## 4 Discussion  
The present study demonstrated that the indices of GV were improved 1 h before and after the LST intervention. The M-value is an index of daily GV, which shows the deviation from an ideal glycemic control [21; 27]. The M-value is a useful clinical parameter that can measure not only GV, but also the quality of the glycemic control [22]. The M-value did not increase in the LST group, whereas it increased in the control group in the same time period that the LST group underwent training. On the contrary, the SD decreased in the LST group, whereas it did not decrease in the control group. The SD value of 24 h glucose levels is a strong independent risk factor of mortality in critically ill patients [28; 29; 30; 31]. The findings of this study suggest that LST has a beneficial effect on short-term GV in healthy individuals. To the best of our knowledge, this is the first study to show the effect of LST on GV using CGMS. Although the underlying mechanism by which resistance training improves GV is not yet fully understood, the following two mechanisms have been proposed in accordance with the current evidence. First, increased growth hormone and catecholamine levels due to resistance training stimulate lipolysis and glycogenolysis, which may lead to stable glycemic control [32; 33]. Second, rapid decreases in glucose levels after exercise are suppressed by gluconeogenesis due to increased lactic acid levels when performing resistance training [34]. LST is a low-intensity resistance training exercise; however, sustained muscular contraction with slow movement restricts muscle blood flow, decreases oxygen delivery to the contracting muscles, and results in the elevation of blood lactate and growth hormone concentrations after training [35]. Moreover, [PERSON] et al. [13] showed that LST can lead to a comparable increase in lactic acid of that caused by high-intensity (approximately 80% of 1-RM) exercise training in young men [13]. These endocrine changes may contribute to the improvement of GV. There were no differences in age, gender ratio, anthropometric parameters, dietary intake, or physical activity between the LST and control groups. There was also no change in physical activity before and after the intervention in either group. Therefore, potential confounding factors such as diet and physical activity appeared to have no influence on GV in this study. However, a few limitations need to be addressed. First, we cannot claim that LST has a favorable effect on GV in patients with diabetes because all study subjects were healthy, young individuals. However, muscle mass declines at a rate of 3-8% every 10 years after the age of 30 [36], and resistance training is an effective strategy for middle-aged and older individuals to counteract age-related declines in muscle mass and insulin sensitivity and to prevent and manage type 2 diabetes [37]. LST may exhibit more beneficial effects on GV in patients with diabetes. Further studies in older patients with diabetes are warranted. Second, the chronic effect of LST on long-term GV or glycemic control is unknown. Third, we did not obtain dietary recall data or physical activity data from the study participants at baseline. Therefore, there may be potential differences in dietary intake and physical activity between groups prior to the study. However, we suggest that physical activity and dietary intake before the study period do not affect the results because the study subjects had a standardized diet during the study period, and no difference in physical activity measured by a triaxial accelerometer between the control group and the intervention group was observed. Despite these limitations, we demonstrated that LST is effective for improving short-term GV. High-intensity resistance exercise increases blood pressure due to the Valsalva maneuver. However, low-intensity resistance exercise such as LST that is equivalent to 30-50% 1-RM does not increase blood pressure in healthy individuals [38].