Obesity may impair protein synthesis rates and cause anabolic resistance to growth factors, hormones, and exercise, ultimately affecting skeletal muscle mass and function. To better understand muscle wasting and anabolic resistance with obesity, we assessed protein 24-h fractional synthesis rates (24-h FSRs) in selected hind-limb muscles of sedentary and resistance-exercised lean and obese Zucker rats. Despite atrophied hind-limb muscles (-28% vs. lean rats), 24-h FSRs of mixed proteins were significantly higher in quadriceps (+18%) and red or white gastrocnemius (+22 or +38%, respectively) of obese animals when compared to lean littermates. Basal synthesis rates of myofibrillar (+8%) and mitochondrial proteins (-1%) in quadriceps were not different between phenotypes, while manufacture of cytosolic proteins (+12%) was moderately elevated in obese cohorts. Western blot analyses revealed a robust activation of p70S6k (+178%) and a lower expression of the endogenous mTOR inhibitor DEPTOR (-28%) in obese rats, collectively suggesting that there is an obesity-induced increase in net protein turnover favoring degradation. Lastly, the protein synthetic response to exercise of mixed (-7%), myofibrillar (+6%), and cytosolic (+7%) quadriceps subfractions was blunted compared to the lean phenotype (+34, +40, and +17%, respectively), indicating a muscle- and subfraction-specific desensitization to the anabolic stimulus of exercise in obese animals.

Metabolic risk factors associated with insulin resistance syndrome may attenuate augmentations in skeletal muscle protein anabolism following contractile activity. The purpose of this study was to investigate whether or not the anabolic response, as defined by an increase in cumulative fractional protein synthesis rates (24-h FSR) following resistance exercise (RE), is blunted in skeletal muscle of a well-established rodent model of insulin resistance syndrome. Four-month-old lean ( Fa/?) and obese ( fa/fa) Zucker rats engaged in four lower body RE sessions over 8 days, with the last bout occurring 16 h prior to muscle harvest. A priming dose of deuterium oxide (2H2O) and 2H2O-enriched drinking water were administered 24 h prior to euthanization for assessment of cumulative FSR. Fractional synthesis rates of mixed (−5%), mitochondrial (−1%), and cytosolic (+15%), but not myofibrillar, proteins (−16%, P = 0.012) were normal or elevated in gastrocnemius muscle of unexercised obese rats. No statistical differences were found in the anabolic response of cytosolic and myofibrillar subfractions between phenotypes, but obese rats were not able to augment 24-h FSR of mitochondria to the same extent as lean rats following RE (+14% vs. +28%, respectively). We conclude that the mature obese Zucker rat exhibits a mild, myofibrillar-specific suppression in basal FSR and a blunted mitochondrial response to contractile activity in mixed gastrocnemius muscle. These findings underscore the importance of assessing synthesis rates of specific myocellular subfractions to fully elucidate perturbations in basal protein turnover rates and differential adaptations to exercise stimuli in metabolic disease.

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Metabolic syndrome has been shown in numerous studies to be related to a higher incidence of coronary artery disease. A study by Jurca and coworkers (Med. Sci. Sports Exerc 36(8):1301-1307, 2004 found a relationship between aerobic fitness and the prevalence of metabolic syndrome in a group of men enrolled in the Aerobics Center Longitudinal Study (ACLS). In addition, recent work in our lab (Int J Exerc Sci 2(1): S43, 2009) has supported these findings. However, research exploring this relationship is still lacking in male firefighters, whose leading cause of line-of-duty deaths is heart attacks. Purpose: To further evaluate the association of metabolic syndrome and aerobic fitness in male fire fighters. Methods: As part of an annual physical exam, 210 male fire fighters (average age = 36) underwent evaluation of risk factors associated with metabolic syndrome as defined by NCEP III. These include the presence of three or more of the following: Waist Circumference > 40", HDL Cholesterol < 40 mg/dL, Triglycerides > 150 mg/dL, Blood Glucose > 110 mg/dL, and Resting Blood Pressure > 130/85 mm Hg. Aerobic Fitness was determined by estimating VO2max from time on treadmill during a Bruce protocol. Results: The subjects were ranked and divided into quartiles based on VO2max. All data were analyzed using a Chi Square test (p < 0.05). Prevalence of metabolic syndrome increased significantly across quartiles as aerobic fitness declined. Conclusion: These data suggest that as aerobic fitness improves, the likelihood of male firefighters having metabolic syndrome decreases.

Docosahexaenoic acid (DHA) is a C22:6 omega‐3 fatty acid that has been shown to reduce inflammation. Our study examined serum inflammatory (GM‐CSF, IL‐6, IL‐8, TNF‐α, interferon‐γ, CRP) and muscle damage (creatine kinase, LDH, ALT, AST, alkaline phosphatase) markers following 2 g/d of supplemented, purified algal DHA (E;n=24) or placebo (P;n=28) in American collegiate football athletes during preseason training. Fasted blood was drawn three different times: 1) Summer (S) before starting supplements (T1); 2) August, pre‐camp (PRE) after 35 d supplementation (T2); and 3) August, post‐camp (POST) after 52 d supplementation (T3). A 2x3 ANCOVA with repeated measures (covaried for race; CRP for weight change). A significant group x time interaction was observed in IL‐8 (p<0.05). Other markers of inflammation showed no differences between groups (p>0.05). POST CRP was significantly higher than PRE (p<0.001). POST levels of creatine kinase, LDH, ALT, AST, alkaline phosphatase were significantly (p<0.001) increased compared to S and PRE in both groups. Preseason training can elevate muscle damage markers. DHA supplementation did affect IL‐8 levels during preseason training of collegiate football athletes.Funding provided by Martek Biosciences Corp., Columbia, MD and The Sydney & J.L. Huffines Institute for Sports Medicine & Human Performance