Reduced Resting and Increased Elevation of Heart Rate Variability With Cognitive Task Performance in Concussed Athletes.

OBJECTIVE: To examine heart rate variability (HRV) at rest and with a 2-Back cognitive task involving executive function and sustained attention in athletes during the acute phase following concussion and compare them with the controls. PARTICIPANTS: Twenty-three male and female collegiate athletes (20 ± 1 years) following (4 ± 1 days) a sports-related concussion and 23 sports- and sex-matched noninjured controls. PROCEDURE: Continuous R-R interval was acquired using 3-lead electrocardiogram for 3 minutes each at rest and during the 2-Back task. HRV was quantified as percent high-frequency (HF) power. RESULTS: At rest, lower percent HF power was observed in the concussed athletes (23 ± 11) compared with the controls (38 ± 14; P = .0027). However, with the 2-Back task, an increase in HF power was observed in the concussed group (39 ± 12; P = .0008) from rest and was comparable with the controls (36 ± 15). No difference in HF power between rest and 2-Back task was observed in the controls. CONCLUSION: Lower HRV was observed at rest following concussion. An increase in HRV, suggestive of enhanced prefrontal cortex (PFC) functioning, was observed during a cognitive task in the concussed athletes. Therefore, cognitive tasks as early as 4 days after injury may increase PFC functioning from rest and expedite return to learn in collegiate athletes.

Autonomic nervous system dysfunction in mild traumatic brain injury: a review of related pathophysiology and symptoms.

The autonomic nervous system (ANS) plays a vital role in maintaining and regulating homeostatic processes. ANS dysfunction has been reported in patients with moderate to severe traumatic brain injury (TBI), but its role in mild TBI (mTBI) is understudied. The objective of this review is to elucidate the role of ANS dysfunction following mTBI and the underlying pathophysiology specifically neuroinflammation, neurodegeneration, oxidative stress, and altered cerebral blood flow. ANS dysfunction is thought to be one of the many factors contributing to clinical features following mTBI including headache, anxiety, cognitive impairment, mood disorders, and sleep disturbances. The ANS has been shown to play a role in the production and regulation of pro-inflammatory molecules. ANS dysfunction most often results in exaggerated sympathetic neural activation (SNA) which contributes to neuroinflammation and oxidative stress. SNA is associated with the production of reactive oxygen species and subsequent neurodegeneration following mTBI. Additionally, changes in cerebral blood flow can be seen in patients with mTBI showing evidence of ANS dysfunction. No Level I studies have explored the relationship between mTBI and ANS dysfunction. Better understanding of the role of the ANS in mTBI will improve the evaluation and clinical management of mTBI by offering additional diagnostic and novel treatment strategies.

The influence of the carotid baroreflex on dynamic regulation of cerebral blood flow and cerebral tissue oxygenation in humans at rest and during exercise.

PURPOSE: This preliminary study tested the hypothesis that the carotid baroreflex (CBR) mediated sympathoexcitation regulates cerebral blood flow (CBF) at rest and during dynamic exercise. METHODS: In seven healthy subjects (26 ± 1 years), oscillatory neck pressure (NP) stimuli of + 40 mmHg were applied to the carotid baroreceptors at a pre-determined frequency of 0.1 Hz at rest, low (10 ± 1W), and heavy (30 ± 3W) exercise workloads (WLs) without (control) and with α - 1 adrenoreceptor blockade (prazosin). Spectral power analysis of the mean arterial blood pressure (MAP), mean middle cerebral artery blood velocity (MCAV), and cerebral tissue oxygenation index (ScO2) in the low-frequency range (0.07-0.20 Hz) was estimated to examine NP stimuli responses. RESULTS: From rest to heavy exercise, WLs resulted in a greater than three-fold increase in MCAV power (42 ± 23.8-145.2 ± 78, p < 0.01) and an almost three-fold increase in ScO2 power (0.51 ± 0.3-1.53 ± 0.8, p = 0.01), even though there were no changes in MAP power (from 24.5 ± 21 to 22.9 ± 11.9) with NP stimuli. With prazosin, the overall MAP (p = 0.0017), MCAV (p = 0.019), and ScO2 (p = 0.049) power was blunted regardless of the exercise conditions. Prazosin blockade resulted in increases in the Tf gain index between MAP and MCAV compared to the control (p = 0.03). CONCLUSION: CBR-mediated changes in sympathetic activity contribute to dynamic regulation of the cerebral vasculature and CBF at rest and during dynamic exercise in humans.

