βeta-endorphin levels following acute physical exercise in young and middle-aged adults

A large and growing body of literature has explored the impact of physical exercise (PE) on human health, shedding light on its crucial role for brain health [1]. Recent research suggests βeta-endorphin (βE) as a promising candidate for mediating the exercise-induced stimulation of neurogenesis [2] Moreover, PE can elevate the levels of brain-derived neurotrophic factor (BDNF), further promoting the process of neurogenesis [3]. To date, few studies have analysed age-related differences in βE secretion following acute PE and no study has investigated its association with BDNF in humans. The purposes of this study were to examine the exercise-induced changes in βE release in two age groups of healthy adult males and to explore potential correlations between βE and BDNF. Thirty-four participants (22 young adults, YA: age, 24.6±3.5 yrs; BMI, 23.2±2.3 kg/m2; peak oxygen uptake (V̇O2peak), 49±9.8 ml/kg/min and 12 middle-aged adults, MA: age, 54.6±5.7 yrs; BMI, 23.4±2.2 kg/m2; V̇O2peak, 44.8±5.1 l/kg/min), underwent an incremental cycling test to exhaustion. Respiratory gases were measured breath-by-breath using a metabolic cart and venous blood samples were collected before the exercise, 15 min, and 24 h post-exercise. Serum levels of βE and BDNF were measured using ELISA kits. Data were analysed with the Mann-Whitney test, Wilcoxon signed-rank test, and Spearman's correlation. βE levels exhibited a significant increase from baseline (YA: 176±21.2 pg/ml; MA: 152.1±21 pg/ml) to 15 post-exercise (YA: 211.7±30.8 pg/ml, p<0.001; MA: 187.2±33.5 pg/ml, p<0.01), followed by a significant decline from 15 min to 24 h post-exercise (YA: 180.2±23.7 pg/ml, p<0.001; MA: 155.7±23 pg/ml, p<0.01). βE concentration before and at 24 h post-exercise was higher in YA than MA (p<0.01 and p<0.05, respectively). However, no significant differences between groups were found at 15 min post-exercise. For all time points evaluated, no correlation was observed between serum βE and BDNF levels (p>0.05). Serum BDNF levels have been previously reported. Despite the impact of chronological ageing on circulating βE levels, our findings demonstrate that acute PE can induce an immediate increase in βE levels in both YA and MA. The lack of correlation between βE and BDNF suggests that these two molecules might independently contribute to the neurogenic effects of PE on the human brain.