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You searched for +publisher:"Temple University" +contributor:("Libonati, Joseph R."). Showing records 1 – 2 of 2 total matches.

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Temple University

1. Witmer, Chad A. Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve.

Degree: PhD, 2011, Temple University

Kinesiology

The purpose of this study was to investigate the effects of acute moderate hypoxia (14.5% inspired oxygen fraction) on the magnitude of fatigue development during the different phases (work, recovery, and both) of a repeated-sprint test (10 x 6-s sprints interspersed with 30-s recovery) in healthy, trained males. This study also sought to investigate the relationship between anaerobic power reserve and fatigue during the aforementioned repeated-sprint test. Fourteen exercise-trained males completed four trials of the repeated-sprint test under each of the following conditions: (a) normoxia (20.93% inspired oxygen fraction), (b) acute hypoxia during the work intervals only, (c) acute hypoxia during the recovery intervals only, and (d) acute hypoxia during both the work and recovery intervals. The order of the experimental conditions was systematically balanced. Fatigue scores were not different between experimental conditions, despite the fact that arterial oxygen saturation values from the acute hypoxia during recovery condition and the acute hypoxia during both work and recovery condition differed significantly from the normoxia and acute hypoxia during work intervals only conditions (p < .001). There was no relationship between anaerobic power reserve and fatigue in any experimental condition. The results of the present study indicate that although the participants experienced different levels of hypoxia during the experimental trials, the degree of hypoxia was insufficient to alter mechanical performance during a repeated-sprint test. The lack of an effect on mechanical performance does not appear to be influenced by an individual's anaerobic power reserve. It may be inferred that the degree of hypoxia employed was neither severe enough as to impair levels of muscle oxygenation beyond what was experienced in normoxia, nor as to induce further fatigue related to central mechanisms.

Temple University – Theses

Advisors/Committee Members: Kendrick, Zebulon V., Libonati, Joseph R., Brown, Michael D., Davis, Shala E., Santiago, Mayra C..

Subjects/Keywords: Kinesiology; Physiology; fatigue; hypoxia; repeated-sprint

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APA (6th Edition):

Witmer, C. A. (2011). Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,135073

Chicago Manual of Style (16th Edition):

Witmer, Chad A. “Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve.” 2011. Doctoral Dissertation, Temple University. Accessed August 14, 2020. http://digital.library.temple.edu/u?/p245801coll10,135073.

MLA Handbook (7th Edition):

Witmer, Chad A. “Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve.” 2011. Web. 14 Aug 2020.

Vancouver:

Witmer CA. Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Aug 14]. Available from: http://digital.library.temple.edu/u?/p245801coll10,135073.

Council of Science Editors:

Witmer CA. Effects of acute exposure to moderate hypoxia during different phases of repeated-sprint cycling on fatigue and anaerobic power reserve. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,135073


Temple University

2. Barr, Larry A. The Role of Calcium in the Regulation of Pathological Hypertrophy.

Degree: PhD, 2014, Temple University

Physiology

Pathological hypertrophy leads to cardiac dysfunction and heart failure. It is not clearly defined how this process occurs in the cardiomyocyte, or how the pathology can be effectively treated. There are numerous processes that lead to pathological hypertrophy. We developed two models to study pathological hypertrophy and the role that Ca2+ plays. In one model, we administered clinical doses of the leukemia therapeutic drug imatinib to neonatal ventricular cardiomyocytes. This drug has recently been found to be cardiotoxic, and we set out to understand if Ca2+ is involved. In the second model, we developed mice with overexpression of the Ca2+ entrance channel, the L-type calcium channel (LTCC), which leads to pathological hypertrophy over time. We instituted a chronic exercise regimen on these mice to learn if physiological hypertrophy can ameliorate detrimental aspects of pathological hypertrophy. After cardiomyocytes were treated with imatinib, they expressed enhanced Ca2+ activity. Levels of atrial natriuretic peptide (ANP) were up, signifying pathological hypertrophy. We determined that Ca2+ was activating Calcineurin, leading to translocation of nuclear factor of activated T-cells (NFAT) into the nucleus, resulting in hypertrophy. This activity was blocked by Ca2+ and Calcineurin inhibitors. We concluded that imatinib causes Ca2+ induced pathological hypertrophy. When mice with LTCC overexpression were exercised, they exhibited enhanced cardiac function. They also had thicker septal walls and increased chamber diameter, hallmarks of physiological hypertrophy. Heart weight to body weight ratio was significantly higher after exercise. When isolated hearts were administered ischemia/reperfusion injury, the exercised hearts showed a significant improvement in recovery compared to sedentary LTCC overexpressed hearts. Calcium activity was enhanced at the cardiomyocyte level in both mouse lines of exercised mice. In conclusion, hearts with a pathological hypertrophic phenotype can enhance function and achieve cardioprotection through chronic exercise.

Temple University – Theses

Advisors/Committee Members: Houser, Steven R., Rizzo, Victor, Chen, Xiongwen, Libonati, Joseph R., Rabinowitz, Joseph;.

Subjects/Keywords: Physiology; Molecular biology; Pharmacology;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Barr, L. A. (2014). The Role of Calcium in the Regulation of Pathological Hypertrophy. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,254617

Chicago Manual of Style (16th Edition):

Barr, Larry A. “The Role of Calcium in the Regulation of Pathological Hypertrophy.” 2014. Doctoral Dissertation, Temple University. Accessed August 14, 2020. http://digital.library.temple.edu/u?/p245801coll10,254617.

MLA Handbook (7th Edition):

Barr, Larry A. “The Role of Calcium in the Regulation of Pathological Hypertrophy.” 2014. Web. 14 Aug 2020.

Vancouver:

Barr LA. The Role of Calcium in the Regulation of Pathological Hypertrophy. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Aug 14]. Available from: http://digital.library.temple.edu/u?/p245801coll10,254617.

Council of Science Editors:

Barr LA. The Role of Calcium in the Regulation of Pathological Hypertrophy. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,254617

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