Does Behavioral Style Influence Learning Strategy in Health Professions Students?

Proficiency in areas of task completion, information processing, and time management are important attributes for successful academic performance and can be assessed using the Learning Assessment Study Strategies Inventory (LASSI). The purpose of this study was to determine if there were differences in learning strategies across four behavioral profiles using the DISC style analysis (Dominance, Influence, Steadiness, Compliance). Graduate health professions students (n=247) were administered the DISC and LASSI to assess study strategy categories based on their natural DISC behavioral style. A one-way ANOVA was used to assess differences for 10 LASSI category scores across the four DISC profiles; scores were also compared with national percentile scores. The D and C profiles were above the 75th percentile for information processing, but below the 50th percentile for self-testing. The S profile had significantly lower scores (p<0.005) for information processing and was below the 50th percentile for anxiety (i.e., higher anxiety). The I profile was below the 50th percentile for time management and concentration to academic tasks. The data are in close agreement with recognized behaviors specific for each behavioral style and suggest that behavioral style should be considered an important factor in academic performance.

Autonomic responses to exercise: where is central command?

A central command is thought to involve a signal arising in a central area of the brain eliciting a parallel activation of the autonomic nervous system and skeletal muscle contraction during exercise. Although much of the neural circuitry involved in autonomic control has been identified, defining the specific higher brain region(s) serving in a central command capacity has proven more challenging. Investigators have been faced with redundancies in regulatory systems, feedback mechanisms and the complexities ofhuman neural connectivity. Several studies have attempted to address these issues and provide more definitive neuroanatomical information. However, none have clearly answered the question, "where is central command?"

The relevance of central command for the neural cardiovascular control of exercise.

This paper briefly reviews the role of central command in the neural control of the circulation during exercise. While defined as a feedforward component of the cardiovascular control system, central command is also associated with perception of effort or effort sense. The specific factors influencing perception of effort and their effect on autonomic regulation of cardiovascular function during exercise can vary according to condition. Centrally mediated integration of multiple signals occurring during exercise certainly involves feedback mechanisms, but it is unclear whether or how these signals modify central command via their influence on perception of effort. As our understanding of central neural control systems continues to develop, it will be important to examine more closely how multiple sensory signals are prioritized and processed centrally to modulate cardiovascular responses during exercise. The purpose of this article is briefly to review the concepts underlying central command and its assessment via perception of effort, and to identify potential areas for future studies towards determining the role and relevance of central command for neural control of exercise.

New insights into central cardiovascular control during exercise in humans: a central command update.

The autonomic adjustments to exercise are mediated by central signals from the higher brain (central command) and by a peripheral reflex arising from working skeletal muscle (exercise pressor reflex), with further modulation provided by the arterial baroreflex. Although it is clear that central command, the exercise pressor reflex and the arterial baroreflex are all requisite for eliciting appropriate cardiovascular adjustments to exercise, this review will be limited primarily to discussion of central command. Central modulation of the cardiovascular system via descending signals from higher brain centres has been well recognized for over a century, yet the specific regions of the human brain involved in this exercise-related response have remained speculative. Brain mapping studies during exercise as well as non-exercise conditions have provided information towards establishing the cerebral cortical structures in the human brain specifically involved in cardiovascular control. The purpose of this review is to provide an update of current concepts on central command in humans, with a particular emphasis on the regions of the brain identified to alter autonomic outflow and result in cardiovascular adjustments.

Changes in regional cerebral blood flow distribution during postexercise hypotension in humans.

