Visceral fat accumulation and metabolic syndrome in children: the impact of Trp64Arg polymorphism of the beta3-adrenergic receptor gene.

AIM: To investigate the association between Trp64Arg polymorphism of the beta3-adrenergic receptor (ADRB3) gene and total fat mass, abdominal fat distribution, other metabolic derangements and metabolic syndrome (MS) in Japanese children. METHODS: Molecular screening of the ADRB3 gene polymorphism (Trp64Trp, Trp64Arg and Arg64Arg) was carried out in 132 children aged 6-12 years: 73 were obese (45 boys) and 59 were not obese (27 boys). Visceral fat (VF) and subcutaneous fat (SF) area were measured using magnetic resonance imaging, blood pressure, lipid and glucose profiles. RESULTS: The frequencies of Arg carriers (Trp64Arg or Arg64Arg) were significantly higher in obese children with MS, compared to obese children without MS and nonobese children. In obese children, Arg carriers had significantly higher VF area, systolic and diastolic blood pressure, and low-density lipoprotein cholesterol and triglyceride than Arg noncarriers (Trp64Trp). However, there were no differences in total fat mass and SF area between the two groups. In nonobese children, none of these parameters differed significantly between Arg carriers and noncarriers. CONCLUSION: Trp64Arg polymorphism of the ADRB3 gene may affect VF accumulation and be associated with MS, a cluster of conditions involving aggravated lipid metabolism and higher blood pressure, in Japanese children.

Pronounced muscle deoxygenation during supramaximal exercise under simulated hypoxia in sprint athletes.

The purpose of this study was to determine whether acute hypoxia alters the deoxygenation level in vastus lateralis muscle during a 30 s Wingate test, and to compare the muscle deoxygenation level between sprint athletes and untrained men. Nine male track sprinters (athletic group, VO2max 62.5 ± 4.1 ml/kg/min) and 9 healthy untrained men (untrained group, VO2max 49.9 ± 5.2 ml·kg(-1)·min(-1)) performed a 30 s Wingate test under simulated hypoxic (FIO2 = 0.164 and PIO2 = 114 mmHg) and normoxic conditions. During the exercise, changes in oxygenated hemoglobin (OxyHb) in the vastus lateralis were measured using near infrared continuous wave spectroscopy. Decline in OxyHb, that is muscle deoxygenation, was expressed as percent change from baseline. Percutaneous arterial oxygen saturation (SpO2), oxygen uptake (VO2), and ventilation (VE) were measured continuously. In both groups, there was significantly greater muscle deoxygenation, lower SpO2, lower peakVO2, and higher peakVE during supramaximal exercise under hypoxia than under normoxia, but no differences in peak and mean power output during the exercise. Under hypoxia, the athletic group experienced significantly greater muscle deoxygenation, lower SpO2, greater decrement in peakVO2 and increment in peakVE during the exercise than the untrained group. When the athletic and untrained groups were pooled, the increment of muscle deoxygenation was strongly correlated with lowest SpO2 in the 30 s Wingate test under hypoxia. These results suggest that acute exposure to hypoxia causes a greater degree of peripheral muscle deoxygenation during supramaximal exercise, especially in sprint athletes, and this physiological response would be explained mainly by lower arterial oxygen saturation. Key pointsThe deoxygenation trends in the vastus lateralis muscle during 30 s Wingate test in track sprinters and untrained men under simulated hypoxic and normoxic conditions was investigated using near infrared spectroscopy.Acute hypoxia caused a greater degree of peripheral muscle deoxygenation than normoxia, whereas there were no changes in performance such as power output during 30 s Wingate test.Sprint athletes show a greater degree of peripheral muscle deoxygenation during 30 s Wingate test in hypoxia when compared with untrained subjects.A larger difference in muscle deoxygenation between hypoxia and normoxia is accompanied by lowest SpO2 at the 30 s Wingate test in hypoxia.