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Skeletal muscle benefits of endurance training: mitochondrial adaptations.


Endurance training results in mitochondrial adaptations within skeletal muscle fibers that cause alterations in submaximal muscle metabolism. These changes in muscle metabolism yield a lower blood lactate concentration and greater utilization of fat as a fuel substrate, as well as spare muscle glycogen and reduce the disturbance of energetic homeostasis. The metabolic changes that occur are specific to the muscle fibers recruited during the training. Additionally, the intensity and duration of the training sessions, coupled with the length of the training program have significant influences on the magnitude of the adaptations.


In order for the human body to sustain activity, energy production within the active muscle must equal the energy used. In other words, the resynthesis of adenosine triphosphate (ATP) must equal ATP utilization. Skeletal muscle can resynthesize ATP required for exercise by nonoxidative (anaerobic) and oxidative (aerobic) means.

During prolonged submaximal exercise, ATP is supplied predominately by oxidative metabolism. The organelles within skeletal muscle cells that are responsible for the production of ATP during oxidative metabolism are the mitochondria. Known as the respiratory centers of the cell, the mitochondria require a sufficient amount of oxygen and fuel to resynthesize ATP from adenosine diphosphate (ADP) and phosphate (Pi). The main fuel substrates of oxidative metabolism are carbohydrate and fatty acids. Endurance training results in skeletal muscle adaptations which may modify muscle metabolism and lead to improved aerobic exercise capacity and physical performance (1), (2), (3). Thus, the mitochondria are involved in many of these training adaptations that occur within skeletal muscle.

Adaptations Involving the Mitochondria

A well-established adaptation to endurance training is an increase in the mitochondrial content of trained muscle fibers (1), (3), (4), (5), a process that more recently has been referred to as mitochondrial biogenesis. Studies have shown an increase in both size and number of skeletal muscle mitochondria due to endurance training (5), (6). Although the increased mitochondrial content may occur in all muscle types (6), it is types I (slow-twitch oxidative) and IIA (fast-twitch oxidative) that see the most gain with endurance training. Because these are the predominant muscle types recruited during submaximal work, it appears that the contraction of muscle fibers is a probable stimulus for adaptation (3), (7). Therefore, interval training would appear to be necessary to cause a significant increase in mitochondrial content of type TIB (fast-twitch glycolytic) fibers (3).

The magnitude of the increased mitochondrial content is influenced by the duration and intensity of training sessions. Exercise sessions of longer duration tend to result in greater increases in mitochondrial content (3, 8); however, this relationship is not linear. As the training sessions become longer, the effectiveness of increasing mitochondrial content becomes less. In addition, exercise intensity interacts with the exercise duration. Dudley et al. (8) have shown that greater increases in mitochondrial content occur within oxidative muscle fibers with higher intensity, shorter duration training sessions. Thus, the increases in performance associated with prolonged training sessions may be due in part to adaptations outside those specific to skeletal muscle fibers (i.e. increased mitochondrial content) (3).

Other adaptations due to endurance training are increases in several mitochondrial enzymes. These include the enzymes of the Kreb's cycle (1) and electron transport chain (4), (9), and the enzymes involved in fatty acid oxidation (1), (9). Associated with these responses is an alteration in mitochondrial composition that makes skeletal muscle mitochondria resemble heart mitochondria (1).

Influence on Muscle Metabolism

The mitochondrial changes that occur due to endurance training have important effects on skeletal muscle metabolism during submaximal exercise, all of which help to improve performance (1), (3), (6). These effects include a decrease in blood lactate accumulation (1), a beneficial shift in fuel substrate utilization (1), (3), (6), and a reduction in the disturbance of homeostasis (1), (2). The same relative exercise intensity as measured by percent of maximal oxygen uptake results in a smaller increase in circulating lactate levels in the trained state (1). The increased respiratory capacity of trained muscles cells due to an increased mitochondrial content may in part be responsible for this reduction in lactate concentration. Holloszy and Coyle (1) proposed that the decreased lactate accumulation may help account for 1) greater endurance at the same relative exercise intensity in the trained state and 2) the ability of highly trained individuals to exercise at a higher relative exercise intensity for a designated period of time. Karlsson et al. (10) demonstrated that the lower concentration of blood lactate during submaximal exercise in the trained state is secondary to a lower lactate concentration in the exercising muscles.

