric handgrip in normal humans

1992 ◽  
Vol 72 (3) ◽  
pp. 1039-1043 ◽  
Author(s):  
V. K. Somers ◽  
K. C. Leo ◽  
R. Shields ◽  
M. Clary ◽  
A. L. Mark
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Endurance Training ◽  
Sympathetic Nerve ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Response ◽  
The Right ◽  
Muscle Chemoreflex

Recent evidence indicates that muscle ischemia and activation of the muscle chemoreflex are the principal stimuli to sympathetic nerve activity (SNA) during isometric exercise. We postulated that physical training would decrease muscle chemoreflex stimulation during isometric exercise and thereby attenuate the SNA response to exercise. We investigated the effects of 6 wk of unilateral handgrip endurance training on the responses to isometric handgrip (IHG: 33% of maximal voluntary contraction maintained for 2 min). In eight normal subjects the right arm underwent exercise training and the left arm sham training. We measured muscle SNA (peroneal nerve), heart rate, and blood pressure during IHG before vs. after endurance training (right arm) and sham training (left arm). Maximum work to fatigue (an index of training efficacy) was increased by 1,146% in the endurance-trained arm and by only 40% in the sham-trained arm. During isometric exercise of the right arm, SNA increased by 111 +/- 27% (SE) before training and by only 38 +/- 9% after training (P less than 0.05). Endurance training did not significantly affect the heart rate and blood pressure responses to IHG. We also measured the SNA response to 2 min of forearm ischemia after IHG in five subjects. Endurance training also attenuated the SNA response to postexercise forearm ischemia (P = 0.057). Sham training did not significantly affect the SNA responses to IHG or forearm ischemia. We conclude that endurance training decreases muscle chemoreflex stimulation during isometric exercise and thereby attenuates the sympathetic nerve response to IHG.

The relationships between exercise intensity, heart rate, and blood pressure during an incremental isometric exercise test

2008 ◽  
Vol 26 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Jonathan D. Wiles ◽  
Simon R. Allum ◽  
Damian A. Coleman ◽  
Ian L. Swaine
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Exercise Intensity ◽  
Exercise Test ◽  
Isometric Exercise

Site of central chemosensitivity in fetal sheep

1975 ◽  
Vol 39 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. H. Jansen ◽  
V. Chernick
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Respiratory Response ◽  
Fetal Sheep ◽  
Central Chemosensitivity ◽  
Cord Clamping ◽  
Chemosensitive Areas ◽  
Ventral Medullary Surface ◽  
Histotoxic Hypoxia

The heart rate, blood pressure, and respiratory response to topically applied cyanide on the ventrolateral medullary surface and upper spinal cord was studied on exteriorized sinaortic-denervated fetal lambs under pentobarbital anesthesia. On all sites tested cyanide produced a rapid increase in heart rate and blood pressure (P smaller than 0.05) which was most pronounced from the area adjacent to the nerve roots IX to XI (mean 32%). Respiratory efforts consisting of 1–8 gasps were induced in half the applications to the medulla but never when the pledgets were applied to the spinal cord. The mean delay to response was 43 s (range 13–102 s). After cautery of the chemosensitive areas, topical application of cyanide failed to stimulate gasping, whereas intravenous cyanide or cord clamping still produced a vigorous respiratory response. It is concluded that sympathetic stimulation of the heart and blood vessels can originate centrally in response to local histotoxic hypoxia of the ventral medulla and upper spinal cord. Furthermore, it is proposed that in the apneic fetus histotoxic hypoxia of the medulla initiates respiration possibly by stimulating a special gasping mechanism which is separate from the respiratory center responsible for rhythmic breathing after birth. The responsible neurons must be located at least 2 mm beneath the ventral medullary surface.

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