Secondary intracranial hypertension (pseudotumor cerebri) presenting as post-traumatic headache in mild traumatic brain injury: a case series.

BACKGROUND: Cerebral edema peaks 36-72 h after moderate traumatic brain injury but thought to be uncommon after mild traumatic brain injury. Post-traumatic headache can develop 48-72 h post-injury, perhaps reflecting the developing cerebral edema. Pseudotumor cerebri can result from various causes, including cerebral edema, and is characterized by increased intracranial pressure, headache, visual, and other common symptoms. Our objective was to report a phenotypically identifiable post-traumatic headache subtype. CASE SERIES PRESENTATION: This case series of six pediatric patients with post-traumatic pseudotumor cerebri was assessed at 48-120 h post-primary injury with new or a change in symptoms such as headache, vision, auditory, balance, and cognition. Clinical findings included slight fever, neck/head pain, papilledema or cranial nerve deficit (6th), and lack of coordination. Elevated cerebral spinal fluid pressure was documented by lumbar puncture, with no infection. Symptoms improved with treatment specific to post-traumatic headache subtype (lumbar puncture, topiramate, or acetazolamide). CONCLUSIONS: Recognition of specific post-traumatic headache subtypes after mild traumatic brain injury will expedite treatment intervention to lower intracranial pressure and resolve symptoms.

Impaired cerebral autoregulation is associated with vasospasm and delayed cerebral ischemia in subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Cerebral autoregulation may be impaired in the early days after subarachnoid hemorrhage (SAH). The purpose of this study was to examine the relationship between cerebral autoregulation and angiographic vasospasm (aVSP) and radiographic delayed cerebral ischemia (DCI) in patients with SAH. METHODS: Sixty-eight patients (54±13 years) with a diagnosis of nontraumatic SAH were studied. Dynamic cerebral autoregulation was assessed using transfer function analysis (phase and gain) of the spontaneous blood pressure and blood flow velocity oscillations on days 2 to 4 post-SAH. aVSP was diagnosed using a 4-vessel conventional angiogram. DCI was diagnosed from CT. Decision tree models were used to identify optimal cut-off points for clinical and physiological predictors of aVSP and DCI. Multivariate logistic regression models were used to develop and validate a risk scoring tool for each outcome. RESULTS: Sixty-two percent of patients developed aVSP, and 19% developed DCI. Patients with aVSP had higher transfer function gain (1.06±0.33 versus 0.89±0.30; P=0.04) and patients with DCI had lower transfer function phase (17.5±39.6 versus 38.3±18.2; P=0.03) compared with those who did not develop either. Multivariable scoring tools using transfer function gain>0.98 and phase<12.5 were strongly predictive of aVSP (92% positive predictive value; 77% negative predictive value; area under the receiver operating characteristic curve, 0.92) and DCI (80% positive predictive value; 91% negative predictive value; area under the curve, 0.94), respectively. CONCLUSIONS: Dynamic cerebral autoregulation is impaired in the early days after SAH. Including autoregulation as part of the initial clinical and radiographic assessment may enhance our ability to identify patients at a high risk for developing secondary complications after SAH.

α1-Adrenergic receptor control of the cerebral vasculature in humans at rest and during exercise.

