Abstract
High-fitness individuals have been suggested to be at risk of a poor vitamin B2 (riboflavin) status due to a potentially higher vitamin B2 demand, as measured by the erythrocyte glutathione reductase (EGR) activation coefficient (EGRAC). Longer-term exercise interventions have been shown to result in a lower vitamin B2 status, but studies are contradictory. Short-term exercise effects potentially contribute to discrepancies between studies but have only been tested in limited study populations. This study investigated if vitamin B2 status, measured by EGRAC, is affected by a single exercise bout in females who differ in fitness levels, and that represents long-term physical activity. At baseline and overnight after a 60-min cycling bout at 70% O2peak, EGR activity and EGRAC were measured in 31 young female adults, divided into a high-fit (O2peak ≥ 47 mL/kg/min, N = 15) and low-fit (O2peak ≤ 37 mL/kg/min, N = 16) group. A single exercise bout significantly increased EGR activity in high-fit and low-fit females (Ptime = 0.006). This response was not affected by fitness level (Ptime*group = 0.256). The effect of exercise on EGRAC was not significant (Ptime = 0.079) and not influenced by EGR activity. The exercise response of EGRAC was not significantly different between high-fit and low-fit females (Ptime*group = 0.141). Thus, a single exercise bout increased EGR activity, but did not affect EGRAC, indicating that vitamin B2 status was not affected. The exercise response on EGRAC and EGR did not differ between high-fit and low-fit females.
Highlights
This study investigates the effect of a single bout of exercise, i.e., short-term exercise, on erythrocyte glutathione reductase activation coefficient (EGRAC) and erythrocyte glutathione reductase (EGR) activity in high-fit compared to low-fit females, i.e., females that differ in long-term physical activity
Our results indicate that the effect of a single bout of exercise on EGRAC and EGR was not different between high- and low-fit females
We hypothesized that the single bout of exercise could affect vitamin B2 status as determined by EGRAC, as the short-term effects (
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Exercise requires chemical energy (adenosine triphosphate, ATP) to enable muscle contractions and relaxations [1]. Exercise generates reactive oxygen species (ROS) as a by-product, which enhance antioxidant defense systems [2,3,4], including those that depend on glutathione [3]. One essential gatekeeper of energy and redox metabolism is vitamin B2 (riboflavin) [5]. Vitamin B2 acts as a precursor for the electron carriers flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), which are both essential mitochondrial cofactors of oxidative phosphorylation (OXPHOS) complexes
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