Protease Supplementation Improves Muscle Function after Eccentric Exercise

Buford, Thomas W.; Cooke, Molly; Redd, Liz; Hudson, Geoffrey M.; Shelmadine, Brian; Willoughby, Darryn S.

doi:10.1249/mss.0b013e3181a518f0

Cited by 33 publications

(36 citation statements)

References 36 publications

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“…However, the TBARS values for the African American group and the Caucasian group were very similar at all time-points. Second, diet was not controlled leading up to the study, but we felt it was not necessary because recent research has shown that in subjects of similar age and health to those in the present study, the day to day differences in macronutrient ingestion are very minimal (2,7). Finally, most exercise studies use more aggressive exercise intensities, and the use of a submaximal exercise test in this study may not replicate the oxidative stress responses to other maximal or exhaustive exercises.…”

Section: Discussionmentioning

confidence: 97%

Differentiating Racial Differences in Time-Course Oxidative Stress Responses to Acute Exercise

Feairheller

Diaz

Williamson

et al. 2010

Medicine &Amp; Science in Sports &Amp; Exercise

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African Americans have disproportionate levels of cardiovascular disease and oxidative stress. The purpose of our study was to examine racial differences between African American and Caucasian adults in time-course oxidative stress responses to a treadmill test. After a 12-hr fast, 18 participants (9 of each ethnic group; 21 ± 0.4 yrs) completed a submaximal treadmill test and underwent serial blood draws: Pre, Post (within 2 min), 30, 60, and 120 min after exercise. At each time-point, superoxide dismutase (SOD, U/mL), total antioxidant capacity (TAC, mM), protein carbonyls (PC, nmol/mg), and thiobarbituric acid-reactive substance (TBARs, μmol/L) were measured. We found no difference between groups for blood pressure, BMI, or exercise capacity (as measured by volume of oxygen consumed, VO2 max). African Americans had significantly (p < 0.05) higher SOD (Pre: 5.45 ± 0.4 vs. 3.69 ± 0.69; 60 min: 8.99 ± 0.7 vs. 4.23 ± 0.6; 120 min: 9.69 ± 1.6 vs. 3.52 ± 0.7), TAC (Pre: 2.31 ± 0.25 vs. 1.16 ± 0.3; Post: 2.39 ± 0.2 vs. 1.34 ± 0.2; 30 min: 2.29 ± 0.2 vs. 1.09 ± 0.2), and PC (Pre: 1.09 ± 0.1 vs. 0.82 ± 0.1; Post: 1.14 ± 0.1 vs. 0.81 ± 0.1; 30 min: 1.13 ± 0.1 vs. 0.85 ± 0.1; 60 min: 1.06 ± 0.1 vs. 0.81 ± 0.05), but not TBARs. Between groups, only SOD exhibited a different time-course response: levels for African Americans rose steadily throughout the 120 min, while levels for Caucasians peaked at 30 min and by 120 min had returned to pre-exercise levels. Race had a greater effect on oxidative stress responses than submaximal exercise did. African Americans had significantly higher TAC, SOD, and PC levels compared to Caucasians.

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Section: Discussionmentioning

confidence: 97%

Differentiating Racial Differences in Time-Course Oxidative Stress Responses to Acute Exercise

Feairheller

Diaz

Williamson

et al. 2010

Medicine &Amp; Science in Sports &Amp; Exercise

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“…The most investigated lipid mediator in human models of exerciseinduced muscle injury has been PGE 2 , likely because of its proinflammatory and hyperalgesic properties and their hypothesized association with sympotomology of DOMs. Although some studies have reported elevated circulating PGE 2 concurrent with the onset of DOMs 24 -72 h following exerciseinduced muscle injury (95,102), others have found no such response (4,9,13,23,24,41). The reasons for this are unclear but may be related to differences in the intensity of skeletal muscle loading [for example, downhill running (13) vs. resistance exercise (95,102)] and/or the volume of active muscle mass [unilateral/isolation (4,9,23,24,41) vs. bilateral/compound exercises (95,102)].…”

Section: Discussionmentioning

confidence: 99%

“…The limited studies available have focused on the potential role of select COX-1 and COX-2 pathway-derived proinflammatory/hyperalgesic PGs (e.g., PGE 2 ) in underlying the symptoms of exercise-induced muscle injury, which occur Ն24 h into recovery. While some studies have reported elevated circulating levels PGE 2 , concurrent with the onset of delayed onset muscle soreness (DOMs) 24 -72 h postexercise (95,102), others have found no such response (4,9,13,23,24,41). Additionally, a large body of research on the use of NSAIDs, the main therapeutic mechanism of action of which is thought to be blockade of the COX-1 and COX-2 pathways to relieve symptoms of DOMs, has yielded conflicting and inconclusive results (reviewed in Ref.…”

