Resistance Training May Raise BDNF More Than Cardio

Resistance training tops the current BDNF ranking

If your goal is to raise circulating BDNF, the best comparative evidence does not put running first. It puts resistance training first.

That result comes from a 2022 Bayesian network meta-analysis by Zhou et al. in Frontiers in Aging Neuroscience. The study pooled 39 randomized controlled trials with 2,031 participants and ranked five exercise modalities for their effect on serum BDNF against inactive control. The hierarchy was resistance training, then HIIT, then combined training, then aerobic plus resistance training, and finally aerobic training alone.

That is the headline. It is also where the easy certainty ends.

The paper provides the strongest modality ranking in this evidence base, but the available publication details here do not include the full table of mean differences, 95% credible intervals, or SUCRA-style ranking metrics. So we can report the order, but not how wide the gap was between adjacent modalities. That matters. A first-place ranking can reflect a real separation, or a slim lead propped up by overlapping uncertainty bands. Without the full quantitative table, readers should treat the ranking as informative, not surgical.

Why this finding surprised people

Most popular discussions of exercise and brain health lean toward cardio. That instinct is not crazy. Exercise does raise BDNF in aggregate, and aerobic exercise has long been the default brain-friendly option. But the network meta-analysis suggests that when you compare modalities head to head across the literature, muscle-loading work may push serum BDNF more than steady-state aerobic training does.

That does not mean aerobic exercise failed. It ranked last among the five options in the network, but last is not the same thing as useless. A 2025 meta-analysis by Gholami et al. found that exercise training significantly increased resting BDNF concentrations in older adults. A 2022 meta-analysis by Caceres Fleitas et al. reached the same broad conclusion for peripheral BDNF in elderly populations. And a 2025 review by Cheng et al. reported that walking, running, and cycling each raised circulating BDNF in older adults.

So the practical interpretation is narrower than the hype version. Resistance training ranked highest for serum BDNF in the comparative model. Aerobic exercise still raised BDNF. The question is relative magnitude, not whether one works and the other does not.

What the network meta-analysis can and cannot tell you

A Bayesian network meta-analysis has one major advantage: it can compare interventions even when few trials tested them directly against each other. It combines direct comparisons with indirect ones through a shared control network. That is useful in exercise science, where you often get resistance training versus control in one paper, aerobic training versus control in another, and very few clean head-to-head trials.

It also creates a vulnerability. Rankings can lean heavily on indirect evidence when some nodes in the network have fewer studies. The available description of the Zhou et al. paper does not provide the per-modality study counts in enough detail to show how balanced the network was. HIIT, in particular, may have been supported by fewer direct comparisons than aerobic training, though that is an inference from how the literature usually looks rather than a published count from the paper itself.

The other major limitation is more concrete: the analysis did not produce a usable dose-response prescription for resistance training. Zhou et al. explicitly reported that they could not run a dose-effect analysis for resistance training because fewer than seven resistance studies had complete single-load intensity and duration data. In plain terms, the ranking says resistance training came out on top, but it does not tell you whether that meant heavy squats, moderate machine circuits, higher-volume hypertrophy work, or something else entirely.

The literature can tell you that resistance training likely wins the BDNF contest. It cannot yet tell you the exact winning program.

Human evidence supports the effect, but protocol detail is thin

The strongest protocol-specific resistance evidence in this set comes from a 2023 randomized trial by Bang et al.. The study followed middle-aged Korean women with obesity for 12 weeks and measured plasma BDNF, nerve growth factor, and metabolic biomarkers under different resistance-training set structures. The trial supports the idea that resistance training can change BDNF in a real-world clinical population and suggests that programming details such as set structure may matter.

That is useful, but it does not settle general practice. This was a specific population, with a specific intervention, in a specific metabolic context. You cannot jump from that trial to a universal rule for young lifters, older adults without obesity, or patients with cognitive impairment.

For the latter group, a 2025 study by Oporto-Colicoi et al. tested resistance exercise in patients with both mild cognitive impairment and sarcopenia. The study adds neurological relevance because it looked at neuroinflammation, cognitive performance, and structural brain changes in a clinically vulnerable population. It broadens the case that resistance training may help the aging brain. Still, it does not answer the narrower question the BDNF ranking raises: which exact resistance dose best increases BDNF?

A 2023 trial by Chia et al. also found BDNF-related effects in older untrained men using concurrent aerobic and resistance training over 12 weeks. That matters because the network meta-analysis ranked aerobic plus resistance training only fourth. Intuitively, combining two decent ideas should not obviously underperform both of them. That oddity may be real, or it may reflect sparse data, mixed protocols, and imprecise estimates.

The mechanism story is plausible, but still incomplete

Several exercise-linked signals could influence BDNF. A 2023 paper by Rodziewicz-Flis et al. discusses irisin, lactate, and IGF-1 as candidate modulators. The popular mechanism goes like this: muscle contraction increases PGC-1 alpha and FNDC5 signaling, irisin rises, irisin reaches the brain, and BDNF expression increases.

That pathway is biologically plausible. It is also not clinched in humans. The same paper notes that human studies have not shown a consistent or direct relationship between BDNF and irisin. So the mechanism that many people use to explain why exercise boosts BDNF still has a loose bolt in the human data. Animal work can suggest a route; it cannot certify that the same route explains a ranking in adults doing real training programs.

Lactate is another candidate worth taking seriously, especially for resistance training and HIIT. Hard efforts increase lactate, and lactate may influence BDNF signaling. But here again, plausible is not the same thing as proven. The biomarker moved; the full causal chain remains under construction.

The biggest problem: BDNF may not track the outcome you actually care about

The sharpest challenge to BDNF worship comes from a 2025 trial by Jimenez-Maldonado et al.. In active college students, high-intensity circuit training improved cognitive performance without a statistically significant change in serum BDNF.

That is not a small footnote. It means serum BDNF may be neither necessary nor sufficient for exercise-induced cognitive benefit. If cognition improved while serum BDNF stayed flat, then BDNF is at best one piece of the story. The training could have helped through other routes: cerebral blood flow, neurotransmitter changes, inflammatory signaling, sleep, mood, or mechanisms we have not pinned down yet.

This is the point where many brain-biomarker stories drift into wishful thinking. A blood marker is attractive because it is measurable. That does not make it the right optimization target. Serum BDNF is still a surrogate outcome, not a patient-centered one. It also tracks central nervous system biology imperfectly and can be influenced by platelet handling, assay methods, hemolysis, and timing of blood collection.

What should a practical reader do with this?

The cleanest reading of the evidence is modest.

• If you want the best current bet for maximizing serum BDNF, resistance training has the top ranking in the strongest comparative analysis available.
• If you prefer aerobic training, the evidence still supports it. Walking, running, and cycling all raised circulating BDNF in older adults.
• If your real goal is cognition, mood, or long-term brain health, do not assume the highest BDNF modality automatically wins those outcomes.
• If you want a BDNF-optimized resistance plan, the literature does not have one yet. The ranking is real; the prescription is missing.

That leaves a very normal conclusion, which is sometimes the hardest one to sell on the internet. Lift if you can. Do cardio too if you will actually keep doing it. High-intensity combined training may help cognition even when your serum BDNF acts unimpressed. Biology rarely rewards a single-number obsession for long.

Right now, resistance training looks like the front-runner for raising serum BDNF. It does not yet look like the whole answer to exercise and brain health. Those are different claims, and the evidence supports only the first one cleanly.