To study the effect of temperature on muscle metabolism during submaximal exercise, six endurance-trained men had one thigh warmed and the other cooled for 40 min prior to exercise using water-perfused cuffs. One cuff was perfused with water at 50-55 degrees C (HL) with the other being perfused with water at 0 degree C (CL). With the cuffs still in position, subjects performed cycling exercise for 20 min at a work load corresponding to 70% VO2,peak (where VO2,peak is peak pulmonary oxygen uptake) in comfortable ambient conditions (20-22 degrees C). Muscle biopsies were obtained prior to and following exercise and forearm venous blood was collected prior to and throughout the exercise period. Muscle temperature (Tmus) was not different prior to treatment, but treatment resulted in a large difference in pre-exercise Tmus (difference = 6.9 +/- 0.9 degrees C; P < 0.01). Although this difference was reduced following exercise; it was nonetheless significant (difference = 0.4 +/- 0.1 degree C; P < 0.05). Intramuscular [ATP] was not affected by either exercise or muscle temperature. [Phosphocreatine] decreased (P < 0.01) and [creatine] increased (P < 0.01) with exercise but were not different when comparing HL with CL. Muscle lactate concentration was not different prior to treatment nor following exercise when comparing HL with CL. Muscle glycogen concentration was not different when comparing the trials before treatment, but the post-exercise value was lower (P < 0.05) in HL compared with CL. Thus, net muscle glycogen use was greater during exercise with heating (208 +/- 23 vs. 118 +/- 22 mmol kg-1 for HL and CL, respectively; P < 0.05). These data demonstrate that muscle glycogen use is augmented by increases in intramuscular temperature despite no differences in high energy phosphagen metabolism being observed when comparing treatments. This suggests that the increase in carbohydrate utilization occurred as a direct effect of an elevated muscle temperature and was not secondary to allosteric activation of enzymes mediated by a reduced ATP content.

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Hypogonadism is the most frequent hormonal deficiency in individuals with Prader‐Willi syndrome (PWS). This often necessitates testosterone treatment, but limited data are available to guide testosterone treatment in adult men with PWS. We aimed to evaluate the serum testosterone concentrations and adverse effects of testosterone treatment in individuals with PWS attending a specialist obesity management service. A retrospective audit was undertaken at Austin Health, Melbourne between January 2010 and April 2021. Main outcome measures were testosterone formulation and dose, serum total testosterone concentration, and prevalence of polycythemia and behavioral disturbance. Data were available for eight individuals with median baseline age 19 years (range, 19–42) and BMI 37 kg/m2 (range, 27–71). Six men had obstructive sleep apnea; none were smokers. Baseline testosterone concentration was 1.8 nmol/L (IQR, 1.1–3.3) with hematocrit 0.43. Testosterone formulations were intramuscular testosterone undecanoate (TU) 1000 mg (n = 5), transdermal testosterone gel 50 mg daily (n = 1), and oral TU 80–120 mg daily (n = 2). Median total testosterone concentration was 9.7 nmol/L (IQR, 8.5–14.7). Nine of 25 (36%) hematocrit results in six patients measured >0.50 (range, 0.50–0.56). Intramuscular TU was well tolerated and was the only formulation to achieve serum total testosterone concentrations in the adult male reference range. Worsening behavioral disturbance resulted in treatment discontinuation in one individual. Our experience reinforces the need to regular monitoring of hematocrit in men with PWS treated with testosterone. However, a worsening of behavior problems was uncommon in this series.