Date of Completion


Embargo Period



inflammation, low carbohydrate, ketogenic, immune, muscle repair

Major Advisor

Carl M. Maresh

Co-Major Advisor

Elaine C. Lee

Associate Advisor

William J. Kraemer

Associate Advisor

Jeff S. Volek

Associate Advisor

Michael F. Joseph

Field of Study



Doctor of Philosophy

Open Access

Campus Access


Background: Low carbohydrate (LC) diets cause dramatic shifts in metabolism toward reliance on fatty acids and ketones. Systemic inflammatory markers in those with chronic constitutive inflammation are reduced with LC diets. Exercise results in a transient pro-inflammatory response reflected in circulating immune cell and cytokine increases that is ideally followed by an anti-inflammatory response to limit damage and enhance repair. It is unknown if LC diets can modulate this response. Purpose: The overall aim of this investigation was to examine the immune, inflammatory and repair responses in elite ultra-endurance athletes consuming LC or high carbohydrate (HC) diets. Methods: Highly trained endurance male athletes who habitually consumed either a LC (n=8) or HC (n=3) diet completed a three hour treadmill run at moderate intensity (65% VO2max). Muscle biopsies from the vastus lateralis and blood samples were obtained to measure markers of muscle damage, inflammation, and muscle regeneration prior to, during, and in the early recovery period of the exercise bout. Due to the low number of HC athletes statistical analysis was only performed for LC athletes over time. Results: Endurance exercise resulted in a biphasic leukocytosis with increased neutrophils and monocytes immediately post exercise and into early recovery, while immediate post-exercise lymphocytosis was followed by lymphocytopenia into recovery. Additionally, circulating IL-6, IL-8 and IL-10 increased following endurance exercise, while IL-12, TNFα, and IL1β were not altered. LC athletes consistently showed higher fat oxidation during exercise with approximately 90% of energy derived from fat. Circulating lymphocytes, and systemic IL-6 and IL-10 appeared increased in LC athletes compared to HC athletes, particularly immediately following exercise. Conclusion: Endurance exercise as a multimodal stressor resulted in acute systemic inflammation as indicated by increased phagocytic cells, pro-inflammatory cytokine IL-6 and chemokine IL-8. This was balanced by an increase in anti-inflammatory cytokine IL-10. Preliminary results indicate acute exercise-induced inflammation may be attenuated with LC diets. Future analysis will determine if this is accurate and if this is seen intramuscularly. Additionally, the implications these effects may have on repair and regeneration in the muscle will be examined.