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

The muscle metabo- and mechanoreflexes have been shown to increase muscle sympathetic nerve activity (MSNA) during exercise. Group III and IV muscle afferents, which are believed to mediate this response, have been shown to be thermosensitive in animals. The purpose of the present study was to evaluate the effect of muscle temperature on MSNA responses during exercise. Eleven subjects performed ischemic isometric handgrip at 30% of maximal voluntary contraction to fatigue, followed by 2 min of postexercise muscle ischemia (PEMI), with and without local heating of the forearm. Local heating of the forearm increased forearm muscle temperature from 34.4 +/- 0.2 to 38.9 +/- 0.3 degree C (P = 0.001). Diastolic and mean arterial pressures were augmented during exercise in the heat. MSNA responses were greater during ischemic handgrip with local heating compared with control (no heating) after the first 30 s. MSNA responses at fatigue were greater during local heating. MSNA increased by 16 +/- 2 and 20 +/- 2 bursts per 30 s for control and heating, respectively (P = 0.03). When expressed as a percent change in total activity (total burst amplitude), MSNA increased 531 +/- 159 and 941 +/- 237% for control and heating, respectively (P = 0.001). However, MSNA was not different during PEMI between trials. This finding suggests that the augmentation of MSNA during exercise with heat was due to the stimulation of mechanically sensitive muscle afferents. These results suggest that heat sensitizes skeletal muscle afferents during muscle contraction in humans and may play a role in the regulation of MSNA during exercise.
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PMID:Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating. 917 32

The etiology of atherosclerosis must explain the development of primary pathological complications (intimal tears, ectasia, tortuosity, aneurysms and stenoses). They are interrelated and associated with destruction of mural architecture and concomitant loss of tensile strength (fragility) attributable to bioengineering fatigue. The complications become manifested clinically by ischemia, hemorrhage and pressure effects developing with greater frequency in association with hypertension, arteriovenous shunts or connective tissue disorders. Moreover they are produced experimentally and iatrogenically by hemodynamic means but are unexplained by other current etiological hypotheses.
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PMID:Mechanisms underlying arterial fragility and the complications of atherosclerosis. 920 Jan 85

Reduced oxygen supply to contracting muscles affects not only the metabolic paths but also modifies the gain of sensorimotor reflex loops initiated from the activation of specialized nervous endings that detect the changes in muscle metabolism and membrane outflow of potassium. Large differences are found between skeletal muscles and the diaphragm with respect to their sensitivity to acute or chronic hypoxia. The diaphragm tolerates much more hypoxemia than do skeletal muscles, namely those constituted by a large proportion of slow twitch oxidative fibers. Acute hypoxemia or ischemia accentuates the inhibitory influences exerted by the afferent paths from muscle metaboreceptors. This adaptative response may be responsible for enhanced muscle wisdom phenomenon during fatiguing contractions under hypoxic conditions. Prolonged and severe chronic hypoxemia markedly reduces muscle force generation by skeletal muscles and their endurance to fatigue. Restoration of normal PaO2 levels in these individuals immediately improves maximal muscle performance, perhaps through more efficient excitation-contraction coupling. Recent data on the consequences of hypoxia on muscle metabolism and the associated changes in sensorimotor control strongly suggest that local acidosis cannot entirely explain all electromyogram changes found during and after fatiguing exercise.
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PMID:Functional consequences of acute and chronic hypoxia on respiratory and skeletal muscles in mammals. 924 11

For over four decades, various methods have been described for the use of electrically stimulated skeletal muscle to pump blood. To date, there has been no way of predicting the efficacy or long-term pumping capabilities of these methods. This article reviews the basic physiological properties of skeletal muscle and relates them to the blood pumping task and illustrates the paradox, namely a high preload is needed for a forceful contraction, but a high prolonged preload produces muscle ischemia and early fatigue. However, the high preload is only required just before muscle contraction. Two methods are described to attain the high preload and high muscle capillary blood flow.
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PMID:The paradox in using electrically stimulated skeletal muscle to pump blood. 927 39

