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Objective. Altered temporal muscle perfusion is implicated in several painful disorders afflicting orofacial and head regions, including temporomandibular joint dysfunctions, bruxism, and headache. Knowledge about the regulation of blood supply to the temporalis muscle is limited, due to methodological difficulties. The study aimed to test the feasibility of near-infrared spectroscopy (NIRS) monitoring of the human temporal muscle. Approach. Twenty-four healthy subjects were monitored with a 2-channel NIRS: a muscle probe placed over the temporal muscle and a brain probe placed on the forehead. A series of teeth clenching at 25, 50, and 75% of maximum voluntary contraction for 20 s and hyperventilation for 90 s at 20 mmHg of end-tidal CO2 were performed, to elicit hemodynamic changes in muscle and brain, respectively. Main results. In twenty responsive subjects, NIRS signals from both probes were consistently different during both tasks. The absolute change in tissue oxygenation index (ΔTOI) as detected by muscle and brain probes was −9.40 ± 12.28 and 0.29 ± 1.54% during teeth clenching (p < 0.01) at 50% maximum voluntary contraction, while −1.03 ± 2.70 and −5.11 ± 3.81% during hyperventilation (p < 0.01), respectively. Significance. Distinct response patterns were observed from the temporal muscle and prefrontal cortex which proves that this technique is adequate to monitor tissue oxygenation and hemodynamic changes in human temporal muscle. Noninvasive and reliable monitoring of hemodynamics in this muscle will help to extend basic and clinical investigations about the peculiar control of blood flow in head muscles. [ABSTRACT FROM AUTHOR]

Simple Summary: Ischemic preconditioning (IPC) is a protective maneuver that alternates short periods of occlusion and reperfusion of tissue blood flow. Nineteen subjects were enrolled in one of the two groups, IPC (3 × 5/5 min right arm ischemia/reperfusion; cuff inflations 250 mmHg) and SHAM (3 × 5/5 min pseudo ischemia/reperfusion; 20 mmHg). The subjects performed a fatiguing contraction protocol before and 30 min after the IPC treatment. Results suggest that IPC may delay fatigue onset by reducing muscle oxygen consumption. The decrease in tissue oxygenation and the increase in deoxygenated hemoglobin were significantly reduced post- vs. pre-IPC (p < 0.05), but not post- vs. pre-SHAM. IPC delays the onset of fatigue, probably due to improved metabolic efficiency of muscles. Ischemic preconditioning (IPC) is a non-invasive protective maneuver that alternates short periods of occlusion and reperfusion of tissue blood flow. Given the heterogeneity in the magnitude and frequency of IPC-induced improvements in physical performance, here we aimed to investigate, in a well-controlled experimental set-up, the local effects of IPC in exposed muscles in terms of tissue oxygenation and muscle fatigue. Nineteen subjects were enrolled in one of the two groups, IPC (3 × 5/5 min right arm ischemia/reperfusion; cuff inflations 250 mmHg) and SHAM (3 × 5/5 min pseudo ischemia/reperfusion; 20 mmHg). The subjects performed a fatiguing contraction protocol before and 30 min after the IPC treatment, consisting of unilateral intermittent isometric elbow flexions (3 s ON/OFF, 80% of maximal voluntary contraction) until exhaustion. While muscle strength did not differ between groups, post- vs. pre-treatment endurance was significantly reduced in the SHAM group (4.1 ± 1.9 vs. 6.4 ± 3.1 repetitions until exhaustion, p < 0.05) but maintained in IPC (7.3 ± 2.0 vs. 7.1 ± 4.3, n.s.). The decrease in tissue oxygenation and the increase in deoxygenated hemoglobin were significantly reduced post- vs. pre-IPC (p < 0.05), but not post- vs. pre-SHAM. The results suggest that IPC delays the onset of fatigue likely through improved metabolic efficiency of muscles. [ABSTRACT FROM AUTHOR]

Purpose: A brief compressive stimulus is known to induce a rapid hyperemia in skeletal muscles, considered to contribute to the initial phase of functional hyperemia. Whether the same mechano-sensitivity characterizes the cutaneous circulation is debated. This study aims to investigate whether a rapid hyperemic response to compressive stimuli is also expressed by skin blood flow in humans.Methods: In 12 subjects, brief compressive stimuli were delivered to the forearm at varying pressures/durations (50/2, 100/2, 200/2, 200/1, 200/5 mmHg/s); the sequence was randomized and repeated with the arm above and below heart level. Laser Doppler flowmetry technique was used to monitor skin blood flow. The response was described in terms of peak skin blood flow normalized to baseline (nSBFpeak), time-to-peak from the release of compression, and excess blood volume (EBV, expressed in terms of seconds of basal flow, s-bf) received during the response.Results: The results consistently evidenced the occurrence of a compression-induced hyperemic response, with nSBFpeak = 2.9 ± 1.1, EBV = 17.0 ± 6.6 s-bf, time-to-peak = 7.0 ± 0.7 s (200 mmHg, 2 s, below heart level). Both nSBFpeak and EBV were significantly reduced (by about 50%) above compared to below heart level (p < 0.01). In addition, EBV slightly increased with increasing pressure (p < 0.05) and duration (p < 0.01) of the stimulus.Conclusions: For the first time, the rapid dilatator response to compressive stimuli was demonstrated in human cutaneous circulation. The functional meaning of this response remains to be elucidated. [ABSTRACT FROM AUTHOR]

