Sam R. Emerson

Does Moderate Intensity Exercise Attenuate the Postprandial Lipemic and Airway Inflammatory Response to a High-Fat Meal?

We investigated whether an acute bout of moderate intensity exercise in the postprandial period attenuates the triglyceride and airway inflammatory response to a high-fat meal (HFM) compared to remaining inactive in the postprandial period. Seventeen (11 M/6 F) physically active (≥150 min/week of moderate-vigorous physical activity (MVPA)) subjects were randomly assigned to an exercise (EX; 60% VO2peak) or sedentary (CON) condition after a HFM (10 kcal/kg, 63% fat). Blood analytes and airway inflammation via exhaled nitric oxide (eNO) were measured at baseline, and 2 and 4 hours after HFM. Airway inflammation was assessed with induced sputum and cell differentials at baseline and 4 hours after HFM. Triglycerides doubled in the postprandial period (~113 ± 18%, P < 0.05), but the increase did not differ between EX and CON. Percentage of neutrophils was increased 4 hours after HFM (~17%), but the increase did not differ between EX and CON. Exhaled nitric oxide changed nonlinearly from baseline to 2 and 4 hours after HFM (P < 0.05,  η 2 = 0.36). Our findings suggest that, in active individuals, an acute bout of moderate intensity exercise does not attenuate the triglyceride or airway inflammatory response to a high-fat meal.

Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise

Postprandial lipemia is an independent risk factor for development of cardiovascular disease. Postprandial inflammation following the prolonged elevation of triglycerides occurring subsequent to ingestion of high-fat meals, provides a likely explanation for increased disease risk. Substantial evidence has shown that acute exercise is an effective modality for attenuation of postprandial lipemia following a high-fat meal. However, much of the evidence pertaining to exercise intensity, duration, and overall energy expenditure for reducing postprandial lipemia is inconsistent. The effects of these different exercise variables on postprandial inflammation is largely unknown. Long-term, frequent exercise, however, appears to effectively reduce systemic inflammation, especially in at-risk or diseased individuals. With regard to an acute postprandial response, without a recent bout of exercise, high levels of chronic exercise do not appear to reduce postprandial lipemia. This review summarizes the current literature on postprandial and inflammatory responses to high-fat meals, and the roles that both acute and chronic exercise play. This review may be valuable for health professionals who wish to provide evidence-based, pragmatic advice for reducing postprandial lipemia and cardiovascular disease risk for their patients. A brief review of proposed mechanisms explaining how high-fat meals may result in pro-inflammatory and pro-atherosclerotic environments is also included.

Magnitude and Timing of the Postprandial Inflammatory Response to a High-Fat Meal in Healthy Adults: A Systematic Review

Research findings over the past several decades have shown that inflammation is a prominent feature of many chronic diseases, with poor diet being one likely inflammatory stimulus. Specifically, a single high-fat meal (HFM) has been suggested to increase inflammation, although there is currently no consensus with regard to the specific changes in many of the proinflammatory markers that are frequently assessed after an HFM. The aim of this systematic review was to objectively describe the postprandial timing and magnitude of changes in 5 common inflammatory markers: interleukin (IL) 6, C-reactive protein (CRP), tumor necrosis factor (TNF) α, IL-1β, and IL-8. Ten relevant databases were searched, yielding 494 results, of which 47 articles met the pre-established inclusion criteria: 1) healthy men and women aged 18-60 y, 2) consuming a single HFM (≥30% fat, ≥500 kcal), and 3) assessing relevant inflammatory markers postmeal for ≥2 h. The only marker found to consistently change in the postprandial period was IL-6: on average, from a baseline of ∼1.4 pg/mL, it peaked at ∼2.9 pg/mL ∼6 h post-HFM (an average relative change of ∼100%). CRP, TNF-α, IL-1β, and IL-8 did not change significantly in 79% (23 of 29), 68% (19 of 28), 67% (2 of 3), and 75% (3 of 4) of included studies, respectively. We conclude that there is strong evidence that CRP and TNF-α are not responsive at the usual time scale observed in postprandial studies in healthy humans younger than age 60 y. However, future research should further investigate the role of IL-6 in the postprandial period, because it routinely increases even in healthy participants. We assert that the findings of this systematic review on markers of inflammation in the postprandial period will considerably aid in informing future research and advancing clinical knowledge.

Decreased Prevalence of Exercise Expiratory Flow Limitation from Pre- to Postpuberty.

