Abstract P297: The Decline in Excess Post-Exercise Oxygen Consumption in Response to Dietary Nitrate is Eliminated With Concurrent Caffeine Intake

Abstract

Introduction: Dietary nitrate has been shown to reduce submaximal oxygen consumption (VO 2 ), but less is known about the changes to excess post-exercise oxygen consumption (EPOC). In contrast, caffeine intake increases both exercise VO 2 and EPOC. Minimal research has reported on the combined effects of dietary nitrate/caffeine on exercise and post-exercise metabolism. Hypothesis: Caffeine will elevate exercise VO 2 and EPOC while dietary nitrate will attenuate the change in exercise VO 2 and EPOC. Methods: Seven healthy individuals participated in a double-blind, placebo controlled, crossover experiment. The first of five visits consisted of a maximal volume of oxygen consumption (VO 2max ) treadmill test. Prior to visit 2 - 5, participants consumed either a dietary nitrate (~12.4 mmol, NIT) or placebo nitrate supplement (PLN) combined with either a caffeine (3 mg/kg, CAF) or placebo caffeine (PLC) dose. Supplements were consumed on each of 4 days and the final doses of NIT or PLN and CAF or PLC were consumed 2.5 and 1-hr pre-exercise, respectively. Visits 2 - 5 consisted of a 30-min treadmill run at ~65% VO 2max followed by a 60-min seated recovery. During exercise, VO 2 and heart rate (HR) were measured continuously. During recovery, EPOC, HR, and peripheral (SBP/DBP) and aortic (cSBP/cDBP) blood pressure (via pulse wave analysis) were measured every 20 min. A linear mixed effects model analysis was performed to determine how each supplementation influenced each dependent variable. Treatments (NIT+CAF, CAF+PLN, NIT+PLC, PLN+PLC) and exercise timepoints (10, 20, 30 min) and recovery timepoints (20, 40, and 60 min post-exercise) served as fixed factors. If p<0.05, p ost-hoc pairwise comparisons were performed. Results: Exercise VO 2 (p=0.450) and HR (p=0.622) were not different between treatments at any timepoint. However, EPOC was different between treatments (p<0.001); NIT+PLC (4.0±0.6 ml/kg/min) was significantly lower than NIT+CAF (4.7±0.7 ml/kg/min, p<0.001), CAF+PLN (4.6±0.7 ml/kg/min p=0.001), and PLN+PLC (4.7±0.8 ml/kg/min, p=0.001). Recovery PLN+PLC brachial SBP (117±8 mmHg) was significantly lower than NIT+CAF (122+7 mmHg, p=0.041), CAF+PLN (123+9 mmHg, p=0.003), and NIT+PLC (122+6 mmHg, p=0.013). Recovery treatment differences were found for cSBP (p=0.005); PLN+PLC (104+7 mmHg) was significantly lower than CAF+PLN (109+9 mmHg, p=0.001), and NIT+PLC (108+7 mmHg, p=0.013), but not NIT+CAF (107+7 mmHg, p=0.063). Recovery HR was elevated in PLN+PLC (91+14 bpm) compared to CAF+PLN (86+15 bpm, p=0.029) and NIT+PLC (86+12 bpm, p=0.002). Conclusion: A modest dose of caffeine (3 mg/kg) did not elevate exercise VO 2 or EPOC. Dietary nitrate reduced EPOC and elevated peripheral and aortic SBP in recovery. When caffeine was consumed alongside nitrate, the decrease in EPOC was abolished. Dietary nitrate alone may not be advised to those seeking additional workout caloric expenditure.