This investigation compared patterns of regional cerebral blood flow (rCBF) during exercise recovery both with and without postexercise hypotension (PEH). Eight subjects were studied on 3 days with randomly assigned conditions: 1) after 30 min of rest; 2) after 30 min of moderate exercise (M-Ex) at 60-70% heart rate (HR) reserve during PEH; and 3) after 30 min of light exercise (L-Ex) at 20% HR reserve with no PEH. Data were collected for HR, mean blood pressure (MBP), and ratings of perceived exertion and relaxation, and rCBF was assessed by use of single-photon-emission computed tomography. With the use of ANOVA across conditions, there were differences (P < 0.05; mean +/- SD) from rest during exercise recovery from M-Ex (HR = +12 +/- 3 beats/min; MBP = -9 +/- 2 mmHg), but not from L-Ex (HR = +2 +/- 2 beats/min; MBP = -2 +/- 2 mmHg). After M-Ex, there were decreases (P < 0.05) for the anterior cingulate (-6.7 +/- 2%), right and left inferior thalamus (-10 +/- 3%), right inferior insula (-13 +/- 3%), and left inferior anterior insula (-8 +/- 3%), not observed after L-Ex. There were rCBF decreases for leg sensorimotor regions after both M-Ex (-15 +/- 4%) and L-Ex (-12 +/- 3%) and for the left superior anterior insula (-7 +/- 3% and -6 +/- 3%), respectively. Data show that there are rCBF reductions within specific regions of the insular cortex and anterior cingulate cortex coupled with a postexercise hypotensive response after M-Ex. Findings suggest that these cerebral cortical regions, previously implicated in cardiovascular regulation during exercise, may also be involved in PEH.

Evidence for central command activation of the human insular cortex during exercise.

The purpose of this investigation was to determine whether central command activated regions of the insular cortex, independent of muscle metaboreflex activation and blood pressure elevations. Subjects (n = 8) were studied during 1) rest with cuff occlusion, 2) static handgrip exercise (SHG) sufficient to increase mean blood pressure (MBP) by 15 mmHg, and 3) post-SHG exercise cuff occlusion (PECO) to sustain the 15-mmHg blood pressure increase. Data were collected for heart rate, MBP, ratings of perceived exertion and discomfort, and regional cerebral blood flow (rCBF) by using single-photon-emission computed tomography. When time periods were compared when MBP was matched during SHG and PECO, heart rate (7 +/- 3 beats/min; P < 0.05) and ratings of perceived exertion (15 +/- 2 units; P < 0.05) were higher for SHG. During SHG, there were significant increases in rCBF for hand sensorimotor (9 +/- 3%), right inferior posterior insula (7 +/- 3%), left inferior anterior insula (8 +/- 2%), and anterior cingluate regions (6 +/- 2%), not found during PECO. There was significant activation of the inferior (ventral) thalamus and right inferior anterior insular for both SHG and PECO. Although prior studies have shown that regions of the insular cortex can be activated independent of mechanoreflex input, it was not presently assessed. These findings provide evidence that there are rCBF changes within regions of the insular and anterior cingulate cortexes related to central command per se during handgrip exercise, independent of metaboreflex activation and blood pressure elevation.

Brain activation by central command during actual and imagined handgrip under hypnosis.

The purpose was to compare patterns of brain activation during imagined handgrip exercise and identify cerebral cortical structures participating in "central" cardiovascular regulation. Subjects screened for hypnotizability, five with higher (HH) and four with lower hypnotizability (LH) scores, were tested under two conditions involving 3 min of 1) static handgrip exercise (HG) at 30% of maximal voluntary contraction (MVC) and 2) imagined HG (I-HG) at 30% MVC. Force (kg), forearm integrated electromyography, rating of perceived exertion, heart rate (HR), mean blood pressure (MBP), and differences in regional cerebral blood flow distributions were compared using an ANOVA. During HG, both groups showed similar increases in HR (+13 +/- 5 beats/min) and MBP (+17 +/- 3 mmHg) after 3 min. However, during I-HG, only the HH group showed increases in HR (+10 +/- 2 beats/min; P < 0.05) and MBP (+12 +/- 2 mmHg; P < 0.05). There were no significant increases or differences in force or integrated electromyographic activity between groups during I-HG. The rating of perceived exertion was significantly increased for the HH group during I-HG, but not for the LH group. In comparison of regional cerebral blood flow, the LH showed significantly lower activity in the anterior cingulate (-6 +/- 2%) and insular cortexes (-9 +/- 4%) during I-HG. These findings suggest that cardiovascular responses elicited during imagined exercise involve central activation of insular and anterior cingulate cortexes, independent of muscle afferent feedback; these structures appear to have key roles in the central modulation of cardiovascular responses.