A second effect of the training-induced mitochondrial adaptations in skeletal muscle is a shift in substrate utilization. During submaximal exercise, enduraned-trained muscle derives a greater percentage of energy from fat oxidation when compared to untrained muscle (1), (3), and this is accompanied by a sparing of muscle glycogen (1), (6).

Increasing the circulating fatty acid concentration has been shown to slow the utilization of glycogen as a fuel source (11); however, circulating fatty acid levels during submaximal exercise have been shown to be lower in trained versus untrained states (12). Regardless, studies have shown that free fatty acid (FFA) rate of appearance and disappearance is greater in individuals after training (13), (14). Additionally, some research indicates that intramuscular triglyceride stores serve as an important fuel source in trained skeletal muscle (15), (16). Thus, the increased fat oxidation in a trained state is likely due to an enhanced oxidation of both plasma FFA (adipose-derived) and intramuscular triglyceride. The sparing of muscle glycogen associated with this increased utilization of lipids is very important to performance because a depletion of muscle glycogen stores is linked to fatigue during prolonged events such a distance running (17).

A final effect of the increases in muscle mitochondrial content is a reduced disturbance in energetic homeostasis during submaximal exercise. The primary factor regulating mitochondrial respiration when oxygen and fuel substrate availability are not limiting factors, is the concentration of ADP (18) or as noted by others, the [ATP]/[ADP]x[Pi] ratio (cellular energy state) (19). With the beginning of exercise, ATP is hydrolyzed, causing a decline of ATP and phosphocreatine concentrations and an increase in ADP and Pi. These changes lead to an increase in respiration. Once a submaximal steady state is reached, the ADP level is attained and ATP breakdown equals ATP resynthesis. The oxygen consumption and energy requirement of a certain submaximal level are approximately the same for trained and untrained individuals of similar body mass; however, trained skeletal muscles have a higher mitochondrial content. Therefore, the amounts of energy production (ATP) needed from each mitochondrion is less and the required stimulus (ADP) for respiration is less (1), (2), (20).

This has been demonstrated in studies by Constable et al. (21) and Dudley et al. (22). Both studies reported that during the same level of submaximal exercise ATP and phosphocreatine decrease less and ADP and Pi increase less in trained versus untrained muscles. In addition, Starnes (2) states that many of the mitochondria produced through training are located near the contractile proteins of the muscle and therefore, there is less diffusion space between ATP-synthesizing and ATP-utilization sites, lessening the disturbance in homeostasis during submaximal exercise.

Time Frame for Mitochondrial Adaptations

The influences of the intensity and duration of an individual training session on mitochondrial adaptations have been addressed. But the duration of the training program may also influence the magnitude of mitochondrial adaptations. Muscle fiber mitochondrial content increases with the length or duration of a training program (3) but this relationship is not linear; mitochondrial content increases seem to plateau after approximately five weeks of training (3). Worth noting is a study by Green et al. (23) in which they demonstrated reductions in both muscle glycogen loss and lactate concentration during sub-maximal exercise after short term training (5 to 7 days). They concluded that other adaptations early in training may promote some of the same metabolic effects that have been observed following increases in muscle mitochondrial content. A suggested mechanism for these metabolic improvements that precede mitochondrial adaptations is an enhancement of the "parallel activation" of ATP supply and ATP consumption (24).

Detraining results in a gradual but fairly rapid loss of muscle mitochondrial content. Studies have demonstrated that approximately 50 percent of the increased muscle mitochondrial content induced by training can be lost within one week of detraining (3). The time period to return muscle mitochondrial content to pre-detraining levels is longer than the detraining time period.


