Water consumption acutely reduces meal energy intake (EI) among middle‐aged and older adults. Our objectives were to determine if premeal water consumption facilitates weight loss among overweight/obese middle‐aged and older adults, and to determine if the ability of premeal water consumption to reduce meal EI is sustained after a 12‐week period of increased water consumption. Adults (n = 48; 55–75 years, BMI 25–40 kg/m²) were assigned to one of two groups: (i) hypocaloric diet + 500 ml water prior to each daily meal (water group), or (ii) hypocaloric diet alone (nonwater group). At baseline and week 12, each participant underwent two ad libitum test meals: (i) no preload (NP), and (ii) 500 ml water preload (WP). Meal EI was assessed at each test meal and body weight was assessed weekly for 12 weeks. Weight loss was ∼2 kg greater in the water group than in the nonwater group, and the water group (β = −0.87, P < 0.001) showed a 44% greater decline in weight over the 12 weeks than the nonwater group (β = −0.60, P < 0.001). Test meal EI was lower in the WP than NP condition at baseline, but not at week 12 (baseline: WP 498 ± 25 kcal, NP 541 ± 27 kcal, P = 0.009; 12‐week: WP 480 ± 25 kcal, NP 506 ± 25 kcal, P = 0.069). Thus, when combined with a hypocaloric diet, consuming 500 ml water prior to each main meal leads to greater weight loss than a hypocaloric diet alone in middle‐aged and older adults. This may be due in part to an acute reduction in meal EI following water ingestion.

Exercise is commonly prescribed as a lifestyle treatment for chronic metabolic diseases as it functions as an insulin sensitizer, cardio-protectant, and essential lifestyle tool for effective weight maintenance. Exercise boosts the production of reactive oxygen species (ROS) and subsequent transient oxidative damage, which also upregulates counterbalancing endogenous antioxidants to protect from ROS-induced damage and inflammation. Exercise elevates heme oxygenase-1 (HO-1) and biliverdin reductase A (BVRA) expression as built-in protective mechanisms, which produce the most potent antioxidant, bilirubin. Together, these mitigate inflammation and adiposity. Moderately raising plasma bilirubin protects in two ways: (1) via its antioxidant capacity to reduce ROS and inflammation, and (2) its newly defined function as a hormone that activates the nuclear receptor transcription factor PPARα. It is now understood that increasing plasma bilirubin can also drive metabolic adaptions, which improve deleterious outcomes of weight gain and obesity, such as inflammation, type II diabetes, and cardiovascular diseases. The main objective of this review is to describe the function of bilirubin as an antioxidant and metabolic hormone and how the HO-1–BVRA–bilirubin–PPARα axis influences inflammation, metabolic function and interacts with exercise to improve outcomes of weight management.

With the aging of the baby-boom generation and increases in life expectancy, the American population is growing older. Aging is associated with adverse changes in glucose tolerance and increased risk of diabetes; the increasing prevalence of diabetes among older adults suggests a clear need for effective diabetes prevention approaches for this population. The purpose of paper is to review what is known about changes in glucose tolerance with advancing age and the potential utility of resistance training (RT) as an intervention to prevent diabetes among middle-aged and older adults. Age-related factors contributing to glucose intolerance, which may be improved with RT, include improvements in insulin signaling defects, reductions in tumor necrosis factor-α, increases in adiponectin and insulin-like growth factor-1 concentrations, and reductions in total and abdominal visceral fat. Current RT recommendations and future areas for investigation are presented.

Weight loss from exercise is often less than expected. Putative compensatory mechanisms may limit exercise-induced reductions in body fat and might be proportional to exercise energy expenditure (ExEE). This study was conducted to determine compensation for (the difference between accumulated exercise energy expenditure and changes in body tissue energy stores) and compensatory responses to 1,500 or 3,000 kcal/wk of ExEE. Overweight-to-obese ( n = 36) sedentary men and women were randomized to groups expending 300 or 600 kcal/exercise session, 5 days/wk, for 12 wk. Fourteen participants in the 300-kcal group and 15 in the 600-kcal group completed the study. The primary outcome was energy compensation assessed through changes in body tissue energy stores. Secondary outcomes were putative compensatory responses of resting metabolic rate, food reinforcement, dietary intake, and serum acylated ghrelin and glucagon-like peptide-1. All measures were determined pre- and posttraining. The 3,000 kcal/wk group decreased ( P < 0.01) percentage and kilograms of body fat, while the 1,500 kcal/wk group did not. The 1,500 and 3,000 kcal/wk groups compensated for 943 (−164 to 2,050) and 1,007 (32 to 1,982) kcal/wk (mean, 95% CI, P ≥ 0.93), or 62.9% and 33.6% of ExEE, respectively. Resting metabolic rate and energy intake did not change. Food reinforcement and glucagon-like peptide-1 decreased ( P < 0.02), whereas acylated ghrelin increased ( P ≤ 0.02). Compensation is not proportional to ExEE. Similar energy compensation occurred in response to1,500 and 3,000 kcal/wk of ExEE. ExEE of 3,000 kcal/wk is sufficient to exceed compensatory responses and reduce fat mass.