Natural infection of white grubs (Coleoptera: Scarabaeidae) with entomopathogenic nematodes in the KwaZulu-Natal province of South Africa.

White grubs are root feeding larvae of beetles (Coleoptera: Scarabaeidae) that are sporadic pests in agriculture and can lead to economic damage. The grubs feed on the roots of plants, while the adult beetle can bore into underground stems, as well as cause defoliation of plants. Sporadic incidence of larvae with symptoms of nematode infections were detected in wattle and sugarcane plantations in the KwaZulu-Natal province of South Africa. The larvae with infection symptoms were isolated, washed, and put on water traps to collect infective juveniles of possible nematode infections. Three species of entomopathogenic nematodes (EPNs) were isolated from the white grub larvae. These included Steinernema bertusi isolated from Maladera sp. 4., Oscheius myriophila from Maladera sp. 4 and Schizonchya affinis, and Steinernema fabii isolated from Maladera sp. 4., Pegylis sommeri, and S. affinis. Of these S. fabii was the most common species in the sample (87%). This is the first report of such a high diversity of locally occurring EPNs found naturally associated with white grub species in this region of South Africa.

Single versus repeated exposure to human polarized intestinal epithelial monolayers for in vitro protein hazard characterization.

Recent studies suggest human-derived intestinal epithelial cell (IEC) lines cultured as polarized monolayers on permeable Transwell® filters are effective at differentiating between hazardous and non-hazardous proteins following a single exposure. In this study, IEC polarized monolayers were subjected to hazardous or non-hazardous proteins in nine exposures over 30 days and compared to a single exposure of the same protein. The objective was to evaluate whether repeated exposures to a protein differently alter barrier integrity or compromise cell viability compared to single exposures. Proteins tested included Clostridium difficile toxin A, Streptolysin O, Wheat Germ Agglutinin, Phaseolus vulgaris Hemagglutinin-E, bovine serum albumin, porcine serum albumin, and fibronectin. Evidence of diminished barrier integrity and/or cell viability following exposure to hazardous proteins was more pronounced in magnitude when IECs were subjected to multiple rather than single exposures. In some cases, an effect on IEC monolayers was observed only with repeated exposures. In general, IEC responses to non-hazardous proteins following either single or repeated exposures were minimal. Results from these studies support the utility of using cultured human IEC polarized monolayers to differentiate between hazardous and non-hazardous proteins and suggest that repeated exposures may reveal a greater magnitude of response when compared to single exposures.

Extended exposure duration of cultured intestinal epithelial cell monolayers in characterizing hazardous and non-hazardous proteins.

Recent studies suggest that human derived intestinal epithelial cells (IECs) cultured as polarized monolayers on Transwell® filters may respond differently when exposed to hazardous and non-hazardous proteins. This experimental platform was based on apical exposure of IEC monolayers to test proteins for 24 h followed by assessment of barrier integrity and cell viability. In this study, Caco-2 and T84 IEC polarized monolayers were evaluated for barrier integrity and cytotoxicity following exposure to hazardous and non-hazardous proteins for 24, 48 and 72 h. Hazardous proteins included Clostridium difficile toxin A (ToxA), Streptolysin O (SLO), Wheat Germ Agglutinin (WGA), and Phaseolus vulgaris haemagglutinin-E (PHA-E). Non-hazardous proteins included bovine serum albumin (BSA), porcine serum albumin (PSA), and fibronectin (Fbn). In general, evidence of diminished barrier integrity or cell viability observed following exposure to hazardous proteins for 24 h was more pronounced after 48 and 72 h for both IEC monolayers. Non-hazardous proteins exhibiting no impact following 24 h of exposure elicited minimal effects over longer exposure durations. These results support the utility of using cultured human IEC polarized monolayers to differentiate between hazardous and non-hazardous proteins and suggest that longer durations of exposure may further improve the ability to distinguish between them.

Primary human polarized small intestinal epithelial barriers respond differently to a hazardous and an innocuous protein.

