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The aim of the present study was to assess the performance of subjects with sickle cell trait (SCT) during brief and explosive exercise involving mainly anaerobic metabolism. One hundred and ninety-six black subjects underwent SCT screening, which revealed the presence of 16 subjects with SCT and 180 subjects with normal hemoglobin (HbAA). All subjects performed four tests: 1) a 100-m sprint, 2) a long-jump, 3) a Leger-Boucher shuttle test and 4) a jump-and-reach test. A control group (n = 18) selected from the 180 subjects with HbAA was matched according to the sex, age, weight and height of the SCT subjects (SCTs). The performances of the SCTs (n = 16) were compared with those of the control group. The performances were similar between the SCTs and control group for the sprint test, long-jump and the Leger-Boucher shuttle test. There was, however, a significant difference for the jump-and-reach test between the two groups: the SCTs (i. e., males plus females, and males and females considered separately) reached a significantly greater height (p < 0.05) than the matched subjects of the control group (63.7 +/- 3.6 vs. 58.6 +/- 3.1 cm, 72.3 +/- 3.9 vs. 67.1 +/- 2.4 cm and 52.7 +/- 3.2 vs. 45.3 +/- 2.0 cm for SCTs versus non-SCTs, for the group, the males and the females, respectively). The results of the present study suggest that the performance of brief and explosive exercise may be enhanced by HbS.

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In pancreatic lesions of non-obese diabetic (NOD) mice the expression of inducible nitric oxide synthase (iNOS) and of the cytokines interferon-gamma and interleukin-4 were studied. Strong iNOS expression as determined at the level of transcription, translation and of enzyme activity was associated with destructive insulitis as seen 8-10 days after cyclophosphamide treatment of 70- to 80-day-old female NOD mice. Immunohistochemistry showed iNOS associated with infiltrating macrophages but not in endocrine cells. The enhancement of iNOS after cyclophosphamide correlated with an increase of T-helper type 1 (Th1) associated interferon-gamma expression while T-helper type 2 (Th2) associated interleukin-4 was the dominant cytokine prior to cyclophosphamide and after diabetes onset. We conclude that insulitis in young NOD mice is carried by Th2 cells while cyclophosphamide enhanced insulitis is determined by Th1 cells. Macrophages show two different functional states in insulitis; strong iNOS expression in macrophages is associated with destructive insulitis.

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