The purpose of this cross-sectional study was to determine the differences in areal bone mineral density (aBMD) based on alcohol consumption behaviors, bone-loading history as assessed by a bone-specific physical activity questionnaire (BPAQ), and the body mass index (BMI). College-aged female students (N = 112) were recruited from the universities in Seoul and Gyeonggi province, South Korea. The aBMD of the lumbar spine and non-dominant side of the proximal femur (total hip, TH; femoral neck, FN; femoral trochanter, FT) were measured using dual energy X-ray absorptiometry (DXA). Alcohol consumption was determined by the frequency and amount of alcohol intake during the past 12 months using a self-reported questionnaire. The X-scan plus II was used to measure height (cm), body mass (kg), fat-free mass (FFM, kg), and % body fat. Drinking two or more times alcohol per week was associated with greater aBMD of the TH (p = 0.04–0.002) and FN (p = 0.043) compared to a lower frequency of alcohol consumption and 2–4 times per month, respectively. Based on the drinking amount per occasion, there were no significant group differences (p > 0.05) in aBMD at any of the sites. The highest group of total BPAQ had greater aBMD of the TH, FN, and FT versus the lowest (p = 0.023–0.009) and mid of total BPAQ groups (p = 0.004–0.009). Additionally, the highest group had greater aBMD of the lumbar spine compared to the mid group (p = 0.001). No significant group differences in aBMD at any of the sites were noted based on the BMI (p > 0.05). Young college-aged women with greater bone-loading physical activity showed greater aBMD at the TH, FN, FT, and lumbar spine, while a moderate alcohol intake was associated with greater aBMD of the TH and FN. These findings have clinical implications for young women who may not participate in high-impact physical activity and are binge drinkers.

Atrial fibrillation (AF) is the most common supraventricular arrhythmia, and it corresponds highly with exercise intensity. Here, we induced AF in mice using acetylcholine (ACh)-CaCl 2 for 7 days and aimed to determine the appropriate exercise intensity (no, low, moderate, high) to protect against AF by running the mice at different intensities for 4 weeks before the AF induction by ACh-CaCl 2 . We examined the AF-induced atrial remodeling using electrocardiogram, patch-clamp, and immunohistochemistry. After the AF induction, heart rate, % increase of heart rate, and heart weight/body weight ratio were significantly higher in all the four AF groups than in the normal control; highest in the high-ex AF and lowest in the low-ex (lower than the no-ex AF), which indicates that low-ex treated the AF. Consistent with these changes, G protein-gated inwardly rectifying K + currents, which were induced by ACh, increased in an exercise intensity-dependent manner and were lower in the low-ex AF than the no-ex AF. The peak level of Ca 2+ current (at 0 mV) increased also in an exercise intensity-dependent manner and the inactivation time constants were shorter in all AF groups except for the low-ex AF group, in which the time constant was similar to that of the control. Finally, action potential duration was shorter in all the four AF groups than in the normal control; shortest in the high-ex AF and longest in the low-ex AF. Taken together, we conclude that low-intensity exercise protects the heart from AF, whereas high-intensity exercise might exacerbate AF.

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