An experimental platform employing human derived intestinal epithelial cell (IEC) line monolayers grown on permeable Transwell® filters was previously investigated to differentiate between hazardous and innocuous proteins. This approach was effective at distinguishing these types of proteins and perturbation of monolayer integrity, particularly transepithelial electrical resistance (TEER), was the most sensitive indicator. In the current report, in vitro indicators of monolayer integrity, cytotoxicity, and inflammation were evaluated using primary (non-transformed) human polarized small intestinal epithelial barriers cultured on Transwell® filters to compare effects of a hazardous protein (Clostridium difficile Toxin A [ToxA]) and an innocuous protein (bovine serum albumin [BSA]). ToxA exerted a reproducible decrease on barrier integrity at doses comparable to those producing effects observed from cell line-derived IEC monolayers, with TEER being the most sensitive indicator. In contrast, BSA, tested at concentrations substantially higher than ToxA, did not cause changes in any of the tested variables. These results demonstrate a similarity in response to certain proteins between cell line-derived polarized IEC models and a primary human polarized small intestinal epithelial barrier model, thereby reinforcing the potential usefulness of cell line-derived polarized IECs as a valid experimental platform to differentiate between hazardous and non-hazardous proteins.

Assessment of beetle diversity, community composition and potential threats to forestry using kairomone-baited traps.

Traps designed to capture insects during normal movement/dispersal, or via attraction to non-specific (plant) volatile lures, yield by-catch that carries valuable information about patterns of community diversity and composition. In order to identify potential native/introduced pests and detect predictors of colonization of non-native pines, we examined beetle assemblages captured in intercept panel traps baited with kairomone lures used during a national monitoring of the woodwasp, Sirex noctilio, in Southern Africa. We identified 50 families and 436 morphospecies of beetles from nine sites sampled in both 2008 and 2009 and six areas in 2007 (trap catch pooled by region) across a latitudinal and elevational gradient. The most diverse groups were mainly those strongly associated with trees, known to include damaging pests. While native species dominated the samples in terms of richness, the dominant species was the introduced bark beetle Orthotomicus erosus (Curculionidae: Scolytinae) (22 ± 34 individuals/site). Four Scolytinae species without previous records in South Africa, namely Coccotrypes niger, Hypocryphalus robustus (formerly Hypocryphalus mangiferae), Hypothenemus birmanus and Xyleborus perforans, were captured in low abundances. Communities showed temporal stability within sites and strong biogeographic patterns across the landscape. The strongest single predictors of community composition were potential evaporation, latitude and maximum relative humidity, while the strongest multifactor model contained elevation, potential evaporation and maximum relative humidity. Temperature, land use variables and distance to natural areas did not significantly correlate with community composition. Non-phytophagous beetles were also captured and were highly diverse (32 families) perhaps representing important beneficial insects.

Pathogen induced chemo-attractant hepoxilin A3 drives neutrophils, but not eosinophils across epithelial barriers.

Pathogen induced migration of neutrophils across mucosal epithelial barriers requires epithelial production of the chemotactic lipid mediator, hepoxilin A3 (HXA3). HXA3 is an eicosanoid derived from arachidonic acid. Although eosinophils are also capable of penetrating mucosal surfaces, eosinophilic infiltration occurs mainly during allergic processes whereas neutrophils dominate mucosal infection. Both neutrophils and eosinophils can respond to chemotactic gradients of certain eicosanoids, however, it is not known whether eosinophils respond to pathogen induced lipid mediators such as HXA3. In this study, neutrophils and eosinophils were isolated from human blood and placed on the basolateral side of polarized epithelial monolayers grown on permeable Transwell filters and challenged by various chemotactic gradients of distinct lipid mediators. We observed that both cell populations migrated across epithelial monolayers in response to a leukotriene B4 (LTB4) gradient, whereas only eosinophils migrated toward a prostaglandin D2 (PGD2) gradient. Interestingly, while pathogen induced neutrophil trans-epithelial migration was substantial, pathogen induced eosinophil trans-epithelial migration was not observed. Further, gradients of chemotactic lipids derived from pathogen infected epithelial cells known to be enriched for HXA3 as well as purified HXA3 drove significant numbers of neutrophils across epithelial barriers, whereas eosinophils failed to respond to these gradients. These data suggest that although the eicosanoid HXA3 serves as an important neutrophil chemo-attractant at mucosal surfaces during pathogenic infection, HXA3 does not appear to exhibit chemotactic activity toward eosinophils.

