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Purpose: Postprandial hyperglycemia is assumed to have a negative impact on flow-mediated dilation (FMD), an index of endothelial function, and blood flow of the peripheral conduit arteries. This study aimed to determine whether the enhancement of postprandial hyperglycemia by skipping breakfast accelerates endothelial dysfunction and reduces the blood flow in the brachial artery in young men., Methods: Using a randomized cross-over design, ten healthy men completed two trials: with and without breakfast (Eating and Fasting trials, respectively). Venous blood sampling and brachial FMD tests were conducted before, 30, 60, 90, and 120 min after a 75-g oral glucose tolerance test (OGTT)., Results: Skipping breakfast boosted post-OGTT glucose levels than having breakfast (P = 0.01). The magnitude of the decrease in FMD via OGTT did not vary between trials (main effect of trial P = 0.55). Although brachial blood flow tended to decrease after OGTT in both trials (interaction and main effect of time P = 0.61 and P = 0.054, respectively), the decrease in blood flow following OGTT was greater in the Fasting trial than in the Eating trial (main effect of trial, mean difference =  - 15.8 mL/min [95%CI =  - 25.6 to - 6.0 mL/min], P < 0.01)., Conclusion: Skipping breakfast did not enhance the magnitude of the decrease in FMD following glucose loading, but did accelerate hyperglycemia-induced reduction in brachial blood flow. Current findings suggest that even missing one breakfast has negative impacts on the blood flow regulation of the peripheral conduit arteries in young men who habitually eat breakfast., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Excessive arterial pressure elevation induced by resistance exercise (RE) attenuates peripheral vasodilatory function, but its effect on cerebrovascular function is unknown. We aimed to evaluate the effect of different pressor responses to RE on hypercapnia-induced vasodilation of the internal carotid artery (ICA), an index of cerebrovascular function. To manipulate pressor responses to RE, 15 healthy young adults (11M/4F) performed two RE: high intensity with low repetitions (HL) and low intensity with high repetitions (LH) dynamic knee extension. ICA dilation, induced by 3 min of hypercapnia, was measured before and 10 min after RE using Doppler ultrasound. HL exercise elicited a greater pressor response than LH exercise. In relaxation phases of RE, ICA blood velocity increased in both HL and LH trials. However, ICA shear rate did not significantly increase in either trial (P = 0.06). Consequently, neither exercise altered post-exercise hypercapnia-induced ICA dilation (HL, 3.9 ± 1.9% to 5.1 ± 1.7%; LH, 4.6 ± 1.4% to 4.8 ± 1.8%; P > 0.05 for all). When viewed individually, the changes in ICA shear rate were positively correlated with changes in end-tidal partial pressure of carbon dioxide (P ET CO 2 ) (r = 0.46, P < 0.01) than with mean arterial pressure (r = 0.32, P = 0.02). These findings suggest that the effects of RE-induced pressor response on cerebrovascular function may be different from peripheral arteries. An increase in P ET CO 2 during the relaxation phase may play a more crucial role than elevated pressure in increasing cerebral shear during dynamic RE., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: Exercise-induced increases in shear rate (SR) across different exercise intensities may differentially affect hypercapnia-induced vasodilation of the internal carotid artery (ICA), a potential index of cerebrovascular function. We aimed to elucidate the effects of exercise intensity on ICA SR during exercise and post-exercise hypercapnia-induced vasodilation of the ICA in young men., Methods: Twelve healthy men completed 30 min of cycling at moderate [MIE; 65 ± 5% of age-predicted maximal heart rate (HR max )] and high (HIE; 85 ± 5% HR max ) intensities. Hypercapnia-induced vasodilation was induced by 3 min of hypercapnia (target end-tidal partial pressure of CO 2  + 10 mmHg) and was assessed at pre-exercise, 5 min and 60 min after exercise. Doppler ultrasound was used to measure ICA diameter and blood velocity during exercise and hypercapnia tests., Results: SR was not altered during either exercise (interaction and main effects of time; both P > 0.05). ICA conductance decreased during HIE from resting values (5.1 ± 1.3 to 3.2 ± 1.0 mL·min -1 ·mmHg -1 ; P < 0.01) but not during MIE (5.0 ± 1.3 to 4.0 ± 0.8 mL·min -1 ·mmHg -1 ; P = 0.11). Consequently, hypercapnia-induced vasodilation declined immediately after HIE (6.9 ± 1.7% to 4.0 ± 1.4%; P < 0.01), but not after MIE (7.2 ± 2.1% to 7.3 ± 1.8%; P > 0.05). Sixty minutes after exercise, hypercapnia-induced vasodilation returned to baseline values in both trials (MIE 8.0 ± 3.1%; HIE 6.4 ± 2.9%; both P > 0.05)., Conclusion: The present study showed blunted hypercapnia-induced vasodilation of the ICA immediately after high-intensity exercise, but not a moderate-intensity exercise in young men. Given that the acute response is partly linked to the adaptive response in the peripheral endothelial function, the effects of aerobic training on cerebrovascular health may vary depending on