Proprioceptive sensory feedback is utilized by the central nervous system for conscious appreciation of the position and movement of the body and limbs. In patients with the hypermobility syndrome (HMS), it has been suggested that there is alteration of proprioceptive acuity. Proprioceptive performance of the knee joint was investigated in 10 female subjects who suffered from HMS using a threshold detection paradigm (accurate determination of the onset and direction of knee joint displacement at constant angular velocity). Compared to age- and sex-matched controls, HMS subjects showed significantly higher detection levels at starting knee flexion angles of 30 degrees P < 0.001) and 5 degrees (P < 0.001). Control subjects showed no significant difference in threshold acuity between the sexes (at 5 degrees P = 0.63, at 30 degrees P = 0.48). The increased acuity in proprioception observed towards full extension in the control population (P < 0.001) was absent in the HMS subjects (P = 0.596). Findings reported here suggest that HMS subjects have poorer proprioceptive feedback than controls. Reduced sensory feedback may lead to biomechanically unsound limb positions being adopted. Such a mechanism may allow acceleration of degenerative joint conditions, and may account for the increased prevalence of such conditions seen with HMS subjects.

Electrical stimulation of the cut distal end of the posterior articular nerve (p.a.n.) of the cat knee joint resulted in significant extravasation of plasma proteins and erythrocytes into the synovial cavity of the knee. This effect was mediated by group IV afferents (C fibres) since stimulation of p.a.n. suprathreshold for group II or III afferents but subthreshold for group IV afferents did not produce extravasation. Unmyelinated sympathetic efferent fibres in the joint nerve did not contribute to the extravasation and were responsible for a diminution of this response as shown by the enhanced extravasation occurring after adrenergic blockade. Plasma and erythrocyte extravasation was mediated by afferents containing substance P (SP), as demonstrated by the reversible abolition of extravasation when the substance P antagonist (D‐Pro4,D‐Trp7,9,10)‐SP (4‐11) was injected into the synovial cavity. In some animals it was observed that electrical stimulation of the cut distal end of p.a.n. in one limb resulted in extravasation in the contralateral knee joint. It is suggested that articular C fibre afferents could make a significant neurogenic contribution to the initiation or maintenance of inflammatory joint disease.

SUMMARYBoth neurogenic influences and the regulatory neuropeptide substance P (SP) have been implicated in the development of joint inflammation. Using the laser Doppler perfusion imaging technique to quantify relative changes in joint blood flow, the effects of nerve stimulation and topical SP application were examined in normal and chronically inflamed rat knee joints. Synovial inflammation was induced by unilateral intra-articular injection of Freund's complete adjuvant and experiments were carried out 1 week and 3 weeks later. Normal knees showed a frequency-dependent vasoconstriction in response to saphenous nerve stimulation over the range of 5-30 Hz and a dose-dependent vasodilatation in response to SP administration. These vasoactive responses were completely abolished in the chronically inflamed knee joint, the abolition persisting throughout the investigation. Since articular cartilage is critically dependent on synovial fluid formation for its nutrition, loss of neurovascular control of the synovial microcirculation could contribute to the degenerative changes that commonly accompany chronic inflammatory joint diseases.

Structured AbstractObjectives -We investigated whether a session of prior exercise could ameliorate postprandial endothelial dysfunction.Background -Endothelial function is impaired following fat ingestion and this may be related to rises in triglyceride concentrations. Exercise reduces postprandial triglyceride concentrations.Methods -Ten lean (waist <90cm) and 10 centrally obese (waist >100cm) middle-aged men each underwent two oral fat tolerance tests (blood taken fasting and for eight hours after a high-fat meal containing 80g fat and 70g carbohydrate). On the afternoon before one test, subjects performed a 90-minute treadmill walk (exercise); no exercise was performed before the control test. Endothelium-dependent and -independent microvascular function was assessed using laser Doppler imaging in the fasted state and at two hourly intervals during the eight-hour postprandial period.Results -Exercise reduced both fasting and postprandial triglyceride concentrations by 25% in both the lean and centrally obese groups (p<0.0005). For all subjects taken together, exercise improved fasting endothelium-dependent function by 25% (p<0.05) and, although there was a significant postprandial decrease in both endotheliumdependent and -independent function in both the control and exercise trials (p<0.01), postprandial endothelium-dependent and -independent function were 15% and 20% higher, respectively, in the exercise trial than the control trial (both p<0.05).Conclusions -A session of prior exercise improves fasting and postprandial vascular function in middle-aged men. This may be one mechanism by which exercise influences cardiovascular risk. KeywordsEndothelial function, exercise, lipids, postprandial JACC061504-1955RR 3 Condensed AbstractEndothelial function is impaired following fat ingestion. We investigated whether a session of prior exercise could ameliorate postprandial endothelial dysfunction in 20 middle-aged men. Subjects performed two oral fat tolerance tests: one on the day following a 90-minute treadmill walk, the other after no exercise. Exercise improved fasting endothelial function by 25% and postprandial endothelial function by 15% (both p<0.05). This may be one mechanism by which exercise influences cardiovascular risk. More recent study has focused on non-lipid disturbances occurring in the postprandial state. It is now evident that systemic inflammation is increased (2,3) and that endothelial function is impaired (4,5) postprandially, with some studies reporting that the postprandial decrement in endothelial function is proportional to the postprandial triglyceride rise (4,5). As endothelial dysfunction and inflammation are central to atherogenic progression (6), it is likely that these transient postprandial changes, repeated on a daily basis, have implications for long-term risk of vascular disease. There is now a large body of evidence indicating that a single session of moderate exercise can reduce subsequent postprandial lipemia by ~20-25% (7). Thus, given the reported relationship between...