Retracing the routes of introduction of invasive species: the case of the Sirex noctilio woodwasp.

Understanding the evolutionary histories of invasive species is critical to adopt appropriate management strategies, but this process can be exceedingly complex to unravel. As illustrated in this study of the worldwide invasion of the woodwasp Sirex noctilio, population genetic analyses using coalescent-based scenario testing together with Bayesian clustering and historical records provide opportunities to address this problem. The pest spread from its native Eurasian range to the Southern Hemisphere in the 1900s and recently to Northern America, where it poses economic and potentially ecological threats to planted and native Pinus spp. To investigate the origins and pathways of invasion, samples from five continents were analysed using microsatellite and sequence data. The results of clustering analysis and scenario testing suggest that the invasion history is much more complex than previously believed, with most of the populations being admixtures resulting from independent introductions from Europe and subsequent spread among the invaded areas. Clustering analyses revealed two major source gene pools, one of which the scenario testing suggests is an as yet unsampled source. Results also shed light on the microevolutionary processes occurring during introductions, and showed that only few specimens gave rise to some of the populations. Analyses of microsatellites using clustering and scenario testing considered against historical data drastically altered our understanding of the invasion history of S. noctilio and will have important implications for the strategies employed to fight its spread. This study illustrates the value of combining clustering and ABC methods in a comprehensive framework to dissect the complex patterns of spread of global invaders.

Can dual energy X-ray absorptiometry provide a valid assessment of changes in thigh muscle mass with strength training in older adults?

OBJECTIVE: To determine how dual-energy X-ray absorptiometry (DXA) compares to computed tomography (CT) for measuring changes in total thigh skeletal muscle (SM) mass with strength training (ST) in older adults. SUBJECTS: Fifty previously sedentary, relatively healthy older men (n=23, 60 (s.d.=7.5) years) and women (n=27, 60 (s.d.=9.3) years). RESULTS: Results indicate that there was a significant increase in thigh SM mass with ST measured by both CT (3.9+/-0.4%) and DXA (2.9+/-0.6%) methods (both P<0.001), and there was not a significant difference in percent change between the two methods, although there was a substantial absolute difference ( approximately 2 kg) at baseline between the two methods. Although Bland-Altman plots indicate overall agreement between the percent thigh SM mass changes of DXA vs CT methods, the 3.4% error associated with DXA was greater than the thigh SM mass change from DXA. However, the CT measured change in thigh SM mass was greater than its error (0.6%). CONCLUSIONS: DXA overestimates baseline and after ST thigh SM mass, and may not be able to detect small changes in thigh SM mass with ST due to its higher error. Although DXA has certain advantages that warrant is used in epidemiologic and intervention studies, improvements to DXA are needed for the accurate assessment of small changes in thigh SM mass.

Adhesion molecules involved in hepoxilin A3-mediated neutrophil transepithelial migration.

A common feature underlying active states of inflammation is the migration of neutrophils (PMNs) from the circulation and across a number of tissue barriers in response to chemoattractant stimuli. Although our group has recently established a discreet role for the PMN chemoattractant, hepoxilin A3 (HXA3) in the process of PMN recruitment, very little is known regarding the interaction of HXA3 with PMNs. To characterize further the event of HXA3-induced PMN transepithelial migration, we sought to determine the adhesion molecules required for migration across different epithelial surfaces (T84 intestinal and A549 airway cells) relative to two well-studied PMN chemoattractants, formyl-methionyl-leucyl-phenylalanine (fMLP) and leukotriene B4 (LTB4). Our findings reveal that the adhesion interaction profile of PMN transepithelial migration in response to HXA3 differs from the adhesion interaction profile exhibited by the structurally related eicosanoid LTB4. Furthermore, unique to PMN transepithelial migration induced by gradients of HXA3 was the critical dependency of all four major surface adhesion molecules examined (i.e. CD18, CD47, CD44 and CD55). Our results suggest that the particular chemoattractant gradient imposed, as well as the type of epithelial cell monolayer, each plays a role in determining the adhesion molecules involved in transepithelial migration. Given the complexities of these interactions, our findings are important to consider with respect to adhesion molecules that may be targeted for potential drug development.

