Reduced physical activity in young and older adults: metabolic and musculoskeletal implications - PubMed (original) (raw)

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Reduced physical activity in young and older adults: metabolic and musculoskeletal implications

Kelly A Bowden Davies et al. Ther Adv Endocrinol Metab. 2019.

Abstract

Background: Although the health benefits of regular physical activity and exercise are well established and have been incorporated into national public health recommendations, there is a relative lack of understanding pertaining to the harmful effects of physical inactivity. Experimental paradigms including complete immobilization and bed rest are not physiologically representative of sedentary living. A useful 'real-world' approach to contextualize the physiology of societal downward shifts in physical activity patterns is that of short-term daily step reduction.

Results: Step-reduction studies have largely focused on musculoskeletal and metabolic health parameters, providing relevant disease models for metabolic syndrome, type 2 diabetes (T2D), nonalcoholic fatty liver disease (NAFLD), sarcopenia and osteopenia/osteoporosis. In untrained individuals, even a short-term reduction in physical activity has a significant impact on skeletal muscle protein and carbohydrate metabolism, causing anabolic resistance and peripheral insulin resistance, respectively. From a metabolic perspective, short-term inactivity-induced peripheral insulin resistance in skeletal muscle and adipose tissue, with consequent liver triglyceride accumulation, leads to hepatic insulin resistance and a characteristic dyslipidaemia. Concomitantly, various inactivity-related factors contribute to a decline in function; a reduction in cardiorespiratory fitness, muscle mass and muscle strength.

Conclusions: Physical inactivity maybe particularly deleterious in certain patient populations, such as those at high risk of T2D or in the elderly, considering concomitant sarcopenia or osteoporosis. The effects of short-term physical inactivity (with step reduction) are reversible on resumption of habitual physical activity in younger people, but less so in older adults. Nutritional interventions and resistance training offer potential strategies to prevent these deleterious metabolic and musculoskeletal effects.

Impact: Individuals at high risk of/with cardiometabolic disease and older adults may be more prone to these acute periods of inactivity due to acute illness or hospitalization. Understanding the risks is paramount to implementing countermeasures.

Keywords: anabolic resistance; body composition; insulin resistance; liver fat; physical inactivity; skeletal muscle.

© The Author(s), 2019.

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Conflict of interest statement

Conflict of interest statement: The authors declare that there is no conflict of interest.

Figures

Figure 1.

Figure 1.

A two-part schematic representing the metabolic effects of habitual physical activity (left) and chronic sedentary behaviour (inactivity; right). Left: a consequence of sedentary behaviour is diminished AMPK activation and glucose uptake into skeletal muscle, inducing insulin resistance. The plasma glucose (not transported into muscle) provides a substrate for de novo lipogenesis in adipose tissue and liver. Consequently, there is expansion of adipose tissue mass, intrahepatic lipid accumulation and increased lipid export from the liver as VLDL triacylglycerol particles and serum triacylglycerol with induction of systemic insulin resistance. Right: being habitually active stimulates AMPK activation and glucose uptake into skeletal muscle; insulin sensitivity is therefore preserved and less glucose is diverted to metabolically unfavourable depots. AMPK, AMP-activated protein kinase; NEFA, nonesterified fatty acids; TG, triglyceride; VLDL, very low-density lipoproteins.

Figure 2.

Figure 2.

A two-part schematic representing the Catabolic Crisis model proposed by English and Paddon-Jones (upper figure) and the reduced activity models (young_versus_ old) proposed by Perkin and colleagues (lower figure). Upper: the Catabolic Crisis model proposes that rather than the traditional linear model of age-related muscle loss (sarcopenia), instead episodes of acute illness or injury can accelerate muscle loss (indicated as a nadir on the graph) and are followed by periods of incomplete recovery. Lower: the reduced activity model suggests that older individuals compared to younger individuals tend to have less muscle mass and may lose muscle mass at a quicker rate (when subject to periods of inactivity), and recovery may be more variable. These two theories contextualize the importance of avoiding periods of prolonged inactivity, particularly in older adults.

Figure 3.

Figure 3.

A schematic to summarize the reported effects of physical inactivity on skeletal muscle atrophy. Physical inactivity and ageing have both been linked with increased inflammation and anabolic resistance; microvascular impairment also has a role due to insulin resistance; and with blunted MPS and increased MPB skeletal muscle atrophy is exacerbated. Physical inactivity can also cause reduced satellite cell activation, also linked to atrophy. MPB, muscle protein breakdown; MPS, muscle protein synthesis.

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