Unilateral lower limb suspension can cause deep venous thrombosis.
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Biomedical subjects
Publications and source records attributed to Maria T E Hopman.
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STUDY DESIGN: Experimental repeated-measures study. OBJECTIVE: To investigate the effect of different extension forces applied to the palm of the hand on electromyographic (EMG) activity of the wrist extensor muscles during hand gripping. BACKGROUND: Lateral epicondylitis is usually caused by repetitive wrist extension that leads to an overuse injury. The current theory is that the process of lateral epicondylitis begins with an overuse injury that leads to microtearing of the extensor carpi radialis brevis muscle and occasionally the extensor digitorum communis muscle. Use of an external wrist extension force might reduce muscle activity during gripping. METHODS: Muscle activity was measured using surface EMG while subjects gripped at an intensity of 10%, 20%, and 30% of the maximum voluntary contraction force without, and with, an applied external wrist extension force of 1%, 2%, and 3% of maximum voluntary contraction. RESULTS: Applying an extension force to the palm of the hand reduced EMG activity of the extensor muscles at the same strength generation during hand gripping. The muscles with the most significant reduction in EMG level, the extensor carpi radialis brevis and extensor digitorum communis, are those muscles that are most often involved with lateral epicondylitis. CONCLUSIONS: This study shows that an external extension force reduces EMG activity of the wrist extensor muscles during gripping in healthy volunteers. As the extension force increased, a greater reduction in muscle activity was noted.
BACKGROUND: Supraspinal sympathetic control of leg vascular tone is lost in spinal cord-injured individuals, but this does not result in a reduced leg vascular tone: Leg vascular resistance is even increased. The aim of this study was to assess the alpha-adrenergic contribution to the increased vascular tone in the lower extremity in patients without central sympathetic control of leg circulation. METHODS AND RESULTS: Upper-leg vascular resistance responses to local infusion of incremental doses of phentolamine (a competitive antagonist of the alpha-adrenoceptor) into the femoral artery were determined in 10 spinal cord-injured individuals (SCI) and 8 healthy age-matched control subjects during local beta-adrenergic receptor blockade with propranolol. Basal leg vascular resistance was higher in SCI than in control subjects (41+/-6 arbitrary units [AU] versus 24+/-4 AU; P=0.034). The same accounts for minimal leg vascular resistance, assessed during reactive hyperemia, which was higher in SCI compared with control subjects (6.9+/-1.0 AU versus 2.5+/-0.2 AU; P<0.01). The maximal phentolamine-induced reduction in leg vascular resistance normalized to each individual's minimal resistance did not differ between the groups (68+/-17% and 51+/-4% for SCI and control subjects, respectively; P>0.1). A decline in mean arterial pressure was observed in both groups with increasing dosage of phentolamine. In response, baroreceptor-mediated vasoconstriction was observed in the noninfused leg of the control subjects, whereas in SCI individuals this reaction was absent. CONCLUSIONS: These results indicate that the alpha-adrenoceptor-mediated vascular tone in the leg is preserved in spinal cord-injured individuals without sympathetic supraspinal control.
It has been shown that peak oxygen uptake (O(2)peak) during leg exercise is enhanced by an increased inspiratory oxygen fraction ( FiO(2)), indicating that oxygen supply is the limiting factor. Whether oxygen supply is a limiting factor in arm exercise performance is unknown. The purpose of this study, therefore, was to examine the effect of different levels of FiO(2 )on O(2)peak during arm exercise in healthy individuals. Nine men successfully performed three incremental arm-cranking exercise tests with FiO(2)15%, FiO(2)21% and FiO(2)50% applied in counterbalanced order. A significant FiO(2 )dependency was observed for O(2)peak ( p=0.02) and power output ( p=0.03) and post hoc tests revealed a significant difference in O(2)peak between 15 and 50% FiO(2 )( p=0.02), but not between 15 and 21% FiO(2), and 21 and 50% FiO(2). The results of this study show that O(2)peak is enhanced with increasing FiO(2), and suggest that O(2)peak during arm exercise is limited by oxygen supply rather than by the metabolic machinery within the muscle itself.
