Smith Joshua R, Didier Kaylin D, Hammer Shane M, Alexander Andrew M, Kurti Stephanie P, Copp Steven W, Barstow Thomas J, Harms Craig A
Department of Kinesiology, Kansas State University, Manhattan Kansas
Department of Kinesiology, Kansas State University, Manhattan Kansas.
J Appl Physiol (1985). 2017 Jul 1;123(1):197-204. doi: 10.1152/japplphysiol.00165.2017. Epub 2017 May 18.
Inspiratory muscle metaboreflex activation increases mean arterial pressure (MAP) and limb vascular resistance (LVR) and decreases limb blood flow (Q̇). Cyclooxygenase (COX) inhibition has been found to attenuate limb skeletal muscle metaboreflex-induced increases in muscle sympathetic nerve activity. We hypothesized that compared with placebo (PLA), COX inhibition would attenuate inspiratory muscle metaboreflex-induced ) increases in MAP and LVR and ) decreases in Q̇ Seven men (22 ± 1 yr) were recruited and orally consumed ibuprofen (IB; 10 mg/kg) or PLA 90 min before performing the cold pressor test (CPT) for 2 min and inspiratory resistive breathing task (IRBT) for 14.9 ± 2.0 min at 65% of maximal inspiratory pressure. Breathing frequency was 20 breaths/min with a 50% duty cycle during the IRBTs. MAP was measured via automated oscillometry, Q̇ was determined via Doppler ultrasound, and LVR was calculated as MAP divided by Q̇ Electromyography was recorded on the leg to ensure no muscle contraction occurred. The 65% IRBT led to greater increases ( = 0.02) in 6-keto-prostaglandin-F with PLA compared with IB. IB, compared with PLA, led to greater ( < 0.01) increases in MAP (IB: 17 ± 7 mmHg vs. PLA: 8 ± 5 mmHg) and LVR (IB: 69 ± 28% vs. PLA: 52 ± 22%) at the final minute of the 65% IRBT. The decrease in Q̇ was not different ( = 0.72) between IB (-28 ± 11%) and PLA (-27 ± 9%) at the final minute. The increase in MAP during the CPT was not different ( = 0.87) between IB (25 ± 11 mmHg) and PLA (24 ± 6 mmHg). Contrary to our hypotheses, COX inhibition led to greater inspiratory muscle metaboreflex-induced increases in MAP and LVR. Cyclooxygenase (COX) products play a role in activating the muscle metaboreflex. It is not known whether COX products contribute to the inspiratory muscle metaboreflex. Herein, we demonstrate that COX inhibition led to greater increases in blood pressure and limb vascular resistance compared with placebo during inspiratory muscle metaboreflex activation.
吸气肌代谢性反射激活会增加平均动脉压（MAP）和肢体血管阻力（LVR），并减少肢体血流量（Q̇）。已发现抑制环氧化酶（COX）可减弱肢体骨骼肌代谢性反射引起的肌肉交感神经活动增加。我们假设，与安慰剂（PLA）相比，抑制COX会减弱吸气肌代谢性反射引起的：）MAP和LVR升高以及）Q̇降低。招募了7名男性（22±1岁），在进行2分钟的冷加压试验（CPT）和以最大吸气压力的65%进行14.9±2.0分钟的吸气阻力呼吸任务（IRBT）前90分钟，口服布洛芬（IB；10mg/kg）或PLA。在IRBT期间，呼吸频率为每分钟20次呼吸，占空比为50%。通过自动示波法测量MAP，通过多普勒超声测定Q̇，并将LVR计算为MAP除以Q̇。记录腿部的肌电图以确保未发生肌肉收缩。与IB相比，PLA组在65%IRBT时6-酮-前列腺素-F的升高幅度更大（P = 0.02）。在65%IRBT的最后一分钟，与PLA相比，IB使MAP（IB：17±7mmHg vs. PLA：8±5mmHg）和LVR（IB：69±28% vs. PLA：52±22%）升高幅度更大（P < 0.01）。在最后一分钟，IB（-28±11%）和PLA（-27±9%）之间Q̇的降低无差异（P = 0.72）。在CPT期间，IB（25±11mmHg）和PLA（24±6mmHg）之间MAP的升高无差异（P = 0.87）。与我们的假设相反，抑制COX导致吸气肌代谢性反射引起的MAP和LVR升高幅度更大。环氧化酶（COX）产物在激活肌肉代谢性反射中起作用。尚不清楚COX产物是否参与吸气肌代谢性反射。在此，我们证明在吸气肌代谢性反射激活期间，与安慰剂相比，抑制COX导致血压和肢体血管阻力升高幅度更大。