We tested the hypothesis that pharmacological blockade of α(1)-adrenoreceptors (by prazosin), at rest and during steady-state dynamic exercise, would impair cerebral autoregulation and result in cerebral vasodilatation in healthy humans. In 10 subjects, beat-to-beat mean arterial pressure and mean middle cerebral artery blood velocity were determined at rest and during low (Ex90) and moderate workload (Ex130) on an upright bicycle ergometer without and with prazosin. Plasma noradrenaline concentrations increased significantly from rest to Ex130 during control conditions (from 1.8 ± 0.2 to 3.2 ± 0.3 pmol (ml plasma)(-1)). In the control conditions, the transfer function gain between mean arterial pressure and mean middle cerebral artery blood velocity in the low-frequency range was decreased at Ex90 (P = 0.035) and Ex130 (P = 0.027) from rest. A significant increase in critical closing pressure (CCP) was also observed in the control conditions from rest to Ex90 to Ex130 (from 18 ± 3 to 24 ± 4 to 31 ± 4 mmHg). An average of 74 ± 2% blockade of blood pressure response was achieved with oral prazosin. Following blockade, plasma noradrenaline concentrations further increased at rest and during Ex130 from the control value (from 2.6 ± 0.3 to 4.4 ± 0.5 pmol (ml plasma)(-1)). Prazosin also resulted in an increase in low-frequency gain (P < 0.003) compared with the control conditions. Prazosin blockade abolished the increases in CCP during Ex130 and increased the cerebrovascular conductance index (P = 0.018). These data indicate that in the control conditions a strengthening of cerebral autoregulation occurred with moderate dynamic exercise that is associated with an increase in CCP as a result of the exercise-mediated augmentation of sympathetic activity. Given that α(1)-adrenergic receptor blockade attenuated the increase in dynamic cerebral autoregulation and CCP, we conclude that increases in sympathetic activity have a role in establishing cerebral vascular tone in humans.

Transcranial Doppler ultrasound: technique and application.

Transcranial Doppler (TCD) ultrasound provides rapid, noninvasive, real-time measures of cerebrovascular function. TCD can be used to measure flow velocity in the basal arteries of the brain to assess relative changes in flow, diagnose focal vascular stenosis, or to detect embolic signals within these arteries. TCD can also be used to assess the physiologic health of a particular vascular territory by measuring blood flow responses to changes in blood pressure (cerebral autoregulation), changes in end-tidal CO2 (cerebral vasoreactivity), or cognitive and motor activation (neurovascular coupling or functional hyperemia). TCD has established utility in the clinical diagnosis of a number of cerebrovascular disorders such as acute ischemic stroke, vasospasm, subarachnoid hemorrhage, sickle cell disease, as well as other conditions such as brain death. Clinical indication and research applications for this mode of imaging continue to expand. In this review, the authors summarize the basic principles and clinical utility of TCD and provide an overview of a few TCD research applications.

The effects of aerobic fitness and beta1-adrenergic receptor blockade on cardiac work during dynamic exercise.

The purpose of this investigation was to determine whether cardiovascular adaptations characteristic of long-term endurance exercise compensate more effectively during cardioselective beta(1)-adrenergic receptor blockade-induced reductions in sympathoadrenergic-stimulated contractility. Endurance-trained (ET) athletes (n = 8) and average-trained (AT; n = 8) subjects performed submaximal cycling exercise at moderate [45% maximum oxygen uptake (Vo(2max))] and heavy (70% Vo(2max)) workloads, with and without metoprolol. Cardiac output (Qc), heart rate (HR), and systolic blood pressure were recorded at rest and during exercise. Cardiac work was calculated from the triple product of HR, stroke volume, and systolic blood pressure, and myocardial efficiency is represented as cardiac work for a given total body oxygen consumption. Metoprolol reduced Qc at 45% Vo(2max) (P = 0.004) and 70% Vo(2max) (P = 0.022) in ET subjects, but did not alter Qc in the AT subjects. In ET subjects at 45% Vo(2max), metoprolol-induced reductions in Qc were a result of decreases in HR (P < 0.05) and the absence of a compensatory increase in stroke volume (P > 0.05). The cardiac work and calculated cardiac efficiency were reduced with metoprolol in ET subjects at both exercise intensities and in the AT subjects during the high-intensity workload (P < 0.01). The cardiac work and the calculated cardiac efficiency were not affected by metoprolol in the AT subjects during the 45% Vo(2max) exercise. Therefore, in AT subjects, beta-blockade reduced the amount of pressure generation necessary to produce the same amount of work during moderate-intensity exercise. In patients with heart disease receiving metoprolol, a decrease in the generation of cardiac pressure necessary to perform a given amount of work during mild-to-moderate exercise would prove to be beneficial.

Reduced heart rate variability and lower cerebral blood flow associated with poor cognition during recovery following concussion.

