All things being equal if you extend life by slowing aging, meaning a slowing of the pace of damage accumulation, then you end up with a longer period of disease and frailty in later life simply because life is longer overall. More time is spent at a given level of damage. All things are not equal, however, and the mechanisms and interaction between damage and biological systems are quite complicated: it isn't a straightforward linear path from youthful function to aged dysfunction. So the end result of slowing aging by altering the operation of metabolism could be either less frailty or more frailty, and the outcome could vary widely by both species and method of slowing aging.
Overall it is better to aim for rejuvenation through repair of damage rather than altering metabolism to slow down aging by reducing the pace of damage accumulation. In the case of damage repair there is no ambiguity about outcomes: there will be a restored set of biological systems with less dsyfunction as a result, and the more comprehensive the repair treatments, the better the outcome for the treated individual.
Despite the fact that there are now many, many ways of lengthening life in lower animals such as the nematode species Caenorhabditis elegans, I don't recall much in the way of examination of time spent in frailty, as is carried out in this study:
Aging research has been very successful at identifying signaling pathways and evolutionarily conserved genes that extend lifespan with the assumption that an increase in lifespan will also increase healthspan. However, it is largely unknown whether we are extending the healthy time of life or simply prolonging a period of frailty with increased incidence of age-associated diseases. Here we use Caenorhabditis elegans, one of the premiere systems for lifespan studies, to determine whether lifespan and healthspan are intrinsically correlated.
We conducted multiple cellular and organismal assays on wild type as well as four long-lived mutants until animals reached 80% maximum lifespan (insulin/insulin-like growth factor-1, dietary restriction, protein translation, mitochondrial signaling) in a longitudinal manner to determine the health of the animals as they age. We find that some long-lived mutants performed better than wild type when measured chronologically (number of days). However, all long-lived mutants increased the proportion of time spent in a frail state.
Together, these data suggest that lifespan can no longer be the sole parameter of interest and reveal the importance of evaluating multiple healthspan parameters for future studies on antiaging interventions. We show lifespan and healthspan can be separated and all of the long-lived mutants extend the period of frailty as a consequence. If applied to humans, this would likely lead to unsustainable healthcare costs and demonstrates the importance of examining healthspan as opposed to lifespan for future research.