The use of periodization in exercise prescriptions for inactive adults: A systematic review.

BACKGROUND: Periodization of exercise is a method typically used in sports training, but the impact of periodized exercise on health outcomes in untrained adults is unclear. PURPOSE: This review aims to summarize existing research wherein aerobic or resistance exercise was prescribed to inactive adults using a recognized periodization method. METHODS: A search of relevant databases, conducted between January and February of 2014, yielded 21 studies published between 2000 and 2013 that assessed the impact of periodized exercise on health outcomes in untrained participants. RESULTS: Substantial heterogeneity existed between studies, even under the same periodization method. Compared to baseline values or non-training control groups, prescribing periodized resistance or aerobic exercise yielded significant improvements in health outcomes related to traditional and emerging risk factors for cardiovascular disease, low-back and neck/shoulder pain, disease severity, and quality of life, with mixed results for increasing bone mineral density. CONCLUSIONS: Although it is premature to conclude that periodized exercise is superior to non-periodized exercise for improving health outcomes, periodization appears to be a feasible means of prescribing exercise to inactive adults within an intervention setting. Further research is necessary to understand the effectiveness of periodizing aerobic exercise, the psychological effects of periodization, and the feasibility of implementing flexible non-linear methods.

A one-year school-based diet/exercise intervention improves non-traditional disease biomarkers in Mexican-American children.

School-based interventions are an effective way to treat childhood obesity. The purpose of the present study was to biologically validate an established school-based intervention designed to reduce standardised body mass index (zBMI) over a period of 12 months. This intervention focused on a subset of Mexican-American children who were participating in a larger clinical weight loss study. Plasma samples were analysed from self-identified Mexican-American children (12-14 years) who were randomised to either a school-based intervention (IN, n = 152) or self-help control (CN, n = 69). Treatment was 4 days week⁻¹ of exercise (45 min day⁻¹) and 1 day week⁻¹ of nutritional counselling for 6 months. Fasting (>8 h) blood samples were collected at baseline, 6 months (end of active intervention) and 12 months (6 months after the end of the active intervention). Plasma resistin, adiponectin and leptin concentration were measured using a multiplex assay. Separate linear mixed models and a P < 0.05 were used to test for significance. Significant group × time interactions were found for resistin (P < 0.0001), adiponectin (P = 0.001) and leptin (P = 0.013). For resistin, IN was 12% lower at 6 months than CN. Adiponectin concentration in IN was greater at 6 months (26%) and 12 months (8%) than CN. Leptin concentration was 22% lower for IN at 12 months than CN. We have previously reported that our school-based intervention reduced zBMI and now reported alterations in biologically relevant disease biomarkers. Some of the observed changes were only present at the end of the active intervention (resistin), while others persisted until 12 months (leptin and adiponectin). These changes underscore the effectiveness of our school-based intervention at not only improving zBMI but also at reducing disease risk.

Obese Mexican American children have elevated MCP-1, TNF-α, monocyte concentration, and dyslipidemia.

BACKGROUND AND OBJECTIVE: Obesity is an independent risk factor for chronic disease. The prevalence of obesity is especially high among Mexican American children. Peripheral blood monocytes are altered with obesity contributing to elevated systemic inflammation and increased risk of chronic disease. In addition, obesity alters the circulating levels of cytokines/chemokines that influence monocyte behavior. The study objective was to investigate alterations in blood monocytes and plasma cytokines/chemokine levels among healthy weight (standardized BMI [zBMI] ≤85th percentile; n = 66), overweight (zBMI 85th-95th percentile; n = 23), and obese (zBMI ≥95th percentile; n = 39) Mexican American children. METHODS: Blood samples were analyzed for total and subset monocyte concentration via flow cytometry. Serum monocyte chemoattractant protein-1 (MCP-1), fractalkine, interleukin-8, and tumor necrosis factor α (TNF-α) were measured by using a Milliplex MagPix assay. Serum cholesterol, high-density lipoproteins, triglycerides, and glucose were measured by using an enzymatic assay. RESULTS: Total monocyte concentration (P = .012), classic monocyte concentration (P = .045), MCP-1 (P = .015), and TNF-α (P = .002) were significantly greater in obese children compared with healthy weight children. Also, overweight and obese children had elevated triglycerides (P = .001) and reduced high-density lipoproteins (P = .033) compared with healthy weight children. CONCLUSIONS: Childhood obesity alters monocytes and circulating chemokines, putting children at a greater risk of developing obesity-related chronic diseases in adulthood. Further characterization of early immune alterations in childhood obesity may provide additional clinical insight into the assessment of obesity-related disease risk.