Although physiological deficits such as altered cerebral blood flow (CBF), and autonomic nervous system (ANS) dysregulation have been reported following a concussion, the relationship between CBF and ANS with functional outcome post-injury remains unclear. Our present study was designed to examine heart-rate variability (HRV) using percentage of successive NN intervals (pNN50) and CBF on day-3 (T1), day-21 (T2), and day-90 (T3) following a concussion in collegiate athletes (N = 31) in comparison to non-injured controls (N = 31). Continuous RR-interval (3-lead electrocardiogram), middle cerebral artery blood velocity (MCAV; transcranial Doppler ultrasonography), mean arterial pressure (MAP; finger photoplethysmography) were obtained at rest. Cerebrovascular conductance index (CVCi) was estimated as a ratio of MCAV to MAP. Cognition was evaluated with standard assessment of concussion (SAC), and Trails A & B. Compared to the controls, lower HRV (43 ±â€¯15 vs. 27 ±â€¯20%; p < 0.0001) was observed at T1 with normalization at T2 and T3. No difference in MCAV between the control and the concussed groups across the three time points were observed. However, post-hoc analyses indicated a positive relationship between MCAV at T1 phase with HRV and CVCi during T2, and T3 phases. Higher MCAV at T1 was also associated with better cognition scores during the asymptomatic T2 phase in the concussed athletes. Therefore, our results indicate ANS dysregulation during the acute recovery phase after a concussion. Differences in CBF may be one of the underlying causes behind heterogeneity in clinical symptoms and functional outcomes after a concussion and future studies are warranted to validate this finding.

Balance Testing Following Concussion: Postural Sway versus Complexity Index.

BACKGROUND: Although postural control deficits are common following a concussion, the current clinical assessments for postural control tend to resolve within 3 to 10 days after injury. There is a lack of sensitive tools to examine subtle changes in postural control during the recovery phase following sports-related concussion. Only a limited number of studies have examined nonlinear dynamics of postural control; no study has examined this metric longitudinally during the recovery phase following a sports-related concussion. OBJECTIVE: To examine sway and complexity index of postural control in collegiate athletes during day 3, day 21, and day 90 following a concussion and compare them with noninjured controls. DESIGN: Prospective longitudinal case-control study. SETTING: University cerebrovascular research laboratory. PARTICIPANTS: Thirty-one male and female collegiate athletes on day 3 following a concussion. Twenty-eight athletes returned on day 21, and 21 completed assessments on day 90. Twenty-nine sports-matched noninjured controls. METHODS: Center of pressure (COP) measurements obtained during 60-second quiet standing on a force plate system with either eyes opened or closed. Postural sway was estimated as range and variability of COP in the anteroposterior (AP) and mediolateral planes. MAIN OUTCOME MEASUREMENTS: Complexity index of AP COP utilizing multiscale entropy analysis. RESULTS: Postural sway measured as AP range (P = .03) and variability (P = .04) during quiet standing with eyes closed were higher on day 3 compared to the controls. Postural sway in the concussed group was comparable to the noninjured controls by day 21 postinjury. However, postural control dynamics utilizing complexity index was lower on day 3 (P < .001) and persisted on day 21 (P < .006) and day 90 (P < .02), despite resolution of abnormal postural sway 21 days postinjury. CONCLUSION: Complexity index utilizing nonlinear dynamics might be a more sensitive objective biomarker for examining postural control following a concussion, with implications for return-to-play and interventions. Future studies with a larger sample size are needed to validate this finding. CLINICAL TRIAL NUMBER: NCT02754206. LEVEL OF EVIDENCE: III.

Impaired Cerebral Vasoreactivity Despite Symptom Resolution in Sports-Related Concussion.

