High-Intensity Locomotor Exercise Increases Brain-Derived Neurotrophic Factor in Individuals with Incomplete Spinal Cord Injury

Abstract

High-intensity locomotor exercise is suggested to contribute to improved recovery of locomotor function after neurological injury. This may be secondary to exercise-intensity-dependent increases in neurotrophin expression demonstrated previously in control subjects. However, rigorous examination of intensity-dependent changes in neurotrophin levels is lacking in individuals with motor incomplete spinal cord injury (SCI). Therefore, the primary aim of this study was to evaluate the effect of locomotor exercise intensity on peripheral levels of brain-derived neurotrophic factor (BDNF) in individuals with incomplete SCI. We also explored the impact of the Val66Met single-nucleotide polymorphism (SNP) on the BDNF gene on intensity-dependent changes. Serum concentrations of BDNF and insulin-like growth factor-1 (IGF-1), as well as measures of cardiorespiratory dynamics, were evaluated across different levels of exercise intensity achieved during a graded-intensity, locomotor exercise paradigm in 11 individuals with incomplete SCI. Our results demonstrate a significant increase in serum BDNF at high, as compared to moderate, exercise intensities (p = 0.01) and 15 and 30 min post-exercise (p < 0.01 for both), with comparison to changes at low intensity approaching significance (p = 0.05). Serum IGF-1 demonstrated no intensity-dependent changes. Significant correlations were observed between changes in BDNF and specific indicators of exercise intensity (e.g., rating of perceived exertion; R = 0.43; p = 0.02). Additionally, the data suggest that Val66Met SNP carriers may not exhibit intensity-dependent changes in serum BDNF concentration. Given the known role of BDNF in experience-dependent neuroplasticity, these preliminary results suggest that exercise intensity modulates serum BDNF concentrations and may be an important parameter of physical rehabilitation interventions after neurological injury.

Keywords: Val66Met polymorphism; brain-derived neurotrophic factor; high-intensity exercise; locomotion; spinal cord injury.

Conflict of interest statement

No competing financial interests exist.

Figures

FIG. 1.

Changes in s[BDNF] and s[IGF-1] with locomotor exercise. Percent change in s[BDNF] (A) and s[IGF-1] (B) during and post-locomotor exercise at different intensities. High levels of exercise intensity led to a significantly larger percent change in s[BDNF] from rest, as compared to that elicited at moderate intensity or post-exercise, with the difference between the change in BDNF at low and high intensities approaching significance. No significant intensity-dependent changes were found in s[IGF-1]. Error bars reflect standard error. BDNF, brain-derived neurotrophic factor; IGF-1, insulin-like growth factor-1; m, minutes; s[BDNF], serum concentration of BDNF; s[IGF-1], serum concentration of IGF-1.

FIG. 2.

Relationships between changes in s[BDNF] and indirect measures of exercise intensity and duration of exercise. Changes in s[BDNF] are significantly and positively correlated to Net VO2 (A), HR (B), and RPE (C;n = 9), but not duration of exercise (D). a.u., arbitrary units; BDNF, brain-derived neurotrophic factor; HR, heart rate; s[BDNF], serum concentration of BDNF; VO2, oxygen consumption.

FIG. 3.

Potential impact of Val66Met SNP on intensity-dependent changes in s[BDNF]. Percent change in s[BDNF] during and post-exercise from resting levels in Val/Val (gray; n = 7) and Val/Met (white; n = 4) subjects. Error bars reflect standard error. BDNF, brain-derived neurotrophic factor; m, minutes; s[BDNF], serum concentration of BDNF; SNP, single-nucleotide polymorphism.