Resistance training alters cytokine gene expression in skeletal muscle of adults with type 2 diabetes.

Resistance training results in muscle hypertrophy and improves glycemic control in patients with type 2 diabetes. Whether resistance training modulates inflammation in muscles of diabetic patients remains unknown. We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. Thirty men and women (67+/-7 years) were randomized to either 16 weeks of resistance training and usual diabetes care (EX) or to usual diabetes care only (CON). Muscle biopsies were obtained from the vastus lateralis muscle prior to the 16-week intervention, and 72 h following the maximal strength test post-intervention. Fiber cross-sectional area (CSA) was determined following ATPase staining. Cytokine and CD18 transcript levels were assessed by real-time PCR. Resistance training increased CSA of type I and II fibers (both P <0.05) and IL-1beta transcript levels (P = 0.05). TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. In both groups, the increase in CD18 transcripts remained minimal. The two groups differ by the relationship between changes in CD18 and changes in cytokine transcripts, suggesting that resistance training affects the source of cytokines in muscle. Our studies establish that resistance training in older adults with type 2 diabetes results in muscle fiber hypertrophy, despite a greater accumulation of inflammatory cytokine transcripts in muscle.

Atherogenic oxidized low-density lipoprotein/beta2-glycoprotein I (oxLDL/beta2GPI) complexes in patients with systemic lupus erythematosus and antiphospholipid syndrome.

Oxidized low-density lipoprotein (oxLDL) interacts in vitro with beta2-glycoprotein I (beta2GPI) via LDL-derived specific ligands forming oxLDL/beta2GPI complexes. Circulating oxLDL/beta2GPI complexes have been demonstrated in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Autoimmune vascular inflammation and oxidative stress contribute to oxLDL/beta2GPI complex formation. Immunohistochemical staining of atherosclerotic lesions suggest that these complexes are formed in the arterial wall and released into circulation. The demonstration of antibodies to oxLDL/beta2GPI complexes indicates that these complexes are immunogenic, and the coexistence of complexes and antibodies suggest an active pro-thrombotic/pro-atherogenic role in the development of autoimmune vascular complications. Circulating oxLDL/beta2GPI complexes can be measured by ELISA using a monoclonal antibody specific to complexed human beta2GPI to capture beta2GPI bound to oxLDL. An enzyme-conjugated monoclonal antibody to human Apo B 100 allows the specific detection of oxLDL/beta2GPI complexes. OxLDL/beta2GPI complexes were common in SLE and APS patients suggesting an underlying process of inflammation and oxidation. Using oxLDL/beta2GPI complexes as capture antigen, antibodies to oxLDL/beta2GPI can be measured by ELISA. Serum levels of IgG anti-oxLDL/beta2GPI antibodies were significantly higher in SLE patients with APS compared to SLE controls without APS. Further, high titers of these IgG antibodies were observed in APS patients with a history of arterial thrombosis. The presence of circulating oxLDL/beta2GPI complexes and IgG antibodies to these complexes indicates significant vascular injury and oxidative stress as well as an active role in autoimmune-mediated atherothrombosis.

Oxidized low-density lipoprotein and beta2-glycoprotein I in patients with systemic lupus erythematosus and increased carotid intima-media thickness: implications in autoimmune-mediated atherosclerosis.