Traumatic brain injury (TBI) is associated with increased risk of later-life neurodegeneration and dementia. However, the underpinning mechanisms are poorly understood, and secondary injury resulting from perturbed physiological processes plays a significant role. Cerebral vasoreactivity (CVR), a measure of hemodynamic reserve, is known to be impaired in TBI. However, the temporal course of this physiological perturbation is not established. We examined CVR and clinical symptoms on day 3 (T1), day 21 (T2), and day 90 (T3) after concussion in collegiate athletes and cross-sectionally in non-injured controls. Changes in middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasonography) were measured during changes in end-tidal CO2 (PetCO2) at normocapnia, hypercapnia (inspiring 8% CO2), and hypocapnia (hyperventilation). CVR was determined as the slope of the linear relationship and expressed as percent change in MCAV per mmHg change in PetCO2. CVR was attenuated during the acute phase T1 (1.8 ± 0.4U; p = 0.0001), subacute phases T2 (2.0 ± 0.4U; p = 0.0017), and T3 (1.9 ± 0.6U; p = 0.023) post-concussion compared to the controls (2.3 ± 0.3U). Concussed athletes exhibited higher symptom number (2.5 ± 3.0 vs. 12.1 ± 7.0; p < 0.0001) and severity (4.2 ± 6.0 vs. 29.5 ± 23.0; p < 0.0001), higher Patient Health Questionnaire-9 score (2.2 ± 2.0 vs. 9.1 ± 6.0; p = 0.0003) at T1. However, by T2, symptoms had resolved. We show that CVR is impaired as early as 4 days and remains impaired up to 3 months post-injury despite symptom resolution. Persistent perturbations in CVR may therefore be involved in secondary injury. Future studies with a larger sample size and longer follow-up period are needed to validate this finding and delineate the duration of this vulnerable period.

Regulation of middle cerebral artery blood velocity during recovery from dynamic exercise in humans.

We sought to examine the regulation of cerebral blood flow during 10 min of recovery from mild, moderate, and heavy cycling exercise by measuring middle cerebral artery blood velocity (MCA V). Transfer function analyses between changes in arterial blood pressure and MCA V were used to assess the frequency components of dynamic cerebral autoregulation (CA). After mild and moderate exercise, the decreases in mean arterial pressure (MAP) and mean MCA V (MCA Vm) were small. However, following heavy exercise, MAP was rapidly and markedly reduced, whereas MCA Vm decreased slowly (-23 +/- 4 mmHg and -4 +/- 1 cm/s after 1 min for MAP and MCA Vm, respectively; means +/- SE). Importantly, for each workload, the normalized low-frequency transfer function gain between MAP and MCA Vm remained unchanged from rest to exercise and during recovery, indicating a maintained dynamic CA. Similar results were found for the systolic blood pressure and systolic MCA V relationship. In contrast, the normalized low-frequency transfer function gain between diastolic blood pressure and diastolic MCA V (MCA Vd) increased from rest to exercise and remained elevated in the recovery period (P < 0.05). However, MCA Vd was quite stable on the cessation of exercise. These findings suggest that MCA V is well maintained following mild to heavy dynamic exercise. However, the increased transfer function gain between diastolic blood pressure and MCA Vd suggests that dynamic CA becomes less effective in response to rapid decreases in blood pressure during the initial 10 min of recovery from dynamic exercise.

Effects of changes in central blood volume on carotid-vasomotor baroreflex sensitivity at rest and during exercise.

The purpose of this investigation was to examine whether the effect of changes in central blood volume on carotid-vasomotor baroreflex sensitivity at rest was the same during exercise. Eight men (means +/- SE: age 26 +/- 1 yr; height 180 +/- 3 cm; weight 86 +/- 6 kg) participated in the present study. Sixteen Torr of lower body negative pressure (LBNP) were applied to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak O2 uptake (104 +/- 20 W). Subsequently, infusions of 25% human serum albumin solution were administered to increase CVP at rest and during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, the maximal gain (G(max)) of the carotid-vasomotor baroreflex function curve was measured using the neck pressure and neck suction technique. LBNP reduced CVP and increased the G(max) of the carotid-vasomotor baroreflex function curve at rest (+63 +/- 25%, P = 0.006) and during exercise (+69 +/- 19%, P = 0.002). In contrast to the LBNP, increases in CVP resulted in the G(max) of the carotid-vasomotor baroreflex function curve being decreased at rest -8 +/- 4% and during exercise -18 +/- 5% (P > 0.05). These findings indicate that the relationship between CVP and carotid-vasomotor baroreflex sensitivity was nonlinear at rest and during exercise and suggests a saturation load of the cardiopulmonary baroreceptors at which carotid-vasomotor baroreflex sensitivity remains unchanged.

