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• W1977227568 endingPage "440" @default.
• W1977227568 startingPage "432" @default.
• W1977227568 abstract "Abstract Both altered sympathetic function and insulin resistance have been observed in amyotrophic lateral sclerosis (ALS). Insulin is a sympathetic stimulator. We recorded muscle sympathetic nerve activity (MSNA) by microneurography in 9 patients with ALS and 9 healthy controls during rest. We also initiated a number of sympathoexcitatory maneuvers, including intake of 100 g of glucose. Patients showed reduced glucose tolerance and a higher heart rate and higher level of MSNA at rest than controls (61.0 ± 15.2 vs. 41.2 ± 5.8 bursts/min, P = 0.006); baroreflex inhibitory influence was present. In contrast, MSNA in ALS patients responded more weakly to maneuvers. This inverse relationship is interpreted as a “ceiling effect,” as ALS patients use nearly maximal MSNA capacity already at rest and do not have sympathetic failure. The increased level of MSNA may be a primary feature of ALS, but insulin stimulation may also contribute. Our findings are assessed in relation to previous, sometimes seemingly contradictory observations. Muscle Nerve, 2011" @default.
• W1977227568 created "2016-06-24" @default.
• W1977227568 creator A5021110701 @default.
• W1977227568 creator A5068328185 @default.
• W1977227568 date "2011-02-08" @default.
• W1977227568 modified "2023-10-16" @default.
• W1977227568 title "High resting level and weak response of baroreflex-governed sympathetic outflow in amyotrophic lateral sclerosis" @default.
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• W1977227568 doi "https://doi.org/10.1002/mus.21894" @default.
• W1977227568 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21305564" @default.
• W1977227568 hasPublicationYear "2011" @default.
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