Brain-derived Neurotrophic Factor (BDNF) is a neurotrophin that plays a pivotal role in memory, learning, and neural plasticity. Its levels can be significantly influenced by various external factors, including physical exercise 1. Many studies have investigated the impact of exercise on BDNF production, in both healthy individuals and various medical conditions 2–5. This study sought to shed light on the temporal dynamics of BDNF production in response to incremental exercise, in particular exploring whether age can influence its release. We enrolled 20 young adults (YA: 24.7 ± 3.6 yrs.; percentage of fat mass (%FM): 11.1 ± 5.4 %; peak oxygen uptake (V̇O2peak): 49.7 ± 9.9 ml/kg/min) and 12 middle-aged adults (MA: 54.6 ± 5.7 yrs.; %FM: 16.7 ± 6.5 %; V̇O2peak: 44.8 ± 5.1 ml/kg/min). Participants underwent a cycling ramp V̇O2max test until volitional exhaustion. Throughout the exercise regimen, gas exchange was continuously recorded using a metabolic cart. Venous blood samples were collected at three-time points: baseline (T0), 15 minutes after exercise (T1), and 24 hours post-exercise (T2). Serum BDNF (sBDNF) levels were quantified using an ELISA kit. Statistical analyses were performed with SPSS (ver. 27). Wilcoxon signed-rank test was employed to analyse the differences in sBDNF concentration throughout time points. Mann-Whitney U test was used to analyse differences in sBDNF concentration between groups. Results were considered significant when p<0.05. Surprisingly, we did not observe significant changes in sBDNF levels from T0 to T1 for both the YA and MA groups. However, a remarkable increase in sBDNF was detected from T0 (YA: 13.3 ± 1.69 ng/ml and MA: 12.7 ± 0.9 ng/ml) to T2 for both groups (YA: 15.5 ± 3.5 ng/ml, p<0.001; MA: 14.4 ± 3 ng/ml; p<0.05). Importantly, there were no statistical differences in sBDNF levels between age groups at any of the time points. This study provides new insights into the age-related effects on sBDNF release following acute strenuous exercise within a substantial cohort of healthy adult males. Contrary to previous findings, our results exhibit that acute exercise can stimulate delayed sBDNF release, irrespective of age, 24h post strenuous exercise. These results emphasize the critical role of physical exercise in promoting neurogenesis and neural plasticity throughout the entire lifespan. Given the importance of exercise induced BDNF release in enhancing cognitive functions, such as memory and spatial learning, regular physical exercise should be included into daily routines, even for middle-aged and older individuals.
Marano, L., Tommasini, E., Missaglia, S., Vago, P., Pecci, C., Rampinini, E., Bosio, A., Morelli, A., Tavian, D., Brain-Derived Neurotrophic Factor Production in Response to Strenuous Incremental Exercise across adulthood, Abstract de <<2024 Padua Days on Muscle and Mobility Medicine (2024 Pdm3)>>, (Padova, 27-February 02-March 2024 ), UGO CARRARO, Padova 2024: 1-113. 10.4081/ejtm.2024.12346 [https://hdl.handle.net/10807/271575]
Brain-Derived Neurotrophic Factor Production in Response to Strenuous Incremental Exercise across adulthood
Marano, Luigi
;Tommasini, Ester;Missaglia, Sara;Vago, Paola;Rampinini, Ermanno;Tavian, Daniela
2024
Abstract
Brain-derived Neurotrophic Factor (BDNF) is a neurotrophin that plays a pivotal role in memory, learning, and neural plasticity. Its levels can be significantly influenced by various external factors, including physical exercise 1. Many studies have investigated the impact of exercise on BDNF production, in both healthy individuals and various medical conditions 2–5. This study sought to shed light on the temporal dynamics of BDNF production in response to incremental exercise, in particular exploring whether age can influence its release. We enrolled 20 young adults (YA: 24.7 ± 3.6 yrs.; percentage of fat mass (%FM): 11.1 ± 5.4 %; peak oxygen uptake (V̇O2peak): 49.7 ± 9.9 ml/kg/min) and 12 middle-aged adults (MA: 54.6 ± 5.7 yrs.; %FM: 16.7 ± 6.5 %; V̇O2peak: 44.8 ± 5.1 ml/kg/min). Participants underwent a cycling ramp V̇O2max test until volitional exhaustion. Throughout the exercise regimen, gas exchange was continuously recorded using a metabolic cart. Venous blood samples were collected at three-time points: baseline (T0), 15 minutes after exercise (T1), and 24 hours post-exercise (T2). Serum BDNF (sBDNF) levels were quantified using an ELISA kit. Statistical analyses were performed with SPSS (ver. 27). Wilcoxon signed-rank test was employed to analyse the differences in sBDNF concentration throughout time points. Mann-Whitney U test was used to analyse differences in sBDNF concentration between groups. Results were considered significant when p<0.05. Surprisingly, we did not observe significant changes in sBDNF levels from T0 to T1 for both the YA and MA groups. However, a remarkable increase in sBDNF was detected from T0 (YA: 13.3 ± 1.69 ng/ml and MA: 12.7 ± 0.9 ng/ml) to T2 for both groups (YA: 15.5 ± 3.5 ng/ml, p<0.001; MA: 14.4 ± 3 ng/ml; p<0.05). Importantly, there were no statistical differences in sBDNF levels between age groups at any of the time points. This study provides new insights into the age-related effects on sBDNF release following acute strenuous exercise within a substantial cohort of healthy adult males. Contrary to previous findings, our results exhibit that acute exercise can stimulate delayed sBDNF release, irrespective of age, 24h post strenuous exercise. These results emphasize the critical role of physical exercise in promoting neurogenesis and neural plasticity throughout the entire lifespan. Given the importance of exercise induced BDNF release in enhancing cognitive functions, such as memory and spatial learning, regular physical exercise should be included into daily routines, even for middle-aged and older individuals.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.