Abstract

In aged humans, low-intensity exercise increases mitochondrial density, function and oxidative capacity, decreases the prevalence of hybrid fibers, and increases lean muscle mass, but these adaptations have not been studied in aged horses. Effects of age and exercise training on muscle fiber type and size, satellite cell abundance, and mitochondrial volume density (citrate synthase activity; CS), function (cytochrome c oxidase activity; CCO), and integrative (per mg tissue) and intrinsic (per unit CS) oxidative capacities were evaluated in skeletal muscle from aged (n = 9; 22 ± 5 yr) and yearling (n = 8; 9.7 ± 0.7 mo) horses. Muscle was collected from the gluteus medius (GM) and triceps brachii at wk 0, 8, and 12 of exercise training. Data were analyzed using linear models with age, training, muscle, and all interactions as fixed effects. At wk 0, aged horses exhibited a lower percentage of type IIx (p = 0.0006) and greater percentage of hybrid IIa/x fibers (p = 0.002) in the GM, less satellite cells per type II fiber (p = 0.03), lesser integrative and intrinsic (p 0.04) CCO activities, lesser integrative oxidative phosphorylation capacity with complex I (PCI; p = 0.02) and maximal electron transfer system capacity (ECI+II; p = 0.06), and greater intrinsic PCI, ECI+II, and electron transfer system capacity with complex II (ECII; p 0.05) than young horses. The percentage of type IIx fibers increased (p < 0.0001) and of type IIa/x fibers decreased (p = 0.001) in the GM, and the number of satellite cells per type II fiber increased (p = 0.0006) in aged horses following exercise training. Conversely, the percentage of type IIa/x fibers increased (p ≤ 0.01) and of type IIx fibers decreased (p ≤ 0.002) in young horses. Integrative maximal oxidative capacity (p ≤ 0.02), ECI+II (p ≤ 0.07), and ECII (p = 0.0003) increased for both age groups from wk 0 to 12. Following exercise training, aged horses had a greater percentage of IIx (p ≤ 0.002) and lesser percentage of IIa/x fibers (p ≤ 0.07), and more satellite cells per type II fiber (p = 0.08) than young horses, but sustained lesser integrative and intrinsic CCO activities (p 0.04) and greater intrinsic PCI, ECI+II, and ECII (p 0.05). Exercise improved mitochondrial measures in young and aged horses; however, aged horses showed impaired mitochondrial function and differences in adaptation to exercise training.

Highlights

  • The three primary myosin heavy chain isoforms in horses are types I, IIa, and IIx (Rivero et al, 1996b), which are most commonly phenotypically characterized by differences in twitch speed and oxidative capacity (Table 1), and often differ in capillarity, fatigability, and other variables

  • We examined 10 aged and eight young horses to characterize the effects of age and 12 wk exercise training on skeletal muscle fiber type, satellite cell abundance, and mitochondrial density, function, and oxidative capacity

  • Before exercise training began, aged horses exhibited a lower percentage of IIx fibers and higher percentage of hybrid type IIa/x fibers, lower indices of satellite cell abundance, lesser mitochondrial function (CCO activity) and integrative oxidative capacity, and greater intrinsic oxidative capacity than young horses

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Summary

Introduction

The three primary myosin heavy chain isoforms in horses are types I, IIa, and IIx (Rivero et al, 1996b), which are most commonly phenotypically characterized by differences in twitch speed and oxidative capacity (Table 1), and often differ in capillarity, fatigability, and other variables. Muscle fibers span a spectrum of twitch speed, size, and oxidative capacity (Rivero et al, 1996a). Research in humans has demonstrated that exercise offers many benefits to skeletal muscle health, including increases in force production, muscle fiber size, and the percentage of fast, fatigue-resistant type IIa fibers (Williams et al, 2002). Improvements in these parameters are, in part, attributed to an increase in satellite cell number and activity with exercise training (Abreu et al, 2017). In agreement with the increase in size and percentage of fatigue-resistant oxidative fibers, exercise increases skeletal muscle oxidative capacity through a number of mechanisms including increases in mitochondrial biogenesis and fusion (Hood et al, 2019)

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