Cardiopulmonary baroreflex is reset during dynamic exercise.

The purpose of this study was to examine the hypothesis that the operating point of the cardiopulmonary baroreflex resets to the higher cardiac filling pressure of exercise associated with the increased cardiac filling volumes. Eight men (age 26 +/- 1 yr; height 180 +/- 3 cm; weight 86 +/- 6 kg; means +/- SE) participated in the present study. Lower body negative pressure (LBNP) was applied at 8 and 16 Torr to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak oxygen uptake (104 +/- 20 W). Subsequently, two discrete infusions of 25% human serum albumin solution were administered until CVP was increased by 1.8 +/- 0.6 and 2.4 +/- 0.4 mmHg at rest and 2.9 +/- 0.9 and 4.6 +/- 0.9 mmHg during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, forearm blood flow and cardiac output were measured. During exercise, forearm vascular conductance increased from 7.5 +/- 0.5 to 8.7 +/- 0.6 U (P = 0.024) and total systemic vascular conductance from 7.2 +/- 0.2 to 13.5 +/- 0.9 l.min(-1).mmHg(-1) (P < 0.001). However, there was no significant difference in the responses of both forearm vascular conductance and total systemic vascular conductance to LBNP and the infusion of albumin between rest and exercise. These data indicate that the cardiopulmonary baroreflex had been reset during exercise to the new operating point associated with the exercise-induced change in cardiac filling volume.

Surface electromyographic amplitude-to-work ratios during isokinetic and isotonic muscle actions.

CONTEXT: Isokinetic and isotonic resistance training exercises are commonly used to increase strength during musculoskeletal rehabilitation programs. Our study was designed to examine the efficacy of isokinetic and isotonic muscle actions using surface electromyographic (EMG) amplitude-to-work ratios (EMG/WK) and to extend previous findings to include a range of isokinetic velocities and isotonic loads. OBJECTIVE: To examine work (WK), surface EMG amplitude, and EMG/WK during concentric-only maximal isokinetic muscle actions at 60, 120, 180, 240, and 300 degrees /s and isotonic muscle actions at 10%, 20%, 30%, 40%, and 50% of the maximal voluntary isometric contraction (MVIC) torque during leg extension exercises. DESIGN: A randomized, counterbalanced, cross-sectional, repeated-measures design. SETTING: A university-based human muscle physiology research laboratory. PATIENTS OR OTHER PARTICIPANTS: Ten women (mean age = 22.0 +/- 2.6 years) and 10 men (mean age = 20.8 +/- 1.7 years) who were apparently healthy and recreationally active. INTERVENTION(S): Using the dominant leg, each participant performed 5 maximal voluntary concentric isokinetic leg extension exercises at randomly ordered angular velocities of 60, 120, 180, 240, and 300 degrees /s and 5 concentric isotonic leg extension exercises at randomly ordered loads of 10%, 20%, 30%, 40%, and 50% of the isometric MVIC. MAIN OUTCOME MEASURE(S): Work was recorded by a Biodex System 3 dynamometer, and surface EMG was recorded from the superficial quadriceps femoris muscles (vastus lateralis, rectus femoris, and vastus medialis) during the testing and was normalized to the MVIC. The EMG/WK ratios were calculated as the quotient of EMG amplitude (muVrms) and WK (J) during the concentric phase of each exercise. RESULTS: Isotonic EMG/WK remained unchanged ( P > .05) from 10% to 50% MVIC, but isokinetic EMG/WK increased ( P < .05) from 60 to 300 degrees /s. Isotonic EMG/WK was greater ( P < .05) than isokinetic EMG/WK for 50% MVIC versus 60 degrees /s, 40% MVIC versus 120 degrees /s, and 30% MVIC versus 180 degrees /s; however, no differences were noted ( P > .05) between 20% MVIC versus 240 degrees /s or 10% MVIC versus 300 degrees /s. An 18% decrease in active range of motion was seen for the isotonic muscle actions, from 10% to 50% MVIC, and a 3% increase in range of motion for the isokinetic muscle actions from 60 to 300 degrees /s was also observed. Furthermore, the peak angular velocities for the isotonic muscle actions ranged from 272.9 to 483.0 degrees /s for 50% and 10% MVIC, respectively. CONCLUSIONS: When considering EMG/WK, peak angular velocity, and range of motion together, our data indicate that maximal isokinetic muscle actions at 240 degrees /s or controlled-velocity isotonic muscle actions at 10%, 20%, or 30% MVIC may maximize the amount of muscle activation per unit of WK done during the early stages of musculoskeletal rehabilitation. These results may be useful to allied health professionals who incorporate open-chain resistance training exercises during the early phases of rehabilitation and researchers who use isotonic or isokinetic modes of resistance exercise to examine muscle function.