exercise intensity., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: This study aimed to test our hypothesis that acute hypotension attenuates brachial flow-mediated dilation (FMD) as an index of endothelial function in healthy humans., Methods: Twelve healthy men (21.8 ± 1.6 years, body mass index; 22.2 ± 1.6 kg/m 2 ) participated in this study. Brachial FMD was measured in three trials: standardized FMD protocol (control trial), abrupt decrease in blood pressure (BP) via thigh cuff inflation-deflation (hypotension trial) and decrease in shear rate (SR) via a shortened forearm occlusion time (SR reduction trial). Brachial diameter and blood velocity were measured using Duplex ultrasound., Results: Mean arterial pressure during reactive hyperaemia showed a marked decrease in the hypotension trial (- 23.7 ± 6.0 mmHg), but not in the control and SR reduction trials. SR area under the curve was attenuated in the SR reduction trial (P < 0.001), but not in the control and hypotension trials (P = 0.316). Consequently, FMD was attenuated in the hypotension and SR reduction trials compared with that in the control trial (P = 0.003 and P = 0.043, respectively), and was attenuated to a greater extent in the hypotension trial compared with the SR reduction trial (P = 0.006; control, 6.9 ± 3.5%; hypotension, 3.5 ± 1.7%; SR reduction, 5.0 ± 2.2%). After adjusting FMD using SR, FMD remained attenuated in the hypotension trial (P = 0.014), but not in the SR reduction trial., Conclusion: Our findings indicate that arterial pressure as well as sympathetic nervous system activation could be an important determinant of FMD. Blunted FMD of peripheral arteries may be a rational response to restore BP and/or prevent further reduction of BP following acute hypotension in healthy humans.

Purpose: This study aimed to elucidate the effects of hypoxia on the pattern of oscillatory blood flow in the inactive limb during constant-load dynamic exercise. We hypothesised that retrograde blood flow in the brachial artery of the inactive limb would increase during constant-load leg cycling under hypoxic conditions., Methods: Three maximal exercise tests were conducted in eight healthy males on a semi-recumbent cycle ergometer while the subjects breathed a normoxic [inspired oxygen fraction (FIO2) = 0.209] or two hypoxic gas mixtures (FIO2 = 0.155 and 0.120). Subjects then performed submaximal exercise at the same relative exercise intensity of 60 % peak oxygen uptake under normoxic or the two hypoxic conditions for 30 min. Brachial artery blood velocity and diameter were recorded simultaneously during submaximal exercise using Doppler ultrasonography., Results: Antegrade blood flow gradually increased during exercise, with no significant differences among the three trials. Retrograde blood flow showed a biphasic response, with an initial increase followed by a gradual decrease during normoxic exercise. In contrast, retrograde blood flow significantly increased during moderate and severe hypoxic exercise, and remained elevated above normoxic conditions during exercise. At 30 min of exercise, the magnitude of the change in retrograde blood flow during exercise was greater as the level of hypoxia increased (normoxia: -18.7 ± 23.5 ml min(-1); moderate hypoxia: -39.3 ± 21.4 ml min(-1); severe hypoxia: -64.0 ± 36.3 ml min(-1))., Conclusion: These results indicate that moderate and severe hypoxia augment retrograde blood flow in the inactive limb during constant-load dynamic leg exercise.

The purpose of this study was to clarify the effect of acute exercise in hypoxia on flow-mediated vasodilation (FMD). Eight males participated in this study. Two maximal exercise tests were performed using arm cycle ergometry to estimate peak oxygen uptake [Formula: see text] while breathing normoxic [inspired O(2) fraction (FIO(2)) = 0.21] or hypoxic (FIO(2) = 0.12) gas mixtures. Next, subjects performed submaximal exercise at the same relative exercise intensity [Formula: see text] in normoxia or hypoxia for 30 min. Before (Pre) and after exercise (Post 5, 30, and 60 min), brachial artery FMD was measured during reactive hyperemia by ultrasound under normoxic conditions. FMD was estimated as the percent (%) rise in the peak diameter from the baseline value at prior occlusion at each FMD measurement (%FMD). The area under the curve for the shear rate stimulus (SR(AUC)) was calculated in each measurement, and each %FMD value was normalized to SR(AUC) (normalized FMD). %FMD and normalized FMD decreased significantly (P < 0.05) immediately after exercise in both condition (mean ± SE, FMD, normoxic trial, Pre: 8.85 ± 0.58 %, Post 5: -0.01 ± 1.30 %, hypoxic trial, Pre: 8.84 ± 0.63 %, Post 5: 2.56 ± 0.83 %). At Post 30 and 60, %FMD and normalized FMD returned gradually to pre-exercise levels in both trials (FMD, normoxic trial, Post 30: 1.51 ± 0.68 %, Post 60: 2.99 ± 0.79 %; hypoxic trial, Post 30: 4.57 ± 0.78 %, Post 60: 6.15 ± 1.20 %). %FMD and normalized FMD following hypoxic exercise (at Post 5, 30, and 60) were significantly (P < 0.05) higher than after normoxic exercise. These results suggest that aerobic exercise in hypoxia has a significant impact on endothelial-mediated vasodilation.