A 30-year follow-up of the Dallas Bedrest and Training Study: I. Effect of age on the cardiovascular response to exercise.

BACKGROUND: Cardiovascular capacity declines with aging, as evidenced by declining maximal oxygen uptake (VO(2)max ), with little known about the specific mechanisms of this decline. Our study objective was to assess the effect of a 30-year interval on body composition and cardiovascular response to acute exercise in 5 healthy subjects originally evaluated in 1966. METHODS AND RESULTS: Anthropometric parameters and the cardiovascular response to acute maximal exercise were assessed with noninvasive techniques. On average, body weight increased 25% (77 versus 100 kg) and percent body fat increased 100% (14% versus 28%), with little change in fat-free mass (66 versus 72 kg). On average, VO(2)max decreased 11% (3.30 versus 2.90 L/min). Likewise, VO(2)max decreased when indexed to total body mass (43 versus 31 mL. kg(-1). min(-1)) or fat-free mass (50 versus 43 mL/kg fat-free mass per minute). Maximal heart rate declined 6% (193 versus 181 bpm) and maximal stroke volume increased 16% (104 versus 121 mL), with no difference observed in maximal cardiac output (20.0 versus 21.4 L/min). Maximal AV oxygen difference declined 15% (16.2 versus 13.8 vol%) and accounted for the entire decrease in cardiovascular capacity. CONCLUSIONS: Cardiovascular capacity declined over the 30-year study interval in these 5 middle-aged men primarily because of an impaired efficiency of maximal peripheral oxygen extraction. Maximal cardiac output was maintained with a decline in maximal heart rate compensated for by an increased maximal stroke volume. Most notably, 3 weeks of bedrest in these same men at 20 years of age (1966) had a more profound impact on physical work capacity than did 3 decades of aging.

A 30-year follow-up of the Dallas Bedrest and Training Study: II. Effect of age on cardiovascular adaptation to exercise training.

BACKGROUND: Aerobic power declines with age. The degree to which this decline is reversible remains unclear. In a 30-year longitudinal follow-up study, the cardiovascular adaptations to exercise training in 5 middle-aged men previously trained in 1966 were evaluated to assess the degree to which the age-associated decline in aerobic power is attributable to deconditioning and to gain insight into the specific mechanisms involved. Methods and Results-- The cardiovascular response to acute submaximal and maximal exercise were assessed before and after a 6-month endurance training program. On average, VO(2max) increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, VO(2max) increased 16% when indexed to total body mass (31 versus 36 mL/kg per minute) or fat-free mass (44 versus 51 mL/kg fat-free mass per minute). Maximal heart rate declined (181 versus 171 beats/min) and maximal stroke volume increased (121 versus 129 mL) after training, with no change in maximal cardiac output (21.4 versus 21.7 L/min); submaximal heart rates also declined to a similar degree. Maximal AVDO(2) increased by 10% (13.8 versus 15.2 vol%) and accounted for the entire improvement of aerobic power associated with training. CONCLUSIONS: One hundred percent of the age-related decline in aerobic power among these 5 middle-aged men occurring over 30 years was reversed by a 6-month endurance training program. However, no subject achieved the same maximal VO(2) attained after training 30 years earlier, despite a similar relative training load. The improved aerobic power after training was primarily the result of peripheral adaptation, with no effective improvement in maximal oxygen delivery.

Hypnotic manipulation of effort sense during dynamic exercise: cardiovascular responses and brain activation.