mentioning

confidence: 99%

Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment

Markworth

Vella

Lingard

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

139

158

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Classical proinflammatory eicosanoids, and more recently discovered lipid mediators with anti-inflammatory and proresolving bioactivity, exert a complex role in the initiation, control, and resolution of inflammation. Using a targeted lipidomics approach, we investigated circulating lipid mediator responses to resistance exercise and treatment with the NSAID ibuprofen. Human subjects undertook a single bout of unaccustomed resistance exercise (80% of one repetition maximum) following oral ingestion of ibuprofen (400 mg) or placebo control. Venous blood was collected during early recovery (0 -3 h and 24 h postexercise), and serum lipid mediator composition was analyzed by LC-MS-based targeted lipidomics. Postexercise recovery was characterized by elevated levels of cyclooxygenase (COX)-1 and 2-derived prostanoids (TXB2, PGE2, PGD2, PGF2␣, and PGI2), lipooxygenase (5-LOX, 12-LOX, and 15-LOX)-derived hydroxyeicosatetraenoic acids (HETEs), and leukotrienes (e.g., LTB4), and epoxygenase (CYP)-derived epoxy/dihydroxy eicosatrienoic acids (EpETrEs/DiHETrEs). Additionally, we detected elevated levels of bioactive lipid mediators with anti-inflammatory and proresolving properties, including arachidonic acid-derived lipoxins (LXA4 and LXB4), and the EPA (E-series) and DHA (D-series)-derived resolvins (RvD1 and RvE1), and protectins (PD1 isomer 10S, 17S-diHDoHE). Ibuprofen treatment blocked exercise-induced increases in COX-1 and COX-2-derived prostanoids but also resulted in off-target reductions in leukotriene biosynthesis, and a diminished proresolving lipid mediator response. CYP pathway product metabolism was also altered by ibuprofen treatment, as indicated by elevated postexercise serum 5,6-DiHETrE and 8,9-DiHETrE only in those receiving ibuprofen. These findings characterize the blood inflammatory lipid mediator response to unaccustomed resistance exercise in humans and show that acute proinflammatory signals are mechanistically linked to the induction of a biological active inflammatory resolution program, regulated by proresolving lipid mediators during postexercise recovery. eicosanoid; exercise; inflammation; nonsteroidal anti-inflammatory drug; resolution LIPID MEDIATORS ARE A DIVERSE class of bioactive autocrine/ paracrine signaling molecules that are synthesized endogenously from essential omega-6 and omega-3 fatty acids. Oxidation of free fatty acid substrates via cyclooxygenase (COX-1 and COX-2), lipoxygenase (5-LOX, 12-LOX, and 15-LOX), epoxygenase (CYP), and nonenzymatic pathways, produces a potential array of more than 100 distinct lipid mediators. Bioactive lipid mediators are involved in a wide range of physiological and pathological processes, one of the best characterized of which is their key role in the inflammatory response (reviewed in Ref. 91). Classical eicosanoids derived from omega-6 arachidonic acid (AA, -6 20:4), including prostaglandins (PGs; synthesized via COX-1 and COX-2) and leukotrienes (LTs, synthesized via 5-LOX), are well established proinflammatory signaling molecules that stimul...

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“…Specific protease supplementation protocols accelerated muscle recovery after strenuous exercises (Miller et al, 2004; Beck et al, 2007; Buford et al, 2009). These findings may indicate that protein digestibility was improved; however, the reported studies lacked direct measurements of protein digestibility.…”

Section: Enzyme and Hormone Supplementation And Use Of Hydrolysates mentioning

confidence: 99%

Personalizing protein nourishment

Dallas

Sanctuary

et al. 2017

Critical Reviews in Food Science and Nutrition

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Proteins are not equally digestible—their proteolytic susceptibility varies by their source and processing method. Incomplete digestion increases colonic microbial protein fermentation (putrefaction), which produces toxic metabolites that can induce inflammation in vitro and have been associated with inflammation in vivo. Individual humans differ in protein digestive capacity based on phenotypes, particularly disease states. To avoid putrefaction-induced intestinal inflammation, protein sources and processing methods must be tailored to the consumer’s digestive capacity. This review explores how food processing techniques alter protein digestibility and examines how physiological conditions alter digestive capacity. Possible solutions to improving digestive function or matching low digestive capacity with more digestible protein sources are explored. Beyond the ileal digestibility measurements of protein digestibility, less invasive, quicker and cheaper techniques for monitoring the extent of protein digestion and fermentation are needed to personalize protein nourishment. Biomarkers of protein digestive capacity and efficiency can be identified with the toolsets of peptidomics, metabolomics, microbial sequencing and multiplexed protein analysis of fecal and urine samples. By monitoring individual protein digestive function, the protein component of diets can be tailored via protein source and processing selection to match individual needs to minimize colonic putrefaction and, thus, optimize gut health.

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Protease Supplementation Improves Muscle Function after Eccentric Exercise

Abstract: Protease supplementation seems to attenuate muscle strength losses after eccentric exercise by regulating leukocyte activity and inflammation.

Cited by 33 publications

References 36 publications

Differentiating Racial Differences in Time-Course Oxidative Stress Responses to Acute Exercise

Differentiating Racial Differences in Time-Course Oxidative Stress Responses to Acute Exercise

Human inflammatory and resolving lipid mediator responses to resistance exercise and ibuprofen treatment

Personalizing protein nourishment

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