Using an integrative approach, this review highlights the benefits of resistance training toward improvements in functional status, health and quality of life among older adults. Sarcopenia (i.e. muscle atrophy) and loss of strength are known to occur with age. While its aetiology is poorly understood, the multifactorial sequelae of sarcopenia are well documented and present a major public health concern to our aging population, as both the quality of life and the likelihood of age-associated declines in health status are influenced. These age-related declines in health include decreased energy expenditure at rest and during exercise, and increased body fat and its accompanying increased dyslipidaemia and reduced insulin sensitivity. Quality of life is affected by reduced strength and endurance and increased difficulty in being physically active. Strength and muscle mass are increased following resistance training in older adults through a poorly understood series of events that appears to involve the recruitment of satellite cells to support hypertrophy of mature myofibres. Muscle quality (strength relative to muscle mass) also increases with resistance training in older adults possibly for a number of reasons, including increased ability to neurally activate motor units and increased high-energy phosphate availability. Resistance training in older adults also increases power, reduces the difficulty of performing daily tasks, enhances energy expenditure and body composition, and promotes participation in spontaneous physical activity. Impairment in strength development may result when aerobic training is added to resistance training but can be avoided with training limited to 3 days/week.

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Findings indicate 3-d x wk(-1) concurrent performance of both strength and endurance training does not impair adaptations in strength, muscle hypertrophy, and neural activation induced by strength training alone. Results provide a physiological basis to support several performance studies that consistently indicate 3-d x wk(-1) concurrent training does not impair strength development over the short term.

Single and double site mutants affecting the presumed catalytic centre of the selenoenzyme PHGPx were subjected to functional analysis. The rate constants k+1 and k'+2, for the oxidation and the regeneration of the ground state enzyme were estimated, respectively. Moreover, the alkylation rate of the reactive centre by iodoacetate (kinact.) was also analysed. The substitution of the catalytically competent selenocysteine 46 by cysteine (PHGPxcys46) decreased k+1 and k'+2 by about three orders of magnitude, although leaving unaffected kinact.. Furthermore, mutations of PHGPxcys46 involving the other residues of the triad decreased both kinact. and k+1, thus highlighting the involvement of Gln 81 and Trp 136 in the dissociation/activation of the nucleophilic cysteine thiol. In general, substitutions of Gln 81 or Trp 136 by acidic residues in PHGPxcys46 most dramatically depressed the k+1 values, because they practically prevented the dissociation of the thiol group, while neutral or positively charged residues in these positions allowed an intermediate dissociation and induced a corresponding reactivity of the thiol. Our data, for the first time, reveal that the presumed triad of selenocysteine, glutamine and tryptophan residues represents a novel type of catalytic centre, whose integrity is essential for the full catalytic function of glutathione peroxidases.

Individual compartments of abdominal adiposity and lipid content within the liver and muscle are differentially associated with metabolic risk factors, obesity and insulin resistance. Subjects with greater intra‐abdominal adipose tissue (IAAT) and hepatic fat than predicted by clinical indices of obesity may be at increased risk of metabolic diseases despite their “normal” size. There is a need for accurate quantification of these potentially hazardous depots and identification of novel subphenotypes that recognize individuals at potentially increased metabolic risk. We aimed to calculate a reference range for total and regional adipose tissue (AT) as well as ectopic fat in liver and muscle in healthy subjects. We studied the relationship between age, body‐mass, BMI, waist circumference (WC), and the distribution of AT, using whole‐body magnetic resonance imaging (MRI), in 477 white volunteers (243 male, 234 female). Furthermore, we used proton magnetic resonance spectroscopy (MRS) to determine intrahepatocellular (IHCL) and intramyocellular (IMCL) lipid content. The anthropometric variable which provided the strongest individual correlation for adiposity and ectopic fat stores was WC in men and BMI in women. In addition, we reveal a large variation in IAAT, abdominal subcutaneous AT (ASAT), and IHCL depots not fully predicted by clinically obtained measurements of obesity and the emergence of a previously unidentified subphenotype. Here, we demonstrate gender‐ and age‐specific patterns of regional adiposity in a large UK‐based cohort and identify anthropometric variables that best predict individual adiposity and ectopic fat stores. From these data we propose the thin‐on‐the‐outside fat‐on‐the‐inside (TOFI) as a subphenotype for individuals at increased metabolic risk.

