Saturday, August 9, 2008

Performance Research for June: Fat loss exercise

Some more uber geeky data from June on the latest and greatest related to Fat/Weight Loss.

The short take away is further data to show that
EXERCISE IS GOOD MEDICINE!

Shocking, I know.

Caloric restriction but not exercise-induced reductions in fat mass decrease plasma triiodothyronine concentrations: a randomized controlled trial.

Weiss EP, Villareal DT, Racette SB, Steger-May K, Premachandra BN, Klein S, Fontana L. Division of Geriatrics and Nutritional Sciences, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri., Department of Nutrition and Dietetics, Saint Louis University, St. Louis, Missouri. Abstract Caloric restriction (CR) decreases circulating triiodothyronine (T(3)) concentration. However, it is not known if this effect is due to body fat mass reductions or due to CR, per se. The purpose of this study was to test the hypothesis that plasma T(3) concentration decreases with CR-induced reductions in fat mass but not in response to similar decreases in fat mass that are induced by exercise. Sedentary, nonobese 50- to 60-year-old men and women with no clinical evidence of cardiovascular or metabolic disease and not taking thyroid medications were randomly assigned to 12 months of caloric restriction (n = 18) or exercise-induced weight loss (n = 17) or to a control group (n = 9). Body weight and composition and plasma concentrations of the thyroid hormones T(3), thyrotropin (TSH), thyroxine (T(4)), and free thyroxine (FT(4)) were measured at baseline and 12 months. Fat mass changed significantly in the CR (-6.3 +/- 1.0 kg) and exercise (-5.5 +/- 1.0 kg) groups but not in the control group (-0.6 +/- 1.4 kg). The changes were not significantly different between the CR and exercise groups. Plasma T(3) concentration decreased in the CR group (-9.8 +/- 2.0 ng/dL, p < p =" 0.07)" p =" 0.65)" style="font-weight: bold;">Conclusion: This effect does not appear to be attributable to changes in body fat mass because a comparable decrease in T(3) concentration was not observed in response to an exercise-induced fat mass reduction.

Effect of weight loss on some serum cytokines in human obesity: increase in IL-10 after weight loss.

Jung SH, Park HS, Kim KS, Choi WH, Ahn CW, Kim BT, Kim SM, Lee SY, Ahn SM, Kim YK, Kim HJ, Kim DJ, Lee KW.Department of Endocrinology and Metabolism, Ajou University School of Medicine, Yongtong Gu, Suwon 443-721, South Korea. Obesity is a major risk factor for hypertension, coronary artery disease and type 2 diabetes. Weight loss is associated with significant metabolic benefits. Our objective was to examine changes in adipocytokines and interleukin (IL) 10 in obese subjects before and after weight loss. We measured anthropometric parameters, adipocytokine and IL-10 in 78 obese people who had visited obesity clinics at five university hospitals (Ajou, Ulsan, Catholic, Hanyang and Yonsei) in Korea. They restricted their caloric intake to less than their usual intake (by 500 kcal), were administered sibutramine and were given a program of exercise for 12 weeks. After 12 weeks, weight, body mass index, waist circumference, hip circumference, waist-to-hip ratio, total body fat, total cholesterol, triglyceride, tumor necrosis factor alpha (TNF-alpha), IL-6, resistin and leptin had significantly decreased, while adiponectin and IL-10 had significantly increased. A bivariate correlation analysis found that increment in IL-10 and baseline IL-10 levels significantly correlated with decrement in TNF-alpha (P<.01) and baseline adiponectin (r=.52, P<.001), respectively. Conclusion: These results were confirmed in a multiple regression analysis. The results suggest that weight loss after caloric restriction and medical treatment in obesity can improve metabolic risk factors through changes in some cytokines.

Cost-sparing effect of twice-weekly targeted endurance training in type 2 diabetics: A one-year controlled randomized trial.

Brun JF, Bordenave S, Mercier J, Jaussent A, Picot MC, Préfaut C.ERI 25, Inserm, 34000 Montpellier, France; EA 4202, UFR de médecine, université Montpellier-1, 34000 Montpellier, France; Service de physiologie clinique (CERAMM), hôpital Lapeyronie, CHU de Montpellier, avenue du doyen Gaston-Giraud, 34295 Montpellier cedex 5, France.

OBJECTIVE: We evaluated the effects of targeted, moderate endurance training on healthcare cost, body composition and fitness in type 2 diabetes patients routinely followed within the French healthcare system.
DESIGN AND METHODS: A total of 25 type 2 diabetic patients was randomly assigned to one of two groups: 13 underwent a training programme (eight sessions, followed by training twice a week for 30-45minutes at home at the level of the ventilatory threshold [V(T)]); and 12 received their usual routine treatment. Both groups were followed for one year to evaluate healthcare costs, exercise effectiveness and a six-minute walking test.
RESULTS: The training prevented loss of maximum aerobic capacity, which decreased slightly in the untrained group (P=0.014), and resulted in a higher maximum power output (P=0.041) and six-minute walking distance (P=0.020). The Voorrips activity score correlated with both [Formula: see text] (r=0.422, P<0.05) r="0.446," r="0.608," r="0.436," p="0.05)" style="font-weight: bold;">
CONCLUSION: Endurance training at V(T) level (my note--pretty intense, so no Oprah watching!!) prevented the decline in aerobic working capacity seen in untrained diabetics over the study period, and resulted in a marked reduction in healthcare costs due to less treatments and fewer hospitalizations.