PURPOSE We recently reported a high prevalence of expiratory flow limitation (EFL) independent of sex in prepubescent children that exceeds the prevalence reported in adults. It is unknown how transpubertal maturation and growth affect pulmonary function, specifically EFL, during exercise. The purpose of this longitudinal study was to investigate the changes in EFL, including sex differences, from pre- to postpuberty. METHODS Twenty-one children (age 12-16 yr, 11 boys and 10 girls) were recruited from 40 prepubescent children who completed testing in our laboratory ∼5 yr ago. Subjects completed pulmonary function tests before and after an incremental exercise test to exhaustion on a cycle ergometer. EFL was determined using the percent tidal volume overlap method. RESULTS Nineteen of 21 subjects (10 boys and 9 girls, ∼90%) exhibited EFL prepuberty, whereas only 7 of 21 subjects (5 boys and 2 girls, 33%) exhibited EFL postpuberty. Boys had a significantly greater forced vital capacity (FVC) than girls both pre- (∼15%) and postpuberty (boys: 4.73 ± 0.53 L; girls: 3.80 ± 0.29 L). Maximal aerobic capacity (V˙O2max) significantly increased (boys: ∼120%; girls: ∼110%) from pre- to postpuberty and was greater (P < 0.05) in boys postpuberty (boys: 2.76 ± 0.43 L·min; girls: 1.94 ± 0.35 L·min). V˙E/V˙CO2 significantly decreased (∼13%) in boys and girls during maximal exercise. Postpuberty, subjects regulated tidal breathing at significantly higher lung volumes (greater expiratory reserve volume/FVC and lower inspiratory reserve volume/FVC) during exercise compared with prepuberty. CONCLUSION Our findings suggest that the prevalence of EFL declines as children mature from pre- to postpuberty, likely because of increases in lung size, decreases in V˙E/V˙CO2, and/or changes in breathing mechanics that are greater than increases in maximal ventilation that occur with increased pulmonary gas exchange.

Absence of Respiratory Muscle Fatigue in High-Intensity Continuous or Interval Cycling Exercise.

Abstract Kurti, SP, Smith, JR, Emerson, SR, Castinado, KM, and Harms, CA. Absence of respiratory muscle fatigue in high-intensity continuous or interval cycling exercise. J Strength Cond Res 29(11): 3171–3176, 2015—Respiratory muscle fatigue (RMF) occurs during prolonged exercise (∼15–20 minutes) at >85% V[Combining Dot Above]O2max. However, RMF has been reported to occur in ∼3–6 minutes in various modes of exercise at a high intensity. It is not known if continuous cycling exercise vs. repeated bouts of high-intensity interval training (HIT) at >85% V[Combining Dot Above]O2max will lead to RMF. We hypothesized that RMF would occur after a constant load test and would be present before end exercise in an HIT protocol. Eight moderately active healthy men (21.7 ± 1.7 years; 181.3 ± 5.2 cm; 81.3 ± 2.3 kg) completed a V[Combining Dot Above]O2max test on a cycle ergometer. Subjects then completed 2 bouts of HIT (7 × 1 minute, 2-minute recovery between intervals) and 3 bouts of continuous exercise (CE) tests at 90% of peak power (determined from an incremental exercise test to exhaustion). Maximal inspiratory pressure (PIMAX) and expiratory pressure (PEMAX) were measured pre- and post-exercise for both HIT and CE and after each interval during HIT. Decreases in postexercise PIMAX and PEMAX compared with baseline were used to determine RMF. There were no differences (p > 0.05) in PIMAX or PEMAX pre- to post-exercise for HIT (PIMAX pre: 134 ± 51, post: 135 ± 50 cmH2O; PEMAX pre: 143 ± 41, post: 148 ± 46 cmH2O) or CE (PIMAX pre: 135 ± 54, post: 133 ± 52 cmH2O; PEMAX pre: 146 ± 46, post: 148 ± 46 cmH2O) indicating RMF was not present following CE and HIT. These data suggest that repeated high-intensity cycling exercise at 90% peak power in a CE or HIT protocol does not lead to RMF.