The purpose of this investigation was to hypnotically manipulate effort sense during dynamic exercise and determine whether cerebral cortical structures previously implicated in the central modulation of cardiovascular responses were activated. Six healthy volunteers (4 women, 2 men) screened for high hypnotizability were studied on 3 separate days during constant-load exercise under three hypnotic conditions involving cycling on a 1) perceived level grade, 2) perceived downhill grade, and 3) perceived uphill grade. Ratings of perceived exertion (RPE), heart rate (HR), blood pressure (BP), and regional cerebral blood flow (rCBF) distributions for several sites were compared across conditions using an analysis of variance. The suggestion of downhill cycling decreased both the RPE [from 13 +/- 2 to 11 +/- 2 (SD) units; P < 0.05] and rCBF in the left insular cortex and anterior cingulate cortex, but it did not alter exercise HR or BP responses. Perceived uphill cycling elicited significant increases in RPE (from 13 +/- 2 to 14 +/- 1 units), HR (+16 beats/min), mean BP (+7 mmHg), right insular activation (+7.7 +/- 4%), and right thalamus activation (+9.2 +/- 5%). There were no differences in rCBF for leg sensorimotor regions across conditions. These findings show that an increase in effort sense during constant-load exercise can activate both insular and thalamic regions and elevate cardiovascular responses but that decreases in effort sense do not reduce cardiovascular responses below the level required to sustain metabolic needs.

Determinants of clinical performance in a physical therapy program.

In admission decisions, allied health programs evaluate various factors that may include overall grade-point average (GPA), science GPA, GPA in the most recent 60 hours of course work, volunteer/work experience, and performance during an admission interview. Most use mathematical formulas based on these parameters, but the rationale for weighting each factor is not always clear. To determine whether pre-admission variables can differentiate between good and poor clinical performances, the authors compared pre-admission data from 118 graduates of a physical therapy (PT) baccalaureate program with their clinical performances. GPA in the PT curriculum was included to determine whether it was related to clinical performance, which was taken as the average of overall performance scores assigned to each student by his or her instructors at four clinical education sites. The students were divided into quartiles by clinical scores. One-way ANOVA was used to identify differences between quartiles for each variable (alpha level of p < 0.05). The interview score was the only pre-admission variable that differentiated between students who did and did not perform well in the clinic (p < 0.003). Those who performed better in the clinic also had higher PT GPAs (p < 0.0001). The interview format and scoring system used may easily be adapted for other programs. Recommendations are made regarding how to utilize interview scores in the admission decision.

Cardiovascular responses to static exercise in patients with Brown-Séquard syndrome.

1. The purpose of this study was to determine the contributions of central command and the exercise pressor reflex in regulating the cardiovascular response to static exercise in patients with Brown-Sequard syndrome. In this rare condition, a hemisection of the spinal cord typically leaves one side of the body with diminished sensation and normal motor function and the other side with diminished motor function and normal sensation. 2. Four, otherwise healthy, patients with Brown-Sequard syndrome and varying degrees of motor and sensory dysfunction were studied during four isometric knee extension protocols involving both voluntary contraction and electrically stimulated contractions of each leg. Heart rate, blood pressure, force production and ratings of perceived exertion were measured during all conditions. Measurements were also made during post-contraction thigh cuff occlusion and during a cold pressor test. 3. With the exception of electrical stimulation of the leg with a sensory deficit, protocols yielded increases in heart rate and blood pressure. Cuff occlusion sustained blood pressure above resting levels only when the leg had intact sensation. 4. While voluntary contraction (or attempted contraction) of the leg with a motor deficit produced the lowest force, it produced the highest ratings of perceived exertion coupled with the greatest elevations in heart rate and blood pressure. 5. These data show that the magnitude of the heart rate and blood pressure responses in these patients was greatly affected by an increased central command; however, there were marked cardiovascular responses due to activation of the exercise pressor reflex in the absence of central command.

Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans.