My Notes: Maybe we should reimburst for exercise! Further data showing that--hey it works!

EXERCISE BUT NOT DIET-INDUCED WEIGHT LOSS DECREASES SKELETAL MUSCLE INFLAMMATORY GENE EXPRESSION IN FRAIL OBESE ELDERLY

Charles P Lambert, Nicole R Wright, Brian N Finck, and Dennis T Villareal. Division of Geriatrics and Nutritional Sciences, Washington University School of Medicine, United States. Division of Geriatrics and Nutritional Sciences, Washington University School of Medicine, St. Louis, Missouri, United States

Many obese elderly persons have impaired physical function associated with an increased chronic inflammatory response. We evaluated 12 weeks of exercise (aerobic and resistance) or 12 weeks of weight loss (~7% reduction) on skeletal muscle mRNAs for toll-like receptor-4, (TLR-4), mechanogrowth factor (MGF), tumor necrosis factor-{alpha} (TNF-{alpha}), and interleukin-6 (IL-6) in 16 obese (BMI: 38±2 kg/m2) older (69±1 yrs) physically frail individuals. m. vastus lateralis biopsies were obtained at 0 and 12 weeks and analyzed by real time RT-PCR. Body composition was assessed by dual x-ray absorptiometry. Body weight decreased (-7.5 ±1.2 kg, p=0.001) in the weight loss group, but not in the exercise group (-0.3±0.8 kg, p=0.74). Fat free mass (FFM) decreased (-2.9±0.6 kg, p=0.010) in the weight loss group and increased (1.6±0.6 kg, p=0.03) in the exercise group. Exercise resulted in a 37% decrease in TLR-4 mRNA (p<0.05) style="font-weight: bold;">
Conclusion: In conclusion, exercise but not weight loss had a beneficial effect on markers of muscle inflammation and anabolism in frail obese elderly individuals.

GO EXERCISE!

Voluntary Exercise Improves Insulin Sensitivity and Adipose Tissue Inflammation in Diet-Induced Obese Mice.

Bradley RL, Jeon JY, Liu FF, Maratos-Flier E. Endocrinology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States. Exercise promotes weight loss and improves insulin sensitivity. However, the molecular mechanisms mediating its beneficial effects are not fully understood. Obesity correlates with increased production of inflammatory cytokines, which in turn, contributes to systemic insulin resistance. To test the hypothesis that exercise mitigates this inflammatory response, thereby improving insulin sensitivity, we developed a model of voluntary exercise in mice made obese by feeding of a high fat/high sucrose diet (HFD). Over four weeks, mice fed chow gained 2.3 +/- 0.3 g, while HFD mice gained 6.8 +/- 0.5 g. After 4 weeks, mice were subdivided into four groups: chow-no exercise, chow-exercise, HFD-no exercise, HFD-exercise and monitored for an additional 6 weeks. Chow-no exercise and HFD-no exercise mice gained an additional 1.2 +/- 0.3 g and 3.3 +/- 0.5 g respectively. Exercising mice had higher food consumption, but did not gain additional weight. As expected, GTT and ITT showed impaired glucose tolerance and insulin resistance in HFD-no exercise mice. However, glucose tolerance improved significantly and insulin sensitivity was completely normalized in HFD-exercise animals. Furthermore, expression of TNF-alpha, MCP-1, PAI-1 and IKKbeta was increased in adipose tissue from HFD mice compared to chow mice, whereas exercise reversed the increased expression of these inflammatory cytokines. In contrast, expression of these cytokines in liver was unchanged among the four groups.

Conclusion: These results suggest that exercise partially reduces adiposity, reverses insulin resistance and decreases adipose tissue inflammation in diet-induced obese mice, despite continued consumption of HFD (high fat diet).

My Notes: Note that they said PARTIALLY, so this is not a free ticket to Krispy Kreme!

Reduced tricarboxylic acid cycle flux in type 2 diabetes mellitus

Schrauwen P, Hesselink MK.Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Department of Human Biology, Maastricht University, PO Box 616, 6200 MD, Maastricht, the Netherlands, p.schrauwen@hb.unimaas.nl.

AIMS/HYPOTHESIS: Mitochondrial dysfunction has been postulated to underlie muscular fat accumulation, leading to muscular insulin sensitivity and ultimately type 2 diabetes mellitus. Here we re-interpret previously published data on [(13)C]acetate recovery in breath gas obtained during exercise in type 2 diabetic patients and control individuals.

METHODS: When infusing [(13)C]palmitate to estimate fat oxidation, part of the label is lost in exchange reactions of the tricarboxylic acid (TCA) cycle. To correct for this loss of label, an acetate recovery factor (ARF) has previously been used, assuming that 100% of the exogenously provided acetate will enter the TCA cycle. The recovery of acetate in breath gas depends on the TCA cycle activity, hence providing an indirect measure of the latter and a marker of mitochondrial function.
RESULTS: Re-evaluation of the available literature reveals that the ARF during exercise is highest in lean, healthy individuals, followed by obese individuals and type 2 diabetic patients.

CONCLUSION: Revisiting previously published findings on the ARF during exercise in type 2 diabetic patients reveals a reduction in muscular TCA cycle flux, reflecting mitochondrial dysfunction, in these patients. How mitochondrial dysfunction is related to type 2 diabetes mellitus-cause or consequence-requires further study..

My Notes: This supports the theory that those with type 2 diabetes have hosed up mitochondria (the little powerhouses of the cell)