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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent evidence indicates that muscle ischemia and activation of the muscle chemoreflex are the principal stimuli to sympathetic nerve activity (SNA) during isometric exercise. We postulated that physical training would decrease muscle chemoreflex stimulation during isometric exercise and thereby attenuate the SNA response to exercise. We investigated the effects of 6 wk of unilateral handgrip endurance training on the responses to isometric handgrip (IHG: 33% of maximal voluntary contraction maintained for 2 min). In eight normal subjects the right arm underwent exercise training and the left arm sham training. We measured muscle SNA (peroneal nerve), heart rate, and blood pressure during IHG before vs. after endurance training (right arm) and sham training (left arm). Maximum work to fatigue (an index of training efficacy) was increased by 1,146% in the endurance-trained arm and by only 40% in the sham-trained arm. During isometric exercise of the right arm, SNA increased by 111 +/- 27% (SE) before training and by only 38 +/- 9% after training (P less than 0.05). Endurance training did not significantly affect the heart rate and blood pressure responses to IHG. We also measured the SNA response to 2 min of forearm ischemia after IHG in five subjects. Endurance training also attenuated the SNA response to postexercise forearm ischemia (P = 0.057). Sham training did not significantly affect the SNA responses to IHG or forearm ischemia. We conclude that endurance training decreases muscle chemoreflex stimulation during isometric exercise and thereby attenuates the sympathetic nerve response to IHG.
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PMID:Forearm endurance training attenuates sympathetic nerve response to isometric handgrip in normal humans. 156 57

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects (n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35 degrees C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 +/- 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 +/- 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.
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PMID:Effects of muscle metaboreceptor stimulation on cutaneous blood flow from glabrous and nonglabrous skin in mildly heated humans. 1253 97

Measurement of skin sympathetic nerve activity (SSNA) during isometric exercise has been previously limited to handgrip. We hypothesized that isometric leg exercise due to the greater muscle mass of the leg would elicit greater SSNA responses than arm exercise because of presumably greater central command and muscle mechanoreceptor activation. To compare the effect of isometric arm and leg exercise on SSNA and cutaneous end-organ responses, 10 subjects performed 2 min of isometric knee extension (IKE) and handgrip (IHG) at 30% of maximal voluntary contraction followed by 2 min of postexercise muscle ischemia (PEMI) in a normothermic environment. SSNA was recorded from the peroneal nerve. Cutaneous vascular conductance (laser-Doppler flux/mean arterial pressure) and electrodermal activity were measured within the field of cutaneous afferent discharge. Heart rate and mean arterial pressure significantly increased by 16 +/- 3 and 23 +/- 3 beats/min and by 22 +/- 2 and 27 +/- 3 mmHg from baseline during IHG and IKE, respectively. Heart rate and mean arterial pressure responses were significantly greater during IKE compared with IHG. SSNA increased significantly and comparably during IHG and IKE (52 +/- 20 and 50 +/- 13%, respectively). During PEMI, SSNA and heart rate returned to baseline, whereas mean arterial pressure remained significantly elevated (Delta12 +/- 2 and Delta13 +/- 2 mmHg from baseline for IHG and IKE, respectively). Neither cutaneous vascular conductance nor electrodermal activity was significantly altered by either exercise or PEMI. These results indicate that, despite cardiovascular differences in response to IHG and IKE, SSNA responses are similar at the same exercise intensity. Therefore, the findings suggest that relative effort and not muscle mass is the main determinant of exercise-induced SSNA responses in humans.
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PMID:Comparison of skin sympathetic nerve responses to isometric arm and leg exercise. 1503 62

Altered frequency of slow (0.04-0.15Hz) arterial pressure and R-R interval oscillations has been observed in various diseases but the mechanisms for this frequency shift are unclear. The median (Med) frequencies of slow R-R interval and blood pressure (BP) oscillations were recorded in 11 healthy subjects with paced breathing (0.25Hz) during muscle metaboreflex and baroreflex mediated sympathetic stimuli: 1) handgrip exercise (HG) followed by post-exercise circulatory occlusion (PECO), 2) handgrip exercise during ischemia by circulatory occlusion (IHG) and 3) passive head-up tilt (TILT). Med(BP) shifted to the higher frequency during HG, PECO and IHG (from 0.070+/-0.009Hz to 0.088+/-0.013, 0.085+/-0.015 and 0.099+/-0.013Hz, respectively, p<0.01 for all) but not during TILT (0.078+/-0.012Hz). Similarly, Med(R-R) shifted to the higher frequency during HG, PECO and IHG (from 0.072+/-0.009Hz to 0.085+/-0.014, 0.085+/-0.016 and 0.095+/-0.015Hz, respectively, p<0.01 for all) but not during TILT (0.075+/-0.012Hz). Med(BP) and Med(R-R) were higher during IHG compared to HG and lower during TILT compared to both HG and IHG (p<0.01 for all). We conclude that the sympathetic stimulus induced by muscle metaboreflex is an important mechanism increasing the frequency of slow oscillations in arterial pressure and R-R intervals. The present results give new insight to understand the physiology underlying the frequency of slow arterial pressure and R-R interval oscillations.
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PMID:Frequency of slow oscillations in arterial pressure and R-R intervals during muscle metaboreflex activation. 1976 47