PURPOSE: The purpose of this study was to determine the cardiac mechanisms involved in cardiovascular adjustments during postexercise circulatory occlusion (OCCL). METHOD: Heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance (total peripheral resistance (TPR)) were assessed in nine healthy volunteers during rest and static exercise at 30% of maximum voluntary contraction followed by either OCCL for 3 min or non-OCCL in a randomized crossover protocol. RESULTS: During handgrip, HR (+20%; P < 0.001), CO (+11%; P = 0.003), MAP (+18%; P = 0.001), and TPR (+6%; P = 0.004) increased, SV (-8%; P = 0.001) and EDV (-5%; P < 0.001) decreased, while ESV did not change (P > 0.05). These responses were similar between conditions (P > 0.05). During OCCL, HR, SV, and CO returned to baseline, whereas MAP (+19%; P < 0.001) and TPR (+9%; P = 0.004) remained elevated. EDV (+12%; P < 0.001) and ESV (+23%; P < 0.001) increased in parallel above resting values. CONCLUSION: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying the involvement of the Frank-Starling mechanism.

Activation of the insular cortex is affected by the intensity of exercise.

The purpose of this investigation was to determine whether there were differences in the magnitude of insular cortex activation across varying intensities of static and dynamic exercise. Eighteen healthy volunteers were studied: eight during two intensities of leg cycling and ten at different time periods during sustained static handgrip at 25% maximal voluntary contraction or postexercise cuff occlusion. Heart rate, blood pressure (BP), perceived exertion, and regional cerebral blood flow (rCBF) distribution data were collected. There were significantly greater increases in insular rCBF during lower (6.3 +/- 1.7%; P < 0.05) and higher (13.3 +/- 3.8%; P < 0.05) intensity cycling and across time during static handgrip (change from rest for right insula at 2-3 min, 3.8 +/- 1.1%, P < 0.05; and at 4-5 min, 8.6 +/- 2.8%, P < 0.05). Insular rCBF was decreased during postexercise cuff occlusion (-5.5 +/- 1.2%; P < 0.05) with BP sustained at exercise levels. Right insular rCBF data, but not left, were significantly related, with individual BP changes (r(2) = 0.80; P < 0.001) and with ratings of perceived exertion (r(2) = 0.79; P < 0.01) during exercise. These results suggest that the magnitude of insular activation varies with the intensity of exercise, which may be further related to the level of perceived effort or central command.

Activation of the insular cortex during dynamic exercise in humans.

1. The insular cortex has been implicated as a region of cortical cardiovascular control, yet its role during exercise remains undefined. The purpose of the present investigation was to determine whether the insular cortex was activated during volitional dynamic exercise and to evaluate further its role as a site for regulation of autonomic activity. 2. Eight subjects were studied during voluntary active cycling and passively induced cycling. Additionally, four of the subjects underwent passive movement combined with electrical stimulation of the legs. 3. Increases in regional cerebral blood flow (rCBF) distribution were determined for each individual using single-photon emission-computed tomography (SPECT) co-registered with magnetic resonance (MR) images to define exact anatomical sites of cerebral activation during each condition. 4. The rCBF significantly increased in the left insula during active, but not passive cycling. There were no significant changes in rCBF for the right insula. Also, the magnitude of rCBF increase for leg primary motor areas was significantly greater for both active cycling and passive cycling combined with electrical stimulation compared with passive cycling alone. 5. These findings provide the first evidence of insular activation during dynamic exercise in humans, suggesting that the left insular cortex may serve as a site for cortical regulation of cardiac autonomic (parasympathetic) activity. Additionally, findings during passive cycling with electrical stimulation support the role of leg muscle afferent input towards the full activation of leg motor areas.

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans.

Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 +/- 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 +/- 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118-136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55-38 ml) mediated the increase in SV.

Eccentric exercise augments the cardiovascular response to static exercise.

