Climate Change, Air Pollution, and Physical Inactivity: Is Active Transportation Part of the Solution?

Active transportation is defined as self-propelled, human-powered transportation modes, such as walking and bicycling. In this article, we review the evidence that reliance on gasoline-powered transportation is contributing to global climate change, air pollution, and physical inactivity and that this is harmful to human health. Global climate change poses a major threat to human health and in the future could offset the health gains achieved over the last 100 yr. Based on hundreds of scientific studies, there is strong evidence that human-caused greenhouse gas emissions are contributing to global climate change. Climate change is associated with increased severity of storms, flooding, rising sea levels, hotter climates, and drought, all leading to increased morbidity and mortality. Along with increases in atmospheric CO2, other pollutants such as nitrogen dioxide, ozone, and particulate matter (e.g., PM2.5) are released by combustion engines and industry, which can lead to pulmonary and cardiovascular diseases. Also, as car ownership and vehicle miles traveled have increased, the shift toward motorized transport has contributed to physical inactivity. Each of these global challenges has resulted in, or is projected to result in, millions of premature deaths each year. One of the ways that nations can mitigate the health consequences of climate change, air pollution, and chronic diseases is through the use of active transportation. Research indicates that populations that rely heavily on active transportation enjoy better health and increased longevity. In summary, active transportation has tremendous potential to simultaneously address three global public health challenges of the 21st century.

Effects of Seasonal Vitamin D3 Supplementation on Strength, Power, and Body Composition in College Swimmers.

The purpose of this study was to evaluate the impact of fall season vitamin D3 supplementation on strength/power, body composition, and anabolic hormones in swimmers with optimal vitamin D status at summer's end. Male and female National Collegiate Athletic Association Division I swimmers (N = 19) with optimal 25-hydroxyvitamin D [25(OH)D] randomly received 5,000 IU of vitamin D3 (VITD) or placebo (PLA) daily for 12 weeks while participating in swimming and strength and conditioning training (August-November). Before and after the intervention, the participants underwent blood sampling for analysis of serum 25(OH)D, parathyroid hormone, total testosterone, free testosterone, sex hormone-binding globulin, and insulin-like growth factor 1, dual-energy X-ray absorptiometry, and strength/power testing (bench press, squat, dead lift, standing broad jump, vertical jump, and dips and pull-ups). Sex was used as a covariate for analyses. The 25(OH)D was decreased by 44% in PLA (p < .05) and increased by 8% in VITD over the 12 weeks. Fat-free mass increased in VITD (56.4-59.1 kg; p < .05), but not PLA (59.4-59.7 kg; p < .01). Significant Group × Time interaction effects were observed for dead lift (F = 21.577, p < .01) and vertical jump (F = 11.219, p < .01), but no other strength/power tests. Total testosterone decreased similarly in both groups, but free testosterone decreased and sex hormone-binding globulin increased only in PLA (p < .01). There were no group differences or changes in insulin-like growth factor 1 with the intervention. The findings suggest that vitamin D supplementation is an efficacious strategy to maintain 25(OH)D during the fall season training and to enhance some aspects of strength/power and fat-free mass in swimmers. Further research on the relationship between vitamin D and anabolic hormones is needed.

Docosahexaenoic acid affects markers of inflammation and muscle damage after eccentric exercise.

The effect of docosahexaenoic acid (DHA) on inflammatory and muscle damage response to acute eccentric exercise and to the subsequent initiation of a resistance training program was studied in 41 untrained men. Subjects consumed either 2 g·d of either DHA or placebo (PL) for 28 days before a 17-day exercise phase (day 1 to day 17) that began with an eccentric exercise bout of the elbow flexors (day 1). For analysis, the exercise period was further divided into an acute response phase (day 1-4). Isometric muscle strength (STR), range of motion (ROM), and delayed onset muscle soreness (DOMS) were measured on days 1, 2, 3, 4, 7, 12, and 17. Fasted blood was measured for interleukin 6 (IL-6), interleukin 1 receptor antagonist, C-reactive protein (CRP), and creatine kinase (CK) on days 1, 2, and 4. Serum CK and CRP were also measured in blood collected on days 7, 12, and 17. In the acute phase, DHA significantly reduced the serum CK (12.5%) and the IL-6 response (32%) but did not affect STR or DOMS. Over the entire 17-day resistance exercise period, DOMS area under the curve was 183.2 ± 96.2 for DHA and 203.2 ± 120.9 for PL (p = 0.054) and the CK response was numerically lower for DHA (p = 0.093). Docosahexaenoic acid supplementation reduced some but not all indicators of muscle damage and inflammation in the 4 days after an acute eccentric exercise bout but did not significantly affect the response to initiation of resistance exercise.

Evidence-based evaluation of potential benefits and safety of beta-alanine supplementation for military personnel.

