Age and sex differences in sympathetic and hemodynamic responses to hypoxia and cold pressor test.

Emerging evidence suggests that sympathetic vasoconstriction is lower in young women. We hypothesized that increases in muscle sympathetic nerve activity (MSNA) during acute physiological stressors induce less vasoconstriction in young women compared to young men. Healthy young men (n = 10, 27 ± 1 years), young women (n = 12, 25 ± 1 years), and older women (n = 10, 63 ± 6 years) performed the cold pressor test (hand in ice for 2 min) and continuous hypoxia (10% O2 , 90% N2 ) for 5 min. MSNA, femoral blood flow velocity, heart rate, and blood pressure were acquired continuously. Femoral artery diameter was obtained every minute and used to calculate femoral blood flow, and femoral vascular resistance and conductance. MSNA responses to cold pressor test (P = 0.345) and hypoxia (P = 0.969) were not different between groups. Young women had greater femoral blood flow (P = 0.002) and vascular conductance (P = 0.041) responses to cold pressor test compared with young men. The femoral blood flow response to hypoxia was not different between the two sexes but the increase in femoral flow was attenuated in older women compared with younger women (P = 0.036). These data show that young women had paradoxical vasodilation to cold pressor test. The mechanisms responsible for the attenuated sympathetic vasoconstriction or for enhanced vasodilation in young women during the CPT require further investigation.

Evaluation of femoral perfusion using dynamic contrast-enhanced MRI after simultaneous initiation of electrical stimulation and steroid treatment in an osteonecrosis model.

This study aimed to evaluate femoral perfusion using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) for two weeks after the simultaneous initiation of electrical stimulation (ES) and steroid treatment in a steroid-induced osteonecrosis (ON) model. A single dose of methylprednisolone was injected into 14 rabbits. Seven rabbits underwent ES (ES group), and seven rabbits did not (control group). DCE-MRI was performed before steroid administration and 1, 5, 10, and 14 days after steroid administration. Regions of interest were set in the bilateral proximal femora. The enhancement ratio, initial slope, and area under the curve were analyzed. These parameters were evaluated after steroid administration in each group and between the two groups, and the ratios of ON in both groups were compared. In the control group, the minimum values of all parameters decreased significantly after steroid administration (P < 0.05), but in the ES group, the parameters did not decrease. In the ES group, all parameter values were significantly increased on the 10th and 14th days (P < 0.05). All parameter values in the ES group were significantly higher than those in the control group on the 14th day (P < 0.05). In the control group, ON was detected in three of five rabbits (in three of ten femora). In the ES group, ON was not detected. These results suggest that increased femoral blood flow elicited by ES may be related to ON prevention after steroid administration.

Voluntary apnea during dynamic exercise activates the muscle metaboreflex in humans.

Voluntary apnea during dynamic exercise evokes marked bradycardia, peripheral vasoconstriction, and pressor responses. However, the mechanism(s) underlying the cardiovascular responses seen during apnea in exercising humans is unknown. We therefore tested the hypothesis that the muscle metaboreflex contributes to the apnea-induced pressor response during dynamic exercise. Thirteen healthy subjects participated in apnea and control trials. In both trials, subjects performed a two-legged dynamic knee extension exercise at a workload that elicited heart rates at ~100 beats/min. In the apnea trial, after reaching a steady state, subjects began voluntary apnea. Immediately after cessation of the apnea, arterial occlusion was initiated at both thighs and the subjects stopped exercising. The occlusion was sustained for 3 min in the postexercise period. In the control trial, the occlusion was started without subjects performing the apnea. The apnea induced marked bradycardia, pressor responses, and decreases in arterial O2 saturation, cardiac output, and total vascular conductance. In addition, arterial blood pressure was significantly higher and total vascular conductance was significantly lower in the apnea trials than the control trials throughout the occlusion period. In separate sessions, we measured apnea-induced changes in exercising leg blood flow in the same subjects. Leg blood flow was significantly reduced by apnea and reached the resting level at the peak of the apnea response. We conclude that the muscle metaboreflex is activated by the decrease in O2 delivery to the working muscle during apnea in exercising humans and contributes to the large pressor response. NEW & NOTEWORTHY We demonstrated that apnea during dynamic exercise activates the muscle metaboreflex in humans. This result indicates that a reduction in O2 delivery to working muscle triggers the muscle metaboreflex during apnea. Activation of the muscle metaboreflex is one of the mechanisms underlying the marked apnea-induced pressor response.