Oxidative stress and LDL modification (oxLDL) are early pro-atherogenic events. OxLDL binds beta2GPI producing immunogenic oxLDL/beta2GPI complexes. Antibodies to these complexes have been associated with arterial thrombosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Circulating oxLDL/beta2GPI complexes, IgG and IgM antibodies to these complexes were measured by ELISA in 30 SLE patients asymptomatic for cardiovascular disease (mean age 31 years) and 27 age/sex matched healthy controls. Carotid intima-media thickness (IMT) was measured by ultrasound in all patients and controls. Forty-seven percent of SLE presented plaques (median IMT of 0.65 +/- 0.12 mm) while only 7% of the controls had plaques (median IMT of 0.50 +/- 0.04 mm, P < 0.001). Median optical density (OD450nm) for oxLDL/beta2GPI complexes in SLE was 0.244 +/- 0.07, higher than controls (0.174 +/- 0.09, P < 0.001). Median OD for IgG anti-oxLDL/beta2GPI antibodies was also higher in SLE (0.297 +/- 0.26) compared to controls (0.194 +/- 0.07, P < 0.001) while the median OD for IgM antibodies in SLE (0.444 +/- 0.46) was not different than controls (0.326 +/- 0.22, P = 0.267). There was no correlation between IMT and oxLDL/beta2GPI complexes, IgG or IgM antibodies, possibly reflecting the complex interrelationship between these serologic elements and tissue factors in the arterial wall. These results support the hypothesis that oxLDL/beta2GPI complexes and IgG (not IgM) anti-oxLDL/beta2GPI antibodies contribute to the development of autoimmune-mediated atherosclerosis.

IGF2 genotype and obesity in men and women across the adult age span.

We studied a previously reported association between the IGF2 gene's ApaI polymorphism and obesity in 500 healthy men and women (19-90 y). We hypothesized that individuals homozygous for the IGF2 A allele (A/A) would exhibit lower body mass, BMI and DEXA-measured fat mass compared to G/G homozygotes. Subjects were categorized as exhibiting the G/G (n = 241), G/A (n = 197) or A/A (n = 62) genotype. Contrary to our hypothesis, no difference was observed in body mass, body mass index (BMI) or fat mass between the G/G and A/A genotype groups in the entire cohort. Surprisingly, Caucasian A/A individuals (n = 427) exhibited significantly higher fat mass compared to Caucasian G/G individuals (P < 0.05). In summary, individuals homozygous for the IGF2 G allele do not exhibit higher body mass, BMI or fat mass compared to A/A individuals; however, Caucasians with the A/A genotype exhibit higher fat mass than G/G individuals.

Does age, sex, or ACE genotype affect glucose and insulin responses to strength training?

The purpose of the present study was to determine whether age, sex, or angiotensin I-converting enzyme (ACE) genotype influences the effects of strength training (ST) on glucose homeostasis. Nineteen sedentary young (age = 20-30 yr) men (n = 10) and women (n = 9) were studied and compared with 21 sedentary older (age = 65-75 yr) men (n = 12) and women (n = 9) before and after a 6-mo total body ST program. Fasting insulin concentrations were reduced in young men and in older men with ST (P < 0.05 in both). In addition, total insulin area under the curve decreased by 21% in young men (P < 0.05), and there was a trend for a decrease (11%) in older men (P = 0.06). No improvements in insulin responses were observed in young or older women. The ACE deletion/deletion genotype group had the lowest fasting insulin and insulin areas under the oral glucose tolerance test (OGTT) curve before training (all P < 0.05), but those with at least one insertion allele had a trend for a greater reduction in total insulin area than deletion homozygotes (P = 0.07). These results indicate that ST has a more favorable effect on insulin response to an OGTT in men than in women and offer some support for the hypothesis that ACE genotype may influence insulin responses to ST.

Shiga toxins induce, superinduce, and stabilize a variety of C-X-C chemokine mRNAs in intestinal epithelial cells, resulting in increased chemokine expression.

