Muscle protein degradation in elderly individuals

With aging, the decline in muscle strength exceeds the decline in muscle mass. Specific strength, defined as strength normalized to the cross-sectional area of a given muscle or muscle group, declines accordingly. However, underlying mechanisms are not well elucidated.


Place: Norges idrettshøgskole

Formal title

The role of muscle protein breakdown in the regulation of muscle mass and muscle quality in elderly


In contrast, specific strength is increased following strength training, even in frail elderly individuals. The relative contribution from factors such as neural activation level and muscle quality is not fully characterized. Interestingly, it has been speculated that inefficient protein quality control may contribute to the reduction in muscle quality observed with aging. Autophagy, a cellular process responsible for the degradation of dysfunctional proteins, mitochondria, and lipid droplets, has been shown to be attenuated in old rodents. Interestingly, training seems to have the opposite effect. Whether or not autophagy is affected by aging and training in humans, has received little attention so far.

The aim of the project is to investigate whether autophagy is affected by aging and frailty in humans. Moreover, the relationship between autophagy and muscle quality will be examined.

We will also investigate how specific strength and autophagy is affected by heavy-load strength training in frail elderly.


A cross-sectional study will be conducted to compare autophagic markers in young, healthy elderly, pre-frail and frail elderly individuals. In addition, other proteins related to cellular stress will be examined. A strength training intervention will be conducted to investigate the effect of heavy-load strength training on a broad number of factors related to specific strength in frail elderly. Endpoints are activation level, muscle density, intermuscular adipose tissue, intramyocellular lipids and single fiber specific tension. Additionally, an acute experiment will be conducted before and after the intervention to assess autophagic regulation acutely and following long-term exercise.


In contrast to several previous studies, our findings suggest that even in pre-frail and frail elderly, most of the variation in muscle strength is explained by differences in muscle cross-sectional area. Moreover, the training-induced increase in muscle strength was primarily due to increased muscle quantity, not quality in our study. Nevertheless, we found indications of impaired autophagy and higher cellular stress in elderly and frail individuals compared to young and healthy individuals. Furthermore, specific strength was lowest in the elderly and frail, and within the elderly there was a correlation between markers of autophagy and specific strength, supporting a possible relation between impaired protein quality control and reduced muscle quality. Altogether, impaired autophagy may play a role in the age-associated decline in specific strength, but muscle mass seems to be the most important determinant of muscle strength and function even in old and frail individuals. It is too early to conclude that strength training does not affect protein quality control systems in this population, and it is possible that a higher frequency or longer duration of training is required to elicit greater changes.