Exercise intensity affects acute neurotrophic and neurophysiological responses poststroke

Abstract

Aerobic exercise may acutely prime the brain to be more responsive to rehabilitation, thus facilitating neurologic recovery from conditions like stroke. This aerobic priming effect could occur through multiple mechanisms, including upregulation of circulating brain-derived neurotrophic factor (BDNF), increased corticospinal excitability, and decreased intracortical inhibition. However, optimal exercise parameters for targeting these mechanisms are poorly understood. This study tested the effects of exercise intensity on acute BDNF and neurophysiological responses. Sixteen ambulatory persons >6 mo poststroke performed three different 20-min exercise protocols in random order, approximately 1 wk apart, including the following: 1) treadmill high-intensity interval training (HIT-treadmill); 2) seated-stepper HIT (HIT-stepper); and 3) treadmill moderate-intensity continuous exercise (MCT-treadmill). Serum BDNF and transcranial magnetic stimulation measures of paretic lower limb excitability and inhibition were assessed at multiple time points during each session. Compared with MCT-treadmill, HIT-treadmill elicited significantly greater acute increases in circulating BDNF and corticospinal excitability. HIT-stepper initially showed BDNF responses similar to HIT-treadmill but was no longer significantly different from MCT-treadmill after decreasing the intensity in reaction to two hypotensive events. Additional regression analyses showed that an intensity sufficient to accumulate blood lactate appeared to be important for eliciting BDNF responses, that the interval training approach may have facilitated the corticospinal excitability increases, and that the circulating BDNF response was (negatively) related to intracortical inhibition. These findings further elucidate neurologic mechanisms of aerobic exercise and inform selection of optimal exercise-dosing parameters for enhancing acute neurologic effects. NEW & NOTEWORTHY Acute exercise-related increases in circulating BDNF and corticospinal excitability are thought to prime the brain for learning. Our data suggest that these responses can be obtained among persons with stroke using short-interval treadmill high-intensity interval training, that a vigorous aerobic intensity sufficient to generate lactate accumulation is needed to increase BDNF, that interval training facilitates increases in paretic quadriceps corticospinal excitability, and that greater BDNF response is associated with lesser intracortical inhibition response.

Effects of Exercise Intensity on Acute Circulating Molecular Responses Poststroke

“…14 A secondary analyses found that an exercise intensity around the onset of blood lactate accumulation was the optimal threshold for discriminating large acute BDNF responses. 14 While these results provide preliminary evidence that BDNF could potentially mediate some intensity-dependent effects of exercise on neurologic function, there are also several other less-studied molecules that could be involved. For example, vascular endothelial growth factor (VEGF) and insulin-like growth factor 1 (IGF1) are 2 additional neurotrophins that accumulate in human blood during exercise, 15,16 and have some evidence of intensity-dependence.…”

“…The purpose of this study was to determine the effect of exercise intensity on acute circulating VEGF, IGF1, and cortisol responses poststroke, using the same data set and serum samples as a previous BDNF analysis. 14 We hypothesized that high-intensity interval training (HIT), whether performed on a treadmill (HIT-treadmill) or seated stepper (HIT-stepper), would elicit significantly greater acute increases in VEGF and IGF1 compared with moderateintensity continuous exercise (MCT-treadmill). We also hypothesized that there would be no significant betweenprotocol difference in cortisol response, based on the limited evidence of psychological stress found in a previous qualitative assessment of treadmill HIT after stroke.…”

“…BDNF response was included as an additional dependent variable in the mediation analyses, because the novel statistical methods used herein provided more direct quantification of mediated effects than the previous BDNF analysis that used the same samples. 14…”

“…40 However, this HIT protocol was designed to enable persons with stroke to sustain vigorous aerobic intensities (ie, >60% heart rate reserve) and has done so consistently. 3,14,40 Seated Stepper High-Intensity Interval Training. HIT-stepper used the same burst and recovery durations as HIT-treadmill, but on a seated stepper (NuStep T5XR).…”

Acute high-intensity and moderate-intensity interval exercise do not change corticospinal excitability in low fit, young adults

“…intermittent) [26]. It was hypothesized that HI would increase corticospinal excitability compared to MOD in low fit young adults, as higher intensity exercise evokes increased BDNF [16][17][18]27] and IGF-1 [14] levels more so than moderate-intensity exercise.…”