Date of Award:


Document Type:


Degree Name:

Doctor of Philosophy (PhD)


Nutrition, Dietetics, and Food Sciences

Committee Chair(s)

Sulaiman K. Matarneh


Sulaiman K. Matarneh


Karin Allen


Charles Carpenter


Daren Cornforth


Kara J. Thornton-Kurth


Among all eating quality characteristics in beef, tenderness is regarded as one of the most important traits. Previous research indicates that consumers are willing to pay a premium for beef guaranteed to be tender. Yet, tenderness is difficult to control and predict as it is influenced by a multitude of factors. Among these factors, meat aging has been shown to be a strong determinant of tenderness. Meat aging describes a process in which muscle tissue is broken down by other proteins within the muscle, resulting in a more tender product after cooking. Two well-recognized proteins that participate in the breakdown of muscle tissue are known as calpains and caspases. The process of breaking down muscle tissue is necessary to achieve the desirable palatability that consumers seek in beef and is an essential phenomenon for converting muscle tissue into edible meat. However, even knowing this, issues with producing meat products that are consistently tender still exist. This suggests that there are other factors that are influencing the aging process that we do not quite understand. Known as the “power house” of a cell, mitochondria are responsible for generating a large portion of the necessary energy that is required for organisms to live. Mitochondria are often ignored for their role in the conversion of muscle to meat due to requiring oxygen to function. However, these organelles can participate in other functions that do not require oxygen, such as sequestering calcium and signaling for cell death in the muscle. Interestingly, these two events are associated with calpain and caspase activities, and hence, could potentially partially explain the variation observed with meat tenderness. Therefore, we hypothesize that mitochondria influence the aging process by limiting available calcium for calpains momentarily but later enhancing tenderness by participating in cell death. To test this hypothesis, we evaluated the effects of calcium uptake by the mitochondria on tenderness, different muscle characteristics and proteins of steaks that vary in tenderness, and the ability of the mitochondria to initiate cell death in meat.

Our results showed that mitochondria could influence meat tenderness by controlling cellular calcium levels, and subsequently, calpain activity. Furthermore, muscles that possess less mitochondria appear to positively impact meat tenderness. Although the results suggest that more mitochondria negatively impact tenderness, our results also indicated that mitochondria could improve tenderness by participating in cell death by activating the caspase system. In conclusion, this project demonstrates that the improvement in meat tenderness may be partly regulated by the presence of mitochondria in the muscle, yet it is important to consider that the observed effects may be species, breed, and muscle dependent.



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