Skeletal muscle contraction during ischemia, such as that experienced by peripheral vascular disease patients, is characterized by rapid fatigue. Using a canine gracilis model, we tested the hypothesis that a critical factor determining force production during ischemia is the metabolic response during the transition from rest to steady state. Dichloroacetate (DCA) administration before gracilis muscle contraction increased pyruvate dehydrogenase complex activation and resulted in acetylation of 80% of the free carnitine pool to acetylcarnitine. After 1 min of contraction, phosphocreatine (PCr) degradation in the DCA group was approximately 50% lower than in the control group (P < 0.05) during conditions of identical force production. After 6 min of contraction, steady-state force production was approximately 30% higher in the DCA group (P < 0.05), and muscle ATP, PCr, and glycogen degradation and lactate accumulation were lower (P < 0.05 in all cases). It appears, therefore, that an important determinant of contractile function during ischemia is the mechanisms by which ATP regeneration occurs during the period of rest to steady-state transition.
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PMID:Metabolic responses from rest to steady state determine contractile function in ischemic skeletal muscle. 927 74

This study evaluated the effects of dexamethasone (DXM) on contractile function of reperfused extensor digitalis longus (EDL) muscles following 3-hour ischemia and 24-hour reperfusion. The rats were divided into four groups: normal muscle, ischemia with saline treatment, ischemia/reperfusion with saline treatment, and ischemia/reperfusion with DXM treatment groups. DXM (0.6 mg kg[-1]) or saline (3.0 ml kg[-1]) was administered at 3 hours prior to ischemia. Results showed that although contractile force in all three treated groups was significantly lower than that of normal EDL, the average isometric tetanic contractile force in the DXM-treated group was significantly greater than that in the saline-treated ischemia and ischemia/reperfusion groups. A significant difference was also seen at the peak force and at 5 seconds of the fatigue trains, and with a longer fatigue half-time (FT1/2) in the DXM-treated group than in the other two groups. Histologically, edema, inflammation and necrosis of muscle fiber were less severe in the DXM-treated group than in the saline-treated group. The results indicate that pretreatment with DXM appears to attenuate, but does not completely reverse, the contractile function deficit of ischemic skeletal muscle during the first 24 hours of reperfusion.
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PMID:Effects of dexamethasone on the contractile function of reperfused skeletal muscle. 930 15

Elevation of muscle temperature has been shown to increase muscle sympathetic nerve activity (MSNA) during isometric exercise in humans. The purpose of the present study was to evaluate the effect of muscle cooling on MSNA responses during exercise. Eight subjects performed ischemic isometric handgrip at 30% of maximal voluntary contraction to fatigue followed by 2 min of postexercise muscle ischemia (PEMI), with and without local cooling of the forearm. Local cooling of the forearm decreased forearm muscle temperature from 31.8 +/- 0.4 to 23.1 +/- 0.8 degrees C (P = 0.001). Time to fatigue was not different during the control and cold trials (156 +/- 11 and 154 +/- 5 s, respectively). Arterial pressures and heart rate were not significantly affected by muscle cooling during exercise, although heart rate tended to be higher during the second minute of exercise (P = 0.053) during muscle cooling. Exercise-induced increases in MSNA were delayed during handgrip with local cooling compared with control. However, MSNA responses at fatigue and PEMI were not different between the two conditions. These findings suggest that muscle cooling delayed the activation of the muscle metaboreflex during ischemic isometric exercise but did not prevent its full expression during fatiguing contraction. These results support the concept that muscle temperature can play a role in the regulation of MSNA during exercise.
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PMID:Muscle cooling delays activation of the muscle metaboreflex in humans. 937 82