Ind PW, Bell JD. Reduction of total lung capacity in obese men: comparison of total intrathoracic and gas volumes. J Appl Physiol 108: 1605-1612, 2010. First published March 18, 2010 doi:10.1152/japplphysiol.01267.2009.-Restriction of total lung capacity (TLC) is found in some obese subjects, but the mechanism is unclear. Two hypotheses are as follows: 1) increased abdominal volume prevents full descent of the diaphragm; and 2) increased intrathoracic fat reduces space for full lung expansion. We have measured total intrathoracic volume at full inflation using magnetic resonance imaging (MRI) in 14 asymptomatic obese men [mean age 52 yr, body mass index (BMI) 35-45 kg/m 2 ] and 7 control men (mean age 50 yr, BMI 22-27 kg/m 2 ). MRI volumes were compared with gas volumes at TLC. All measurements were made with subjects supine. Obese men had smaller functional residual capacity (FRC) and FRC-to-TLC ratio than control men. There was a 12% predicted difference in mean TLC between obese (84% predicted) and control men (96% predicted). In contrast, differences in total intrathoracic volume (MRI) at full inflation were only 4% predicted TLC (obese 116% predicted TLC, control 120% predicted TLC), because mediastinal volume was larger in obese than in control [heart and major vessels (obese 1.10 liter, control 0.87 liter, P ϭ 0.016) and intrathoracic fat (obese 0.68 liter, control 0.23 liter, P Ͻ 0.0001)]. As a consequence of increased mediastinal volume, intrathoracic volume at FRC in obese men was considerably larger than indicated by the gas volume at FRC. The difference in gas volume at TLC between the six obese men with restriction, TLC Ͻ 80% predicted (OR), and the eight obese men with TLC Ͼ 80% predicted (ON) was 26% predicted TLC. Mediastinal volume was similar in OR (1.84 liter) and ON (1.73 liter), but total intrathoracic volume was 19% predicted TLC smaller in OR than in ON. We conclude that the major factor restricting TLC in some obese men was reduced thoracic expansion at full inflation. magnetic resonance imaging; restricted total lung capacity; mediastinal volume ABOUT 50 YEARS AGO, IT WAS established that functional residual capacity (FRC) and expiratory reserve volume (ERV) are reduced in most seated obese subjects (14, 32). More recently, reduction in total lung capacity (TLC), formerly thought only to occur in massively obese subjects (28), has been found in some subjects with less severe obesity (17). Consistent with the development of a restrictive pattern of lung function in some obese subjects, prospective studies have shown that weight gain is associated with loss of vital capacity (VC) (6,7,34), while weight loss is associated with increase in VC (22,28,29,31).The mechanical factors reducing VC and TLC in obesity are uncertain, but it has been speculated that increased abdominal volume in some way reduces inspiratory descent of the diaphragm and consequent expansion of the thorax. Recent studies of induced ascites in dogs have shown that, at FRC, the lung-expanding action of the diaphragm was r...

An inverse relationship has been shown between running and cycling exercise economy and maximum oxygen uptake (VO2max). The purposes were: 1) determine the relationship between walking economy and VO2max; and 2) determine the relationship between muscle metabolic economy and muscle oxidative capacity and fiber type. Subjects were 77 premenopausal normal weight women. Walking economy (1/VO2max) was measured at 3 mph and VO2max during graded treadmill test. Muscle oxidative phosphorylation rate (OxPhos), and muscle metabolic economy (force/ATP) were measured in calf muscle using 31P MRS during isometric plantar flexion at 70 and 100% of maximum force, (HI) and (MI) respectively. Muscle fiber type and citrate synthase activity were determined in the lateral gastrocnemius. Significant inverse relationships (r from -0.28 to -0.74) were observed between oxidative metabolism measures and exercise economy (walking and muscle). Type IIa fiber distribution was inversely related to all measures of exercise economy (r from -0.51 to -0.64) and citrate synthase activity was inversely related to muscle metabolic economy at MI (r = -0.56). In addition, Type IIa fiber distribution and citrate synthase activity were positively related to VO2max and muscle OxPhos at HI and MI (r from 0.49 to 0.70). Type I fiber distribution was not related to any measure of exercise economy or oxidative capacity. Our results support the concept that exercise economy and oxidative capacity are inversely related. We have demonstrated this inverse relationship in women both by indirect calorimetry during walking and in muscle tissue by 31P MRS.

These data suggest that differences in Hb and aerobic capacity of muscle are related to reduced VO2max in AA women. However, Hb and aerobic capacity of the muscle can only partially explain the racial differences in VO2max.