Moderate-intensity, premeal cycling blunts postprandial increases in monocyte cell surface CD18 and CD11a and endothelial microparticles following a high-fat meal in young adults.

High-fat meals promote transient increases in proatherogenic factors, implicating the postprandial state in cardiovascular disease (CVD) progression. Although low-grade inflammation is associated with CVD, little research has assessed postprandial inflammation. Because of its anti-inflammatory properties, premeal exercise may counteract postprandial inflammation. The purpose of this study was to determine postprandial alterations in monocytes and circulating markers of endothelial stress and inflammation following a high-fat meal in young adults with or without premeal cycle exercise. Each subject completed two trials and was randomized to rest or cycle at a moderate intensity prior to eating a high-fat meal. Flow cytometry was used to assess monocyte cell surface receptor expression and concentration of endothelial microparticles (EMP). Plasma cytokines were assessed using Luminex MagPix. Statistical analysis was completed using separate linear mixed models analyses with first-order autoregressive (AR(1)) heterogeneous covariance structure. Significance was set at P ≤ 0.05. Percentage increases in classic monocyte CD11a and CD18 were greater overall in the postprandial period in the meal-only condition compared with the meal + exercise condition (P < 0.05). EMP concentration was 47% greater 3 h after the meal compared with premeal values in the meal-only condition (P < 0.05); no significant increase was observed in the meal + exercise condition. Premeal cycling blunted postprandial increases in EMP and CD11a and CD18. Acute, moderate-intensity exercise may help counteract possibly deleterious postprandial monocyte and endothelial cell activation.

Aged mice have increased inflammatory monocyte concentration and altered expression of cell-surface functional receptors.

The expression of monocyte cell-surface receptors represents one index of immune dysfunction, which is common with aging. Although mouse models of aging are prevalent, monocyte subset assessment is rare. Our purpose was to compare cell receptor expression on classic (CD115+/Gr-1 high) and non-classic (CD115+/Gr-1 low) monocytes from 80- or 20-week-old CD-1 mice. Three-colour flow cytometry was used to determine the concentration of monocyte subsets and their respective cell-surface expression of TLR2, TLR4, CD80, CD86, MHC II and CD54. These receptors were selected because they have been previously associated with altered monocyte function. Data were analysed with independent t-tests; significance was set at P less than 0.05. Old mice had a greater concentration of both classic (258%, P=0.003) and non-classic (70%, P=0.026) monocytes. The classic : non-classic monocyte ratio doubled in old as compared with that in young mice (P=0.006), indicating a pro-inflammatory shift. TLR4 ( 27%, P=0.001) and CD80 ( 37%, P=0.004) were decreased on classic monocytes from old as compared with those from young mice. TLR2 ( 24%, P=0.002) and MHCII ( 21%, P=0.026) were altered on non-classic monocytes from old as compared with those from young mice. The increased classic : non-classic monocyte ratio combined with changes in the cell-surface receptor expression on both monocyte subsets is indicative of immune dysfunction, which may increase age-associated disease risk.

Effects of exercise on weight loss and monocytes in obese mice.

