Author(s): MORGAN, P., PRATT, J., SMEUNINX, B., QUINLAN, J., NIELSEN, J., BREEN, L., Institution: MANCHESTER METROPOLITAN UNIVERSITY, Country: UNITED KINGDOM, Abstract-ID: 1059

INTRODUCTION:
Excessive intramyocellular lipid droplet (LD) storage and mitochondrial dysfunction may represent hallmarks of both ageing and obesity. Heterogeneity in lipid droplet morphology and positioning at the subcellular and single fibre level obscures whether obesity worsens age related declines in muscle ‘quality’. The exercise-induced motility of LDs and the associated structural and metabolic alterations in LD composition, size, and interactions with mitochondria and other organelles likely also underpin their capacity for substrate oxidation and association with impairments in metabolic health. Therefore, this study examined age- and obesity-related differences in intramyocellular LD organisation and LD-mitochondrial interactions at the single-fibre level at rest and following a bout of physical activity.
METHODS:
To assess age- and obesity-related differences in LD organisation and LD–mitochondrial interactions, quantitative transmission electron microscopy was used to analyse intramuscular LDs at the single-fibre level in muscle biopsy samples from 15 young non-obese (23 ± 4 years, Body mass index [BMI]; 24 ± 3 kg·m-2, Body fat: 13 ± 5%), 10 older non-obese (69 ± 5 years, BMI; 25 ± 2 kg·m-2, Body fat: 20 ± 3%) and 10 older obese (73 ± 5 years, BMI; 31 ± 3 kg·m-2, Body fat: 33 ± 3%). LD morphology, subcellular distribution, and LD-mitochondrial contacts were assessed at rest and immediately following the completion of a 45-min bout of brisk walking. Z-disc width was used to indicate muscle fiber type.
RESULTS:
Ageing was associated with greater total LD volume density, driven primarily by increased intermyofibrillar lipid accumulation. This effect was confined to type II fibres. In contrast, older obese individuals exhibited a compartment-specific increase in subsarcolemmal LD volume density, likely reflecting larger LD size rather than increased LD number, and potentially also showing a bias towards type II fibres. Brisk walking did not alter LD volume density in any subcellular compartment but did reduce IMF LD size across all groups. Absolute LD-mitochondrial contact decreased post-brisk walking but was maintained relative to LD size.
CONCLUSION:
In conclusion, ageing and obesity impose distinct yet converging disruptions to intramyocellular lipid architecture. Ageing seems to drive intermyofibrillar lipid accumulation, whereas obesity preferentially expands subsarcolemmal stores. These compartment specific alterations show minimal responsiveness to acute moderate intensity walking. Together, the findings identify subcellular lipid distribution and LD–mitochondrial coupling as mechanistic features that may underpin the accelerated age related decline in skeletal muscle metabolic health in older adults with obesity.