Does chronic physical activity level modify the airway inflammatory response to an acute bout of exercise in the postprandial period

Recent studies have confirmed that a single high-fat meal (HFM) leads to increased airway inflammation. However, exercise is a natural anti-inflammatory and may modify postprandial airway inflammation. The postprandial airway inflammatory response is likely to be modified by chronic physical activity (PA) level. This study investigated whether chronic PA modifies the airway inflammatory response to an acute bout of exercise in the postprandial period in both insufficiently active and active subjects. Thirty-nine nonasthmatic subjects (20 active, 13 males/7 females) who exceeded PA guidelines (≥150 min moderate-vigorous PA/week) and 19 insufficiently active (6 males/13 females) underwent an incremental treadmill test to exhaustion to determine peak oxygen uptake. Subjects were then randomized to a condition (COND), either remaining sedentary (CON) or exercising (EX) post-HFM. Exercise was performed at the heart rate corresponding to 60% peak oxygen uptake on a treadmill for 1 h post-HFM (63% fat, 10 kcal/kg body weight). Blood lipids and exhaled nitric oxide (eNO: marker of airway inflammation) were measured at baseline and 2 h and 4 h post-HFM. Sputum differential cell counts were performed at baseline and 4 h post-HFM. The mean eNO response for all groups increased at 2 h post-HFM (∼6%) and returned to baseline by 4 h (p = 0.03). There was a time × COND interaction (p = 0.04), where EX had a greater eNO response at 4 h compared with CON. Sputum neutrophils increased at 4 h post-HFM (p < 0.05). These findings suggest that airway inflammation occurs after an HFM when exercise is performed in the postprandial period, regardless of habitual activity level.

Household Air Pollution Exposure and Influence of Lifestyle on Respiratory Health and Lung Function in Belizean Adults and Children: A Field Study

Household air pollution (HAP) contributes to the global burden of disease. Our primary purpose was to determine whether HAP exposure was associated with reduced lung function and respiratory and non-respiratory symptoms in Belizean adults and children. Our secondary purpose was to investigate whether lifestyle (physical activity (PA) and fruit and vegetable consumption (FV)) is associated with reported symptoms. Belizean adults (n = 67, 19 Male) and children (n = 23, 6 Male) from San Ignacio Belize and surrounding areas participated in this cross-sectional study. Data collection took place at free walk-in clinics. Investigators performed initial screenings and administered questionnaires on (1) sources of HAP exposure; (2) reported respiratory and non-respiratory symptoms and (3) validated lifestyle questionnaires. Participants then performed pulmonary function tests (PFTs) and exhaled breath carbon monoxide (CO). There were no significant associations between HAP exposure and pulmonary function in adults. Increased exhaled CO was associated with a significantly lower forced expiratory volume in 1-s divided by forced vital capacity (FEV1/FVC) in children. Exposed adults experienced headaches, burning eyes, wheezing and phlegm production more frequently than unexposed adults. Adults who met PA guidelines were less likely to experience tightness and pressure in the chest compared to those not meeting guidelines. In conclusion, adults exposed to HAP experienced greater respiratory and non-respiratory symptoms, which may be attenuated by lifestyle modifications.

Post-prandial systemic 8-isoprostane increases after consumption of moderate and high-fat meals in insufficiently active males

A single high-fat meal (HFM) leads to an increase in triglycerides and oxidative stress. Oxidative stress can be assessed via 8-isoprostane generation, which is associated with the development of asthma and cardiovascular disease. No previous research has investigated whether airway and systemic 8-isoprostane increases postprandially in nonasthmatic participants according to the energy and fat content of a meal. Our purpose was to assess airway and systemic 8-isoprostane after a HFM and a true-to-life moderate-fat meal (MFM). We hypothesized that airway and systemic 8-isoprostane would increase after a HFM and a MFM, with the greatest increase in the HFM condition. Eight nonasthmatic men (25.8±6.9years) completed the HFM and MFM trials in a randomized crossover design. After a 10-hour fast, participants consumed either a HFM (71.13kJ/kg body mass, 60% fat, 23% CHO) or a MFM (35.56kJ/kg body mass, 30% fat, 52% CHO). Exhaled breath condensate to assess airway 8-isoprostane was collected at baseline and at 3 and 6hours postmeal. Venous blood samples were collected at baseline and hourly until 6hours postmeal to assess triglycerides, and every 3hours for systemic 8-isoprostane. Airway 8-isoprostane responses were not significant as a main effect of time (P=.072), between conditions (P=.365), or between time and condition (P=.319) postmeal. Systemic 8-isoprostane increased over time (P<.001), but not between conditions (P=.124) or between time and condition (P=.649) postmeal. Triglyceride incremental area under the curve was different in the HFM compared to the MFM condition (P=.013). After a HFM and a MFM, 8-isoprostane increases systemically; however, airway 8-isoprostane does not change.

