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This study investigated the middle cerebral artery blood velocity (MCAv) response to constant work-rate moderate-intensity cycling exercise in 21 children (9.3±0.8 years), 17 adolescents (12.3±0.4 years) and 20 young adults (23.6±2.4 years). Participants completed an incremental ramp test to exhaustion on a cycle ergometer, to determine maximal oxygen uptake and gas exchange threshold (GET), before completing three 6-minute transitions at a moderate-intensity (90% GET), on separate visits. On each visit, bilateral MCAv was measured by transcranial Doppler ultrasonography and breath-by-breath end-tidal carbon dioxide (P ET CO 2 ) via a metabolic cart. Data were ensemble-averaged for each participant and analysed using a mono-exponential model. Absolute MCAv was significantly higher throughout exercise in children and adolescents, compared to adults (P<0.001). Children had a significantly lower relative increase in MCAv from baseline (~12%) compared to adolescents (~20%) and adults (~18%, P<0.040). All adolescents and adults had a mono-exponential rise in MCAv and P ET CO 2 , but this was observed in only eight children. Children and adolescents had a significantly faster MCAv time constant (τ , 12±6 and 14±8 s, respectively) compared to adults (27±9 s, P<0.001). MCAv τ was positively associated with faster P ET CO 2 τ in adolescents (r=0.70, P=0.002) but not children (r=-0.20, P=0.640).Time- and amplitude-based response parameters of MCAv kinetics were significantly associated with P ET CO 2 kinetics in adults (r=0.50 to 0.74, P≤0.025), but not in children (r=-0.19 to -0.48, P>0.227). These findings suggest that the transition from childhood to adulthood impacts the MCAv response to exercise, and the relationships between P ET CO 2 and MCAv kinetics during exercise.

We examined the temporal longitudinal associations of carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT) with the risk of elevated resting heart rate (RHR) and high-sensitivity C-reactive protein (hsCRP). We studied 3,862 adolescents, mean age 17.7 (SD 0.3 yr), followed-up for 7 yr until age 24.5 (0.7) yr, from the Avon Longitudinal Study of Parents and Children, UK. RHR, fasting plasma hsCRP, cfPWV, and cIMT were repeatedly assessed and analyzed using logistic regression, linear mixed-effect, and structural equation models adjusting for important covariates. Among 3,862 adolescents [2,143 (55.5%) female], 10% and 44% were at moderate-to-high risk of elevated RHR and hsCRP at 24.5 yr, respectively. Higher cfPWV at 17.7 yr was associated with elevated RHR risk at follow-up [odds-ratio (OR) 1.58 (CI 1.20-2.08); P = 0.001], whereas cIMT at 17.7 yr was associated with elevated hsCRP risk [OR 2.30 (1.18-4.46); P = 0.014] at follow-up, only among females. In mixed model, 7-yr progression in cfPWV was directly associated with 7-yr increase in RHR [effect-estimate 6 beats/min (1-11); P = 0.017] and hsCRP. cIMT progression was associated with 7-yr increase in RHR and hsCRP. In cross-lagged model, higher cfPWV at 17.7 yr was associated with higher RHR (β = 0.06, standard error = 3.85, P < 0.0001) at 24.5 yr but RHR at 17.7 yr was unassociated with cfPWV at 24.5 yr. Baseline cIMT or RHR was unassociated with either outcome at follow-up. Higher hsCRP at 17.7 yr was associated with higher cfPWV and cIMT at 24.5 yr. In conclusion, adolescent arterial stiffness but not cIMT appears to precede higher RHR in young adulthood, whereas elevated hsCRP in adolescence preceded higher cfPWV and cIMT. NEW & NOTEWORTHY Higher arterial stiffness but not carotid-intima media thickness in adolescence preceded higher resting heart rate in young adulthood, however, elevated high sensitivity C-reactive protein in adolescence preceded higher arterial stiffness and carotid intima-thickness in young adulthood in the temporal causal path. Low-grade inflammation during adolescence may be causally associated with the development of subclinical arteriosclerosis and atherosclerosis in young adulthood.

