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Author ORCID Identifier

https://orcid.org/0000-0001-7293-4214

Document Type

Open Access Dissertation

Degree Name

Doctor of Philosophy (PhD)

Degree Program

Kinesiology

Year Degree Awarded

2019

Month Degree Awarded

September

First Advisor

Jane Kent

Second Advisor

Mark Miller

Third Advisor

Edward Debold

Fourth Advisor

Alexander Gerson

Subject Categories

Biochemistry | Exercise Physiology | Exercise Science

Abstract

Skeletal muscle oxidative capacity plays a critical role in human health and disease. Although current models of oxidative phosphorylation sufficiently describe skeletal muscle energetics during moderate-intensity contractions, much is still unknown about the mechanisms that control and limit oxidative phosphorylation during high-intensity contractions. In particular, the oxygen cost of force generation is augmented during exercise at workloads above the lactate threshold. Presently, it is unclear whether this augmentation in muscle oxygen consumption is driven by increased rates of oxidative ATP synthesis (ATPOX) or by decreases in the efficiency of ATPOX due to mitochondrial uncoupling. To address this gap, 31P-MRS was used in two separate studies to measure rates of ATPOX at the end of: 1) repeated bouts of supramaximal knee extensions, and 2) each stage of an isotonic stepwise knee extension protocol. In both studies, high-intensity contractions impaired the maximal capacity for ATPOX and reduced the sensitivity of ATPOX to changes in ADP and cytosolic phosphorylation potential. However, high-intensity contractions did not cause rates of ATPOX to increase relative to workload, suggesting that the increased oxygen cost of exercise above the lactate threshold is due to changes in mitochondrial coupling control (i.e., P/O ratio).

DOI

https://doi.org/10.7275/3r7y-r561

Creative Commons License

Creative Commons Attribution-Share Alike 4.0 License
This work is licensed under a Creative Commons Attribution-Share Alike 4.0 License.

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