The exact relationship between the bed rest-induced loss of skeletal muscle and reductions in muscle strength and physical performance in the older individuals is still unclear. We examined the effect of 10 days of bed rest on changes in regional body composition, muscle strength, and functional status, and the relationship between these variables in older individuals. Regional body composition was measured using dual energy x-ray absorptiometry. We also determined changes in leg strength and several indices of functional status, including walking speed. Body weight, body mass index, and total and lower extremity lean mass decreased with bed rest. There were also significant reductions in knee extension one repetition maximum, isometric knee extension, knee extension 60° concentric, stair ascent time, stair ascent power, stair descent time, VO₂ max, floor transfer test, 5-minute walk time, and chair stand. The overall change in total and lower extremity lean mass was also directly related to bed rest-induced reductions in one repetition maximum knee extension. Bed rest promoted overall declines in muscle mass, muscle strength, and physical function in older individuals. The changes in lean tissue were closely correlated with the bed rest-induced decline of muscle strength.

The age‐related concomitant loss of skeletal muscle and accumulation of excess adipose tissue have been commonly referred to as sarcopenic obesity. While weight loss may help mitigate the metabolic abnormalities linked to obesity, low fitness levels and muscle atrophy complicate the effectiveness of lifestyle interventions. Because of low levels of compliance, suboptimal economic efficiency, and low functional capacity, there has been no consensus on optimal therapy. This includes the use of high‐protein diets that do not ensure muscle preservation during weight loss in this segment of the population. The primary objectives of this review are to discuss the relevance of sarcopenic obesity, examine the feasibility of weight loss in the elderly, and highlight new approaches to the problem.

The purpose of this study was to evaluate pre- and post-season measures of body composition, skeletal muscle, and blood parameters/liver lipid in wildland firefighters (WLFF) over the fire season. Alaskan WLFF (N = 27) crews were evaluated pre and post wildfire season, which included 63 ± 10 operational days. Body composition, thigh muscle area and liver lipid were quantified using dual energy x-ray absorptiometry and MRI, respectively. Blood metabolic and lipid panels were also collected and analyzed. Total body, fat, and visceral fat mass increased from pre to post season (p < 0.05). Total cholesterol, LDL and total globulin also increased (p < 0.05). There was a trend (p = 0.06) towards an increase in IHL. The observed maladaptive changes in adipose tissue, blood lipids and hepatic function may reflect adaptations/consequences to occupational demands/conditions and warrant evaluation of appropriate countermeasures.

Ism. The purpose of the study was to evaluate the influence of the Yukon Arctic Ultra (430-mile event) on potential activators of brown fat, metabolites, and body composition in healthy individuals. Methods Eight male and female participants (mean ± SEM: age, 44 ± 3 yr; body mass index, 23.4 ± 0.9) were recruited for participation. Blood samples were collected at pre-event, mid-event, and post-event checkpoints. Results The temperature during the event ranged from −45°C to −8°C. Because of these extremely challenging conditions, 50% of the participants withdrew from competition by the 300-mile mark, and those that surpassed 300 miles lost a significant (P = 0.002; P = 0.01) amount of body weight (76 ± 5 kg to 73 ± 4 kg) and fat mass (13 ± 1 kg to 12 ± 3 kg), respectively. With respect to serum irisin, there was a trend (P = 0.06) toward significance from pre-event (1033 ± 88 ng·mL−1), mid-event (1265 ± 23 ng·mL−1) to post-event (1289 ± 24 ng·mL−1). Serum meteorin-like and fibroblast growth factor-21 remained stable throughout the event. There were no changes in creatinine, acetoacetate, acetate, and valine. Serum lactate decreased (P = 0.04) during the event. Conclusions The influence of cold exposure and extreme physical exertion may promote substantial increases in serum irisin, and specific alterations in substrate metabolism that largely preserve skeletal muscle and physiological resilience....

The role of catecholamines in the control of hepatic glucose production was studied during heavy exercise in dogs, using a technique to selectively block hepatic α- and β-adrenergic receptors. Surgery was done >16 days before the study, at which time catheters were implanted in the carotid artery, portal vein, and hepatic vein for sampling and the portal vein and vena cava for infusions. In addition, flow probes were implanted on the portal vein and hepatic artery. Each study consisted of a 100-min equilibration, a 30-min basal, a 20-min heavy exercise (∼85% of maximum heart rate), a 30-min recovery, and a 30-min adrenergic blockade test period. Either saline (control; n= 7) or α (phentolamine)- and β (propranolol)-adrenergic blockers (Blk; n = 6) were infused in the portal vein. In both groups, epinephrine (Epi) and norepinephrine (NE) were infused in the portal vein during the blockade test period to create supraphysiological levels at the liver. Isotope ([3-³H]glucose) dilution and arteriovenous differences were used to assess hepatic function. Arterial Epi, NE, glucagon, and insulin levels were similar during exercise in both groups. Endogenous glucose production (R_a) rose similarly during exercise to 7.9 ± 1.2 and 7.5 ± 2.0 mg ⋅ kg⁻¹⋅ min⁻¹in control and Blk groups at time = 20 min. Net hepatic glucose output also rose to a similar rate in control and Blk groups with exercise. During the blockade test period, arterial plasma glucose and R_arose to 164 ± 5 mg/dl and 12.0 ± 1.4 mg ⋅ kg⁻¹⋅ min⁻¹, respectively, but were essentially unchanged in Blk. The attenuated response to catecholamine infusion in Blk substantiates the effectiveness of the hepatic adrenergic blockade. In conclusion, these results show that direct hepatic adrenergic stimulation does not participate in the increase in R_a, even during the exaggerated sympathetic response to heavy exercise.

To test whether hepatic insulin action and the response to an insulin-induced decrement in blood glucose are enhanced in the immediate postexercise state as they are during exercise, dogs had sampling (artery, portal vein, and hepatic vein) catheters and flow probes (portal vein and hepatic artery) implanted 16 days before a study. After 150 min of moderate treadmill exercise or rest, dogs were studied during a 150-min hyperinsulinemic (1 mU · kg⁻¹· min⁻¹) euglycemic ( n = 5 exercised and n = 9 sedentary) or hypoglycemic (65 mg/dl; n = 8 exercised and n = 9 sedentary) clamp. Net hepatic glucose output (NHGO) and endogenous glucose appearance (R_a) and utilization (R_d) were assessed with arteriovenous and isotopic ([3-³H]glucose) methods. Results show that, immediately after prolonged, moderate exercise, in relation to sedentary controls: 1) the glucose infusion rate required to maintain euglycemia, but not hypoglycemia, was higher; 2) R_dwas greater under euglycemic, but not hypoglycemic conditions; 3) NHGO, but not R_a, was suppressed more by a hyperinsulinemic euglycemic clamp, suggesting that hepatic glucose uptake was increased; 4) a decrement in glucose completely reversed the enhanced suppression of NHGO by insulin that followed exercise; and 5) arterial glucagon and cortisol were transiently higher in the presence of a decrement in glucose. In summary, an increase in insulin action that was readily evident under euglycemic conditions after exercise was abolished by moderate hypoglycemia. The means by which the glucoregulatory system is able to overcome the increase in insulin action during moderate hypoglycemia is related not to an increase in R_abut to a reduction in insulin-stimulated R_d. The primary site of this reduction is the liver.