One in six individuals worldwide will be 60 years or older by 2030. The number of individuals 60 years and older worldwide is expected to increase from 1 billion in 2020 to 2.1 billion in 2050. By 2050, 426 million people will be 80 years or older [1]. Sarcopenia is often considered an important factor in senior frailty and mobility loss. It is characterised by decreased muscle mass, strength, and functionality with age ^{[2][3][4][5][6][7][8]}[2,3,4,5,6,7,8]. An estimation in 2019 suggested that the economic burden of sarcopenia-associated disability was USD 40.4 billion in the United States, with an average cost of USD 260 per person. These expenses include hospitalisation, nursing home admissions, and home healthcare costs [9]. In addition to disability, sarcopenia is associated with multiple comorbidities, such as osteoporosis [10], obesity [11], and type II diabetes mellitus [12].

To effectively prevent sarcopenia, it is essential to have a thorough understanding of its pathophysiology and to use this knowledge to develop appropriate treatment strategies. The pathogenesis of sarcopenia includes impaired myofiber metabolism and adverse changes to muscle satellite cells, which lead to defective myogenesis and the loss of skeletal muscle homeostasis [13]. The reductions in muscle quality and strength associated with sarcopenia are also accompanied by neurological impairments affecting motor neurons and neuromuscular junctions, which result in denervated muscle fibers [14]. Additionally, persistent low-grade inflammation, poor anabolic signaling mediated by the growth hormone (GH)/insulin growth factor-1 (IGF-1) pathway, lower protein consumption, and vitamin D deficiency all contribute to the deterioration of muscle quality with age ^[15][16][17][15,16,17].

Skeletal muscle, the body’s primary metabolic organ, requires a lot of oxygen, micronutrients, and macronutrients to generate ATP for contraction ^[18][19][18,19]. In fact, during vigorous exercise, skeletal muscle tissue consumes 60% of the body’s total oxygen intake. On the other hand, skeletal muscle cells continuously break down glycogen and phosphocreatine to guarantee that anaerobic energy is available [18]. Skeletal muscle ageing is related to tissue metabolism reprogramming, affecting glucose, fat, and protein use and ultimately energy production [20]. Men lose more skeletal muscle and experience an increased visceral adipose with age, while women have less capillarisation of type II glycolytic myofibers [21]. The composition of the muscle fibres has an impact on the metabolism of macronutrients in aged skeletal muscle. In fact, type II fast-twitch fibres preferentially metabolise glucose anaerobically, while type I slow-twitch fibres preferentially metabolise fatty acids and are characterised by oxidation [22]. In the ageing skeletal muscle, decreased capillarisation and decreased nutrition transport to muscle cells have been observed ^[23][24][23,24].

With age, aerobic capacity, which is the maximum capacity to use oxygen to meet energy needs during both rest and exercise, tends to decline. In correspondence, their skeletal muscle energy metabolism decreases [25]. The mitochondria are crucial for the bioenergetic efficiency of skeletal muscle, and mitochondrial failure is widely acknowledged as a key indicator of ageing [26]. Age-related decrease in skeletal muscle mass and strength is caused by mitochondrial dysfunction. Maintaining mitochondrial health is essential for maintaining proteostasis in skeletal muscle. So far, studies on both animals and humans have contributed to a growing body of information regarding mitochondrial dysfunction in sarcopenia ^{[27][28][29][30][31]}[27,28,29,30,31]. Both ATP depletion and ROS/RNS excess are linked to dysfunctional mitochondria, which cause the activation of dangerous cellular pathways. Aged skeletal muscle tissue exhibits a reduction in mitochondrial bulk, tricarboxylic acid cycle enzyme activity, oxygen consumption, and ATP generation [32]. Furthermore, apoptosis is triggered by mitochondrial dysfunction, which may degrade the quality of skeletal muscle [33].

Persistent low-grade inflammation has been recently demonstrated to impact both muscle protein synthesis and breakdown through several signaling pathways, which has an impact on sarcopenia [34]. Low-grade inflammation is a symptom of cells entering the senescent phase of the cell cycle and exiting the cell cycle. The pro-inflammatory tumour necrosis factor (TNF), IL-6, and C-reactive protein (CRP) are modestly elevated in the circulation in the course of ageing [34]. In conjunction, elderly people with sarcopenia are reported to have significantly higher levels of circulating IL-6 and TNF-α [35]. It was further revealed that elevated IL-6 and CRP levels increased the risk of losing muscle strength [36]. In addition, the plasma concentrations of TNF-α, IL-6, and IL-1 were reliable indicators of morbidity and mortality in senior participants in a 10-year longitudinal research study [37].

The conventional approach to sarcopenia management revolves around lifestyle changes, particularly through physical exercise and nutrition [38]. Due to growing awareness of the potential health benefits of natural products, the use of nutraceuticals, dietary supplements, and functional foods for disease prevention has been increasingly popular worldwide in recent years [39]. Given the importance of oxidative stress and inflammation in the aetiology of sarcopenia, compounds with antioxidant and anti-inflammatory characteristics have the potential to complement the current approach in treating this condition. Curcumin is one of the potential compounds with these qualities [40]. The turmeric-derived polyphenol curcumin (diferuloylmethane) has a variety of therapeutic uses. Since ancient times, turmeric has been used to relieve inflammation in traditional Chinese and Ayurvedic medicine [41]. According to recent scientific investigation, curcumin is reported to have antioxidant, anti-inflammatory, antimutagenic, antimicrobial, and anticancer properties ^{[42][43][44][45][46]}[42,43,44,45,46]. Additionally, the precise molecular mechanisms of curcumin’s activity have been demonstrated through scientific studies [47]. Curcumin is demonstrate.

2. Therapeutic Effects of Curcumin on Muscle Health

Curcumin has been linked to a plethora of health advantages, including muscle health, in various studies ^[48][49]. Preserving muscle mass during ageing is the most important step in preventing sarcopenia. Receno et al. (2019) reported that curcumin (0.2% diet for 4 months) increased the muscular mass of supplemented rats without altering the body mass of 32-month-old male F344xBN rats, which is in line with previous studies ^{[49][50][51][52]}[50,51,52,53]. In another study on contusion-induced muscular injury, 5 mg/kg body weight of curcumin for 7 days in 8-week-old male ICR mice was shown to dramatically enhance muscle mass. Similarly, curcumin supplementation boosted muscle mass but it had no discernible effect on body weight ^[53][54]. The higher skeletal muscle mass of curcumin-supplemented rats was consistent with earlier studies using various models of muscle wasting, by reducing both oxidative stress and inflammation ^[54][55][55,56]. The animals showed improved strength as a result of increased muscle strength. In a study, treatment of 150 mg/kg curcumin for over a period of 2 months resulted in improved muscle endurance, grip strength, and fat/lean mass ratio in 12-month-old male Sprague Dawley rats with LPS-induced sarcopenia ^[56][57]. Curcumin (40 and 80 mg/kg) administered 30 min before forced exercise for 28 days could complement exercise-based therapy to prevent muscular issues such as sarcopenia by regulating the expression of genes related to protein synthesis, apoptosis, and inflammation in chronic forced exercise executed 10-month-old ICR mice ^[57][58]. The effects of curcumin on muscle health are summarised in Table 1.