The present study aimed to compare sympathetic hemodynamic effects in masticatory and limb muscles in response to different stressors. Twelve healthy participants were subjected to a randomized series of stressors, including cold pressor test (CPT), mental arithmetic test, apnea, isometric handgrip (IHG) and post-handgrip muscle ischemia (PHGMI), while in the supine position. Spatially-resolved near-infrared spectroscopy was used to measure relative changes in blood volume and oxygenation (TOI) of the resting masseter and biceps muscles. Cardiac output, heart rate, and arterial blood pressure (ABP) were also monitored. Except apnea, all tests increased ABP. Different response patterns were observed in the 2 muscles: TOI significantly increased during contralateral IHG (1.24 ± 1.17%) but markedly decreased during CPT (−4.84 ± 4.09%) and PHGMI (−6.65 ± 5.31%) in the biceps muscle, while exhibiting consistent increases in the masseter (1.88 ± 1.85%; 1.60 ± 1.75%; 1.06 ± 3.29%, respectively) (p < 0.05). The results allow us to infer differential control of blood flow in head and limb muscles. In general, the masseter appears more prone to dilatation than the biceps, exhibiting opposite changes in response to painful stimuli (CPT and PHGMI). Several mechanisms may mediate this effect, including reduced sympathetic outflow to the extracranial vasculature of the head, generally exposed to lower hydrostatic loads than the rest of the body. • Acute stress differently affected blood flow in head and limb muscles. • Vasoconstrictory responses were generally observed in limbs. • No evidence of vasoconstriction was observed in the masseter muscle. • Masseter perfusion was consistently increased in response to painful stimuli. [ABSTRACT FROM AUTHOR]

Recent evidence suggests that the mechano-sensitivity of the vascular network may underlie rapid dilatory events in skeletal muscles. Previous investigations have been mostly based either on in vitro or on whole-limb studies, neither preparation allowing one to assess the musculo-vascular specificity under physiological conditions. The aim of this work is to characterize the mechanosensitivity of an exclusively-muscular vascular bed in vivo. In five anesthetized rabbits, muscle blood flow was continuously monitored in the masseteric artery, bilaterally (n=10). Hyperaemic responses were evoked by compressive stimuli of different extent (50, 100 and 200 mm Hg) and duration (0.5, 1, 2 and 5 s) exerted by a servo-controlled motor on the masseter muscle. Peak amplitude of the hyperaemic response ranged from 340 ± 30% of baseline (at 50 mm Hg) to 459 ± 57% (at 200 mm Hg) (P < 0.05), did not depend on stimulus duration and exhibited very good reliability (ICC = 0.98) when reassessed at 30 min intervals. The time course of the response depended neither on applied pressure nor on the duration of the stimulus. In conclusion, for its high sensitivity and reliability this technique is adequate to characterize mechano-vascular reactivity and may prove useful in the investigation of the underlying mechanisms, with implications in the control of vascular tone and blood pressure in health and disease. [ABSTRACT FROM AUTHOR]

Abstract: In the complex neurovascular control of the orofacial area, the only vasoconstrictor action is mediated by the sympathetic nervous system; however, its functional role is still unclear as little evidence exists of vasoconstrictor responses to physiological stimuli in both animal and human models. Aim of the present study was to investigate, orofacial vascular responses to acute stress in conscious rabbits. Twenty rabbits, implanted with chronic perivascular flow probes on the facial artery and with a telemetric probe for arterial blood pressure, were subjected to different alerting/stress stimuli, i.e., noise, taps on the rabbit''s box, air jet, noxious cutaneous stimuli. Smaller groups of animal also underwent electromyographic (EMG) activity recording from the masseter muscle, unilateral section of the cervical sympathetic nerve (n =8), and alpha-adrenergic blockade with phentolamine (n =6). On average, all stressors evoked a pressor response accompanied by variable changes in heart rate and induced a marked, short-latency reduction in facial artery blood flow, corresponding to a decrease of 37–50% in vascular conductance of the facial artery. Local sympathetic denervation abolished the short-latency (<15s) vasoconstrictor response to all stressors and attenuated the late (>15s) phase of the long-lasting response to the air jet. All vasoconstrictor effects were blocked by phentolamine. Increases in blood flow were observed only in concomitance with masseter EMG activity either during masticatory activity or in the form of brief occasional spontaneous contractions. This study provides evidence of an effective vasoconstrictor control by the sympathetic system in the orofacial area under stress conditions. [Copyright &y& Elsevier]

[Display omitted] • Visual stimulation was administered to med-high and med-low hypnotizable Ss. • Blood flow velocity and vascular reactivity (CVR) did not differ between them. • Hypnotizability and CVR negatively correlated only among med-highs. • Higher hypnotizability is associated with lower cerebral metabolic demand. Hypnotizability is a trait associated with several physiological correlates including cardiovascular control. The present study aimed to investigate the posterior cerebral artery flow velocity (PCAv) in basal closed eyes (B) and during visual stimulation (VS) conditions in med-highs and med-lows. Twenty-four healthy volunteers were submitted to the hypnotic assessment through the Stanford Hypnotic Susceptibility Scale, form A which classified 13 low-to-medium (med-lows) and 10 high-to-medium (med-highs) hypnotizable participants. One subject scoring 6 out of 12 was excluded from the comparisons between groups. Arterial blood pressure, heart rate, and partial pressure of end-tidal CO 2 were monitored during both B and VS conditions. Simultaneously, PCAv was assessed by transcranial Doppler. Cerebrovascular Reactivity (CVR) was computed as a percentage of the PCAv change occurring during VS with respect to B (ΔPCAv). During VS both groups increased their PCAv (mean ± SD: 7.9 ± 5.2 %) significantly with no significant group difference. However, among med-highs, CVR was negatively correlated with hypnotizability scores. Thus, higher hypnotizability may be associated with lower metabolic demand in response to VS only within med-highs hypnotizable participants. [ABSTRACT FROM AUTHOR]