Aerobic exercise training is an effective tool to protect against age-related metabolic disorders, including mitochondrial dysfunction. The optimal exercise intensity for promoting beneficial mitochondrial adaptations, particularly in sedentary middle-aged adults, is currently unknown. This study aims to compare the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on skeletal muscle mitochondrial adaptations in sedentary middle-aged adults.
Thirty-two sedentary, middle-aged (45 to 65 years; 3 male, 29 female) adults performed one of two 12-week, work-matched aerobic exercise interventions (randomised allocation): HIIT (4 to 7 × 4 min, ~90% of peak power) or MICT (36 to 48 min, ~60% peak power). Resting muscle samples were collected before and after the intervention to measure mitochondrial respiratory function (using an Oxygraph-2k high-resolution respirometer) and citrate synthase activity. Markers of mitochondrial biogenesis and complexes were assessed by Western Blots.
Both MICT and HIIT significantly increased peak oxygen uptake (V̇O2peak) and maximum power (Ẇmax), with a greater effect reported in HIIT. Citrate synthase activity, protein content of mitochondrial complexes, and mitochondrial respiratory function improved with training in both groups, with no difference between groups. Conversely, mitochondrial-specific respiration decreased with training in both groups, with no difference between groups. Following training, Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) protein content was unchanged, while Optic atrophy 1 (OPAI) increased in both groups.
Both MICT and HIIT significantly enhanced V̇O2peak in middle-aged adults, and this response was augmented with HIIT. However, the between-group difference had no bearing on mitochondrial adaptations in either group. These findings suggest limited effects of exercise training intensity on mitochondrial adaptations and aerobic fitness in this demographic, however further investigation into their distinct impacts on mitochondrial function is warranted.