It has been well documented that ischemic preconditioning limits ischemic-reperfusion injury in cardiac muscle, but the ability of ischemic preconditioning to limit skeletal muscle injury is less clear. Previous reports have emphasized the beneficial effects of ischemic preconditioning on skeletal muscle structure and capillary perfusion but have not evaluated muscle function. We investigated the morphologic and functional consequences of ischemic preconditioning, followed by a 2-hour period of tourniquet ischemia on muscles in the rat hindlimb. The 2-hour ischemia was imposed without preconditioning, or was preceded by three brief (10 minutes on/10 minutes off) preischemic conditioning intervals. We compared muscle morphology, isometric contractile function, and muscle fatigue properties in predominantly fast-twitch, tibialis anterior muscles 3 (n = 8) and 7 (n = 8) days after ischemia-reperfusion. Two hours of ischemia, followed by reperfusion, results in a 20 percent reduction of muscle mass (p < 0.05) and a 33 percent reduction in tetanic tension (p < 0.05) when compared with controls (n = 8) at 3 days. The same protocol, when preceded by ischemic preconditioning, results in similar decreases in muscle mass and contractile function. Neuromuscular transmission was also impaired in both ischemic groups 7 days after ischemia. Nerve-evoked maximum tetanic tension was 69 percent of the tension produced by direct muscle stimulation in the ischemia group and 65 percent of direct tension in the ischemic preconditioning/ischemia group. In summary, ischemic preconditioning, using the same protocol reported to be effective in limiting infarct size in porcine muscle, had no significant benefit in limiting injury or improving recovery in the ischemic rat tibialis anterior. The value of ischemic preconditioning in reducing imposed ischemic-reperfusion-induced functional deficits in skeletal muscle remains to be demonstrated.
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PMID:The effect of ischemic preconditioning on the recovery of skeletal muscle following tourniquet ischemia. 939 74

We have demonstrated previously that dichloroacetate can attenuate skeletal muscle fatigue by up to 35% in a canine model of peripheral ischemia (Timmons, J.A., S.M. Poucher, D. Constantin-Teodosiu, V. Worrall, I.A. Macdonald, and P.L. Greenhaff. 1996. J. Clin. Invest. 97:879-883). This was thought to be a consequence of dichloroacetate increasing acetyl group availability early during contraction. In this study we characterized the metabolic effects of dichloroacetate in a human model of peripheral muscle ischemia. On two separate occasions (control-saline or dichloroacetate infusion), nine subjects performed 8 min of single-leg knee extension exercise at an intensity aimed at achieving volitional exhaustion in approximately 8 min. During exercise each subject's lower limbs were exposed to 50 mmHg of positive pressure, which reduces blood flow by approximately 20%. Dichloroacetate increased resting muscle pyruvate dehydrogenase complex activation status by threefold and elevated acetylcarnitine concentration by fivefold. After 3 min of exercise, phosphocreatine degradation and lactate accumulation were both reduced by approximately 50% after dichloroacetate pretreatment, when compared with control conditions. However, after 8 min of exercise no differences existed between treatments. Therefore, it would appear that dichloroacetate can delay the accumulation of metabolites which lead to the development of skeletal muscle fatigue during ischemia but does not alter the metabolic profile when a maximal effort is approached.
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PMID:Substrate availability limits human skeletal muscle oxidative ATP regeneration at the onset of ischemic exercise. 942 69

Conduction velocity (CV) and median frequency (MDF) during tetanic electrical stimulation of the tibialis anterior muscle were evaluated in patients with uncomplicated peripheral arterial occlusive disease. Results were analyzed with respect to biopsy determination of diameter and proportion of types 1 and 2 muscles fibers. Initial MDF and CV correlated positively with type 2, but not type 1 fiber diameter. Initial MDF was reduced bilaterally in patients with unilateral peripheral arterial occlusive disease as compared to normal subjects, indicating that chronic ischemia alone cannot explain the altered myoelectric signal. Physical training increased pain-free walking distance and raised initial MDF, though CV remained unchanged. Fatigue indices were highly interrelated, but showed no correlation with any of the other evaluation variables. Thus, initial MDF, a correlate of type 2 muscle fiber distribution in chronically ischemic tibialis anterior muscles, is altered in peripheral vascular disease. However, muscle ischemia alone cannot explain all aspects of this abnormality.
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PMID:Altered surface myoelectric signals in peripheral vascular disease: correlations with muscle fiber composition. 946 95


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