Exercise-induced reversal of age-related declines of oxidative reactions, mitochondrial yield, and flavins in skeletal muscle of the rat

Abstract

The ability of gastrocnemius muscle homogenates to catalyze the oxidation of succinate, glutamate + malate, pyruvate + malate, palmitoyl-coenzyme A, decanoylcarnitine and palmitoylcarnitine in the presence of ADP decreased by approximately 32% in sedentary male Sprague-Dawley rats between the ages of 9 and 25 months. Following 21 weeks of treadmill training (running), such homogenates from 25-month-old animals catalyzed oxidations 55% more rapidly than those from 25-month-old sedentary rats, and 17% faster than those from 9-month-old sedentary rats. Total and peptide-bound flavin of gastrocnemius muscles also declined between 9 and 25 months of age and were elevated in the 25-month-old endurance trained rats to levels greater than both 9- and 25-month-old sedentary animals. The yield of protein in the mitochondrial fraction from the quadriceps femoris muscle decreased between 9 and 25 months and was restored to the 9-month level by endurance training. The kinetic characteristics of the isolated mitochondria were not influenced by age or exercise. These data indicate that 2-year-old rats retain the capacity to increase skeletal muscle oxidative capacity and mitochondrial population density in response to endurance training.

Alterations in proton leak, oxidative status and uncoupling protein 3 content in skeletal muscle subsarcolemmal and intermyofibrillar mitochondria in old rats

“…On the other hand, intermyofibrillar mitochondria, that provide ATP for muscle contraction, are less prone to oxidative damage. This could explain why it has been found that 2-year-old rats retain the capacity to increase skeletal muscle oxidative capacity and mitochondrial population density in response to endurance training [35]. …”

Training Influence on Age-Dependent Changes in the Gait of Rats

“…In the latter, endurance training improved the oxidative metabolism of skele tal muscles [33], retarded the skeletal muscle atrophy [34], diminished the decrease of the cardiac output [10], and prevented the changes in the neuromuscular synapses [35]. In the central nervous system, physical activ ity counteracted the age-dependent decline in the striatal dopaminergic system [36], in creased the regional blood flow to motorrelated areas of the brain [37,38], and com pensated for the decrease of the muscarinic receptor density in the hippocampus [39], The neural plasticity persisted into old age and was sensitive to exercise training [40,41], The number of synaptic dendrites of pyramidal neurons was positively correlated with the amount of daily wheel running in rats starting to run at the age of 26 months [41], The effects of exercise training to the central nervous system are presumably me diated by both the improved cardiovascular function and by the higher aerobic capacity which maintain the cerebral circulation and the neurons supplying skeletal muscle fibers [30,41], The effectiveness of the training schedule used in the present study was shown by an enhanced myocardial response to (3-adrenergic stimulation [9].…”

Age-related changes in mitochondrial UCP, ANT and COX III gene expression in the breast muscle of quails (Coturnix coturnix japonica)

“…Studies show that mitochondrial proteins are reduced with age (Beyer et al, 1984;Kerner et al, 2001). A lower UCP mRNA expression has been observed in the skeletal muscle of older rats (Barazzoni and Nair, 2001;Iritani et al, 2002).…”