## 4 Discussion
This impaired in their ability to capture and transport oxygen in the cardiorespiratory system and the ability to capture oxygen in skeletal muscle by mitochondria [37,38]. Indeed, this leads to a decrease in mitochondrial fatty acid oxidation by increasing intracellular levels of fatty acyl-CoA and diacylglycerol, inhibiting PI3-kinase activity and causing suppression of insulin-stimulated glucose transport [36,38]. Therefore, there is a close relationship between decreased cardiorespiratory fitness with decreased fat oxidation and the development of IR [8-10]. In accordance with the above, however, we did not find a relationship between body composition and MFO. In this regard, [PERSON] et al. [22] studied the relationship between anthropometric characteristics and MFO by comparing men with normal weight (\(n=12\); 17.2 \(\pm\) 5.7 FM%) and overweight (\(n=12\); 30.0 \(\pm\) 5.3%FM) recreationally trained matched in cardiorespiratory fitness (VO2 max 39.0 \(\pm\) 5.5 vs. 41.4 \(\pm\) 7.6 mL\(\cdot\)kg\(\cdot\)min\({}^{-1}\); \(p=0.31\)) and age (\(p=0.93\)). Among the results, as in our results, they found no correlations between FM, FFM, and BMI (\(p>0.05\)) with MFO. These results could be explained by the fact that in both obese and lean individuals, IR states are characterized by inefficient utilization of energy substrates (metabolic flexibility), both glucose and fat, instead of fatty acid absorption favoring triglyceride accumulation in skeletal muscles [7]. Furthermore, as demonstrated in the study by [PERSON] et al. [39], intermyofibmilar mitochondria size, electron transport chain activity, and insulin sensitivity are related to IR [39]. Therefore, VO2 max, as described by [PERSON] et al. [22], may be an independent indicator of body weight and fat mass in the development of IR in an overweight or obese state. On the other hand, it is well accepted that a high percentage of FM or BMI and a low percentage of FFM increases the risk of developing IR [40,41]. However, whether or not IR develops will also depend on the distribution and location of body fat, i.e., where it accumulates. Accumulation of visceral adipose tissue, muscle intracellular fat deposition, or, in particular, intrahepatic lipid accumulation has been identified as contributing to or potentially triggering IR [40,41]. Consistent with the above, [PERSON] et al. [42] reported correlations of different adipose tissue depots/obesity indices with IR according to HOMA-IR. Specifically, the authors showed a significant correlation between HOMA-IR and FM (\(r=0.49\), 95% CI 0.407 to 0.570) and BMI (\(r=0.48\), 95% CI 0.44 to 0.51) [42]. Our results revealed similar results although our correlations were low to moderate, not significant, between the percentage of FFM, FM, and BMI with HOMA-IR. Therefore, body composition analyses such as BMI, FM and FFM may be independently indicative of the metabolic health of people with IR who are physically inactive. Regarding BMI, despite the questions about its use due to its limited representativeness of body adiposity and/or muscle mass, it is still one of the preferred measures in clinical practice [12], although we recommend the use of FM and FFM which better represents metabolically active tissues [16]. Therefore, the use of different, mainly low-cost technologies, such as bioelectrical impedance to analyze body composition, could be more useful in the field to address the prevalence of IR and type 2 diabetes. In fact, FFM percentage could serve as a proxy indicator of VO2 max independently of age and sex in the development or risk of developing IR.