Exposure of humans to Shiga toxins (Stxs) is a risk factor for hemolytic-uremic syndrome (HUS). Because Stx-producing Escherichia coli (STEC) is a noninvasive enteric pathogen, the extent to which Stxs can cross the host intestinal epithelium may affect the risk of developing HUS. We have previously shown that Stxs can induce and superinduce IL-8 mRNA and protein in intestinal epithelial cells (IECs) in vitro via a ribotoxic stress response. We used cytokine expression arrays to determine the effect of Stx1 on various C-X-C chemokine genes in IECs. We observed that Stx1 induces multiple C-X-C chemokines at the mRNA level, including interleukin-8 (IL-8), GRO-alpha, GRO-beta, GRO-gamma, and ENA-78. Like that of IL-8, GRO-alpha and ENA-78 mRNAs are both induced and superinduced by Stx1. Furthermore, Stx1 induces both IL-8 and GRO-alpha protein in a dose-response fashion, despite an overall inhibition in host cell protein synthesis. Stx1 treatment stabilizes both IL-8 and GRO-alpha mRNA. We conclude that Stxs are able to increase mRNA and protein levels of multiple C-X-C chemokines in IECs, with increased mRNA stability at least one mechanism involved. We hypothesize that ribotoxic stress is a pathway by which Stxs can alter host signal transduction in IECs, resulting in the production of multiple chemokine mRNAs, leading to increased expression of specific proteins. Taken together, these data suggest that exposing IECs to Stxs may stimulate a proinflammatory response, resulting in influx of acute inflammatory cells and thus contributing to the intestinal tissue damage seen in STEC infection.

Shiga toxin translocation across intestinal epithelial cells is enhanced by neutrophil transmigration.

Shiga toxin-producing E. coli (STEC) is a food-borne pathogen that causes serious illness, including hemolytic-uremic syndrome (HUS). STEC colonizes the lower intestine and produces Shiga toxins (Stxs). Stxs appear to translocate across intestinal epithelia and affect sensitive endothelial cell beds at various sites. We have previously shown that Stxs cross polarized intestinal epithelial cells (IECs) via a transcellular route and remain biologically active. Since acute inflammatory infiltration of the gut and fecal leukocytes is seen in many STEC-infected patients and since polymorphonuclear leukocyte (PMN) transmigration across polarized IECs diminishes the IEC barrier function in vitro, we hypothesized that PMN transmigration may enhance Stx movement across IECs. We found that basolateral-to-apical transmigration of neutrophils significantly increased the movement of Stx1 and Stx2 across polarized T84 IECs in the opposite direction. The amount of Stx crossing the T84 barrier was proportional to the degree of neutrophil transmigration, and the increase in Stx translocation appears to be due to increases in paracellular permeability caused by migrating PMNs. STEC clinical isolates applied apically induced PMN transmigration across and interleukin-8 (IL-8) secretion from T84 cells. Of the 10 STEC strains tested, three STEC strains lacking eae and espB (eae- and espB-negative STEC strains) induced significantly more neutrophil transmigration and significantly greater IL-8 secretion than eae- and espB-positive STEC or enteropathogenic E. coli. This study suggests that STEC interaction with intestinal epithelia induces neutrophil recruitment to the intestinal lumen, resulting in neutrophil extravasation across IECs, and that during this process Stxs may pass in greater amounts into underlying tissues, thereby increasing the risk of HUS.

Skeletal muscle satellite cell characteristics in young and older men and women after heavy resistance strength training.

Skeletal muscle satellite cell proportions and morphology were assessed in healthy, sedentary young and older men and women in response to heavy resistance strength training (HRST). Fourteen young (20-30 years) men (n = 7) and women (n = 7) and 15 older (65-75 years) men (n = 8) and women (n = 7) completed 9 weeks of unilateral knee extension exercise training 3 days per week. Muscle biopsies were obtained from each vastus lateralis before and after training, with the nondominant leg serving as an untrained control. All four groups demonstrated a significant increase in satellite cell proportion in response to HRST (2.3 +/- 0.4% vs 3.1 +/- 0.4% for all subjects combined, before and after training, respectively; p < .05), with older women demonstrating the greatest increase (p < .05). Morphology data indicated a significant increase in the proportion of active satellite cells in after-training muscle samples compared with before-training samples and with control leg samples (31% vs 6% and 7%, respectively; p < .05). The present results indicate that the proportion of satellite cells is increased after HRST in young and older men and women, with an exaggerated response in older women. Furthermore, the proportion of satellite cells that appear morphologically active is increased as a result of HRST.

