The effectiveness of body age-based intervention in workplace health promotion: Results of a cohort study on 9851 Danish employees.

INTRODUCTION: The aging population emphasize the need for effective health promotion interventions. The workplace is a prioritized setting for health promotion to reach widely within a population. Body age can be used as a health-risk estimate and as a motivational tool to change health behavior. In this study we investigate body age-based intervention including motivational interview and its effect on health, when applied to real life workplace health promotion. MATERIAL AND METHODS: Body age-based intervention was performed in 90 companies on 9851 Danish employees from 2011-2017. Metabolic risk factors were assessed, body age score was determined and an individualized motivational interview was conducted at baseline and follow-up. Change in body age score, single risk factors, smoking habits and metabolic syndrome were analyzed. The body age score is a composite score comprising 11 weighted variables. A body age score ≤ 0 is preferred, as this elicit a younger/healthier or equal body age compared to chronological age. RESULTS: At 1.3 year follow-up the unhealthiest employees were less likely to participate. Within follow-up participants (39%, n = 3843) body age had improved by a decline in mean body age score of -0.6 and -0.7 years for men and women, respectively (p<0.001). Number of employees with metabolic syndrome had decreased from 646 at baseline to 557 at follow-up (p = 0.005) and 42% of smokers had quit smoking (p<0.001). CONCLUSION: On the basis of this study, we suggest that body age assessment motivates to participate in workplace health promotion, affect high risk behavior such as smoking thus have potential in public health promotion.

Simvastatin-Induced Insulin Resistance May Be Linked to Decreased Lipid Uptake and Lipid Synthesis in Human Skeletal Muscle: the LIFESTAT Study.

BACKGROUND: A prevalent side-effect of simvastatin is attenuated glucose homeostasis. The underlying mechanism is unknown, but impaired lipid metabolism may provide the link. The aim of this study was to investigate whether simvastatin-treated patients had a lower capacity to oxidize lipids and reduced expression of the major proteins regulating lipid uptake, synthesis, lipolysis, and storage in skeletal muscle than matched controls. MATERIALS AND METHODS: Ten men were treated with simvastatin (HbA1c: 5.7 ± 0.1%), and 10 healthy men (HbA1c: 5.2 ± 0.1%) underwent an oral glucose tolerance test and a muscle biopsy was obtained. Fat oxidation rates were measured at rest and during exercise. Western blotting was used to assess protein content. RESULTS: Patients treated with simvastatin had impaired glucose tolerance compared with control subjects, but fat oxidation at rest and during exercise was compatible. Skeletal muscle protein content of CD36, lipoprotein lipase (LPL), and diacylglycerol acyltransferase (DGAT) 1 were lower, and DGAT 2 tended to be lower in patients treated with simvastatin. CONCLUSIONS: Patients treated with simvastatin had a reduced capacity to synthesize FA and diacylglycerol (DAG) into triacylglycerol in skeletal muscle compared to matched controls. Decreased lipid synthesis capacity may lead to accumulation of lipotoxic intermediates (FA and DAG) and hence impair glucose tolerance.

Determinants of maximal whole-body fat oxidation in elite cross-country skiers: Role of skeletal muscle mitochondria.

