Victor Forge
Obesity is a pressing public health issue, affecting a large proportion of older adults. It is associated with a range of health complications, including metabolic syndrome, cardiovascular disease, type 2 diabetes, and cancer. Beyond these well-known complications, obesity also impacts skeletal muscle function and performance, reducing mobility and quality of life. While obese individuals may have greater absolute maximum muscle strength, when normalized to body mass, they exhibit decreased muscle strength, potentially due to reduced mobility, neural adaptations, and changes in muscle morphology. This relative weakness is further exacerbated by the presence of sarcopenia, a condition characterized by the loss of muscle mass and strength, commonly affecting older adults. The interplay between obesity and sarcopenia results in functional limitations and an increased risk of physical disabilities. Understanding the relationship between obesity and muscle strength is crucial for developing interventions to improve physical performance and overall quality of life in obese individuals, particularly as they age.
| Characteristics | Values |
|---|---|
| Definition of Obesity | Abnormal or excessive fat accumulation that may impair health, indicated by a body mass index (BMI) ≥30 |
| Impact of Obesity on Muscle Strength | Obese individuals have greater absolute maximum muscle strength, but when normalized to body mass, they appear weaker due to reduced mobility, neural adaptations, and changes in muscle morphology |
| Obesity and Sarcopenia | Obese individuals with sarcopenia (muscle loss) have a greater risk for complications and functional limitations, such as walking and climbing stairs |
| Obesity and Skeletal Muscle Function | Obesity can affect skeletal muscle function, reducing mobility and quality of life, especially in older adults |
| Mechanisms of Reduced Muscle Function | Alterations in myofilament protein function, cellular contractile properties, morphological adaptations, shifts in fiber type composition, and increased intramyocellular lipid content within skeletal muscle |
| Obesity and Intramuscular Fat | Obesity is associated with increased intramuscular fat content, which can lead to a loss of muscle strength and physical function |
| Comorbidities | Obesity-related muscle strength decline may contribute to cardiometabolic complications, increased risk of cancer, type 2 diabetes, and cardiovascular disease |
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What You'll Learn
Obesity and sarcopenia
Obesity is defined by the World Health Organization as the abnormal or excessive accumulation of fat that may impair health, as indicated by a body mass index (BMI) of ≥30. Obesity is associated with functional limitations in muscle performance and an increased likelihood of developing functional disabilities.
Sarcopenia is the medical term for the gradual loss of muscle mass, strength, and function. It is thought to be caused by the ageing process, with muscle mass beginning to decrease sometime in a person's 30s or 40s, and this process accelerating between the ages of 65 and 80. Sarcopenia can greatly reduce a person's quality of life, impacting their ability to perform daily tasks and leading to a loss of independence.
The coexistence of obesity and sarcopenia is referred to as sarcopenic obesity. Sarcopenic obesity is associated with a higher risk of complications than obesity or sarcopenia alone. The exact mechanisms of sarcopenic obesity are not yet fully understood, but it is believed to be related to metabolic changes, a sedentary lifestyle, adipose tissue derangements, and comorbidities. Studies have found that obese individuals have a greater absolute maximum muscle strength than non-obese persons, but when normalized to body mass, obese individuals appear weaker. This relative weakness may be caused by reduced mobility, neural adaptations, and changes in muscle morphology.
The European Society for Clinical Nutrition and Metabolism (ESPEN) and the European Association for the Study of Obesity (EASO) have recognized the urgent need to define diagnostic tools and criteria for sarcopenic obesity. The lack of a universally established definition and inconsistent diagnostic procedures have hampered efforts to develop effective prevention and treatment strategies.
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Intramuscular fat content
Intramuscular fat, also known as intramuscular adipose tissue (IMAT), refers to the storage of lipids in adipocytes located between muscle fibres and between muscle groups. It is a type of fatty infiltration in the muscle, and its presence can be detected using MRI or CT technology.
Increased levels of IMAT are associated with muscle injury, obesity, age, disease, and physical inactivity. High levels of IMAT can impair mobility and increase the risk of developing disabilities in older adults. Specifically, individuals with high baseline IMAT levels were found to be 50 to 80% more likely to develop mobility limitations over a period of two and a half years compared to those with low baseline IMAT levels.
While obesity is linked to increased IMAT, studies have shown that IMAT levels can also increase with weight loss or remain unchanged with age. This paradox suggests that lipids stored within muscle cells may not always be harmful. For instance, increased levels of intramyocellular lipids (IMCL), a type of lipid stored within muscle cells, are found in both obese, insulin-resistant individuals and highly trained endurance athletes.
The presence of intramuscular fat can have metabolic, muscle, and mobility implications. Specifically, increased IMAT in locomotor muscles can affect metabolism, muscle strength, and mobility. However, the literature also suggests that intramuscular fat content increases irrespective of changes in body mass and subcutaneous fat in the thigh.
