The prevalence of obesity in combination with sarcopenia (the age-related loss of muscle mass and strength or physical function) is increasing in adults aged 65 years and older. A major subset of adults over the age of 65 is now classified as having sarcopenic obesity, a high-risk geriatric syndrome predominantly observed in an ageing population that is at risk of synergistic complications from both sarcopenia and obesity. This Review discusses pathways and mechanisms leading to muscle impairment in older adults with obesity. We explore sex-specific hormonal changes, inflammatory pathways and myocellular mechanisms leading to the development of sarcopenic obesity. We discuss the evolution, controversies and challenges in defining sarcopenic obesity and present current body composition modalities used to assess this condition. Epidemiological surveys form the basis of defining its prevalence and consequences beyond comorbidity and mortality. Current treatment strategies, and the evidence supporting them, are outlined, with a focus on calorie restriction, protein supplementation and aerobic and resistance exercises. We also describe weight loss-induced complications in patients with sarcopenic obesity that are relevant to clinical management. Finally, we review novel and potential future therapies including testosterone, selective androgen receptor modulators, myostatin inhibitors, ghrelin analogues, vitamin K and mesenchymal stem cell therapy.

Sarcopenic obesity in older adults: aetiology, epidemiology and treatment strategies.

Principles of exercise testing and interpretation

Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including cancer, and is increasingly recognized as a growing cause of preventable cancer risk. Chronic inflammation, a well-known mediator of cancer, is a central characteristic of obesity, leading to many of its complications, and obesity-induced inflammation confers additional cancer risk beyond obesity itself. Multiple mechanisms facilitate this strong association between cancer and obesity. Adipose tissue is an important endocrine organ, secreting several hormones, including leptin and adiponectin, and chemokines that can regulate tumor behavior, inflammation, and the tumor microenvironment. Excessive adipose expansion during obesity causes adipose dysfunction and inflammation to increase systemic levels of proinflammatory factors. Cells from adipose tissue, such as cancer-associated adipocytes and adipose-derived stem cells, enter the cancer microenvironment to enhance protumoral effects. Dysregulated metabolism t...

Obesity, Inflammation, and Cancer

Exercise provides clear beneficial effects for the prevention of numerous diseases. However, many of the molecular events responsible for the curative and protective role of exercise remain elusive. The recent discovery of FNDC5/irisin protein that is liberated by muscle tissue in response to exercise might be an important finding with regard to this unsolved mechanism. The most striking aspect of this myokine is its alleged capacity to drive brown-fat development of white fat and thermogenesis. However, the nature and secretion form of this new protein is controversial. The present study reveals that rat skeletal muscle secretes a 25 kDa form of FNDC5, while the 12 kDa/irisin theoretical peptide was not detected. More importantly, this study is the first to reveal that white adipose tissue (WAT) also secretes FNDC5; hence, it may also behave as an adipokine. Our data using rat adipose tissue explants secretomes proves that visceral adipose tissue (VAT), and especially subcutaneous adipose tissue (SAT), express and secrete FNDC5. We also show that short-term periods of endurance exercise training induced FNDC5 secretion by SAT and VAT. Moreover, we observed that WAT significantly reduced FNDC5 secretion in fasting animals. Interestingly, WAT of obese animals over-secreted this hormone, which might suggest a type of resistance. Because 72% of circulating FNDC5/irisin was previously attributed to muscle secretion, our findings suggest a muscle-adipose tissue crosstalk through a regulatory feedback mechanism.

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FNDC5/irisin is not only a myokine but also an adipokine.