Elite endurance athletes possess a high capacity for whole-body maximal fat oxidation (MFO). The aim was to investigate the determinants of a high MFO in endurance athletes. The hypotheses were that augmented MFO in endurance athletes is related to concomitantly increments of skeletal muscle mitochondrial volume density (MitoVD ) and mitochondrial fatty acid oxidation (FAOp ), that is, quantitative mitochondrial adaptations as well as intrinsic FAOp per mitochondria, that is, qualitative adaptations. Eight competitive male cross-country skiers and eight untrained controls were compared in the study. A graded exercise test was performed to determine MFO, the intensity where MFO occurs (FatMax ), and V ˙ O 2 Max . Skeletal muscle biopsies were obtained to determine MitoVD (electron microscopy), FAOp , and OXPHOSp (high-resolution respirometry). The following were higher (P < 0.05) in endurance athletes compared to controls: MFO (mean [95% confidence intervals]) (0.60 g/min [0.50-0.70] vs 0.32 [0.24-0.39]), FatMax (46% V ˙ O 2 Max [44-47] vs 35 [34-37]), V ˙ O 2 Max (71 mL/min/kg [69-72] vs 48 [47-49]), MitoVD (7.8% [7.2-8.5] vs 6.0 [5.3-6.8]), FAOp (34 pmol/s/mg muscle ww [27-40] vs 21 [17-25]), and OXPHOSp (108 pmol/s/mg muscle ww [104-112] vs 69 [68-71]). Intrinsic FAOp (4.0 pmol/s/mg muscle w.w/MitoVD [2.7-5.3] vs 3.3 [2.7-3.9]) and OXPHOSp (14 pmol/s/mg muscle ww/MitoVD [13-15] vs 11 [10-13]) were, however, similar in the endurance athletes and untrained controls. MFO and MitoVD correlated (r2  = 0.504, P < 0.05) in the endurance athletes. A strong correlation between MitoVD and MFO suggests that expansion of MitoVD might be rate-limiting for MFO in the endurance athletes. In contrast, intrinsic mitochondrial changes were not associated with augmented MFO.

Influence of maximal fat oxidation on long-term weight loss maintenance in humans.

Impaired maximal fat oxidation has been linked to obesity and weight regain after weight loss. The aim was to investigate the relationship between maximal fat oxidation (MFO) and long-term weight loss maintenance. Eighty subjects [means (SD): age, 36(13) yrs; BMI, 38(1) kg/m2] were recruited from a total of 2,420 former participants of an 11- to 12-wk lifestyle intervention. Three groups were established based on percent weight loss at follow-up [5.3(3.3) yr]: clinical weight loss maintenance (CWL), >10% weight loss; moderate weight loss (MWL), 1-10% weight loss; and weight regain (WR). Body composition (dual X-ray absorptiometry) and fat oxidation (indirect calorimetry) during incremental exercise were measured at follow-up. Blood and a muscle biopsy were sampled. At follow-up, a U-shaped parabolic relationship between MFO and percent weight loss was observed (r = 0.448; P < 0.001). Overall differences between CWL, MWL, and WR were observed in MFO (mean [95% confidence interval], in g/min, respectively: 0.46 [0.41-0.52]; 0.32 [0.27-0.38]; 0.45 [0.38-0.51]; P = 0.002), maximal oxygen uptake (V̇o2max, in ml·min-1·FFM-1, respectively; 49 [46-51]; 43 [40-47]; 41 [39-44]; P = 0.007), HAD-activity (in µmol·g-1·min-1, respectively: 123 [113-133]; 104 [91-118]; 97 [88-105]; P < 0.001), muscle protein content of CD36 (in AU, respectively: 1.1 [1.0-1.2]; 0.9 [0.8-1.0]; 0.9 [0.8-0.9]; P = 0.008) and FABPpm (in AU, respectively, 1.0 [0.8-1.2]; 0.7 [0.5-0.8]; 0.7 [0.5-0.9]; P = 0.008), body fat (in %, respectively: 33 [29-38]; 42 [38-46]; 52 [49-55]; P < 0.001), and plasma triglycerides (in mM, respectively: 0.8 [0.7-1.0]; 1.3 [0.9-1.7]; 1.6 [1.0-2.1]; P = 0.013). CWL and WR both had higher MFO compared with MWL, but based on different mechanisms. CWL displayed higher V̇o2max and intramuscular capacity for fat oxidation, whereas abundance of lipids at whole-body level and in plasma was higher in WR.NEW & NOTEWORTHY Impaired maximal fat oxidation has been linked to obesity and weight regain after weight loss. Noteworthy, maximal fat oxidation was equally high after clinical weight loss maintenance and weight regain compared with moderate weight loss. A high maximal fat oxidation after clinical weight loss maintenance was related to higher maximal oxygen updake, content of key proteins involved in transport of lipids across the plasma membrane and ß-oxidation. In contrast, a high maximal fat oxidation after weight regain was related to higher availability of lipids, i.e., general adiposity and plasma concentration of triglycerides.

