With tremendous advances in public health as well as science and technology, life expectancy is increasing and the number of people over 80 years old is expected to triple globally by 2050, making global aging an increasingly serious problem[1]. Diseases caused by aging, such as sarcopenia, geriatric diabetes, obesity, and cardiovascular disease, place a huge burden on the healthcare system and have led to an increasing focus on “healthy aging” as a major public health topic [2]. Among these, aging and sarcopenia are associated with loss of bioenergy, and mitochondrial dysfunction is a major hallmark of aging [3]. Mitochondria are a key organelle in the regulation of the metabolic state of skeletal muscle, producing ATP through oxidative phosphorylation, which is essential for life. Impaired mitochondrial function affects cellular energy conversion, leading to excessive accumulation of reactive oxygen species (ROS), and excessive accumulation of ROS under mitochondrial dysfunction or oxidative stress is, in turn, a driver of aging [4]. Cardiolipin (CL) is a unique phospholipid in mitochondria that is essential for mitochondrial energy metabolism and structural integrity, and in normal human skeletal and cardiac muscle mitochondria cardiolipin is mainly present as tetralinoleoyl cardiolipin (TL-CL) [5], which plays an important role in maintaining mitochondrial membrane potential and morphology, participating in oxidative phosphorylation and composition of electron transport chain (ETC) complexes, regulation of mitochondrial autophagy and apoptosis [6]. CL is used as a validated biomarker to study mitochondrial content and function [7], and alterations in its structure or content are thought to contribute to mitochondrial dysfunction and decreased muscle mass, strength, and physical performance [8], [9].

In addition to medications, lifestyle changes such as increased physical activity or calorie restriction are currently of interest for the treatment of diseases associated with aging [10]. Studies have shown that regular participation in physical activity or exercise training can reduce the loss of muscle strength, decrease the incidence of age-related diseases [11], improve quality of life, and even increase the average and maximum life span of humans [12]. Long-term exercise training promotes the accumulation of ROS and reaches levels at which the body induces tolerable damage, thereby stimulating cellular antioxidant and oxidative damage repair systems [13] and inducing beneficial adaptations in the body. The study found that high-intensity interval exercise (HIIT) in young and older adults promotes mitochondrial biosynthesis in skeletal muscle, improves insulin sensitivity, increases mitochondrial respiratory capacity and muscle strength, and improves age-related decline in muscle mitochondrial function [14]. In addition, regular exercise can cause upregulation of CL levels [15] and improve physical health, and athletes who performed regular exercise had higher levels of CL [16] and showed a higher antioxidant capacity. It has been shown that 12 weeks of aerobic exercise combined with resistance exercise-induced changes in the intramuscular phospholipid profile of obese women with enhanced mitochondrial function and increased content, accompanied by increased CL content and improved mitochondrial respiration, in addition to a decrease in the incidence of type 2 diabetes [17]. Also found in animal experiments that exercise training promoted positive remodeling of the mitochondrial phospholipidome in skeletal muscle of rats with skin cancer in the urinary tract, causing an increase in CL content and positively influencing the ability of mitochondria to generate ATP [18]. However, several studies have found that short-term exercise [19], [20] did not induce significant changes in total skeletal muscle CL content in humans. Although several studies have examined the effects of different types of exercise on CL biosynthesis, it is difficult to determine whether exercise promotes CL biosynthesis in human skeletal muscle because of inconsistent results due to limited sample size, different physical characteristics of the subjects, and differences in age ranges. Therefore, it is necessary to conduct an integrated analysis of this type of study, aiming to assess the effect of exercise on CL synthesis.