Regular physical activity and exercise training have long been known to cause adaptations to white adipose tissue (WAT), including decreases in cell size and lipid content and increases in mitochondrial proteins. In this article, we discuss recent studies that have investigated the effects of exercise training on mitochondrial function, the “beiging” of WAT, regulation of adipokines, metabolic effects of trained adipose tissue on systemic metabolism, and depot-specific responses to exercise training. The major WAT depots in the body are found in the visceral cavity (vWAT) and subcutaneously (scWAT). In rodent models, exercise training increases mitochondrial biogenesis and activity in both these adipose tissue depots. Exercise training also increases expression of the brown adipocyte marker uncoupling protein 1 (UCP1) in both adipose tissue depots, although these effects are much more pronounced in scWAT. Consistent with the increase in UCP1, exercise training increases the presence of brown-like adipocytes in scWAT, also known as browning or beiging. Training results in changes in the gene expression of thousands of scWAT genes and an altered adipokine profile in both scWAT and vWAT. Transplantation of trained scWAT in sedentary recipient mice results in striking improvements in skeletal muscle glucose uptake and whole-body metabolic homeostasis. Human and rodent exercise studies have indicated that exercise training can alter circulating adipokine concentration as well as adipokine expression in adipose tissue. Thus, the profound changes to WAT in response to exercise training may be part of the mechanism by which exercise improves whole-body metabolic health.

https://diabetes.diabetesjournals.org/content/diabetes/64/7/2361.full.pdf

Exercise Effects on White Adipose Tissue: Beiging and Metabolic Adaptations

Leptin and adiponectin represent two newly discovered adipose tissue derived hormones; that are both associated with health status and glucose and free fatty acid (FFA) metabolism. Moreover, acute and chronic exercises affect body composition, carbohydrate and lipid metabolism. It is thus interesting to evaluate the effects of physical exercise and training on leptin and adiponectin levels. It seems that leptin concentration is not modified after short-term exercise ( or =60 min) stimulating FFA release, or after exercise that generates energy expenditure higher than 800 kcal. Adiponectin concentration presents a delayed increase (30 min) after short-term intense exercise ( or =60 min). Short-term training ( or =12 weeks) show contrasting results regarding leptin and adiponectin. Most training studies which improve fitness levels and affect body composition could decrease leptin and increase adiponectin concentrations.

https://bjsm.bmj.com/content/bjsports/early/2010/05/10/bjsm.2008.046151.full.pdf

Review on leptin and adiponectin responses and adaptations to acute and chronic exercise

Leptin, a hormone synthesized by fat tissue had been noted to regulate energy balance and metabolism and thus to influence body weight. The influence of acute exercise and chronic exercise training on circulating leptin and its relationship with hormonal and metabolic changes that induce energy balance are presented. Research that has examined the influence of exercise under various experimental conditions on leptin and the conflicts in the literature are presented. It appears that a significant caloric perturbation (> 800 kcals) is necessary for acute exercise to result in a significant reduction in leptin. In contrast, exercise training can result in a leptin decline but typically this manifests a reduction in adipose tissue stores. In addition, future directions are presented. Key PointsPhysical exercise and training have both inhibitory and stimulatory effects on leptin.Exercise with energy expenditure higher than 800 kcal can decrease leptinemia.Acute training may cause a decline in circulating leptin levels.

https://www.jssm.org/hfpdf.php?volume=05&issue=2&page=172

Leptin, its implication in physical exercise and training: a short review.

Parathyroid hormone (PTH) is the major hormone regulating calcium metabolism and is involved in both catabolic and anabolic actions on bone. Intermittent PTH exposure can stimulate bone formation and bone mass when PTH has been injected. In contrast, continuous infusion of PTH stimulates bone resorption. PTH concentration may be affected by physical exercise and our review was designed to investigate this relationship. The variation in PTH concentration appears to be influenced by both exercise duration and intensity. There probably exists a stimulation threshold of exercise to alter PTH. PTH regulation is also influenced by the initial bone mineral content, age, gender, training state, and other hormonal and metabolic factors (catecholamines, lactic acid and calcium concentrations). Key PointsPhysical exercise can improve PTH secretion.PARATHYROID HORMONE HAS BOTH ANABOLIC AND CATABOLIC EFFECTS ON BONE: intermittent treatment of PTH is anabolic whereas continuous treatment is catabolic.

