Muscle myonuclear domain, but not oxidative stress, decreases with age in a long-lived seabird with high activity costs.
Ana Gabriela JimenezErin S O'ConnorKyle H ElliottPublished in: The Journal of experimental biology (2019)
In birds, many physiological parameters appear to remain constant with increasing age, showing no deterioration until 'catastrophic' mortality sets in. Given their high whole-organism metabolic rate and the importance of flight in foraging and predator avoidance, flight muscle deterioration and accumulated oxidative stress and tissue deterioration may be an important contributor to physiological senescence in wild birds. As a by-product of aerobic respiration, reactive oxygen species are produced and can cause structural damage within cells. The anti-oxidant system deters oxidative damage to macromolecules. We examined oxidative stress and muscle ultrastructure in thick-billed murres aged 8 to 37 years (N=50) in pectoralis muscle biopsies. When considered in general linear models with body mass, body size and sex, no oxidative stress parameter varied with age. In contrast, there was a decrease in myonuclear domain similar to that seen in human muscle aging. We conclude that for wild birds with very high flight activity levels, muscle ultrastructural changes may be an important contributor to demographic senescence. Such gradual, linear declines in muscle morphology may eventually contribute to 'catastrophic' failure in foraging or predator avoidance abilities, leading to demographic senescence.
Keyphrases
- oxidative stress
- skeletal muscle
- dna damage
- induced apoptosis
- endothelial cells
- reactive oxygen species
- diabetic rats
- magnetic resonance
- type diabetes
- computed tomography
- coronary artery disease
- magnetic resonance imaging
- cardiovascular disease
- endoplasmic reticulum stress
- stress induced
- high intensity
- cell death
- ultrasound guided
- contrast enhanced