This study examined acute cerebral hemodynamic and circulating neurotrophic factor responses to moderate intensity continuous exercise (MICT), guideline-based high intensity interval exercise (HIIT), and sprint interval exercise (SIT). We hypothesized that the pattern of middle cerebral artery velocity (MCAv) response would differ between interval and continuous exercise, with SIT inducing the smallest increase from rest, while increases in neurotrophic factors would be intensity-dependent. In a randomized crossover design, 24 healthy adults (nine females) performed three exercise protocols: (i) MICT (30 min), (ii) HIIT (4 × 4 min at 85% HRmax), and (iii) SIT (4 × 30 s supramaximal). MCAv significantly increased from rest across MICT (Δ13.1 ± 8.5 cm⋅s–1, p < 0.001) and all bouts of HIIT (Δ15.2 ± 9.8 cm⋅s–1, p < 0.001), but only for the initial bout of SIT (Δ17.3 ± 11.6 cm⋅s–1, p < 0.001). Immediately following each interval bout, MCAv increased (i.e., rebounded) for the SIT (9–14% above rest, p ≤ 0.04), but not HIIT protocol. SIT alone induced significant elevations from rest to end-exercise in vascular endothelial growth factor (VEGF; Δ28 ± 36%, p = 0.017) and brain-derived neurotrophic factor (BDNF, Δ149% ± 162%, p < 0.001) and there were greater increases in lactate than in either other protocol (>5-fold greater in SIT, p < 0.001), alongside a small significant reduction at the end of active recovery in insulin-like growth factor 1 (IGF-1, Δ22 ± 21%, p = 0.002). In conclusion, while the nature of the response may differ, both guideline-based and sprint-based interval exercise have the potential to induce significant changes in factors linked to improved cerebrovascular and brain health.

The optimal exercise intensity and modality for maximizing cerebral blood flow (CBF) and hence potential exposure to positive, hemodynamically derived cerebral adaptations is yet to be fully determined. This study compared CBF velocity responses between running and cycling across a range of exercise intensities. Twenty‐six participants (12 females; age: 26 ± 8 years) completed four exercise sessions; two mode‐specific maximal oxygen consumption (VO 2max ) tests, followed by (order randomized) two incremental exercise protocols (3‐min stages at 35%, 50%, 65%, 80%, 95% VO 2max ). Continuous measures of middle cerebral artery velocity (MCAv), oxygen consumption, end‐tidal CO 2 (P ET CO 2 ), and heart rate were obtained. Modality‐specific MCAv changes were observed for the whole group (interaction effect: p = .01). Exercise‐induced increases in MCAv mean during cycling followed an inverted‐U pattern, peaking at 65% VO 2max (Δ12 ± 7 cm/s from rest), whereas MCAv mean during running increased linearly up to 95% VO 2max (change from rest: Δ12 ± 13 vs. Δ7 ± 8 cm/s for running vs. cycling at 95% VO 2max ; p = .01). In contrast, both modalities had an inverted‐U pattern for P ET CO 2 changes, although peaked at different intensities (running: 50% VO 2max , Δ6 ± 2 mmHg; cycling: 65% VO 2max , Δ7 ± 2 mmHg; interaction effect: p = .01). Further subgroup analysis revealed that the running‐specific linear MCAv mean response was fitness dependent (Fitness*modality*intensity interaction effect: p = .04). Above 65% VO 2max , fitter participants ( n = 16; male > 45 mL/min/kg and female > 40 mL/min/kg) increased MCAv mean up to 95% VO 2max , whereas in unfit participants ( n = 7, male < mL/min/kg and female < 35 mL/min/kg) MCAv mean returned toward resting values. Findings demonstrate that modality‐ and fitness‐specific profiles for MCAv mean are seen at exercise intensities exceeding 65% VO 2max .

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