Weights and cardio may tune ageing muscle's mitochondria in different ways

Cellular ageing is a multifactorial process, and one of its signatures is a decline in the function of mitochondria, the structures that supply muscle cells with energy. That decline is bound up with how older muscle performs. Physical exercise has been proposed as an effective and safe intervention to improve the mitochondrial network in muscle cells, but exercise comes in very different flavours: endurance work, resistance training and combinations of the two. Whether these modalities change mitochondria in different ways in older adults is the question this review tackled.

The authors systematically searched five databases (PubMed, Scopus, Web of Science, Cochrane and PEDro) in November 2021 for randomised controlled trials in healthy older people comparing endurance training, resistance training or combined training against other exercise modalities or physical inactivity. Outcomes were mitochondrial quality, density and dynamics, oxidative capacity and antioxidant capacity. From 2,940 records, six studies met the criteria, together covering 164 elderly participants, and each was assessed for quality and risk of bias.

Exercise produced significant positive effects across the board: mitochondrial quality, density, dynamics, oxidative capacity and antioxidant capacity all improved, though to different degrees depending on the type of training. Resistance training was the modality most associated with improvements in mitochondrial density and dynamics, while endurance training was linked to gains in antioxidant capacity. On quality assessment, only one of the six studies was rated good, with the other five rated fair, which tempers how firmly any of these patterns can be stated.

The idea that exercise rejuvenates muscle mitochondria is not new, but this review is a reminder of how thin the randomised evidence is in older adults specifically: six trials and 164 people in total. The suggestion that lifting and endurance work favour different mitochondrial adaptations is intriguing and, if confirmed, would strengthen the case for mixing training styles. The authors are explicit that the overall low quality of the studies means further research is needed before any type-specific conclusions can be drawn.

For anyone thinking about ageing muscle, this is a reason to believe that training reaches all the way down to the cellular machinery that powers movement, and that more than one kind of training does so. It also hints that weights and cardio may each contribute something the other does not at the mitochondrial level. Given how small and mixed in quality the evidence base is, treat the modality-specific patterns as an early sketch rather than a settled map.