Parathyroid Hormone and Physical Exercise: a Brief Review

Although High-intensity interval training (HIIT) has shown its effectiveness in improving body composition, cardio-respiratory fitness and lipid profile in obese adults, evidences remain limited in overweight/obese youth. This study was conducted to investigate the effect of a 12-week HIIT program without caloric restriction on body composition and lipid profile among young overweight/obese men. Twenty healthy obese youth were randomly allocated into two groups; experimental group (HIIT) and control group. The HIIT program consisted in 3 exercises sessions per week (30 sec of work at 100% maximal aerobic velocity [MAV]) interspersed by 30 sec of active recovery at 50% MAV, starting by 15 repetitions to reach 27 by the end of the program. Aerobic capacity (MAV and maximum oxygen uptake [VO2max]), body composition (body mass index [BMI], waist circumference [WC], and fat mass percent) and lipid profile (triglycerides [TG] and total, high-density lipoprotein [HDL] and low-density lipoprotein [LDL] cholesterol) were determined before and after the HIIT program. Following 12 weeks of HIIT, WC, BMI (P<0.01), and fat mass percent (P<0.05) were significantly decreased. MAV and VO2max were significantly improved in the HIIT group, only. Total cholesterol (P<0.05) and TG (P<0.05) decreased significantly in the HIIT group, while LDL and HDL cholesterol levels remained unchanged in both groups. HIIT may be particularly useful in overweight/obese youth to improve body composition, aerobic fitness and lipid profile.

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Impact of a 12-week high-intensity interval training without caloric restriction on body composition and lipid profile in sedentary healthy overweight/obese youth.

To examine the effects of short high-intensity interval training (HIIT) on body composition, physical performance and plasma lipids in overweight/obese compared to normal-weight young men. Nine overweight/obese and nine normal-weight men (control group) aged 17 to 20 years underwent a HIIT programme three times per week for eight weeks. Body composition, indices of aerobic [maximal aerobic velocity (MAV) and maximal oxygen uptake (VO2max)] and anaerobic [squat jump (SJ), counter-movement jump (CMJ), five-jump test (FJT), 10-m and 30-m sprint] performances, as well as fasting plasma lipids, were assessed in the two groups at PRE and POST HIIT. The HIIT programme resulted in significant reductions in body mass (-1.62%, P=0.016, ES=0.11) and fat mass (-1.59%, P=0.021, ES=0.23) in obese, but not in normal-weight subjects. MAV (+5.55%, P=0.005, ES=0.60 and +2.96%, P=0.009, ES=0.82), VO2max (+5.27%, P=0.006, ES=0.63 and +2.88%, P=0.009, ES=0.41), FJT (+3.63%, P=0.005, ES=0.28 and +2.94%, P=0.009, ES=0.52), SJ (+4.92%, P=0.009, ES=0.25 and +6.94%, P=0.009, ES=0.70) and CMJ (+6.84%, P=0.014, ES=0.30 and +6.69%, P=0.002, ES=0.64) significantly increased in overweight/obese and normal-weight groups, respectively. 30-m sprint time significantly decreased in both groups (-1.77%, P=0.038, ES=0.12 and -0.72%, P=0.030, ES=0.16). Plasma total cholesterol (-11.8%, P=0.026, ES=0.96), LDL cholesterol (-11.9%, P=0.050, ES=0.77) and triglycerides (-21.3%, P=0.023, ES=1.08) significantly decreased in the obese group, but not in the normal-weight group. The eight-week HIIT programme resulted in a slight improvement in physical fitness and a significant decrease in plasma lipids in the obese. Short duration HIIT may contribute to an improved cardiometabolic profile in the obese.

https://www.termedia.pl/Journal/-78/pdf-30526-10?filename=11_24255 Article_c.pdf

Effects of high-intensity interval training on body composition, aerobic and anaerobic performance and plasma lipids in overweight/obese and normal-weight young men.

Anissa Bouassida

Papers

Review on leptin and adiponectin responses and adaptations to acute and chronic exercise

Leptin, its implication in physical exercise and training: a short review.

Parathyroid Hormone and Physical Exercise: a Brief Review

Impact of a 12-week high-intensity interval training without caloric restriction on body composition and lipid profile in sedentary healthy overweight/obese youth.

Effects of high-intensity interval training on body composition, aerobic and anaerobic performance and plasma lipids in overweight/obese and normal-weight young men.