High-force eccentric exercise induces neuromuscular dysfunction and may augment the cardiovascular response to exercise. This investigation sought to determine whether changes in strength and sense of force following high-force eccentric exercise alter heart rate and blood pressure responses during isometric contractions. Subjects (4F,6M) performed 50 maximum resistance eccentric actions with one arm (ECC arm). Contractions at 10% of the ECC arm maximum were held for 7 min on two pre-exercise days. The force output perceived to be the same as 10% of the pre-exercise maximum was determined using a force matching task. This force, 35.6, 27.2, and 21.1% lower on days 1, 3, and 5 post-exercise, was held during isometric contractions on these days, respectively. Despite a lowering of absolute contraction force, heart rate (P < 0.05) and blood pressure (P < 0.001) responses during contractions using the ECC arm were consistently elevated relative to the control arm. However, subjects perceived that they were exerting forces similar to those achieved before eccentric exercise-induced neuromuscular dysfunction. These findings suggest that perceived effort following strength loss induced by mechanically stressful exercise dictates the cardiovascular responses during isometric contractions.

Facial cooling-induced bradycardia: attenuating effect of central command at exercise onset.

Facial cooling (FC) elicits a marked bradycardia at rest that appears to be reduced during exercise. This study was done to delineate the effects of exercise mediated central command from those of muscle afferent feedback and sympathetic stimulation on the attenuation of the bradycardic effect of FC during the onset of exercise. Ten healthy subjects (26 +/- 2 yr) were exposed to FC under five different conditions: 1) seated rest on the cycle ergometer, 2) onset of mild exercise (resting HR + 20 beats.min-1), 3) onset of moderate exercise (resting HR + 50 beats.min-1), 4) seated rest on the ergometer during electrical stimulation, and 5) seated rest on the ergometer during a cold immersion test (CT) (one hand immersed in an ice slurry at 0 degree C). The two exercise intensities were presumed to provide different degrees of central command. Electrical stimulation of the quadriceps was assumed to provide isolated muscle afferent feedback, while the CT served as a sympathetic stimulus. Beat-by-beat data were recorded for HR and mean arterial blood pressure for the duration of each test (50 s), and a rating of perceived pain was taken after each FC. FC elicited significant increases in mean arterial pressure during mild and moderate exercise compared with resting control (P < 0.05) and during moderate exercise compared to exercise without FC (P < 0.05). Mean decreases in HR during FC were similar for resting control (-12 +/- 3 beats.min-1), electrical stimulation (-10 +/- 3 beats.min-1), and CT (-9 +/- 3 beats.min-1). The HR response to FC during mild exercise (-7 +/- 2 beats.min-1) was significantly different (P < 0.05) from the rest condition; however, there was no significant bradycardia (-2 +/- 2 beats.min-1; P > 0.05) during onset of moderate exercise. These findings suggest that the magnitude of cold face-induced bradycardia may be attenuated at exercise onset by neural signals related to the higher levels of central motor command associated with heavier exercise.

Mechanisms regulating regional cerebral activation during dynamic handgrip in humans.

Dynamic hand movement increases regional cerebral blood flow (rCBF) of the contralateral motor sensory cortex (MS1). This increase is eliminated by regional anesthesia of the working arm, indicating the importance of afferent neural input. The purpose of this study was to determine the specific type of afferent input required for this cerebral activation. The rCBF was measured at +5.0 and +9.0 cm above the orbitomeatal (OM) plane in 13 subjects during 1) rest; 2) dynamic left-hand contractions; 3) postcontraction ischemia (metaboreceptor afferents); and 4) biceps brachii tendon vibration (muscle spindles). The rCBF increased only during dynamic hand contraction; contralateral MS1 (OM +9) by 15% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05); supplementary motor area (OM +9) by 11% to 69 +/- 9.8 ml.100 g-1.min-1 (P < 0.05); and there were also bilateral increases at MS2 (OM +5) [by 16% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05)]. These findings suggest that the rCBF increase during dynamic hand contraction does not require neural input from muscle spindles or metabolically sensitive nerve fibers, although the involvement of mechanoreceptors (group III or Ib) cannot be excluded.