No effect of NOS inhibition on skeletal muscle glucose uptake during in situ hindlimb contraction in healthy and diabetic Sprague-Dawley rats.

Nitric oxide (NO) has been shown to be involved in skeletal muscle glucose uptake during contraction/exercise, especially in individuals with Type 2 diabetes (T2D). To examine the potential mechanisms, we examined the effect of local NO synthase (NOS) inhibition on muscle glucose uptake and muscle capillary blood flow during contraction in healthy and T2D rats. T2D was induced in Sprague-Dawley rats using a combined high-fat diet (23% fat wt/wt for 4 wk) and low-dose streptozotocin injections (35 mg/kg). Anesthetized animals had one hindlimb stimulated to contract in situ for 30 min (2 Hz, 0.1 ms, 35 V) with the contralateral hindlimb rested. After 10 min, the NOS inhibitor, N(G)-nitro-l-arginine methyl ester (l-NAME; 5 µM) or saline was continuously infused into the femoral artery of the contracting hindlimb until the end of contraction. Surprisingly, there was no increase in skeletal muscle NOS activity during contraction in either group. Local NOS inhibition had no effect on systemic blood pressure or muscle contraction force, but it did cause a significant attenuation of the increase in femoral artery blood flow in control and T2D rats. However, NOS inhibition did not attenuate the increase in muscle capillary recruitment during contraction in these rats. Muscle glucose uptake during contraction was significantly higher in T2D rats compared with controls but, unlike our previous findings in hooded Wistar rats, NOS inhibition had no effect on glucose uptake during contraction. In conclusion, NOS inhibition did not affect muscle glucose uptake during contraction in control or T2D Sprague-Dawley rats, and this may have been because there was no increase in NOS activity during contraction.

Femoral perfusion after pulsed electromagnetic field stimulation in a steroid-induced osteonecrosis model.

This study was designed to evaluate femoral perfusion after pulsed electromagnetic field (PEMF) stimulation in a steroid-induced osteonecrosis rabbit model by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). Steroid-induced osteonecrosis was produced by single intramuscular injection of methylprednisolone in 15 rabbits. Eight rabbits underwent PEMF stimulation (PEMF group) and seven did not (control group). DCE-MRI was performed before PEMF stimulation, immediately before steroid administration, and 1, 5, 10, and 14 days after steroid administration. Regions of interest were set in the bilateral proximal femora. Enhancement ratio (ER), initial slope (IS), and area under the curve (AUC) were analyzed. ER, IS, and AUC in the control group significantly decreased after steroid administration compared with before administration (P<0.05). In PEMF group, IS significantly decreased; however, ER and AUC showed no significant differences after steroid administration compared with before. ER and IS in PEMF group were higher than in control group until 10th day, and AUC was higher until 5th day after steroid administration (P<0.05). PEMF stimulation restrains the decrease in blood flow after steroid administration.

Femoral Vessel Blood Flow Is Preserved Throughout Direct Anterior Total Hip Arthroplasty.

Posterolateral and anterolateral approach THA disrupts femoral vessel blood flow, however, this has not been established for the direct anterior (DA) approach. Ten patients undergoing primary DA THA had peak vascular flow rates for the femoral artery and vein calculated via Doppler ultrasound at specified points: incision, acetabular preparation, femoral preparation and final reduction. Peak femoral arterial and venous flow decreased over baseline, but not significantly, during acetabular preparation (P=0.88, P=0.98) and femoral preparation (P=0.97, P=0.97). At final reduction, arterial peak flow was restored (P=1) with an increase in venous flow (P=0.55). Although there were alterations to peak flow, no vessel occlusion occurred at any point during DA THA.