A single-trial place conditioning procedure, one treatment and one non-treatment during two daily conditioning sessions followed by a single test session on the 3rd day, was used to examine the place conditioning effects of intracerebrally administered nicotine. In the first series of experiments, Sprague-Dawley male rats were implanted unilaterally with guide cannulas aimed at the lateral ventricle. After 1 week, rats received either "treatment" (nicotine in 2 microliters phosphate buffer or 2 microliters of buffer alone) or "no treatment" (no injections) before being placed in the black or white compartment of a three-compartment place-conditioning apparatus for 20 min. The next day the rats received the opposite treatment before being conditioned in the opposite compartment. On day 3, animals had free access to the entire apparatus for 15 min and the time spent in each compartment was recorded automatically. Even though the rats exhibited a baseline bias for the black compartment, intracerebroventricular nicotine induced positive place preferences relative to buffer control, i.e. if treatments were paired with the black compartment, nicotine enhanced the preference for the black compartment, and if the treatments were paired with the white compartment, nicotine induced a preference for the white compartment. In addition, the nicotine-induced preference response was antagonized by the co-intraventricular administration of mecamylamine. In a second series of experiments, animals were implanted unilaterally with guide cannulas aimed at the pendunculopontine tegmental nucleus of the mesopontine tegmentum. Nicotine microinjection, 1.2-18.5 nmol in 0.5 microliter buffer, induced a dose-dependent positive place preference response.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of morphine, phencyclidine, and nicotine on motor activity in rats were characterized using both observational and automated methods. Activity was scored observationally using a time-sampling method that tabulates discrete response categories (still, locomotion, rearing, sniffing, licking, gnawing, head down, swaying, grooming, falling). Behavior was assessed automatically using an activity monitor that records both the time and activity counts spent in large and small (less than 3 cm) movements, rearing, and resting. The following results using male Sprague-Dawley rats represent significant differences from saline-treated controls. Morphine (1-4 mg/kg SC) increased the incidence of locomotion, sniffing, swaying, and grooming depending on the time after drug injection. These changes corresponded to an increase in large and small movement counts and time as measured by the activity monitor. Phencyclidine (1.25-5 mg/kg SC) caused dose-related increases in the incidence of locomotion, sniffing, swaying, and falling, and induced greater large and small activity movement counts and time especially after the 5 mg/kg dose. Nicotine (0.033-0.33 mg/kg SC) decreased the incidence of rearing and increased the frequency of sniffing and grooming. These changes corresponded to a decrease of rearing activity and to a slight increase in small activity. The present data indicate that morphine, phencyclidine, and nicotine exert dose-related and time-related appearances of various categories of behavior in the rat, and that the data from the automated method complement the findings of the direct observational method.

The effects of phencyclidine (PCP) on locomotor activity were compared to those of the stereoisomers of N-allylnormetazocine (NAN) after acute administration to rats. PCP produced swaying and falling movements, increased sniffing behavior, and enhanced horizontal locomotor activity. d-NAN also induced swaying, falling, sniffing behavior and locomotion, and decreased rearing behavior. l-NAN decreased rearing activity, depressed locomotion, antagonized morphine antinociception and precipitated the morphine-withdrawal syndrome. Sensitization to drug-induced sniffing, rearing and locomotion developed after four daily injections of PCP, d-NAN or l-NAN in rats. Rats which were sensitized to PCP-induced locomotion, sniffing, and rearing were also cross-sensitized to both d-NAN and l-NAN. Animals sensitized to the effects of either d- or l-NAN exhibited cross-sensitization to PCP. There was little evidence that the cross-sensitization between the three agents was stereoselective. These data indicate that the acute effects of PCP are similar to those of d-NAN, but differ from l-NAN, the only agent of the three with opioid antagonist properties. The data further indicate that as sensitization to the motor effects develops during repeated administration of PCP, d-NAN or l-NAN, the differences among the three agents become less apparent.