This Department of Defense-sponsored evidence-based review evaluates the safety and putative outcomes of enhancement of athletic performance or improved recovery from exhaustion in studies involving beta-alanine alone or in combination with other ingredients. Beta-alanine intervention studies and review articles were collected from 13 databases, and safety information was collected from adverse event reporting portals. Due to the lack of systematic studies involving military populations, all the available literature was assessed with a subgroup analysis of studies on athletes to determine if beta-alanine would be suitable for the military. Available literature provided only limited evidence concerning the benefits of beta-alanine use, and a majority of the studies were not designed to address safety. Overall, the strength of evidence in terms of the potential for risk of bias in the quality of the available literature, consistency, directness, and precision did not support the use of beta-alanine by military personnel. The strength of evidence for a causal relation between beta-alanine and paresthesia was moderate.

Effect of capsaicin supplementation on repeated sprinting performance.

Performance in many team sports is partially dependent on the ability to perform repeatedly at high intensity. Previous research demonstrates that capsaicin (CAP) has physiological and metabolic effects that could influence exercise performance and inflammation. The purpose of this study was to investigate the influence of CAP on performance of and the interleukin-6 (IL-6) response to repeated sprints. Nineteen healthy male experienced athletes, age 18-30 years, participated in a placebo (PCB)-controlled, crossover study. During 1 trial, they consumed 3 g·d(-1) cayenne (25.8 mg·d(-1) CAP) and the other a PCB for days. Directly after the supplementation period, they completed a repeated sprint test (RST) consisting of 15 30-m maximal effort sprints on 35-second intervals with sprint times measured via an electronic dual-beam timing system. Fasted blood draws for IL-6 were taken at baseline before supplementation, 45 minute pre-RST, and immediately post-RST. Rate of perceived exertion (RPE), muscle soreness (MS), and gastrointestinal distress (GD) for 5 symptom subscales were measured 1-minute pretest, during, posttest, and 1-minute posttest. The MS was additionally measured for 3-day posttest. Relative to the PCB, CAP significantly increased the sum of ratings of GD symptoms by 6.3-fold. There was no difference between treatments in fastest or mean sprint time, fatigue, IL-6 response, RPE, or MS. In summary, CAP did not influence repeated sprint performance or the IL-6 response but caused substantial GD. The CAP is not recommended for athletes involved in repeated sprinting.

Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults.

BACKGROUND: Studies show that obese individuals have prolonged elevations in postprandial lipemia and an exacerbated inflammatory response to high fat meals, which can increase risk for cardiovascular diseases. As epidemiological studies indicate an association between type of fat and circulating inflammatory markers, the purpose of this study was to investigate the acute effect of different fat sources on inflammation and oxidative stress in overweight and obese individuals. METHODS: Eleven overweight and obese subjects consumed three high fat milkshakes rich in monounsaturated fat (MFA), saturated fat (SFA), or long-chain omega 3 polyunsaturated fat (O3FA) in random order. Blood samples collected at baseline, 1, 2, 4, and 6 hours postprandial were analyzed for markers of inflammation (soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tumor necrosis factor- α (TNF-α), and C-reactive protein (CRP)), oxidative stress (8-epi-prostaglandin-F2α (8-epi) and nuclear factor-κB (NF-κB)), and metabolic factors (glucose, insulin, non-esterified free fatty acids, and triglycerides (TG)). RESULTS: O3FA enhanced NF-kB activation compared to SFA, but did not increase any inflammatory factors measured. Conversely, SFA led to higher ICAM-1 levels than MFA (p = 0.051), while MFA increased TG more than SFA (p < 0.05). CRP increased while TNF-α and 8-epi decreased with no difference between treatments. CONCLUSIONS: While most of the inflammatory factors measured had modest or no change following the meal, ICAM-1 and NF-κB responded differently by meal type. These results are provocative and suggest that type of fat in meals may differentially influence postprandial inflammation and endothelial activation.

American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults.

Overweight and obesity affects more than 66% of the adult population and is associated with a variety of chronic diseases. Weight reduction reduces health risks associated with chronic diseases and is therefore encouraged by major health agencies. Guidelines of the National Heart, Lung, and Blood Institute (NHLBI) encourage a 10% reduction in weight, although considerable literature indicates reduction in health risk with 3% to 5% reduction in weight. Physical activity (PA) is recommended as a component of weight management for prevention of weight gain, for weight loss, and for prevention of weight regain after weight loss. In 2001, the American College of Sports Medicine (ACSM) published a Position Stand that recommended a minimum of 150 min wk(-1) of moderate-intensity PA for overweight and obese adults to improve health; however, 200-300 min wk(-1) was recommended for long-term weight loss. More recent evidence has supported this recommendation and has indicated more PA may be necessary to prevent weight regain after weight loss. To this end, we have reexamined the evidence from 1999 to determine whether there is a level at which PA is effective for prevention of weight gain, for weight loss, and prevention of weight regain. Evidence supports moderate-intensity PA between 150 and 250 min wk(-1) to be effective to prevent weight gain. Moderate-intensity PA between 150 and 250 min wk(-1) will provide only modest weight loss. Greater amounts of PA (>250 min wk(-1)) have been associated with clinically significant weight loss. Moderate-intensity PA between 150 and 250 min wk(-1) will improve weight loss in studies that use moderate diet restriction but not severe diet restriction. Cross-sectional and prospective studies indicate that after weight loss, weight maintenance is improved with PA >250 min wk(-1). However, no evidence from well-designed randomized controlled trials exists to judge the effectiveness of PA for prevention of weight regain after weight loss. Resistance training does not enhance weight loss but may increase fat-free mass and increase loss of fat mass and is associated with reductions in health risk. Existing evidence indicates that endurance PA or resistance training without weight loss improves health risk. There is inadequate evidence to determine whether PA prevents or attenuates detrimental changes in chronic disease risk during weight gain.

