Endothelium-dependent and -independent vasodilation of the superficial femoral artery in spinal cord-injured subjects.

Extreme inactivity of the legs in spinal cord-injured (SCI) individuals does not result in an impairment of the superficial femoral artery flow-mediated dilation (FMD). To gain insight into the underlying mechanism, the present study examined nitric oxide (NO) responsiveness of vascular smooth muscles in controls and SCI subjects. In eight healthy men (34 +/- 13 yr) and six SCI subjects (37 +/- 10 yr), superficial femoral artery FMD response was assessed by echo Doppler. Subsequently, infusion of incremental dosages of sodium nitroprusside (SNP) was used to assess NO responsiveness. Peak diameter was examined on a second day after 13 min of arterial occlusion in combination with sublingual administration of nitroglycerine. Resting and peak superficial femoral artery diameter in SCI subjects were smaller than in controls (P < 0.001). The FMD response in controls (4.2 +/- 0.9%) was lower than in SCI subjects (8.2 +/- 0.9%, P < 0.001), but not after correcting for area under the curve for shear rate (P = 0.35). When expressed as relative change from baseline, SCI subjects demonstrate a significantly larger diameter increase compared with controls at each dose of SNP. However, when expressed as a relative increase within the range of diameter changes [baseline (0%) - peak diameter (100%)], both groups demonstrate similar changes in response to SNP. Changes in diameter during SNP infusion and FMD response are larger in SCI subjects compared with controls. When these results are corrected, superficial femoral artery FMD and NO sensitivity in SCI subjects are not different from those in controls. This illustrates the importance of appropriate data presentation and suggests that, subsequent to structural inward remodeling of conduit arteries as a consequence of extreme physical inactivity, arterial function is normalized.

Flow-mediated dilatation in the superficial femoral artery is nitric oxide mediated in humans.

Flow-mediated dilatation (FMD) of the brachial and radial arteries is an important research tool for assessment of endothelial function in vivo, and is nitric oxide (NO) dependent. The leg skeletal muscle vascular bed is an important territory for studies in exercise physiology. However, the role of endothelial NO in the FMD response of lower limb arteries has never been investigated. The purpose of this study was to examine the contribution of NO to FMD in the superficial femoral artery in healthy subjects. Since physical inactivity may affect endothelial function, and therefore NO availability, spinal cord-injured (SCI) individuals were included as a model of extreme deconditioning. In eight healthy men (34 +/- 13 years) and six SCI individuals (37 +/- 10 years), the 5 min FMD response in the superficial femoral artery was assessed by echo-Doppler, both during infusion of saline and during infusion of the NO synthase blocker N(G)-monomethyl-L-arginine (L-NMMA). In a subset of the controls (n = 6), the 10 min FMD response was also examined using the same procedure. The 5 min FMD response in controls (4.2 +/- 0.3%) was significantly diminished during L-NMMA infusion (1.0 +/- 0.2%, P < 0.001). In SCI, L-NMMA also significantly decreased the FMD response (from 8.2 +/- 0.4% during saline to 2.4 +/- 0.5% during L-NMMA infusion). The hyperaemic flow response during the first 45 s after cuff deflation was lower in both groups during infusion of L-NMMA, but the effect of L-NMMA on FMD persisted in both groups after correction for the shear stress stimulus. The 10 min FMD was not affected by L-NMMA (saline: 5.4 +/- 1.6%, L-NMMA: 5.6 +/- 1.5%). Superficial femoral artery FMD in response to distal arterial occlusion for a period of 5 min is predominantly mediated by NO in healthy men and in the extremely deconditioned legs of SCI individuals.

Vascular adaptations to 8-week cycling training in older men.