Postprandial Metabolic Responses Differ by Age Group and Physical Activity Level

ObjectivesTo compare the postprandial metabolic responses to a high-fat meal in healthy adults who differ by age and physical activity level.DesignCross-sectional, quasi-experimental design.SettingPhysical Activity and Nutrition Clinical Research Consortium (PAN-CRC) at Kansas State University (Manhattan, KS, USA).ParticipantsTwenty-two healthy adults: 8 younger active (YA) adults (4M/4W; 25 ± 5 yr), 8 older active (OA) adults (4M/4W; 67 ± 5 yr), and 6 older inactive (OI) adults (3M/3W; 68 ± 7 yr).InterventionFollowing an overnight (10-hour) fast and having abstained from exercise for 2 days, participants consumed a high-fat meal (63% fat, 34% CHO; 12 kcal/kg body mass; 927 ± 154 kcal). To assess the metabolic response, blood draws were performed at baseline and each hour following the meal for 6 hours.MeasurementsFasting and postprandial triglycerides (TG), glucose, Total-C, and HDL-C were measured. Metabolic load index (MLI) and LDL-C were calculated.ResultsThere were significant group x time interactions for TG (p < 0.0001) and MLI (p = 0.004). The TG total area-under-the-curve (tAUC) response was significantly lower in YA (407.9 ± 115.1 mg/dL 6 hr) compared to OA (625.6 ± 169.0 mg/dL 6 hr; p = 0.02) and OI (961.2 ± 363.6 mg/dL 6 hr; p = 0.0002), while the OA group TG tAUC was lower than the OI group (p = 0.02). The TG peak was significantly lower in YA (90.5 ± 27.0 mg/dL) than OA (144.0 ± 42.2 mg/dL; p = 0.03) and OI (228.2 ± 96.1 mg/dL; p = 0.0003), and was lower in the OA group compared to the OI group (p = 0.03). Glucose was significantly lower 1 hour after the meal in YA (89.4 ± 10.1 mg/dL; p = 0.01) and OA (87.3 ± 22.3 mg/dL; p = 0.005) versus OI (110.7 ± 26.9 mg/dL). MLI tAUC was significantly lower in YA (936.8 ± 137.7 mg/dL 6 hr; p = 0.0007) and OA (1133.0 ± 207.4 mg/dL; p = 0.01) versus OI (1553.8 ± 394.3 mg/dL), with no difference (p = 0.14) between YA and OA groups. Total-C and LDL-C were generally lower in younger compared to older participants at baseline and throughout the postprandial period, while no group or time effects were evident in HDL-C.ConclusionBoth physical activity status and aging appear to affect the postprandial metabolic, namely TG, response to a high-fat meal. These findings point to an inherently diminished metabolic capacity with aging, but suggest that physical activity may help minimize this decrement.

Older women exhibit greater airway 8-isoprostane responses to strenuous exercise compared to older men and younger controls

Development of late-onset respiratory diseases is associated with elevated 8-isoprostane, a marker of oxidative stress, in the airways. However, sex differences exist in development of these diseases. Using an exhaustive exercise bout as a physiological stressor may elucidate whether there is a sex difference with aging in pre- to postexercise airway 8-isoprostane generation. The purpose of this study was to determine whether older women exhibit a greater airway 8-isoprostane response to exhaustive exercise compared with older men and younger controls. Thirty-six individuals completed the study (12 postmenopausal older women (OW) and 12 age-matched older men (OM), 65 ± 4 years of age; and 12 younger controls (YC), 21 ± 2 years of age). Baseline measurements included exhaled breath condensate (EBC) for assessment of airway 8-isoprostane and standard pulmonary function tests (PFTs) to assess forced expiratory volume in 1-s (FEV1), forced vital capacity (FVC), FEV1/FVC, and forced expiratory flow at 25%-75% of FVC. Subjects then performed a peak oxygen uptake test to exhaustion on a cycle ergometer. Immediately postexercise, PFTs and EBC were performed. The generation of airway 8-isoprostane from pre- to postexercise was greater in OW compared with OM and YC (p < 0.01), increasing ∼74% ± 77% in OW, while decreasing in OM (∼12% ± 50%) and YC (∼20.9% ± 30%). The OW exhibited a greater airway 8-isoprostane response to exhaustive exercise compared with OM and YC, which may suggest that sex differences in oxidative stress generation following exhaustive exercise may provide a mechanistic rationale for sex differences in late-onset respiratory diseases.