The acute effect of exercise intensity on cerebrovascular reactivity and whether this mirrors changes in peripheral vascular function have not been investigated. The aim of this study was to explore the acute effect of exercise intensity on cerebrovascular reactivity (CVR) and peripheral vascular function in healthy young adults ( n = 10, 6 females, 22.7 ± 3.5 yr). Participants completed four experimental conditions on separate days: high-intensity interval exercise (HIIE) with intervals performed at 75% maximal oxygen uptake (V̇o 2max ; HIIE1), HIIE with intervals performed at 90% V̇o 2max (HIIE2), continuous moderate-intensity exercise (MIE) at 60% V̇o 2max and a sedentary control condition (CON). All exercise conditions were completed on a cycle ergometer and matched for time (30 min) and average intensity (60% V̇o 2max ). Brachial artery flow-mediated dilation (FMD) and CVR of the middle cerebral artery were measured before exercise, and 1- and 3-h after exercise. CVR was assessed using transcranial Doppler ultrasonography to both hypercapnia (6% carbon dioxide breathing) and hypocapnia (hyperventilation). FMD was significantly elevated above baseline 1 and 3 h following both HIIE conditions ( P < 0.05), but FMD was unchanged following the MIE and CON trials ( P > 0.33). CVR to both hypercapnia and hypocapnia, and when expressed across the end-tidal CO 2 range, was unchanged in all conditions, at all time points (all P > 0.14). In conclusion, these novel findings show that the acute increases in peripheral vascular function following HIIE, compared with MIE, were not mirrored by changes in cerebrovascular reactivity, which was unaltered following all exercise conditions in healthy young adults. NEW & NOTEWORTHY This is the first study to identify that acute improvements in peripheral vascular function following high-intensity interval exercise are not mirrored by improvements in cerebrovascular reactivity in healthy young adults. High-intensity interval exercise completed at both 75% and 90% V̇o 2max increased brachial artery flow-mediated dilation 1 and 3 h following exercise, compared with continuous moderate-intensity exercise and a sedentary control condition. By contrast, cerebrovascular reactivity was unchanged following all four conditions.

The aim of this study was to compare the kinetic response of middle cerebral artery blood velocity (MCAv) to moderate- and heavy-intensity cycling in adults, and explore the relationship between maximal oxygen uptake (V̇o 2max ) and MCAv kinetics. Seventeen healthy adults (23.8 ± 2.4 yr, 9 females) completed a ramp incremental test to exhaustion on a cycle ergometer to determine V̇o 2max and the gas exchange threshold (GET). Across six separate visits, participants completed three 6-min transitions at a moderate intensity (90% GET) and three at a heavy intensity (40% of the difference between GET and V̇o 2max ). Bilateral MCAv was measured using transcranial Doppler (TCD) ultrasonography and analyzed using a monoexponential model with a time delay. The time constant (τ) of the MCAv response was not different between moderate- and heavy-intensity cycling (25 ± 10 vs. 26 ± 8 s, P = 0.82), as was the time delay (29 ± 11 vs. 29 ± 10 s, P = 0.95). The amplitude of the exponential increase in MCAv from baseline was greater during heavy-intensity cycling (23.9 ± 10.0 cm·s -1 , 34.1 ± 14.4%) compared with moderate-intensity cycling (12.7 ± 4.4 cm·s -1 , 18.7 ± 7.5%; P < 0.01). Following the exponential increase, a greater fall in MCAv was observed during heavy-intensity exercise compared with moderate-intensity exercise (9.5 ± 6.9 vs. 2.8 ± 3.8 cm·s -1 , P < 0.01). MCAv after 6 min of exercise remained elevated during heavy-intensity exercise compared with moderate-intensity exercise (85.2 ± 9.6 vs. 79.3 ± 7.7 cm·s -1 , P ≤ 0.01). V̇o 2max was not correlated with MCAv τ or amplitude ( r = 0.11-0.26, P > 0.05). These data suggest that the intensity of constant-work rate exercise influences the amplitude, but not time-based, response parameters of MCAv in healthy adults, and found no relationship between cardiorespiratory fitness and MCAv kinetics. NEW & NOTEWORTHY This is the first study to model the MCAv kinetic response to moderate- and heavy-intensity cycling in healthy adults. This study found that the amplitude of the exponential rise in MCAv at exercise onset was greater during heavy-intensity exercise (∼34%) compared with moderate-intensity exercise (∼19%), but the time-based characteristics of the responses were similar between intensities. Higher cardiorespiratory fitness was not associated with a greater or faster MCAv response to moderate- or heavy-intensity exercise.

