## 1 Introduction  
Moderate-intensity continuous training (MICT) is defined by sustained aerobic exercise performed at a moderate intensity [1]. Research indicates that MICT significantly enhances cardiovascular health, improves aerobic capacity, and reduces blood pressure [2]. Furthermore, MICT has been linked to reductions in waist circumference, visceral fat, body weight, body fat percentage, and blood lipid levels [3,4]. In contrast, high-intensity continuous training (HICT) conducted over comparable durations has demonstrated improvements in fitness and physical function, particularly affecting outcomes such as VO2 max, blood pressure, and walking speed. Nonetheless, the effects of HICT remain inadequately studied, with only a limited number of investigations addressing this training modality [5].  
The intensity of exercise elevates the demand for oxygen, nutrients, and other essential compounds in cardiac and skeletal muscles. This physiological response triggers processes that stimulate the formation of new blood vessels to meet the increased metabolic demands, thereby facilitating exercise-induced metabolic adaptations [6]. Tumstatin (Col-IV\(\alpha\)3), a fragment derived from type IV collagen, is a key anti-angiogenic molecule that inhibits angiogenesis by suppressing blood vessel formation and endothelial cell proliferation within capillaries. While its direct role in exercise-induced angiogenesis is not well established, tumstatin is known to regulate vascular remodeling and plays a critical role in controlling the balance between angiogenesis and vascular stability [7,8]. Recent studies suggest that angiogenesis-related factors are also linked to lipid metabolism and body composition. Given that tumstatin may influence endothelial function and vascular homeostasis, its relationship with lipid parameters becomes relevant [9]. Dysregulation in these biomarkers is often associated with metabolic disorders, and the impact of exercise and dietary supplements like coenzyme Q\({}_{10}\) (CoQ\({}_{10}\)) on these interactions remains an important area of investigation.  
Dietary supplements are a crucial component of contemporary exercise culture. When combined with regular physical activity, these supplements are known to enhance performance, expedite recovery, promote the clearance of metabolic by-products, and support critical metabolic functions. Among the various supplementation compounds, coenzyme Q\({}_{10}\) holds particular significance due to its essential role in cellular energy metabolism. CoQ\({}_{10}\) serves as a coenzyme for mitochondrial enzymes in the electron transport chain, playing a vital role in energy production within the mitochondrial respiratory system. This function helps alleviate ATP deficits caused by reduced mitochondrial oxygenation during physical exertion [10, 11, 12]. Additionally, CoQ\({}_{10}\) supplementation protects against exercise-induced lipid peroxidation and oxidative stress by reducing inflammation and muscle damage, while also promoting the release of growth factors and downregulating the expression of angiogenesis-related proteins [13,14]. In this study, we examined how the different exercise modalities of MICT and HITC along with CoQ\({}_{10}\) supplementation affect tumstatin levels, lipid metabolism, and body weight regulation, providing insights into the potential interplay between angiogenesis inhibition, metabolic adaptations, and vascular health. Therefore, this study aims to investigate the effects of CoQ\({}_{10}\) supplementation in conjunction with MICT and HICT on these parameters, providing insight into its potential role in metabolic regulation in rats.