Venous occlusion strain gauge plethysmography (VOP) is based on the assumption that the veins are occluded and arterial inflow is undisturbed by the venous cuff pressure. Literature is not clear concerning the pressure that should be used. The purpose of this study was to determine the optimal venous occlusion pressure at which the highest arterial inflow is achieved in the forearm, calf, and leg by using VOP. We hypothesized that, for each limb segment, an optimal (range of) venous cuff pressure can be determined. Arterial inflow in each limb segment was measured in nine healthy individuals by VOP by using pressures ranging from 10 mmHg up to diastolic blood pressure. Arterial inflows were similar at cuff pressures between 30 and 60 mmHg for the forearm, leg, and calf. Arterial inflow in the forearm was significantly lower at 10 mmHg compared with the other cuff pressures. In addition, arterial inflows at 20 mmHg tended to be lower in each limb segment than flow at higher cuff pressures. In conclusion, no single optimum venous cuff pressure, at which a highest arterial inflow is achieved, exists, but rather a range of optimum cuff pressures leading to a similar arterial inflow. Venous cuff pressures ranging from 30 mmHg up to diastolic blood pressure are recommended to measure arterial inflow by VOP.
PURPOSE: The aim of the present study was to assess the time course of vascular adaptations to inactivity and paralyses in humans. The spinal cord-injured (SCI) population offers a unique "human model of nature" to assess peripheral vascular adaptations and its time course to extreme inactivity and paralyses. METHODS: Arterial diameters and red blood cell velocity of the carotid artery (CA), common femoral artery (FA), and brachial artery (BA) were measured using echo Doppler ultrasound. Fifteen SCI persons with lesions varying from 6 wk to 13 months postinjury participated in a cross-sectional study (SCI-CS), 6 SCI individuals were included for longitudinal measurements (SCI-L) at weeks 6, 8, 12, 16, 20, and 24 after the trauma, and 16 able-bodied individuals served as a control group (C). RESULTS: Within 6 wk after the SCI, diameter (SCI-CS: 0.68 +/- 0.09 cm, SCI-L: 0.67 +/- 0.04 cm, C: 0.95 +/- 0.07 cm) and blood flow (SCI-CS: 299 +/- 112 mL x min(-1), SCI-L 279: +/- 52 mL x min(-1), C: 405 +/- 97 mL x min(-1)) of the femoral artery were significantly reduced (P < 0.001), and local femoral wall shear rate was almost doubled in SCI-CS and SC-L compared with C (P < 0.001). No further changes in femoral arterial properties were observed between week 6 and 13 months postinjury in SCI-L as well as SCI-CS. Carotid and brachial artery diameter and flow were similar in SCI and C and did not change between 6 wk and 13 months after the injury. CONCLUSION: We conclude that the process of vascular adaptations to inactivity and paralyses in humans seems to be largely completed within weeks.
The purpose of this study was to assess the relationship between inactivity and shear stress, the frictional force of blood against the endothelium, in spinal cord injury (SCI) subjects. SCI group offers a unique "model of nature" to study the effects of inactivity. Nine SCI subjects with upper (SCI-U) and 5 with a lower (SCI-L) motoneuron lesion and 10 able-bodied controls (C) were included. A venous blood sample was withdrawn to determine blood viscosity. Red blood cell velocities and arterial diameters of the common carotid artery (CCA) and common femoral artery (CFA) were measured by using echo-Doppler ultrasound in a supine position. No differences were observed in wall shear stress in the CCA between groups. In the CFA, peak and mean wall shear stress were significantly increased in SCI (14.1 and 1.2 Pa, respectively) compared with C (10.2 and 0.9 Pa, respectively). Because SCI-U and SCI-L showed no differences in shear stress levels, inactivity and not nerve degeneration seems to cause the elevated shear stress levels in the CFA in SCI. However, the lack of central neural control as a causal factor cannot be ruled out.
The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.