(PO29-06-22) The Food Nutrient Index and Inflammation Are Not Linked to Eccentric Exercise-Induced Muscle Damage

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Presenting Author(s)

David C. Nieman, DrPH
– Professor, Appalachian State University, Kannapolis, North Carolina, United States

Co-Author(s)

AS

Andrew Simonson
– Appalachian State University
JW

Joshua Williams
– Appalachian State University
MA

Matthew Arnold
– Appalachian State University
LA

Lathan Arnett
– Appalachian State University
TB

Tondra Blevins
– Appalachian State University
GV

Giuseppe Valacchi, PhD
– North Carolina State University, Kannapolis, North Carolina, United States
ML

Mary a. Lila, PhD
– North Carolina State University, Kannapolis, North Carolina, United States

Disclosure(s):

David C. Nieman, DrPH: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Variation in muscle damage following eccentric exercise is wide-ranging and largely unexplained. This study investigated linkages between eccentric exercise-induced increases in the muscle damage biomarker creatine kinase (CK) and diet quality, body composition and fitness test performance, diagnostic chemistries, oxidative stress, and inflammation.

Methods: Participants included 53 healthy, non-obese male (n=30) and female adults (n=23) (20-55 y, BMI < 30 kg/m²) who were not engaged in regular resistance training. After familiarization, participants engaged in a 90-min bout of whole-body eccentric exercise (90-EE) (17 exercises). Changes in muscle soreness (DOMS, 1-10 scale) and damage biomarkers (serum CK, myoglobin), exercise performance, oxidative stress (4-hydroxynonenal or 4HNE), inflammation (CRP, IL-18, IL-16, IL-10), serum cortisol, and diagnostic chemistries were monitored immediately post-90-EE, and then each morning during a 4-d recovery period. Blood samples were collected in an overnight fasted state, with serum CK, myoglobin, cortisol, and diagnostic chemistries measured at a clinical lab. IL-18, IL-6, IL-10, and 4HNE were assayed by ELISA. Participants entered food and beverage intake in 3-d food records with nutrient and flavonoid intake assessed and the Food Nutrient Index (FNI) calculated using eight under-consumed nutrients.

Results: The 90-EE bout induced significant DOMS and muscle damage, inflammation and oxidative stress, and decreases in strength and anaerobic power. CK increased throughout the 4-d recovery period, with the highest levels measured on the 4^th day (range, 60-17,040 U/L; mean±SD, 1,565±3,132 U/L). CK was correlated with other tissue damage biomarkers including aspartate aminotransferase (r=0.946), lactate dehydrogenase (r=0.884), and myoglobin (r=0.763). Under linear regression analysis with non-tissue damage outcomes including FNI (68.7±15.7), DOMS and serum cortisol emerged as the best predictors of post-90-EE CK variance [R²=0.367, F(2,50)=14.48, p< 0.001].

Conclusions: The CK response to 90-EE varied widely between participants with 37% of the variance related to perceptions of muscle soreness and the stress hormone cortisol, but not diet quality, inflammation, oxidative stress, or fitness test performance.

Funding Sources: MegaFood