Summary: A recent human study finds that an intravenous (IV) infusion of lactate — the metabolite produced during intense exercise — raises circulating levels of pro-BDNF, a precursor of brain-derived neurotrophic factor associated with neural growth and resilience. The infusion recreated lactate concentrations typical of moderate to high-intensity exercise and triggered a sustained increase in pro-BDNF in blood plasma, but it did not increase mature BDNF (mBDNF). Researchers emphasize that while lactate infusion partially mimics exercise-related biochemical signals, regular high-intensity exercise remains the most reliable way to support long-term brain health.
Exercise is known to benefit brain function by improving blood flow, lowering stress hormones, and promoting release of mood-enhancing chemicals. One important pathway involves brain-derived neurotrophic factor (BDNF), a protein produced in tissues including the brain, liver, muscle, and fat that supports neuron survival, growth, and synaptic plasticity. Elevated lactate in the bloodstream, a by-product of carbohydrate metabolism during oxygen-limited conditions such as high-intensity exercise, has been proposed as an upstream signal that helps trigger BDNF release.
Researchers conducted a randomized crossover study with 18 healthy adults aged 20–40. Twelve participants completed both a one-hour IV infusion of sodium lactate and a one-hour saline infusion on separate occasions, while a control group of six received saline only. Blood samples were collected frequently before, during, and up to two hours after each infusion. Muscle biopsies were taken before, immediately after, and during recovery to assess tissue-level changes.
During the lactate infusion, plasma lactate levels rose to peaks comparable to those reached after vigorous exercise. Importantly, circulating pro-BDNF increased within 15 minutes after the end of the lactate infusion and remained elevated throughout the two-hour recovery period. In contrast, levels of mature BDNF (mBDNF) in serum and plasma did not change, and muscle pro-BDNF levels remained unaltered by the infusion. The trial reported a significant rise in plasma pro-BDNF (approximately 55%–68% higher than saline), while mBDNF showed no significant difference.
The investigators interpret these results to mean that lactate acting in isolation can drive an increase in circulating pro-BDNF but is insufficient to raise mature BDNF. Because pro-BDNF and mBDNF have distinct biological roles, the infusion replicated only part of the biochemical response produced by exercise. The authors suggest the increased pro-BDNF likely originates from skeletal muscle or other peripheral tissues responding to elevated lactate.
What this means for brain health and exercise
While the study opens the possibility of harnessing lactate’s signaling properties for clinical applications, the researchers caution that lactate infusion is not a replacement for physical activity. High-intensity exercise triggers a complex network of physiological responses beyond lactate release, including improved cardiovascular fitness, hormonal shifts, and neural activity that together support brain health. The study supports the view that exposing the brain to episodic high lactate levels through intense exercise may help promote healthy neurological aging.
The authors note potential future directions: more research to determine how lactate regulates BDNF metabolism in humans, exploration of individualized exercise prescriptions for people with impaired brain health, and the long-term effects of modulating pro-BDNF versus mBDNF. Pharmacological approaches that mimic lactate’s hormonal-like effects could be considered later, but such strategies would require careful investigation of mechanism, safety, and clinical benefit.
Key facts
- Lactate infusion: Raised blood lactate to levels seen after high-intensity exercise and increased circulating pro-BDNF.
- Partial match: Mature BDNF (mBDNF) did not increase, indicating the infusion reproduced only part of exercise’s molecular effects.
- Practical takeaway: High-intensity exercise remains the best-established method to support brain health and trigger the broader, beneficial physiological responses associated with BDNF.
About this neuroscience research news
Author: Mischa Dijkstra
Source: Frontiers
Contact: Mischa Dijkstra – Frontiers
Image: The image is credited to Neuroscience News
Original Research: Open access. Title: “Lactate Infusion Increases Circulating pro-Brain-Derived Neurotrophic Factor Levels in Humans” by Marcus Moberg et al., published in Frontiers in Cellular Neuroscience. DOI and publisher details are available via the journal.
Abstract
Lactate Infusion Increases Circulating pro-Brain-Derived Neurotrophic Factor Levels in Humans
Brain-derived neurotrophic factor (BDNF) is a central mediator of neuroplasticity and responds acutely to physical exercise, linking exercise to improved brain health. Lactate, a metabolite that rises during intense exercise, has been proposed as one mediator of the exercise-induced BDNF response, but its isolated role in humans was previously unclear.
In this controlled infusion study, 18 young healthy volunteers (50% female) received a one-hour venous infusion of sodium lactate or isotonic saline while blood and muscle samples were taken before, during, and for two hours after the infusion. Plasma lactate peaked at mean values similar to those seen after high-intensity exercise. Plasma pro-BDNF increased significantly 15 minutes after lactate infusion and remained elevated during recovery (55%–68% increase vs saline), while plasma and serum mBDNF showed no significant change. Muscle pro-BDNF and mBDNF levels were unchanged by the infusion; however, baseline muscle pro-BDNF correlated with participants’ proportion of type I muscle fiber area.
These results indicate that lactate alone can increase circulating pro-BDNF but does not alter circulating mature BDNF, suggesting lactate may partially mediate the exercise-induced pro-BDNF response in humans.