Effect of strength training on resting metabolic rate and physical activity: age and gender comparisons.

PURPOSE: The purpose of this study was to compare age and gender effects of strength training (ST) on resting metabolic rate (RMR), energy expenditure of physical activity (EEPA), and body composition. METHODS: RMR and EEPA were measured before and after 24 wk of ST in 10 young men (20-30 yr), 9 young women (20-30 yr), 11 older men (65-75 yr), and 10 older women (65-75 yr). RESULTS: When all subjects were pooled together, absolute RMR significantly increased by 7% (5928 +/- 1225 vs 6328 +/- 1336 kJ.d-1, P < 0.001). Furthermore, ST increased absolute RMR by 7% in both young (6302 +/- 1458 vs 6719 +/- 1617 kJ x d(-1), P < 0.01) and older (5614 +/- 916 vs 5999 +/- 973 kJ x d(-1), P < 0.05) subjects, with no significant interaction between the two age groups. In contrast, there was a significant gender x time interaction (P < 0.05) for absolute RMR with men increasing RMR by 9% (6645 +/- 1073 vs 7237 +/- 1150 kJ x d(-1), P < 0.001), whereas women showed no significant increase (5170 +/- 884 vs 5366 +/- 692 kJ x d(-1), P = 0.108). When RMR was adjusted for fat-free mass (FFM) using ANCOVA, with all subjects pooled together, there was still a significant increase in RMR with ST. Additionally, there was still a gender effect (P < 0.05) and no significant age effect (P = NS), with only the men still showing a significant elevation in RMR. Moreover, EEPA and TEE estimated with a Tritrac accelerometer and TEE estimated by the Stanford Seven-Day Physical Activity Recall Questionnaire did not change in response to ST for any group. CONCLUSIONS: In conclusion, changes in absolute and relative RMR in response to ST are influenced by gender but not age. In contrast to what has been suggested previously, changes in body composition in response to ST are not due to changes in physical activity outside of training.

Insulin action after resistive training in insulin resistant older men and women.

OBJECTIVES: To determine the effects of resistive training (RT) on insulin action and assess the determinants of the changes in insulin action. DESIGN: Longitudinal study. SETTING: Outpatient setting. PARTICIPANTS: Eighteen older men and older postmenopausal women (65-74 years) with normal (6 men and 5 women) or impaired glucose tolerance (4 men and 3 women). INTERVENTION: Six months of progressive whole-body RT. MEASUREMENTS: Upper and lower body strength was assessed by the one repetition maximum test. Total body fat and fat-free mass (FFM) were determined by dual-energy x-ray absorptiometry before and after 6 months of RT. Insulin sensitivity was estimated from the relationship of glucose utilization (M) to the concentration of insulin (I) during the last 30 minutes of 3-hour hyperinsulinemic-euglycenic clamps (240 pmol x min(-2) x min(-1)) (M/I) before and after RT. RESULTS: RT significantly improved upper- and lower-body muscular strength (P < .005). FFM increased after RT in the entire group (P < .01) with no significant change in body fat. Although the change in M was larger in men (13%) than women (3%), the difference was not significant. The change in M was a function of initial M (r = -0.53, P < .05). There was a trend (0.060+/-0.006 vs 0.066+/-0.006 micromol x kg(-1) x min(-1)/pmol/l, n = 18) for M/I to increase after RT in the combined group of men and women (P = .06). There were no significant relationships between changes in M or M/I with changes in body composition or strength. CONCLUSION: A 6-month RT program tends to improve insulin action in insulin-resistant older adults. These results suggest that RT may be useful in ameliorating insulin resistance that often occurs with physical inactivity, obesity, and loss of muscular strength in older insulin resistant men and women.