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Muscle morphology
Obesity is associated with an increase in muscle size, particularly in the antigravity muscles, such as the quadriceps and calf muscles. This increase in muscle size is a result of the chronic overload stimulus caused by increased adiposity. However, when normalised to body mass, obese individuals may exhibit decreased muscle strength relative to their non-obese counterparts. This relative weakness is suggested to be linked to reduced mobility, neural adaptations, and changes in muscle morphology.
The specific morphological changes associated with obesity include an increase in intramuscular fat content, a shift from slow to fast muscle fibre types, and alterations in muscle fibre size distribution. These changes can impact the contractile function of skeletal muscles, leading to reduced mobility and increased health risks.
The shift from slow to fast muscle fibre types is influenced by several factors. One key factor is the disruption in calcium signalling and 5'-adenosine monophosphate-activated protein kinase (AMPK) activity caused by obesity. This disruption affects excitation-contraction coupling and excitation-transcription coupling in muscle cells. Additionally, obesity-induced decreases in adiponectin levels contribute to decreased insulin sensitivity and increased circulating insulin levels, which further impact AMPK activity and slow fibre type expression.
The impact of obesity on muscle morphology and function is complex and may vary depending on individual factors such as age, physical activity levels, and the presence of other conditions. Further research is needed to comprehensively understand the interplay between obesity and muscle morphology, especially in the context of ageing and pre-sarcopenic individuals. Sarcopenia refers to the gradual loss of muscle mass, strength, and function commonly associated with ageing. Obesity coupled with sarcopenia can exacerbate functional limitations and negatively affect an individual's quality of life.
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Neural adaptations
While obesity may lead to increased absolute maximum muscle strength compared to non-obese individuals, this is not the case when maximum muscular strength is normalised to body mass. Obese individuals appear to be weaker in this case, and this relative weakness may be caused by reduced mobility, neural adaptations, and changes in muscle morphology.
One study by Blimkie et al. (1990) examined the neural and muscular components of force-generating capacity in obese and non-obese adolescent males. The study found that obese adolescents had lower quadriceps femoris muscle activation compared to their non-obese counterparts. This suggests that obesity may impact the nervous system's ability to activate muscles effectively.
Another study by Bosco et al. (1986) found that neural adaptations, such as increased motor unit firing rate, additional recruitment of motor units, and synchronisation of these motor units, contributed to increased performance in resistance training. However, it is important to note that this study was conducted on healthy normal-weight individuals, and the adaptations in obese individuals may differ due to the gradual and sustained increases in fat mass.
Overall, while the specific mechanisms are not yet fully understood, neural adaptations play a role in the relationship between obesity and muscle strength. Further research is needed to fully understand how obesity impacts neural adaptations and their effect on muscle strength.
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Mobility and quality of life
Obesity is associated with functional limitations in muscle performance and an increased likelihood of developing functional disabilities, such as mobility issues, reduced strength, and postural and dynamic balance limitations. The consensus is that obese individuals, regardless of age, have a greater absolute maximum muscle strength compared to non-obese individuals. This is because increased adiposity acts as a chronic overload stimulus on the antigravity muscles (e.g. quadriceps and calf muscles), resulting in increased muscle size and strength.
However, when maximum muscular strength is normalised to body mass, obese individuals appear weaker. This relative weakness may be caused by reduced mobility, neural adaptations, and changes in muscle morphology. Obesity can also lead to a decrease in muscle mass and lower muscle quality. The presence of obesity, coupled with sarcopenia (the gradual loss of muscle mass, strength, and function), has been shown to exacerbate functional limitations, making it more difficult to perform physical functions that require strength. Sarcopenia commonly affects older adults and is considered a major factor in increased frailty, falls, and fractures, which can lead to hospitalisations and surgeries, increasing the risk of complications, including death.
Obesity-related declines in physical performance are due, in part, to compromised muscle strength and power. These declines are associated with alterations in myofilament protein function and cellular contractile properties, which may be related to morphological adaptations, such as shifts in fibre type composition and increased intramyocellular lipid content within skeletal muscle. Obesity leads to increased visceral adipose tissue deposits, which result in disrupted secretions of adiponectin and increased production of inflammatory cytokines and chemokines. These disruptions can decrease the production of contractile proteins in myotubes and affect muscle fibre size distribution.
Overall, obesity can negatively impact mobility and quality of life, particularly in older adults, by reducing muscle strength and function and increasing the risk of developing functional disabilities.
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Frequently asked questions
Obesity is associated with functional limitations in muscle performance and an increased likelihood of developing functional disabilities such as mobility, strength, postural and dynamic balance limitations.
Obesity has well-known metabolic effects and leads to serious health complications such as metabolic syndrome, cardiovascular disease, type 2 diabetes, and an increased risk of cancer.
Obese individuals have a greater absolute maximum muscle strength compared to non-obese persons. However, when maximum muscular strength is normalised to body mass, obese individuals appear weaker. This relative weakness may be caused by reduced mobility, neural adaptations, and changes in muscle morphology.
