No abstract

The aim was to investigate the effects of low-load resistant training combined with vascular occlusion or normobaric hypoxic exposure, on neuromuscular function. In a randomised controlled trial, well-trained athletes took part in a 5-week training of knee flexor/extensor muscles in which low-load resistant exercise (20% of one repetition maximum, 1-RM) was combined with either (1) an occlusion pressure of approximately 230 mmHg (KT, n = 10), (2) hypoxic air to generate an arterial blood oxygen saturation of ~80% (HT, n = 10), or (3) with no additional stimulus (CT, n = 10). Before and after training, participants completed the following tests: 3-s maximal voluntary contraction (MVC₃), 30-s MVC, and an endurance test (maximal number of repetitions at 20% 1-RM, Reps₂₀). Electromyographic activity (root mean square, RMS) was measured during tests and the cross-sectional area (CSA) of the quadriceps and hamstrings was measured pre- and post-training. Relative to CT, KT, and HT showed likely increases in MVC₃ (11.0 ± 11.9 and 15.0 ± 13.1%, mean ± 90% confidence interval), MVC₃₀ (10.2 ± 9.0 and 18.3 ± 17.4%), and Reps₂₀ (28.9 ± 23.7 and 23.3 ± 24.0%). Compared to the CT group, CSA increased in the KT (7.6 ± 5.8) and HT groups (5.3 ± 3.0). KT had a large effect on RMS during MVC₃, compared to CT (effect size 0.8) and HT (effect size 0.8). We suspect hypoxic conditions created within the muscles during vascular occlusion and hypoxic training may play a key role in these performance enhancements.

We have previously described two patients with a congenital defect in neutrophil function characterized by an inability to form pus. The patients' neutrophils lack a membrane glycoprotein of mol wt 150,000 daltons (GP-150) on analysis by SDS-PAGE. This glycoprotein is part of a membrane antigen complex recognized by the murine monoclonal antibody (MoAb) 60.3. Addition of MoAb 60.3 to normal neutrophils produces defects in chemotaxis and phagocytosis in vitro similar to those observed in the patients. Since neutrophil adherence to vascular endothelium is prerequisite to neutrophil emigration in vivo, we examined the interaction of the patients' neutrophils and normal neutrophils treated with MoAb 60.3 with cultured endothelium. Adherence was determined as the percentage of 51Cr-labeled purified peripheral blood neutrophils which remained adherent to plastic wells or endothelial monolayers after a 45-minute incubation at 37 degrees C. The percentage of neutrophils from patient 1 remaining adherent to uncoated, fibronectin-coated, or laminin-coated plastic was similar to that observed in normal neutrophils (55% to 84% adherence with normal neutrophils v 73% to 78% adherence with the patient's neutrophils and 63% to 82% adherence with MoAb 60.3-treated normal neutrophils). The adherence of the neutrophils from patient 1 and MoAb 60.3-treated normal neutrophils to human or bovine endothelium in serum-free medium was also not significantly different from that observed in normal neutrophils (less than 10% adherence with normal, MoAb 60.3-treated, and patient neutrophils). In medium containing 10% autologous or heterologous human plasma, however, the adherence of neutrophils from patient 1 or MoAb 60.3-treated normal neutrophils to endothelial monolayers was significantly reduced (35% +/- 7% of normal neutrophils in seven experiments). Although phorbol myristate acetate (PMA) (10 ng/mL) and calcium ionophore A23187 (10(-5) mol/L) markedly increased the adherence of normal neutrophils to endothelial monolayers in serum- free medium (40% to 85% adherence), neither agent increased the adherence of the neutrophils from patient 1 or normal neutrophils treated with MoAb 60.3 (less than 5% adherence). The adherence of PMA- activated neutrophils from patient 2 to endothelial monolayers was also markedly decreased when compared with that of normal neutrophils. Postsecretory cell-free supernatants from PMA-activated normal neutrophils failed to augment adherence of neutrophils from patient 1 (less than 5% adherence).(ABSTRACT TRUNCATED AT 400 WORDS)

Although it is well established that patients with cervical spinal cord injury are prone to acute, marked, hypertensive episodes, i.e., autonomic hyperreflexia, the specific mechanisms mediating this sometimes-fatal phenomenon are not completely understood. In this report, we describe the preparation and characterization of a rat model of chronic cervical spinal cord injury and autonomic hyperreflexia. Adult male Sprague-Dawley rats were chronically instrumented with arterial, venous, and gastric catheters. Beginning the first day after a complete cervical spinal transection (CST) and continuing for 1 wk, acute hypertensive responses to a modest increase of urinary bladder pressure (0-20 mmHg) were studied. Mean arterial pressure increased 25.9 +/- 4.8 mmHg during bladder distension the first day after CST. This response was not significantly different 3, 5, and 7 days after CST (overall average = 18.0 +/- 2.3 mmHg). The pressor response to bladder distension was completely abolished by intravesical lidocaine and autonomic ganglionic blockade (atropine + hexamethonium). Responses to bladder distension were not observed after the administration of chloralose anesthesia. We conclude that after cervical spinal transection the rat exhibits autonomic hyperreflexia similar to that seen in humans with spinal injury. Furthermore, autonomic hyperreflexia is completely established within 24 h after CST in the rat. Finally, some spinal autonomic reflexes are suppressed by chloralose anesthesia in the rat.

