Structural and functional changes occur in skeletal muscle with age and result in a loss of muscle force. Contributors to the loss of muscle force with age include decrease in muscle mass (atrophy), structural changes in the extracellular matrix and increase in fat and fibrotic tissue. The extracellular matrix as well as fibrotic tissue contain a relatively large fraction of macromolecules (primarily collagen). Magnetic Resonance Imaging (MRI) provides a way to map free protons in tissue while protons bound to macromolecules (e.g. to myelin, collagen) are not visible on routine MRI due to their ultra-short T2 values. Magnetization transfer contrast (MTC) enables an indirect evaluation of the macromolecular content by selective saturation of bound protons. It is hypothesized that collagen is the primary macromolecular pool responsible for the MTC effect in skeletal muscle. Collagen content in muscle increases with aging and thus, a non-invasive marker of collagen in muscle tissue has the potential to identify aging differences. The main focus of this thesis is to extract MTsat (a semi-quantitative index of MTC) and T1 to explore age related changes in muscle structure/composition of the lower calf muscles. A cohort of 10 healthy young subjects (5M/5F, 24.5±3 years) and eight healthy senior subjects (7M/1F, 65±8 years) were imaged in a 3T scanner (Siemens Prisma). T1 derived from the fat saturated sequence was significantly different from T1 derived from the other three sequences (no fat suppression, water excitation fast and normal). The decreased T1 values from the fat saturated sequence is attributed to the magnetization transfer effects of the off-resonance pulse at 440 Hz offset from the Larmor frequency. The increase in T1 values with age is hypothesized to reflect inflammatory changes in skeletal muscle and could potentially be an imaging biomarker. In conclusion, fat suppressed T1 and MTsat values were significantly different with age in skeletal muscle though the direction of the change in MTsat cannot be explained due to a lack of knowledge about the macromolecular pool responsible for the MTC effect in skeletal muscle.