Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Johnson, Ariel M.; Kurti, Stephanie P.; Smith, Joshua R.; Rosenkranz, Sara K.; Harms, Craig A.

doi:10.1139/apnm-2015-0314

Cited by 20 publications

(16 citation statements)

References 106 publications

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“…TNF-α may increase postprandially in overweight participants [37], and in participants with metabolic syndrome [45]. However, other studies have reported no change [38, 46] or even a small decrease [35] in TNF-α postprandially. These conflicting results are most likely due to differences in participant characteristics between studies.…”

Section: Postprandial Inflammatory Responsementioning

confidence: 99%

“…Diet is obviously a very important factor to control leading up to a PPL session. The extent to which diet is controlled varies across studies, ranging from tightly controlled studies that provide meals for multiple days [76], to studies that only require participants to log food their food intake and/or keep meals consistent between trials [46]. However, even more important than controlling diet is the requirement of ensuring that individuals fast (for at least 8 h, but typically 10–12 h) prior to their test meal.…”

Section: Assessment Of Ppl and Postprandial Inflammationmentioning

confidence: 99%

“…Additionally, Zhang et al (2004) showed an attenuation of PPL in participants that exercised 12 h, but not 24 h prior to a high-fat meal [90]. However, Johnson et al (2015) found that exercise 12 h prior to a HFM was ineffective for attenuating PPL even though Johnson et al and Zhang et al both had participants exercise at 60% VO 2 max for 60 min [46]. Additionally, exercise performed immediately before ingestion of a HFM has also been shown to be effective for attenuating PPL [90, 91].…”

Section: Acute Exercise Timing and Pplmentioning

confidence: 99%

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

et al. 2016

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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.

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Section: Postprandial Inflammatory Responsementioning

confidence: 99%

Section: Assessment Of Ppl and Postprandial Inflammationmentioning

confidence: 99%

Section: Acute Exercise Timing and Pplmentioning

confidence: 99%

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

et al. 2016

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“…Even after a single high-fat meal (HFM), airway inflammation (measured via exhaled nitric oxide (eNO) (Rosenkranz et al 2010; Johnson et al 2015)) and sputum neutrophils increase in non-asthmatic individuals (Kurti et al 2015). Researchers have also reported an increase in airway inflammation in asthmatic individuals (Wood et al 2011).…”

Section: Introductionmentioning

confidence: 99%

“…We recently reported that active, non-asthmatic individuals experience airway inflammation post-HFM, and an acute bout of exercise does not modify this response (Kurti et al 2015; Johnson et al 2015). However given that ROS can increase after a single HFM (Mohanty et al 2002; Tushuizen et al 2006) and may result in airway inflammation, individuals who are insufficiently active, with reduced antioxidant defenses, may have a greater magnitude of the cellular oxidative stress and inflammatory response to a HFM as compared to physically active individuals.…”

Section: Introductionmentioning

confidence: 99%

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

Kurti

Rosenkranz

Chapes

et al. 2017

Appl. Physiol. Nutr. Metab.

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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 post-prandial airway inflammation. The post-prandial airway inflammatory response is likely to be modified by chronic physical activity (PA) level. Purpose To investigate whether chronic PA modifies the airway inflammatory response to an acute bout of exercise in the post-prandial period in both insufficiently active and active subjects. Methods Thirty-nine non-asthmatic subjects (twenty active (ACT), 13M/7F) who exceeded PA guidelines (≥150 min moderate-vigorous PA/week) and (nineteen insufficiently active (IN), 6M/13F) underwent an incremental treadmill test to exhaustion to determine VO2peak. 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% VO2peak on a treadmill one-hour post-HFM (63% fat, 10kcal/kgbw). Blood lipids and exhaled nitric oxide (eNO: marker of airway inflammation) were measured at baseline, 2 h and 4 h post-HFM. Sputum differential cell counts were performed at baseline and 4 h post-HFM. Results 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 hours compared to CON. Sputum neutrophils increased at 4 hours post-HFM (p<0.05). Conclusion These findings suggest that airway inflammation occurs after a HFM when exercise is performed in the postprandial period, regardless of habitual activity level.

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

et al. 2017

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Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Cited by 20 publications

References 106 publications

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

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

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

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

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