Biomedical subjects

Jim Hansen

Publications and source records attributed to Jim Hansen.

10 recordsLinked to original sources

PubMed2005

Association between regional quadriceps oxygenation and blood oxygen saturation during normoxic one-legged dynamic knee extension.

It is not clear whether muscle oxygenation (O(2-NIRS)) measured by near-infrared spectroscopy (NIRS) correlates with femoral venous SO2 (S(fv)o2) during normoxic exercise. Therefore, the purpose of this study was to compare physiologically calibrated O(2-NIRS) with S(fv)o2 in subjects performing one-legged dynamic knee extension exercise (1L-KEE). Five healthy male subjects (age 25+/-2 year, height 177.8+/-4.8 cm, body weight 67.1 +/- 5.0 kg; mean +/- SD) performed 1L-KEE at 20, 40, and 60% of peak work rate (WR-peak) each for 4 min. S(fv)o2 was measured at rest and during the 3rd minute of each work rate. O(2-NIRS) was continuously monitored in a proximal region of the vastus lateralis (VL-p), a distal region of VL (VL-d), and a proximal region of the rectus femoris (RF-p). S(fv)o2 was 56.0% at rest and decreased to 36.6 at 20% WR-peak, 35.8 at 40% WR-peak, and 31.1 at 60% WR-peak. There was a significant correlation between O(2-NIRS) and S(fv)o2(VL-p: r (2) = 0.62, VL-d: r2 = 0.35, RF-p: r2 = 0.62, with a moderate variation among individuals at each site; residual values = 4.83 - 11.75). These data indicate that NIRS measurement provides a reflection of S(fv)o2 during 20-60% WR-peak of normoxic 1L-KEE.

Adult↗

PubMed2004

Circulating ATP-induced vasodilatation overrides sympathetic vasoconstrictor activity in human skeletal muscle.

Despite increases in muscle sympathetic vasoconstrictor activity, skeletal muscle blood flow and O2 delivery increase during exercise in humans in proportion to the local metabolic demand, a phenomenon coupled to local reductions in the oxygenation state of haemoglobin and concomitant increases in circulating ATP. We tested the hypothesis that circulating ATP contributes to local blood flow and O2 delivery regulation by both inducing vasodilatation and blunting the augmented sympathetic vasoconstrictor activity. In eight healthy subjects, we first measured leg blood flow (LBF) and mean arterial pressure (MAP) during three hyperaemic conditions: (1) intrafemoral artery adenosine infusion (vasodilator control), (2) intrafemoral artery ATP infusion (vasodilator), and (3) mild knee-extensor exercise (approximately 20 W), and then compared the responses with the combined infusion of the vasoconstrictor drug tyramine, which evokes endogenous release of noradrenaline from sympathetic nerve endings. In all three hyperaemic conditions, LBF equally increased from approximately 0.5 +/- 0.1 l min(-1) at rest to approximately 3.6 +/- 0.3 l min(-1), with no change in MAP. Tyramine caused significant leg vasoconstriction during adenosine infusion (53 +/- 5 and 56 +/- 5% lower LBF and leg vascular conductance, respectively, P < 0.05), which was completely abolished by both ATP infusion and exercise. In six additional subjects resting in the sitting position, intrafemoral artery infusion of ATP increased LBF and leg vascular conductance 27 +/- 3-fold, despite concomitant increases in venous noradrenaline and muscle sympathetic nerve activity of 2.5 +/- 0.2- and 2.4 +/- 0.1-fold, respectively. Maximal ATP-induced vasodilatation at rest accounted for 78% of the peak LBF during maximal bicycling exercise. Our findings in humans demonstrate that circulating ATP is capable of regulating local skeletal muscle blood flow and O2 delivery by causing substantial vasodilatation and negating the effects of increased sympathetic vasoconstrictor activity.

Adenosine↗

PubMed2003

Sympathetic neural overactivity in healthy humans after prolonged exposure to hypobaric hypoxia.

Acute exposure to hypoxia causes chemoreflex activation of the sympathetic nervous system. During acclimatization to high altitude hypoxia, arterial oxygen content recovers, but it is unknown to what degree sympathetic activation is maintained or normalized during prolonged exposure to hypoxia. We therefore measured sympathetic nerve activity directly by peroneal microneurography in eight healthy volunteers (24 +/- 2 years of age) after 4 weeks at an altitude of 5260 m (Chacaltaya, Bolivian Andes) and at sea level (Copenhagen). The subjects acclimatized well to altitude, but in every subject sympathetic nerve activity was highly elevated at altitude vs. sea level (48 +/- 5 vs. 16 +/- 3 bursts min(-1), respectively, P < 0.05), coinciding with increased mean arterial blood pressure (87 +/- 3 vs. 77 +/- 2 mmHg, respectively, P < 0.05). To examine the underlying mechanisms, we administered oxygen (to eliminate chemoreflex activation) and saline (to reduce cardiopulmonary baroreflex deactivation). These interventions had minor effects on sympathetic activity (48 +/- 5 vs. 38 +/- 4 bursts min(-1), control vs. oxygen + saline, respectively, P < 0.05). Moreover, sympathetic activity was still markedly elevated (37 +/- 5 bursts min(-1)) when subjects were re-studied under normobaric, normoxic and hypervolaemic conditions 3 days after return to sea level. In conclusion, acclimatization to high altitude hypoxia is accompanied by a striking and long-lasting sympathetic overactivity. Surprisingly, chemoreflex activation by hypoxia and baroreflex deactivation by dehydration together could account for only a small part of this response, leaving the major underlying mechanisms unexplained.

Acclimatization↗

PubMed2002

Nitric oxide-dependent modulation of sympathetic neural control of oxygenation in exercising human skeletal muscle.

Nitric oxide (NO) attenuates alpha-adrenergic vasoconstriction in contracting rodent skeletal muscle, but it is unclear if NO plays a similar role in human muscle. We therefore hypothesized that in humans, NO produced in exercising skeletal muscle blunts the vasoconstrictor response to sympathetic activation. We assessed vasoconstrictor responses in the microcirculation of human forearm muscle using near-infrared spectroscopy to measure decreases in muscle oxygenation during reflex sympathetic activation evoked by lower body negative pressure (LBNP). Experiments were performed before and after NO synthase inhibition produced by systemic infusion of N(G)-nitro-L-arginine methyl ester (L-NAME). Before L-NAME, LBNP at -20 mmHg decreased muscle oxygenation by 20 +/- 2 % in resting forearm and by 2 +/- 3 % in exercising forearm (n = 20), demonstrating metabolic modulation of sympathetic vasoconstriction. As expected, L-NAME increased mean arterial pressure by 17 +/- 3 mmHg, leading to baroreflex-mediated suppression of baseline muscle sympathetic nerve activity (SNA). The increment in muscle SNA in response to LBNP at -20 mmHg also was attenuated after L-NAME (before, +14 +/- 2; after, +8 +/- 1 bursts min(-1); n = 6), but this effect of L-NAME was counteracted by increasing LBNP to -40 mmHg (+19 +/- 2 bursts min(-1)). After L-NAME, LBNP at -20 mmHg decreased muscle oxygenation similarly in resting (-11 +/- 3 %) and exercising (-10 +/- 2 %) forearm (n = 12). Likewise, LBNP at -40 mmHg decreased muscle oxygenation both in resting (-19 +/- 4 %) and exercising (-21 +/- 5 %) forearm (n = 8). These data advance the hypothesis that NO plays an important role in modulating sympathetic vasoconstriction in the microcirculation of exercising muscle, because such modulation is abrogated by NO synthase inhibition with L-NAME.

Adult↗

PubMed2002