Cocoa flavanols protect humans against vascular disease, as evidenced by improvements in peripheral endothelial function, likely through nitric oxide signalling. Emerging evidence also suggests that flavanol-rich diets protect against cognitive aging, but mechanisms remain elusive. In a randomized double-blind within-subject acute study in healthy young adults, we link these two lines of research by showing, for the first time, that flavanol intake leads to faster and greater brain oxygenation responses to hypercapnia, as well as higher performance only when cognitive demand is high. Individual difference analyses further show that participants who benefit from flavanols intake during hypercapnia are also those who do so in the cognitive challenge. These data support the hypothesis that similar vascular mechanisms underlie both the peripheral and cerebral effects of flavanols. They further show the importance of studies combining physiological and graded cognitive challenges in young adults to investigate the actions of dietary flavanols on brain function.
Purpose Red wine polyphenols (RWP) are plant-based molecules that have been extensively studied in relation to their protective effects on vascular health in both animals and humans. The aim of this review was to quantify and compare the efficacy of RWP and pure resveratrol on outcomes measures of vascular health and function in both animals and humans. Methods Comprehensive database searches were carried out through PubMed, Web of Science and OVID for randomised, placebo-controlled studies in both animals and humans. Meta-analyses were carried out on acute and chronic studies of RWP in humans, alongside subgroup analysis where possible. Risk-of-bias assessment was carried out for all included studies based on randomisation, allocation, blinding, outcome data reporting, and other biases. Results 48 animal and 37 human studies were included in data extraction following screening. Significant improvements in measures of blood pressure and vascular function following RWP were seen in 84% and 100% of animal studies, respectively. Human studies indicated significant improvements in systolic blood pressure overall (− 2.6 mmHg, 95% CI: [− 4.8, − 0.4]), with a greater improvement in pure-resveratrol studies alone (− 3.7 mmHg, 95% CI: [− 7.3, − 0.0]). No significant effects of RWP were seen in diastolic blood pressure or flow-mediated dilation (FMD) of the brachial artery. Conclusion RWP have the potential to improve vascular health in at risk human populations, particularly in regard to lowering systolic blood pressure; however, such benefits are not as prevalent as those observed in animal models.
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.
Purpose This study investigated whether intermittent post-exercise sauna bathing across three-weeks endurance training improves exercise heat tolerance and exercise performance markers in temperate conditions, compared to endurance training alone. The subsidiary aim was to determine whether exercise-heat tolerance would further improve following 7-Weeks post-exercise sauna bathing. Methods Twenty middle-distance runners (13 female; mean ± SD, age 20 ± 2 years, $$V$$ V O2max 56.1 ± 8.7 ml kg−1 min−1) performed a running heat tolerance test (30-min, 9 km h−1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [$$V$$ V O2max], speed at 4 mmol L−1 blood lactate concentration ([La−]) before (Pre) and following three-weeks (3-Weeks) normal training (CON; n = 8) or normal training with 28 ± 2 min post-exercise sauna bathing (101–108 °C, 5–10%RH) 3 ± 1 times per week (SAUNA; n = 12). Changes from Pre to 3-Weeks were compared between-groups using an analysis of co-variance. Six SAUNA participants continued the intervention for 7 weeks, completing an additional HTT (7-Weeks; data compared using a one-way repeated-measures analysis of variance). Results During the HTT, SAUNA reduced peak rectal temperature (Trec; − 0.2 °C), skin temperature (− 0.8 °C), and heart rate (− 11 beats min−1) more than CON at 3-Weeks compared to Pre (all p < 0.05). SAUNA also improved $$V$$ V O2max (+ 0.27 L−1 min−1; p = 0.02) and speed at 4 mmol L−1 [La−] (+ 0.6 km h−1; p = 0.01) more than CON at 3-Weeks compared to Pre. Only peak Trec (− 0.1 °C; p = 0.03 decreased further from 3-Weeks to 7-Weeks in SAUNA (other physiological variables p > 0.05). Conclusions Three-weeks post-exercise sauna bathing is an effective and pragmatic method of heat acclimation, and an effective ergogenic aid. Extending the intervention to seven weeks only marginally improved Trec.
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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