The purpose of this study was to examine cardiac function during three consecutive bouts of prolonged endurance exercise (PEE) in healthy collegeaged males for the determination of cardiac myocyte damage indicative of cardiac fatigue. Additionally, multiple bouts were performed in order to examine the cardioprotective effect of exercise and ascertain whether preconditioning was induced. In order to avoid the limitations of previous studies, the exercise sessions were completed in a controlled laboratory setting at a predetermined intensity. Likewise the 3rd generation cTnT ELISA was used in order to validate previous positive results. The present study involved ten male, untrained runners (VO2 max 50.7 ± 3.8 ml/kg/min). During the experimental phase, subjects completed three consecutive treadmill runs to exhaustion separated by twenty-four hours. The average total exercise time for the three bouts combined was 204.5 ± 71.49 minutes and the individual exercise bout times were 70.6 ± 31.44, 70.0 ± 25.39, and 63.90 ± 23.95 minutes respectively. The mean peak VO2 achieved during the exercise bouts was 41.9 ± 4.8 ml/kg-1/min-1 (3.4 ± 0.4 L/min-1) which is 81.92 ± 4.4% of estimated VO2 max. Evaluation of cardiac markers and electrocardiographic data revealed no signs of cardiac fatigue. Electrocardiographic examination focused primarily on signs of myocardial damage and ischemia (ST segment, Q wave, and T wave). Data from the present study suggests that prolonged endurance exercise does not induce myocardial damage in healthy, untrained male subjects. The chosen intensity of 81.92 ± 4.4% of estimated VO2 max may have inhibited the completion of a duration sufficient to induce cardiac fatigue. Additionally, it can be hypothesized that repetitive bouts of exercise did not result in a compounding effect as cardiac fatigue was not noted during any of the exercise bouts. While no significance was found in the current study, heat shock protein 70 (Hsp 70) values increased following exercise possibly providing enhanced myocardial protection and future resistance to the damage of ischemia or infarction. / A Thesis submitted to the Department of Nutrition, Food, and Exercise Sciences in partial fulfillment of the requirements for the degree of Master of
Science. / Fall Semester, 2004. / April 7, 2003. / HSP 70, Heat Shock Protein, Consecutive Bouts, Prolonged Endurance Exercise, Myocyte Damage / Includes bibliographical references. / Robert J. Moffatt, Professor Directing Thesis; Laurie Grubbs, Outside Committee Member; Emily Haymes, Committee Member.
| Identifer | oai:union.ndltd.org:fsu.edu/oai:fsu.digital.flvc.org:fsu_181892 |
| Contributors | Bograd, Benjamin A. (authoraut), Moffatt, Robert J. (professor directing thesis), Grubbs, Laurie (outside committee member), Haymes, Emily (committee member), Department of Nutrition, Food, and Exercise Science (degree granting department), Florida State University (degree granting institution) |
| Publisher | Florida State University, Florida State University |
| Source Sets | Florida State University |
| Language | English, English |
| Detected Language | English |
| Type | Text, text |
| Format | 1 online resource, computer, application/pdf |
| Rights | This Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). The copyright in theses and dissertations completed at Florida State University is held by the students who author them. |
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