## 3 Results
### Effect of 8-Week Low-Volume RT Intervention on Lipid Profile and Glycemic Control  
No significant differences were observed between the groups for total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, or atherogenic index at the baseline (total cholesterol: \(p\) = 0.221, \(g\) = 0.576; HDL: \(p\) = 0.596; LDL: \(p\) = 0.195, \(g\) = 0.603; triglycerides: \(p\) = 0.994; atherogenic index: \(p\) = 0.258, \(g\) = 0.578) or post-test (total cholesterol: \(p\) = 0.077, \(g\) = 0.789; HDL: \(p\) = 0.845; LDL: \(p\) = 0.120, \(g\) = 0.690; triglycerides: \(p\) = 0.282; atherogenic index: \(p\) = 0.126, \(g\) = 0.698). Figure 4 shows a significant and moderate increase in the HDL cholesterol levels in the 1 SET group, from 43.0 (35.0, 46.0) mg/dL to 45.0 (42.0, 52.0) mg/dL, reaching values within the normal reference range. Additionally, a significant and moderate reduction in the atherogenic index was observed in the 1 SET group (from 3.44 \(\pm\) 0.81 to 3.05 \(\pm\) 0.59), as well as a significant and small reduction in the CON group (from 4.02 \(\pm\) 1.13  
Figure 2: Dot plots showing effects of intervention on creatine kinase (**a**) and lactate dehydrogenase (**b**). Significance values are reported for within-group comparisons. Effect sizes (\(g\)) only apply to normally distributed variables. Dashed lines represent reference ranges. Blue and green dashed lines indicate creatine kinase reference values for men (46–171 U/L) and women (34–145 U/L), respectively; black dashed line indicates reference range for lactate dehydrogenase (120–146 U/L). Clinically meaningful thresholds are also indicated where applicable. to 3.69 \(\pm\) 1.16). No significant changes were detected in the total cholesterol, LDL cholesterol, and triglyceride levels in either group after the intervention. The post-hoc power analysis of total cholesterol (effect size f = 0.395), the atherogenic index (effect size f = 0.349), and LDL cholesterol (effect size f = 0.345) revealed statistical powers of 0.52, 0.43, and 0.42, respectively. No significant differences were observed between the groups in HbA1c or the estimated average glucose levels at the baseline (HbA1c: \(p\) = 0.732, \(g\) = 0.065; estimated glucose: \(p\) = 0.742; \(g\) = 0.059) or post-test (HbA1c: \(p\) = 0.508, \(g\) = 0.283; estimated glucose: \(p\) = 0.499, \(g\) = 0.287). Figure 5 shows that the intervention did not result in significant changes in HbA1c and the estimated glucose levels in the 1 SET (HbA1c: from 6.08 \(\pm\) 0.39% to 6.14 \(\pm\) 0.45%; estimated average glucose: from 127.73 \(\pm\) 11.23 mg/dL to 129.60 \(\pm\) 12.99 mg/dL) and CON groups (HbA1c: from 6.05 \(\pm\) 0.62% to 5.99 \(\pm\) 0.56%; estimated average glucose: from 126.85 \(\pm\) 17.66 mg/dL to 125.31 \(\pm\) 16.12 mg/dL). The HbA1c values were within the normal reference range (<6.5%) in both the groups. The estimated average glucose levels, derived from HbA1c, reflected the same pattern. The post-hoc power analysis of HbA1c (effect size f = 0.141) and estimated average glucose (effect size f = 0.143) revealed a statistical power of 0.11 for both the outcome measures. Figure 3: Dot plots showing effects of intervention on aspartate aminotransferase (AST; (**a**)), alanine aminotransferase (ALT; (**b**)), and AST/ALT ratio (**c**). Significance values are reported for within-group comparisons. Effect sizes (\(g\)) only apply to normally distributed variables. Dashed lines represent reference ranges. Black dashed lines indicate clinical reference ranges for AST (<34 U/L) and ALT (10–49 U/L) for both men and women. Clinically meaningful thresholds are also indicated where applicable. Figure 4: Dot plots showing effects of intervention on total cholesterol (**a**), HDL cholesterol (**b**), LDL cholesterol (**c**), triglycerides (**d**), and atherogenic index (**e**). Significance values are reported for within-group comparisons. Effect sizes (\(g\)) only apply to normally distributed variables. Dashed lines represent reference ranges.