Mitochondrial adaptations which occur within skeletal muscle fibers in response to endurance training are specific to the muscle fibers recruited during the training. Resulting from these adaptations are several important effects on skeletal muscle metabolism during submaximal exercise that improve performance and reduce fatigue. Therefore, it is important that an endurance training program be designed to maximize these benefits. This can be done by focusing on three principles of training. First, understand that muscle contraction is a probable stimulus for adaptation and when applying the principle of specificity, the bulk of your training should simulate the event in which you plan to participate. This will train the muscle groups required for the event. Second, understand that the intensity and duration of training sessions along with the length of the training program all have influences on the magnitude of these adaptations. Third, it is important to understand the impact of detraining. Detraining that occurs due to sickness or injury will compromise the training adaptations and the time to regain these losses may be greater than the time it took to lose them.


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(13.) Friedlander AL, Casazza GA, Horning MA, Buddinger TF, Brooks GA. Effects of exercise intensity and training on lipid metabolism in young women. Am J Physiol 1998; 275(5 Pt 1): E853-63.

(14.) Friedlander AL, Casazza GA, Horning MA, Usaj A, Brooks GA. Endurance training increases fatty acid turnover, but not fat oxidation, in young men. J Appl Physiol 1999; 86(6): 2097-2105.

(15.) Hurley BF, Nemeth PM, Martin WH, Hagberg, JM, Dalsky GP, Holloszy, JO. Muscle triglyceride utilization during exercise: effect of training. J Appl Physiol 1986; 60:562-7.

(16.) van Loon LJ, Koopman R, Stegen JH, Wagenmakers AJ, Keizer HA, Saris WH. Intramyocellular lipids form an important substrate source during moderate intensity exercise in endurance-trained males in a fasted state. J Physiol 2003; 553(Pt 2): 611-25.

(17.) Costill DL, Gollnick PD, Jansson ED, Saltin B, Stein EM. Glycogen depletion pattern in human muscle fibers during distance running. Acta Physiol Scand 1973; 89(3): 374-83.

(18.) Jacobus WE, Moreadith RW, Vandegaer KM. Mitochondrial respiratory control. Evidence against the regulation of respiration by extramitochondrial phosphorylation potentials or by |ATP|/|ADP| ratios. J Biol Chem 1982; 257: 2397-2402.

(19.) Wilson DF. Energy metabolism in muscle approaching maximal rates of oxygen utilization. Med Sci Sports Exerc 1995; 27: 54-9.

(20.) Burelle Y, Hochachka PW. Endurance training induces muscle-specific changes in mitochondrial function in skinned muscle fibers. J Appl Physiol 2002; 92, 2429-38.

(21.) Constable SH, Favier RJ, McLane JA, Fell RD, Chen M, Holloszy JO. Energy metabolism in contracting rat skeletal muscle: adaptation to exercise training. Am J Physiol 1987; 253: C316-22.

(22.) Dudley GA, Tullson PC, Terjung RL. Influence of mitochondrial content on the sensitivity of respiratory control. J Biol Chem 1987; 262: 9104-14.

(23.) Green HJ, Helyar, R, Ball-Burnett M, Kowalchuk N, Symon S, Farrance B. Metabolic adaptations to training precede changes in muscle mitochondrial capacity. J Appl Physiol 1992; 72: 484-91.

(24.) Zoladz JA, Korzeniewski B, Grassi B. Training-induced acceleration of oxygen uptake kinetics in skeletal muscle: The underlying mechanisms. J Physiol Pharmacol 2006; 57 Suppl 10: 67-84.

Trey Hoyt, PhD

Department of Kinesiology, Mississippi State University,

Mississippi State, MS

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Author:Hoyt, Trey
Publication:AMAA Journal
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Geographic Code:1USA
Date:Sep 22, 2009
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