Impaired cerebrovascular hemodynamics are associated with cerebral white matter damage.

White matter hyperintensities (WMH) in elderly individuals with vascular diseases are presumed to be due to ischemic small vessel diseases; however, their etiology is unknown. We examined the cross-sectional relationship between cerebrovascular hemodynamics and white matter structural integrity in elderly individuals with vascular risk factors. White matter hyperintensity volumes, fractional anisotropy (FA), and mean diffusivity (MD) were obtained from MRI in 48 subjects (75±7years). Pulsatility index (PI) and dynamic cerebral autoregulation (dCA) was assessed using transcranial Doppler ultrasound of the middle cerebral artery. Dynamic cerebral autoregulation was calculated from transfer function analysis (phase and gain) of spontaneous blood pressure and flow velocity oscillations in the low (LF, 0.03 to 0.15 Hz) and high (HF, 0.16 to 0.5 Hz) frequency ranges. Higher PI was associated with greater WMH (P<0.005). Higher phase across all frequency ranges was associated with greater FA and lower MD (P<0.005). Lower gain was associated with higher FA in the LF range (P=0.001). These relationships between phase and FA were significant in the territories limited to the middle cerebral artery as well as across the entire brain. Our results show a strong relationship between impaired cerebrovascular hemodynamics (PI and dCA) and loss of cerebral white matter structural integrity (WMH and DTI metrics) in elderly individuals.

The functional role of the alpha-1 adrenergic receptors in cerebral blood flow regulation.

Cerebral vasculature is richly innervated by the α-1 adrenergic receptors similar to that of the peripheral vasculature. However, the functional role of the α-1adrenergic receptors in cerebral blood flow (CBF) regulation is yet to be established. The traditional thinking being that during normotension and normocapnia sympathetic neural activity does not play a significant role in CBF regulation. Reports in the past have stated that catecholamines do not penetrate the blood brain barrier (BBB) and therefore only influence cerebral vessels from outside the BBB and hence, have a limited role in CBF regulation. However, with the advent of dynamic measurement techniques, beat-to-beat CBF assessment can be done during dynamic changes in arterial blood pressure. Several studies in the recent years have reported a functional role of the α-1adrenergic receptors in CBF regulation. This review focuses on the recent developments on the role of the sympathetic nervous system, specifically that of the α-1 adrenergic receptors in CBF regulation.

Acute effects of static stretching on characteristics of the isokinetic angle - torque relationship, surface electromyography, and mechanomyography.

The aims of this study were to examine the acute effects of static stretching on peak torque, work, the joint angle at peak torque, acceleration time, isokinetic range of motion, mechanomyographic amplitude, and electromyographic amplitude of the rectus femoris during maximal concentric isokinetic leg extensions at 1.04 and 5.23 rad x s(-1) in men and women. Ten women (mean +/- s: age 23.0 +/- 2.9 years, stature 1.61 +/- 0.12 m, mass 63.3 +/- 9.9 kg) and eight men (age 21.4 +/- 3.0 years, stature 1.83 +/- 0.11 m, mass 83.1 +/- 15.2 kg) performed maximal voluntary concentric isokinetic leg extensions at 1.04 and 5.23 rad x s(-1). Following the initial isokinetic tests, the dominant leg extensors were stretched using four static stretching exercises. After the stretching, the isokinetic tests were repeated. Peak torque, acceleration time, and electromyographic amplitude decreased (P< or = 0.05) from pre- to post-stretching at 1.04 and 5.23 rad . s(-1); there were no changes (P > 0.05) in work, joint angle at peak torque, isokinetic range of motion, or mechanomyographic amplitude. These findings indicate no stretching-related changes in the area under the angle - torque curve (work), but a significant decrease in peak torque, which suggests that static stretching may cause a "flattening" of the angle - torque curve that reduces peak strength but allows for greater force production at other joint angles. These findings, in conjunction with the increased limb acceleration rates (decreased acceleration time) observed in the present study, provide tentative support for the hypothesis that static stretching alters the angle - torque relationship and/or sarcomere shortening velocity.