Inflammatory response to a high-fat, low-carbohydrate weight loss diet: effect of antioxidants.

The objective of this study was to test the hypothesis that the inflammatory response to a high-fat, low-carbohydrate weight loss diet (HF) we previously observed was due to oxidative stress. Nineteen overweight subjects (BMI>27 kg/m(2)) were randomly assigned to either an antioxidant supplement (AS) (1 g vitamin C/800 IU vitamin E) or a placebo (P) group and provided with a HF for 7 days. Fasted pre- and post serum samples were measured for markers of inflammation (C-reactive protein (CRP), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1)), oxygen radical absorbance capacity (ORAC), and glucose, whereas urine was measured for oxidative stress (8-epi-prostaglandin-F(2alpha) (8-epi)). HF resulted in significant reductions in weight (-3.2%), glucose (-18.7%), and MCP-1 (-15%) (all P<0.01), with no difference between groups. There was a trend for a differential effect between groups for CRP as it decreased 32% in the AS group but increased 50% for P (P=0.076). Inverse correlations were noted between initial values and changes in several inflammatory and oxidative stress markers, including CRP (r= -0.501), 8-epi (r= -0.863), and ORAC (r= -0.546) (all P<0.05). It was concluded that weight loss on a short-term HF caused reduction of some but not all markers of inflammation. A role for oxidative stress in causing inflammation was not confirmed; however, longer term diet-controlled studies are necessary to further explore the trend for a differential response in CRP with antioxidant supplementation.

Low carbohydrate, high fat diet increases C-reactive protein during weight loss.

OBJECTIVE: Chronic inflammation is associated with elevated risk of heart disease and may be linked to oxidative stress in obesity. Our objective was to evaluate the effect of weight loss diet composition (low carbohydrate, high fat, LC or high carbohydrate, low fat, HC) on inflammation and to determine whether this was related to oxidative stress. METHODS: Twenty nine overweight women, BMI 32.1 +/- 5.4 kg/m(2), were randomly assigned to a self-selected LC or HC diet for 4 wks. Weekly group sessions and diet record collections helped enhance compliance. Body weight, markers of inflammation (serum interleukin-6, IL-6; C-reactive protein, CRP) oxidative stress (urinary 8-epi-prostaglandin F2alpha, 8-epi) and fasting blood glucose and free fatty acids were measured weekly. RESULTS: The diets were similar in caloric intake (1357 kcal/d LC vs. 1361 HC, p=0.94), but differed in macronutrients (58, 12, 30 and 24, 59, 18 for percent of energy as fat, carbohydrate, and protein for LC and HC, respectively). Although LC lost more weight (3.8 +/- 1.2 kg LC vs. 2.6 +/- 1.7 HC, p=0.04), CRP increased 25%; this factor was reduced 43% in HC (p=0.02). For both groups, glucose decreased with weight loss (85.4 vs. 82.1 mg/dl for baseline and wk 4, p<0.01), while IL-6 increased (1.39 to 1.62 pg/mL, p=0.04). Urinary 8-epi varied differently over time between groups (p<0.05) with no consistent pattern. CONCLUSION: Diet composition of the weight loss diet influenced a key marker of inflammation in that LC increased while HC reduced serum CRP but evidence did not support that this was related to oxidative stress.

Energy restriction but not protein source affects antioxidant capacity in athletes.

The primary purpose of this study was to examine the effect of energy restriction on antioxidant capacity in trained athletes. Secondly, our study determined whether dietary protein source influenced the antioxidant response, performance, and immunity. Twenty male cyclists consumed either whey or casein supplement (40 g/day) in addition to their diet for 17 days. All subjects subsequently underwent 4 days of energy restriction using a formula diet (20 kcal/kg) while continuing protein supplementation. Energy restriction caused 2.7 +/- 0.3 kg weight loss, increased lymphocyte total glutathione (tGSH) 37%, red blood cell glutathione peroxidase 48%, plasma cysteine 12%, and decreased whole blood reduced to oxidized GSH (rGSH/GSSG) ratio by 52%. The only immunity factor altered by energy restriction was an increase in stimulated phagocytosis (65%). Acute submaximal exercise reduced blood tGSH but increased glutathione peroxidase. Performance of a high intensity cycle test following 45 min of moderate exercise tended to be reduced by energy restriction (P = 0.06) but was unaffected by protein source. Energy restriction caused a negative nitrogen balance with no difference from dietary protein source. In conclusion, acute energy restriction increased plasma cysteine and several markers of the glutathione antioxidant system in trained athletes. A high cysteine dietary protein source did not influence these responses.