Can short sprints during moderate intensity exercise reduce the incidence of exercise mediated hypoglycaemia in individuals with type 1 diabetes?

M.Ed ThesisBackground: Short sprints have been shown to reduce exercise induced hypoglycaemia in controlled laboratory settings. This study tested the hypothesis that incorporating sprinting into moderate intensity exercise can reduce the incidence of exercise mediated hypoglycaemia in individuals with T1D in a free-living setting. Methods: Individuals with T1D were recruited into a prospective randomised controlled cross over study. Participants completed three 14-day periods in random order. In one period participants undertook moderate intensity exercise for a minimum of 30 minutes, at least 3 times a week (control period). In the other periods, participants incorporated 10s (every 20 mins) or 4s sprints (every 2 mins) into the exercise regimen. The primary outcome was the incidence of hypoglycaemia, defined as sensor glucose readings <3.5mmol/L for ≥ 20 minutes over the 14-day period. Secondary outcome measures included the incidence of hypoglycaemia <3.1mmol/L and percentage time <3.1mmol/L and <3.5mmol/L. Results: 24 participants completed the study. There was no difference in hypoglycaemic events (<3.5mmol/L) between the 4s and control period (p=0.28) or the 10s and control period (p=0.05). The 10s period was associated with fewer hypoglycaemia events <3.1mmol/L than the control period (p=0.04), with an incidence rate of 0.40 (95% CI 0.26- 0.55), 0.33 (95% CI 0.21-0.45) and 0.28 (95% CI 0.17-0.38) events per day in control, 4s and 10s periods respectively. The 10s period was associated with a reduction in time spent <3.5mmol/L (3.1% vs. 2.1%, p=0.03) and time spent <3.1mmol/L (1.9% vs 1.2%, p= 0.03). There was no increase in nocturnal hypoglycaemia during the sprinting periods. Conclusion: In a free-living setting, the inclusion of 10s sprints into moderate intensity exercise did not reduce hypoglycaemic events <3.5mmol/L but reduced hypoglycaemia <3.1mmol/l and the percentage time spent in hypoglycaemia. These observations may help active people with T1D to exercise more safely by reducing the risk of hypoglycaemia

Prolonged exposure to acetaminophen reduces testosterone production by the human fetal testis in a xenograft model

Most common male reproductive disorders are linked to lower testosterone exposure in fetal life, although the factors responsible for suppressing fetal testosterone remain largely unknown. Protracted use of acetaminophen during pregnancy is associated with increased risk of cryptorchidism in sons, but effects on fetal testosterone production have not been demonstrated. We used a validated xenograft model to expose human fetal testes to clinically relevant doses and regimens of acetaminophen. Exposure to a therapeutic dose of acetaminophen for 7 days significantly reduced plasma testosterone (45% reduction; P = 0.025) and seminal vesicle weight (a biomarker of androgen exposure; 18% reduction; P = 0.005) in castrate host mice bearing human fetal testis xenografts, whereas acetaminophen exposure for just 1 day did not alter either parameter. Plasma acetaminophen concentrations (at 1 hour after the final dose) in exposed host mice were substantially below those reported in humans after a therapeutic oral dose. Subsequent in utero exposure studies in rats indicated that the acetaminophen-induced reduction in testosterone likely results from reduced expression of key steroidogenic enzymes (Cyp11a1, Cyp17a1). Our results suggest that protracted use of acetaminophen (1 week) may suppress fetal testosterone production, which could have adverse consequences. Further studies are required to establish the dose-response and treatment-duration relationships to delineate the maximum dose and treatment period without this adverse effect