Acute Effects of Static and Proprioceptive Neuromuscular Facilitation Stretching on Muscle Strength and Power Output.

Context: Stretching is commonly used as a technique for injury prevention in the clinical setting. Our findings may improve the understanding of the neuromuscular responses to stretching and help clinicians make decisions for rehabilitation progression and return to play.Objective: To examine the short-term effects of static and proprioceptive neuromuscular facilitation stretching on peak torque (PT), mean power output (MP), active range of motion (AROM), passive range of motion (PROM), electromyographic (EMG) amplitude, and mechanomyographic (MMG) amplitude of the vastus lateralis and rectus femoris muscles during voluntary maximal concentric isokinetic leg extensions at 60 and 300 degrees .s.Design: A randomized, counterbalanced, cross-sectional, repeated-measures design.Setting: A university human research laboratory.Patients or Other Participants: Ten female (age, 23 +/- 3 years) and 9 male (age, 21 +/- 3 years) apparently healthy and recreationally active volunteers.Intervention(s): Four static or proprioceptive neuromuscular facilitation stretching exercises to stretch the leg extensor muscles of the dominant limb during 2 separate, randomly ordered laboratory visits.Main Outcome Measure(s): The PT and MP were measured at 60 and 300 degrees .s, EMG and MMG signals were recorded, and AROM and PROM were measured at the knee joint before and after the stretching exercises.Results: Static and proprioceptive neuromuscular facilitation stretching reduced PT (P = .051), MP (P = .041), and EMG amplitude (P = .013) from prestretching to poststretching at 60 and 300 degrees .s (P < .05). The AROM (P < .001) and PROM (P = .001) increased as a result of the static and proprioceptive neuromuscular facilitation stretching. The MMG amplitude increased in the rectus femoris muscle in response to the static stretching at 60 degrees .s (P = .031), but no other changes in MMG amplitude were observed (P > .05).Conclusions: Both static and proprioceptive neuromuscular facilitation stretching caused similar deficits in strength, power output, and muscle activation at both slow (60 degrees .s) and fast (300 degrees .s) velocities. The effect sizes, however, corresponding to these stretching-induced changes were small, which suggests the need for practitioners to consider a risk-to-benefit ratio when incorporating static or proprioceptive neuromuscular facilitation stretching.

The effect of changes in cardiac output on middle cerebral artery mean blood velocity at rest and during exercise.

We examined the relationship between changes in cardiac output and middle cerebral artery mean blood velocity (MCA V(mean)) in seven healthy volunteer men at rest and during 50% maximal oxygen uptake steady-state submaximal cycling exercise. Reductions in were accomplished using lower body negative pressure (LBNP), while increases in were accomplished using infusions of 25% human serum albumin. Heart rate (HR), arterial blood pressure and MCA V(mean) were continuously recorded. At each stage of LBNP and albumin infusion was measured using an acetylene rebreathing technique. Arterial blood samples were analysed for partial pressure of carbon dioxide tension (P(a,CO2). During exercise HR and were increased above rest (P < 0.001), while neither MCA V(mean) nor P(a,CO2) was altered (P > 0.05). The MCA V(mean) and were linearly related at rest (P < 0.001) and during exercise (P = 0.035). The slope of the regression relationship between MCA V(mean) and at rest was greater (P = 0.035) than during exercise. In addition, the phase and gain between MCA V(mean) and mean arterial pressure in the low frequency range were not altered from rest to exercise indicating that the cerebral autoregulation was maintained. These data suggest that the associated with the changes in central blood volume influence the MCA V(mean) at rest and during exercise and its regulation is independent of cerebral autoregulation. It appears that the exercise induced sympathoexcitation and the change in the distribution of between the cerebral and the systemic circulation modifies the relationship between MCA V(mean) and .