A new study at The University of Texas Health Science Centre (UTHSC), San Antonio, may provide some answers on muscle loss with ageing.
The study, conducted in mice with accelerated muscle loss, found less protection from antioxidants and more damage from oxidative stress results in impairment to cells' energy centres (powerhouses) called mitochondria, which slowly leads to death of muscle cells.
A team directed by Holly Van Remmen, found that without a certain antioxidant enzyme to balance the formation of harmful reactive oxygen species (ROS), cellular energy centers called mitochondria fail to work properly. The mitochondria even add to the spate of ROS molecules and release factors leading to cell death.
"The impaired function of mitochondria also has a detrimental effect on the way motor neurons 'talk' to the muscle to achieve muscle contraction. This interaction occurs at a specialized synapse where the nerve and muscle come in close contact," Dr. Van Remmen said.
This key structure is called the neuromuscular junction, she said.
Youngmok C. Jang, a leading author in the study, probed mice genetically engineered to lack an antioxidant enzyme called copper-zinc superoxide dismutase.
He compared mitochondria from these mice and normal mice and found reduced function of the energy centres in the enzyme-deficient mice.
This contributed to more cell death and muscle atrophy in the rodents. "As a result, their muscles were a lot smaller and weaker," Van Remmen said.
If a muscle-preserving therapy is one day developed, future generations of young men will be able to keep their muscle shirts a bit longer.