Acute Effects of Caffeine on Repeated Sprint Performance and Energy Distribution

Overview

The goal of this study is to learn if low-dose caffeinated coffee improves repeated sprint performance and affects energy system contributions in combat sports athletes. The main questions it aims to answer are: * Does low-dose caffeinated coffee (1.5 or 3 mg·kg-¹) improve peak power, mean power, and fatigue index during repeated sprint tests? * What physiological responses (heart rate, blood lactate, perceived exertion, and energy system contributions) do participants have when consuming caffeinated coffee? Researchers compared caffeinated coffee at two doses (1.5 and 3 mg·kg-¹ body mass) to a placebo (decaffeinated coffee of identical taste and appearance) to see if low

This investigation examined whether acute ingestion of low-dose caffeine delivered through commercially available regular coffee would alter repeated sprint capacity and metabolic energy system dynamics in athletes who compete in combat disciplines. A within-subject, double-blind, placebo-controlled crossover framework was adopted to ensure methodological rigor and minimize order and expectation biases. Eligible participants were physically active male combat sports competitors (n = 15; aged 18-25 years) with a documented competitive history spanning at least five years at the regional and national levels. Volunteers were excluded if they reported recent use of performance-modifying agents, stimulant or psychotropic medications, tobacco products, or any diagnosed condition affecting cardiovascular, metabolic, or musculoskeletal function. To standardize caffeine baseline, all participants were instructed to abstain from caffeinated products for a minimum of two weeks prior to the study onset and throughout the entire data collection period. Each participant attended the laboratory on four separate occasions. The initial visit served as a familiarization session and included anthropometric assessment. The subsequent three sessions were assigned in a randomized, counterbalanced order, with a minimum 48-hour recovery interval separating each visit. During these sessions, participants received one of three coded supplementation conditions - placebo (decaffeinated coffee), low-dose caffeine (1.5 mg·kg-¹ body mass), or moderate-low-dose caffeine (3 mg·kg-¹ body mass) - each dissolved in 250 mL of hot water and consumed over a 10-minute period. The caffeine content of both the caffeinated and decaffeinated coffee products (Nescafe Gold) was verified by an accredited food analysis laboratory. To maintain identical volume, appearance, and taste across all conditions, decaffeinated and caffeinated coffees were blended in varying proportions for each dose level. Supplementation was administered 60 minutes before the commencement of exercise testing. Performance testing comprised a standardized cycling-based repeated sprint protocol: six 10-second maximal effort sprints, each separated by a 30-second passive recovery period, performed on a mechanically braked cycle ergometer (Monark 894E) with resistance set at 10% of individual body mass. A structured warm-up preceded each testing bout. Primary performance variables derived from sprint testing included peak power output, mean power output, and fatigue index. Perceptual and physiological responses were documented via the Borg rating of perceived exertion scale, peak heart rate, and capillary blood lactate concentration measured at rest and immediately following the final sprint. Breath-by-breath oxygen uptake data were collected continuously using a portable metabolic system (COSMED K5) to facilitate estimation of energy system contributions. The relative and absolute contributions of the phosphocreatine (ATP-PCr), glycolytic, and oxidative metabolic pathways were quantified using established indirect methods. Excess post-exercise oxygen consumption (EPOC) kinetics were modeled with mono-exponential curve fitting to isolate the fast EPOC component, which served as a proxy for PCr resynthesis. Glycolytic contribution was estimated from the net change in blood lactate concentration, applying an established oxygen-equivalent conversion factor. Oxidative metabolism was derived from the net elevation in VO₂ above resting values during exercise. Total energy expenditure was computed as the cumulative sum of all three pathway contributions. To control for dietary and diurnal confounders, participants replicated identical pre-test meal patterns documented during the first testing session, and all laboratory visits were conducted between 08:00 and 11:00 h. Dietary adherence was verified through structured diet logs reviewed by the research team. Data were analyzed using one-way repeated-measures ANOVA with Bonferroni-adjusted pairwise comparisons, and partial eta squared (η²p) was reported as the measure of effect magnitude. The study received full ethical clearance from the Trabzon Eurasia University Ethics Committee and was conducted in accordance with the principles outlined in the Declaration of Helsinki. Informed consent form obtained from all the participants.