Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

Abstract

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

Exercise training increases glucose transporter protein GLUT‐4 in skeletal muscle of obese Zucker (fa/fa) rats

“…One of the primary biochemical adaptations to endurance exercise training is an increase in mitochondrial protein and oxidative capacity of the muscle [23]. Our results now show that adaptation to chronic endurance training also results in the synthesis of a specific protein which facilitates glucose transport into the muscle cell.…”

Impact of cardiac rehabilitation and exercise training programs in coronary heart disease

“…46 Increased mitochondrial content in muscle promotes fat oxidation preferentially over carbohydrate oxidation. 66 This adaptation decreases lactate as a byproduct and permits a longer duration of ET at increased aerobic capacity. 67 In addition, ET favorably impacts cardiac remodeling and results in improvements in cardiac performance.…”

Pulmonary oxygen uptake and muscle deoxygenation kinetics during recovery in trained and untrained male adolescents

“…In the adult population, training has been shown to result in both faster muscle phosphocreatine (Forbes et al 2008;Takahashi et al 1995;Yoshida 2002) and pulmonary oxygen uptake (Fukuoka et al 2002;Fukuoka et al 2006) kinetics during recovery from moderate-intensity exercise, suggestive of enhanced oxidative capacity of the exercising muscle (Barker et al 2008;Paganini et al 1997;Rossiter et al 2002). The favourable adaptations to oxygen delivery, mitochondrial density and oxidative enzyme activity and thus aerobic fitness that appropriate training permits (Holloszy and Coyle 1984;Murias et al 2010;Phillips et al 1995;Russell et al 2002) are likely to explain the faster recovery kinetics relative to the untrained state. However, to our knowledge no previous study has examined the effect of training status on pulmonary oxygen uptake kinetics during recovery from exercise in adolescents.…”