Maintaining a clinical weight loss after intensive lifestyle intervention is the key to cardiometabolic health.

OBJECTIVE: Intensive lifestyle interventions (ILI) are criticised for ineffective obesity treatment because weight loss over time is modest and thus of limited clinical relevance. However, a subgroup (5-30%) maintains a clinical weight loss >10%, but it is not clear if cardiometabolic health follows this pattern. The aim was to study the effect of different magnitudes of weight loss maintenance after ILI on cardiometabolic health. METHODS: Eighty out of 2420 former participants (age: 36±1, BMI: 38±1, (means ±SE)) in an 11-12-week ILI were recruited into 3 groups; clinical weight loss maintenance (>10% weight loss), moderate maintenance (1-10%), and weight regain based on weight loss at follow-up (5.3±0.4years). Weight loss during the ILI was achieved by increased physical activity and hypo-caloric diet. Dual X-ray Absorptiometry, blood sample, skeletal muscle biopsy and VO2max test were used to determine cardiometabolic health at follow-up. RESULTS: At follow-up, the clinical weight loss maintenance group scored better in the following variables compared to the other groups: BMI (31±1, 33±2, 43±2kg/m2), composition (34±2, 40±1, 49±1% fat), visceral adipose tissue (0.8±0.2, 1.7±0.5, 2.4±0.4kg), plasma triglycerides (0.8±0.2, 1.3±0.4, 1.6±0.3mmol/L), plasma glucose (4.9±0.1, 5.9±0.4, 5.9±0.1mmol/L), Hb1Ac (5.1±0.0, 5.6±0.2, 5.8±0.2%), protein content in skeletal muscle of GLUT4 (1.5±0.2, 0.9±0.1, 1.0±0.1 AU) and hexokinase II (1.6±0.2, 1.0±0.2, 0.7±0.1 AU), citrate synthase activity (155±6, 130±5, 113±5µmol/g/min) and VO2max (49±1, 43±1, 41±1mL/min/FFM) (p<0.05). CONCLUSION: Cardiometabolic health is better in participants who have maintained >10% weight loss compared to moderate weight loss and weight regain.

[Effect of lifestyle changes on weight loss and weight loss maintenance].

Weight loss and weight loss maintenance can be achieved through lifestyle changes such as a hypocaloric diet and increased physical activity. Hypocaloric diet alone as well as training alone can induce weight loss; however, the combination of these result in the greatest weight loss. Whereas a hypocaloric diet plays a major role in weight loss, physical activity seems to be of great importance during weight loss maintenance. In Denmark, there are private and public offers to achieve weight loss, but the focus on weight loss in the maintenance period after treatment is limited.

The influence of anti-inflammatory medication on exercise-induced myogenic precursor cell responses in humans.

The consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) is widespread among athletes when faced with muscle soreness or injury, but the effects of NSAIDs on satellite cell activity in humans are unknown. To investigate this, 14 healthy male endurance athletes (mean peak oxygen consumption 62 ml x kg(-1) x min(-1)) volunteered for the study, which involved running 36 km. They were divided into two groups and received either 100 mg indomethacin per day or placebo. Muscle biopsies collected before the run and on days 1, 3, and 8 afterward were analyzed for satellite cells by immunohistochemistry with the aid of neural cell adhesion molecule (NCAM) and fetal antigen-1 (FA1) antibodies. Muscle biopsies were also collected from untrained individuals for comparison. Compared with preexercise levels, a 27% increase in the number of NCAM+ cells was observed on day 8 postexercise in the placebo group (P < 0.05), while levels remained similar at all time points in the NSAID group. No change was seen in the proportion of FA1+ cells, although lower levels were found in the muscle of endurance-trained athletes compared with untrained individuals (P < 0.05). These results suggest that ingestion of anti-inflammatory drugs attenuates the exercise-induced increase in satellite cell number, supporting the role of the cyclooxygenase pathway in satellite cell activity.