We measured renal, splenogastric, and lumbar multiunit sympathetic activities in chloralose-anesthetized, paralyzed, and artificially respired Sprague-Dawley rats. Acute spinal transection reduced arterial pressure and lumbar sympathetic activity. However, renal and splenogastric activities were doubled after transection. We conclude that spinal systems exist in the rat that are capable of maintaining renal and splenogastric, but not lumbar, sympathetic activities after spinal transection. Cross-correlation and power spectral analysis of simultaneously recorded sympathetic activities indicated that renal and splenogastric activities often, but not always, shared periodicities near the respiratory rate. These shared periodicities were responsible for high correlations between renal and splenogastric activities. After spinal transection, the shared periodicities usually disappeared, and correlations were reduced. Renal and lumbar activities were rarely strongly correlated, and they rarely shared major periodicities. We conclude that brain stem systems often provide synchronization of abdominal sympathetic activities. However, these activities can be independently generated in both intact and spinally transected rats.

dall. Heart rate-arterial blood pressure relationship in conscious rat before vs. after spinal cord transection. Am J Physiol Regul Integr Comp Physiol 283: R748-R756, 2002. First published April 18, 2002 10.1152/ajpregu.00003. 2002This experiment quantified the initial disruption and subsequent adaptation of the blood pressure (BP)-heart rate (HR) relationship after spinal cord transection (SCT). BP and HR were recorded for 4 h via an implanted catheter in neurally intact, unanesthetized rats. The animals were then anesthetized, and their spinal cords were severed at T1-T2 (n ϭ 5) or T4-T5 (n ϭ 6) or sham lesioned (n ϭ 4). BP was recorded for 4 h daily over the ensuing 6 days. The neurally intact rat showed a positive cross correlation, with HR leading BP at the peak by 1.8 Ϯ 0.8 (SD) s. The cross correlation in unanesthetized rats (n ϭ 2) under neuromuscular blockade was also positive, with HR leading. After SCT at T1-T2, the cross correlation became negative, with BP leading HR, and did not change during the next 6 days. The cross correlation also became negative 1-3 days after SCT at T4-T5, but in four rats by day 6 and thereafter the cross correlation progressively reverted to a positive value. We propose that the positive cross correlation with HR leading BP in the intact rat results from an open-loop control that depends on intact supraspinal input to sympathetic preganglionic neurons in the spinal cord. After descending sympathetic pathways were severed at T1-T2, the intact vagal pathway to the sinoatrial node dominated BP regulation via the baroreflex. We suggest that reestablishment of the positive correlation after SCT at T4-T5 was attributable to the surviving sympathetic outflow to the heart and upper vasculature reasserting some effective function, perhaps in association with decreased spinal sympathetic hyperreflexia. The HR-BP cross correlation may index progression of sympathetic dysfunction in pathological processes. sympathetic; parasympathetic; dysautonomia; cross correlation; baroreflex SHORT-TERM STABILITY of arterial blood pressure (BP) is achieved in large part by appropriate adjustments in sympathetic and parasympathetic outflow from the central nervous system to the cardiovascular effector mechanisms. Many of these neuroregulatory mechanisms, including the baroreflex, are integrated within the medulla oblongata or within more rostral regions of the brain. Spinal cord transection (SCT), depending on the level, severs the descending sympathetic pathways targeted to the heart and arterial resistance vessels. Such injury compromises BP stability (for review, see Ref. 15) and would be expected to manifest itself in alterations in the relationship between changes in BP and heart rate (HR).The precise nature and degree of the changes in the integrity of BP stability after SCT depend on the site and severity of the injury (9). For instance, complete SCT at T 1 in rat virtually disconnects descending supraspinal sympathetic outflow from all effectors, whereas SCT at T 5 preserves most of the ...

The present study was conducted to determine whether sympathetic vasoconstrictor activity is a determinant of mean arterial pressure (MAP) hours and days after cervical spinal transection (CST) in unanesthetized rats. MAP on the 2 days before CST was 107.2 +/- 3.6 and 103.3 +/- 3.0 mmHg, respectively, and fell to 77.7 +/- 1.1 mmHg on day 1 after CST. MAP returned to control levels over the course of the study and, by day 9 after CST, was not statistically different from control (98.6 +/- 3.4 mmHg). Neither autonomic ganglionic blockade nor alpha-adrenergic blockade affected MAP the 1st day after CST. Similarly, alpha-adrenergic blockade was without effect on days 3, 5, and 7 after CST. Administration of a vasopressin V1-antagonist had no effect on MAP on day 1 or day 8 after CST. However, blockade of angiotensin-converting enzyme with captopril decreased arterial pressure both on day 1 (-22.1 +/- 2.6 mmHg) and day 8 (-23.3 +/- 2.9 mmHg) after CST. We conclude that neither sympathetic nor vasopressin vasoconstrictor activity affected MAP within the 1st wk after CST. Although the vasoconstrictor actions of angiotensin II were important, these effects were not responsible for the normalization of MAP observed after CST.

A B S T R A C T We have developed