Regulation of cerebral blood flow during exercise in youth is poorly understood. This study investigated the cerebrovascular and ventilatory responses to a ramp incremental cycle test to exhaustion in 14 children (means ± SD age: 9.4 ± 0.9 yr), 14 adolescents (12.4 ± 0.4 yr), and 19 adults (23.4 ± 2.5 yr). Middle cerebral artery blood velocity (MCAv), partial pressure of end-tidal CO 2 ([Formula: see text]), and ventilatory parameters were analyzed at baseline, gas exchange threshold (GET), respiratory compensation point (RCP), and exhaustion. The increase in minute ventilation relative to CO 2 production during exercise was also calculated (V̇e/V̇co 2 slope). Relative change from baseline (Δ%) in MCAv was lower in children, compared with adolescents and adults at GET [15 ± 10% vs. 26 ± 14%, and 24 ± 10%, respectively, P ≤ 0.03, effect size ( d ) = 0.9] and RCP (13 ± 11% vs. 24 ± 16% and 27 ± 15%, respectively, P ≤ 0.05, d  ≥   0.8). Δ%MCAv was similar in adults and adolescents at all intensities and similar in all groups at exhaustion. The magnitude of the V̇ E /V̇co 2 slope was negatively associated with Δ%MCAv at GET and RCP across all participants ( P ≤ 0.01, r = -0.37 to -0.48). Δ%[Formula: see text] was smaller in children and adolescents compared with adults at GET and RCP ( P ≤ 0.05, d  ≥   0.6). In children, Δ%[Formula: see text] and Δ%MCAv were not associated from baseline-GET ( r¯  = 0.14) and were moderately associated from RCP-exhaustion ( r¯  = 0.49). These relationships strengthened with increasing age and were stronger in adolescents (baseline-GET: r¯  = 0.47, RCP-exhaustion: r¯  = 0.62) and adults (baseline-GET: r¯  = 0.66, RCP-exhaustion: r¯  = 0.78). These findings provide the first evidence on the development of the regulatory role of [Formula: see text] on MCAv during exercise in children, adolescents, and adults. NEW & NOTEWORTHY This is the first study to observe similar increases in cerebral blood flow during incremental exercise in adolescents and adults. Increases in cerebral blood flow during exercise were smaller in children compared with adolescents and adults and were associated with a greater V̇ E /V̇co 2 slope. This study also provides the first evidence on the progressive development of the regulatory role of end-tidal CO 2 on cerebral blood flow during exercise during the transition from childhood to adulthood.

The present study examined the effect of priming exercise on O(2) uptake (Vo(2)) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O(2) delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II Vo(2) tau, 3) elevate the phase II Vo(2) total amplitude, and 4) reduce the magnitude of the Vo(2) slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests Vo(2), muscle oxygenation (near infrared spectroscopy), and cardiac output (Q) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q at baseline and throughout the second exercise bout. The phase II Vo(2) tau was not altered by priming exercise (bout 1: 22 + or - 7 s vs. bout 2: 20 + or - 4 s; P = 0.30). However, the time constant describing the entire Vo(2) response from start to end of exercise was accelerated (bout 1: 43 + or - 8 s vs. bout 2: 36 + or - 5 s; P = 0.002) due to an increased total phase II Vo(2) amplitude (bout 1: 1.73 + or - 0.33 l/min vs. bout 2: 1.80 + or - 0.59 l/min; P = 0.002) and a reduced Vo(2) slow component amplitude (bout 1: 0.18 + or - 0.08 l/min vs. bout 2: 0.12 + or - 0.09 l/min; P = 0.048). These results suggest that phase II Vo(2) kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the Vo(2) total phase II and slow component amplitudes may be O(2) delivery sensitive.

The splitting of muscle phosphocreatine (PCr) plays an integral role in the regulation of muscle O2 utilization during a "step" change in metabolic rate. This study tested the hypothesis that the kinetics of muscle PCr would be faster in children compared with adults both at the onset and offset of moderate-intensity exercise, in concert with the previous demonstration of faster phase II pulmonary O2 uptake kinetics in children. Eighteen peri-pubertal children (8 boys, 10 girls) and 16 adults (8 men, 8 women) completed repeated constant work-rate exercise transitions corresponding to 80% of the Pi/PCr intracellular threshold. The changes in quadriceps [PCr], [Pi], [ADP], and pH were determined every 6 s using 31P-magnetic resonance spectroscopy. No significant (P>0.05) age- or sex-related differences were found in the PCr kinetic time constant at the onset (boys, 21+/-4 s; girls, 24+/-5 s; men, 26+/-9 s; women, 24+/-7 s) or offset (boys, 26+/-5 s; girls, 29+/-7 s; men, 23+/-9 s; women 29+/-7 s) of exercise. Likewise, the estimated theoretical maximal rate of oxidative phosphorylation (Qmax) was independent of age and sex (boys, 1.39+/-0.20 mM/s; girls, 1.32+/-0.32 mM/s; men, 2.36+/-1.18 mM/s; women, 1.51+/-0.53 mM/s). These results are consistent with the notion that the putative phosphate-linked regulation of muscle O2 utilization is fully mature in peri-pubertal children, which may be attributable to a comparable capacity for mitochondrial oxidative phosphorylation in child and adult muscle.