Muscle sympathetic nerve activity (MSNA) was investigated 1 week before (pre-training), 1 week after, and 4-6 weeks after strength training using fatigue-inducing handgrip exercises and post-exercise forearm occlusion. Eighteen volunteers underwent forearm training, which consisted of 30 maximal effort, 10-s-duration static handgrips, 4 days per week for 4 weeks. A second group of 18 volunteers served as a control. MSNA was recorded from the tibial nerve by microneurography. Maximal handgrip force increased at 1 week post-training. The MSNA response during fatigued handgrip also increased at 1 week post-training, as compared to pre-training (52.6 +/- 5.8 vs. 40.6 +/- 4.4 bursts min(-1) (mean +/- SEM), respectively). However, at 4 weeks post-training, MSNA activity returned to the pre-training level (44.0 +/- 5.2 bursts min(-1); p < 0.0001 by ANOVA), while the control group showed no changes throughout this period. The MSNA response during post-exercise forearm occlusion was constant throughout the experiment in both groups. Our results indicate that an increased MSNA response after strength training is likely to be the result of central neural factors rather than the muscle metaboreflex.

Cyclic adenosine monophosphate (cAMP) production during a 5-hour incubation using porcine thyroid cells (PTC) was stimulated significantly more by polyethylene glycol (PEG) 22.5% precipitated fractions (ppt frs) than by PEG 12.5% ppt frs from almost all Graves' sera. However, the thyrotropin (TSH) binding inhibition (TBI) activities of the PEG 12.5% and 22.5% ppt frs using porcine thyroid membranes were similar, and did not change in the 5-hour incubation. When the PEG 12.5% ppt fr from Graves' serum and the PEG 22.5% ppt fr from normal human serum (NHS) were coincubated, cAMP production was also stimulated as much as by the PEG 22.5% ppt fr from Graves' serum. When purified thyroid stimulating antibody (TSAb)-immunoglobulin G (IgG) and the PEG 22.5% ppt fr from NHS were coincubated, increased cAMP production was also observed, whereas bovine thyrotropin (bTSH) did not produce this effect. When purified TSAb-IgG and PEG solutions were coincubated, maximum increases in cAMP production (approximately 10-fold) with 5% PEG were found, whereas no increase was observed using bTSH. The stimulatory effect of high PEG concentrations on thyroid stimulating activity was observed by TSAb-IgG in salt-free or salt-containing medium (<0.15 mol/L NaCl concentration) but not by either TSAb-IgG conjugated to protein A-sepharose 4B or the inactivated TSAb-IgG by the treatment of 70 degrees C for 10 minutes. No stimulatory action by PEG was found with the thyroid stimulating substances such as GTPgammaS, forskolin, or pituitary adenylate-cyclase activating polypeptide (PACAP). The increased thyroid stimulating activity of Graves (IgG) at high PEG concentrations suggests the existence of some factors influencing the ability of TSAb to stimulate thyroid cells, although the exact mechanism remains to be clarified.

These results suggest that changes in selective deep calf oxygenated-Hb can be utilized to estimate calf muscle blood flow changes that are most likely caused by vasoconstriction during graded LBNP.

In this report we describe the characteristics of auto-antibodies to bovine TSH (bTSH) detected in the serum of 2 females among 102 patients with Graves' disease. These patients had never been injected with bTSH. One patient had high LATS activity and high bTSH binding activity after isotope therapy. The other patient showed no detectable LATS activity. Interestingly, the antibody showed a specifically high binding activity for the labelled TSH preparation purified by receptor. The auto-antibody could be demonstrated by the double antibody method, polyethylene glycol method, and by gel-filtration. The antibody was polyclonal immunoglobulin G (IgG). Because the binding of [125I]bTSH with the patient's antibody was inhibited by pituitary extracts from mammalian species other than human, this antibody may cross-react with bovine, rat, dog, rabbit and whale TSH.

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