AIM: Because age-related changes in the large conduit arteries (increased wall thickness, and attenuated arterial compliance and endothelial function) are associated with cardiovascular pathology, prevention is of paramount importance. The effects of endurance training (i.e. walking or cycling) in older humans are assessed in cross-sectional studies, examining the brachial and carotid arteries (supplying non-trained areas). The purpose of this study was to assess the effects of 8-week endurance training in older men on conduit artery characteristics in the trained and non-trained vascular beds. METHODS: In eight healthy sedentary older men (70 +/- 3 years), characteristics of the large conduit arteries [common femoral (CFA), superficial femoral (SFA), carotid (CA), and brachial artery (BA)] were measured before and after 8-week cycling training. Functional [arterial compliance and flow-mediated dilation (FMD)] and structural (diameter and intima-media thickness) conduit artery properties were measured using echo-Doppler. Peak blood flow, representing structural peripheral adaptations, was measured using venous occlusion plethysmography. RESULTS: After training, peak leg blood flow was increased (P < 0.01) and baseline diameter and flow were increased in the CFA (P < 0.05). Cycling training enhanced arterial compliance of the SFA (P = 0.03), but did not affect the FMD (P = 0.32) or the intima-media thickness of the SFA. Exercise training did not alter characteristics of the BA or CA. CONCLUSION: Eight weeks of endurance training in older men altered functional and structural characteristics of the lower extremity vasculature, whereas no changes are reported for the conduit arteries in the non-trained areas (BA or in the CA).

Effects of 18 days of bed rest on leg and arm venous properties.

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6 degrees head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 +/- 0.007 ml x 100 ml(-1) x mmHg(-1), post: 0.033 +/- 0.007 ml x 100 ml(-1) x mmHg(-1); P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 +/- 1.08 mmHg x ml(-1) x 100 ml x min, post: 3.10 +/- 1.00 mmHg x ml(-1) x 100 ml x min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure x time), decreased in all subjects after bed rest (pre: 932 mmHg x min, post: 747 mmHg x min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.

Effect of training intensity on physical capacity, lipid profile and insulin sensitivity in early rehabilitation of spinal cord injured individuals.

STUDY DESIGN: Pre-post training intervention. OBJECTIVES: To evaluate the effect of training intensity on physical capacity, lipid profile and insulin sensitivity in early rehabilitation of spinal cord injured (SCI) patients, and to assess the correlation between peak aerobic capacity (VO(2Peak)) and insulin sensitivity. SETTING: Spinal Cord Rehabilitation Unit, Sunnaas Hospital, Nesoddtangen, Norway. METHOD: Six recently injured SCI individuals participated in the arm training intervention and were randomly admitted to a high-intensity (HI; 70-80% heart rate reserve (HRR)) and low-intensity (LI; 40-50% HRR) group. The 1 h interval training consisted of 3 min exercise bouts interspersed with 2 min of rest, three times a week for 8 weeks. In addition, a correlation coefficient was obtained between VO(2Peak) and insulin sensitivity in 11 SCI patients. RESULTS: The 8-week training program resulted in a significant increase in VO(2Peak) and maximal power output (PO(Max)) for the group as a whole (P<0.05). VO(2Peak) increased significantly more and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio and triglycerids decreased significantly more in the HI group than in the LI group (P=0.05). Training-induced changes in insulin sensitivity were significantly different between the groups (P=0.05), which was due to a nonsignificant decline in insulin sensitivity in the HI group and a nonsignificant improvement in the LI group. A significant positive correlation was found between VO(2peak) and insulin sensitivity (r=0.68, P=0.02). CONCLUSION: The interval arm training protocol as used in the present study enables recently injured SCI patients to do substantial work at a relatively high intensity. Results indicate that improvements in physical capacity and lipid profile were more pronounced in response to high-intensity training. The significant correlation between maximal oxygen consumption and insulin sensitivity indicates that, as in the able-bodied population, peak aerobic capacity is a predictive value with regard to insulin sensitivity in SCI. Future studies with larger groups assessing the role of exercise intensity on insulin sensitivity in SCI are suggested.