Obesity causes innate immune dysfunction, contributing to increased disease risk. Weight loss from a combination of caloric restriction and exercise is the most effective treatment of obesity. We compared forced and voluntary exercise as weight-loss treatments in diet-induced obese (DIO) mice and assessed the effects of weight loss on monocyte concentration and cell-surface expression of Toll-like receptor (TLR) 2, TLR4, CD80, and CD86. DIO CD1 male mice were allocated randomly to 1 of 3 groups (n = 6 per group): voluntary wheel running (VEX); forced treadmill running (FEX); and sedentary (S). A fourth (control) group (CN, n = 6) of nonDIO mice was included also. During the 8-wk weight-loss treatment, all 4 groups consumed a low-fat (10% fat) diet. Nonlethal saphenous vein blood samples collected at baseline, week 4, and week 8 were analyzed by flow cytometry to assess monocyte concentration and functional receptor expression. The VEX and FEX groups lost significantly more body weight (36% and 27%, respectively) over the 8 wk of treatment than did other groups. VEX mice ran 4.4 times more than did FEX animals. VEX mice had higher monocyte concentrations (48% and 58%, respectively) than did the CN and FEX groups. Compared with baseline, week 8 cell-surface expression of TLR2 (22%), TLR4 (33%), and CD86 (18%) was increased in VEX mice. At week 4, CD80 expression was 42% greater for VEX than S mice. The present study confirms that short-term exercise and low-fat diet consumption cause significant weight loss and altered immune profiles.

Comparison of blood monocytes and adipose tissue macrophages in a mouse model diet-induced weight gain.

Diet-induced weight gain causes changes in adipose tissue that alter blood monocytes and adipose tissue macrophages, increasing disease risk. The purpose of this study was to compare the effects of 24 wk of diet-induced weight gain on the percentages of blood monocytes and adipose tissue macrophages as well as the cell-surface expression of toll-like receptors 2 and 4 and leptin receptor, which are associated with inflammation and homing to adipose tissue. Crl:CD1(ICR) male mice were assigned to either a diet-induced weight gain (60% of calories from fat; n = 12) or control (10% of calories from fat; n = 13) group. After 24 wk of dietary treatment, whole blood and bilateral perigonadal fat pads were collected. Whole blood or SVF were separately labeled for monocytes (CD11b(+)CD14-) or macrophages (CD11b(+)F4/80(+)) and receptor expression by using 3-color flow cytometry. Data were analyzed by using univariate ANOVA. Compared with control mice, those in the weight-gain group had greater body weight, fat mass, and percentages of monocytes and macrophages compared with CN. Regardless of cell type, monocytes and macrophages from mice in the weight-gain group expressed significantly less toll-like receptor 2 and leptin receptor than did control mice. The present study demonstrates that monocytes and macrophages are similarly affected by diet-induced weight gain. More research is needed to confirm how monocytes might be used as a proxy measure of macrophages.

Leveraging Online Learning Resources to Teach Core Research Skills to Undergraduates at a Diverse Research University.

Today's students have unique learning needs and lack knowledge of core research skills. In this program report, we describe an online approach that we developed to teach core research skills to freshman and sophomore undergraduates. Specifically, we used two undergraduate kinesiology (KIN) courses designed to target students throughout campus (KIN1304: Public Health Issues in Physical Activity and Obesity) and specifically kinesiology majors (KIN1252: Foundations of Kinesiology). Our program was developed and validated at the 2nd largest ethnically diverse research university in the United States, thus we believe that it would be effective in a variety of student populations.

Longitudinal, Diet-induced Weight Gain is Associated with Increased Blood Monocytes and Reduced TLR4 Expression.

Excessive weight gain increases systemic inflammation resulting in increased disease risk. Toll-like receptor 4 (TLR4) reportedly mediates increases in inflammation; however, its role in obesity-induced inflammation has not been fully evaluated. The purpose of this study was to determine the longitudinal effect of diet-induced weight gain on blood monocyte concentration and cell-surface TLR4 expression. Male CD-1 mice were randomly assigned to high-fat (HF, n = 12) or low-fat (LF, n = 13) groups. Non-lethal, saphenous vein blood samples were collected at 0, 4, 8 and 12 weeks of treatment. Three-color flow cytometry was used to measure monocyte (CD11b+/CD14+) concentration and TLR4 cell-surface expression. Data were analyzed with a repeated measures ANOVA; significance was set at P<0.05. Body weight at week 12 was 21% greater in HF than LF (P<0.05). At week 12 HF had 155% more monocytes (P<0.05) with 24% less TLR4 than LF; Monocyte concentration and body weight at week 12 was negatively correlated with TLR4 gMFI (P<0.05). The observed effects of high-fat feeding on blood monocytes are consistent with a phenotype, which may be associated with premature morbidity. The observed monocyte responses may be associated with immune dysfunction and diminished response to infection.