Age-Related Changes in Skeletal Muscle Oxygen Utilization

The cardiovascular and skeletal muscle systems are intrinsically interconnected, sharing the goal of delivering oxygen to metabolically active tissue. Deficiencies within those systems that affect oxygen delivery to working tissues are a hallmark of advancing age. Oxygen delivery and utilization are reflected as muscle oxygen saturation (SmO(2)) and are assessed using near-infrared resonance spectroscopy (NIRS). SmO(2) has been observed to be reduced by ~38% at rest, ~24% during submaximal exercise, and ~59% during maximal exercise with aging (>65 y). Furthermore, aging prolongs restoration of SmO(2) back to baseline by >50% after intense exercise. Regulatory factors that contribute to reduced SmO(2) with age include blood flow, capillarization, endothelial cells, nitric oxide, and mitochondrial function. These mechanisms are governed by reactive oxygen species (ROS) at the cellular level. However, mishandling of ROS with age ultimately leads to alterations in structure and function of the regulatory factors tasked with maintaining SmO(2). The purpose of this review is to provide an update on the current state of the literature regarding age-related effects in SmO(2). Furthermore, we attempt to bridge the gap between SmO(2) and associated underlying mechanisms affected by aging.