首页> 外文期刊>The Journal of Physiology >Human skeletal muscle sympathetic nerve activity, heart rate and limb haemodynamics with reduced blood oxygenation and exercise.
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Human skeletal muscle sympathetic nerve activity, heart rate and limb haemodynamics with reduced blood oxygenation and exercise.

机译:人骨骼肌交感神经活动,心率和肢体血流动力学降低血氧合和运动。

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摘要

Acute systemic hypoxia causes significant increases in human skeletal muscle sympathetic nerve activity (MSNA), heart rate and ventilation. This phenomenon is thought to be primarily mediated by excitation of peripheral chemoreceptors sensing a fall in arterial free oxygen partial pressure (Pa,O2). We directly tested the role of Pa,O2 on MSNA (peroneal microneurography), heart rate, ventilation and leg haemodynamics (n = 7-8) at rest and during rhythmic handgrip exercise by using carbon monoxide (CO) to mimic the effect of systemic hypoxia on arterial oxyhaemoglobin (~20 % lower O2Hba), while normalising or increasing Pa,O2 (range 40-620 mmHg). The four experimental conditions were: (1) normoxia (Pa,O2 ~110 mmHg; carboxyhaemoglobin (COHb) ~2 %); (2) hypoxia (Pa,O2 ~40 mmHg; COHb ~2 %); (3) CO + normoxia (Pa,O2 ~110 mmHg; COHb ~23 %); and (4) CO + hyperoxia (Pa,O2 ~620 mmHg; COHb ~24 %). Acute hypoxia augmented sympathetic burst frequency, integrated MSNA, heart rate and ventilation compared to normoxiaover the entire protocol (7-13 bursts min-1, 100-118 %, 13-17 beats min-1, 2-4 l min-1, respectively, P < 0.05). The major new findings were: (1) CO + normoxia and CO + hyperoxia also elevated MSNA compared to normoxia (63-144 % increase in integrated MSNA; P < 0.05) but they did not increase heart rate (62-67 beats min-1) or ventilation (6.5-6.8 l min-1), and (2) despite the 4-fold elevation in MSNA with hypoxaemia and exercise, resting leg blood flow, vascular conductance and O2 uptake remained unchanged. In conclusion, the present results suggest that increases in MSNA with CO are not mediated by activation of the chemoreflex, whereas hypoxia-induced tachycardia and hyperventilation are mediated by activation of the chemoreflex in response to the decline in Pa,O2. Our findings also suggest that Pa,O2 is not an obligatory signal involved in the enhanced MSNA with reduced blood oxygenation.
机译:急性系统性缺氧会导致人体骨骼肌交感神经活动(MSNA),心率和通气量显着增加。据认为,这种现象主要是由周围化学感受器的激发介导的,从而感应到动脉游离氧分压(Pa,O2)的下降。我们通过使用一氧化碳(CO)模仿全身性作用,直接测试了Pa,O2在静止和节律性手握锻炼过程中对MSNA(腓骨微神经造影),心率,通气和腿部血流动力学(n = 7-8)的作用氧合血红蛋白低氧(O2Hba降低约20%),同时使Pa,O2正常化或升高(范围40-620 mmHg)。四个实验条件是:(1)常氧(Pa,O2〜110 mmHg;羧基血红蛋白(COHb)〜2%); (2)缺氧(Pa,O2〜40 mmHg; COHb〜2%); (3)CO +常氧(Pa,O2〜110 mmHg; COHb〜23%); (4)CO +高氧(Pa,O2〜620 mmHg; COHb〜24%)。在整个实验方案中,与正常氧相比,急性低氧增加了交感神经的猝发频率,综合MSNA,心率和通气(7-13次min-1、100-118%,13-17次min-1、2-4 l min-1,分别为P <0.05)。主要的新发现是:(1)与正常氧相比,CO +正常氧和CO +高氧也使MSNA升高(综合MSNA升高63-144%; P <0.05),但它们并未增加心率(62-67次/分, 1)或通气(6.5-6.8 l min-1),以及(2)尽管低氧血症和运动导致MSNA升高了4倍,但腿部静息血流,血管电导率和O2摄取保持不变。总之,目前的结果表明,CO引起的MSNA的增加不是由化学反射激活引起的,而缺氧诱导的心动过速和过度换气是由化学反射激活引起的,对Pa,O2的降低做出反应。我们的研究结果还表明,Pa,O2不是与血液氧合降低相关的MSNA增强所必需的信号。

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