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.