We recently reported that collaborative testing (i.e., group test taking) increased student performance on quizzes. It is unknown, however, whether collaborative testing improves student retention of course content. Therefore, this study was designed to test the hypotheses that collaborative-group testing improves student retention of course content. To test this hypothesis, our undergraduate exercise physiology class of 38 students was randomly divided into two groups: group A (n = 19) and group B (n = 19). During exam 1, students from both groups answered questions in the traditional format as individuals. Immediately after completing the exam as individuals, students from group A answered a randomly selected subset of questions from exam 1 in groups of two (1 group had 3 students) to test the effectiveness of collaborative-group testing on test performance and level of student retention. On the next exam (exam 2, 4 wk later), students from both groups answered questions in the traditional format as individuals and responded to the same subset of questions from exam 1. The subset of questions was analyzed to determine the level of retention of the original test material. In addition, immediately after completing the exam as individuals, students from group B answered a randomly selected subset of questions from exam 2 in groups of two (1 group had 3 students). Finally, on the next exam (exam 3, 4 wk later), students from both groups answered questions in the traditional format as individuals and responded to the same subset of questions from exam 2. This protocol followed a randomized crossover design to control for time and order effects. Student retention of course content was reduced when students completed the original examinations individually. In sharp contrast, student retention was improved (P < 0.05) when students completed the original examinations in groups. Results suggest that collaborative testing is an effective strategy to enhance learning and increase student retention of course content.

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We tested the hypothesis that dynamic exercise resets the operating point and attenuates the gain of the arterial baroreflex regulation of heart rate (HR) in rats. Seven adult female spontaneously hypertensive rats (SHR) were chronically instrumented with left carotid arterial catheters. After the rats recovered, arterial baroreflex function was examined by recording reflex changes in HR in response to spontaneous changes in arterial pressure (AP) during a preexercise condition and during steady-state treadmill running at 6 and 18 m/min. Dynamic exercise at 6 and 18 m/min, respectively, reduced the spontaneous range (by 55 and 70%) and spontaneous gain (by 64 and 82%) of the arterial baroreflex control of HR. Dynamic exercise at 6 and 18 m/min, respectively, also increased the pressure at the midpoint of the spontaneous pressure range (by 7 and 12%), the spontaneous minimum HR response (by 35 and 59%), the HR at the midpoint of the spontaneous HR range (by 31 and 52%), and the spontaneous maximum HR response (by 27 and 46%). Sinoaortic denervation eliminated the relationship between AP and HR by reducing the spontaneous gain 95%. These results demonstrate that dynamic exercise shifted the operating point of the arterial baroreflex to a higher pressure and reduced the spontaneous gain in female SHR.

Traditional review sessions are typically focused on instructor-based learning. However, experts in the field of higher education have long recommended teaching modalities that incorporate student-based active-learning strategies. Given this, we developed an educational game in pulmonary physiology for first-year medical students based loosely on the popular television game show Who Wants To Be A Millionaire. The purpose of our game, Who Wants To Be A Physician, was to provide students with an educational tool by which to review material previously presented in class. Our goal in designing this game was to encourage students to be active participants in their own learning process. The Who Wants To Be A Physician game was constructed in the form of a manual consisting of a bank of questions in various areas of pulmonary physiology: basic concepts, pulmonary mechanics, ventilation, pulmonary blood flow, pulmonary gas exchange, gas transport, and control of ventilation. Detailed answers are included in the manual to assist the instructor or player in comprehension of the material. In addition, an evaluation instrument was used to assess the effectiveness of this instructional tool in an academic setting. Specifically, the evaluation instrument addressed five major components, including goals and objectives, participation, content, components and organization, and summary and recommendations. Students responded positively to our game and the concept of active learning. Moreover, we are confident that this educational tool has enhanced the students' learning process and their ability to understand and retain information.

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact ( n = 10) and paraplegic ( n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact ( n = 8) and paraplegic ( n = 8) rats. Paraplegia significantly ( P < 0.05) reduced AV interval (–25%), sinus cycle length (–24%), SNRT (–28%), cSNRT (–53%), WCL (–19%), and the electrical stimulation threshold to induce ventricular arrhythmia (–48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (–28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.