Research: Understanding the cell’s energy power plant.
The mitochondrion (plural: mitochondria) is a specialized organelle found in most eukaryotic cells (cells that contain a nucleus). It is often referred to as a cell’s energy power plant. Essential for human existence, mitochondria are involved in numerous cell processes that rely on energy sustenance—for example, cell growth, cell messaging, aging and replication (Schardt 2008).
For this same reason, mitochondria are known to be associated with several diseases of energy-demanding organs and tissues of the body, including the heart, brain and skeletal muscle (Hood et al. 2006). For instance, heart disease, dementia and most muscle weakness disorders are all associated with mitochondria maladies.
Most human cells contain several hundred to a couple of thousand mitochondria (Schardt 2008). They have incredible bioenergetic capacity. Tonkonogi and Sahlin (2002) state that during cardiorespiratory exercise the energy output (i.e., work output) of these microscopic organelles can be 400 times higher than it is at rest. As a result, mitochondria oxygen consumption and utilization (to help accomplish the work) can be 100 times higher than they are at rest. This research column presents a brief review of mitochondria’s vital energy function capabilities in the human body.
German cell and structure researcher Richard Altmann discovered mitochondria in the 19th century. Carl Benda, a German physician, later gave them the name mitochondria. Altman correctly hypothesized from his research observations that mitochondria (which he called bioblasts) had metabolic and genetic self-sufficiency characteristics (meaning they adapt independently to various stimuli).
Lynn Margulis (previously Sagan) (Sagan 1967), an American biologist from the department of geosciences at the University of Massachusetts, Amherst, is recognized for her theoretical explanation of mitochondria development with the endosymbiotic (from the Greek root endo, meaning “inside,” and the word symbiosis, meaning “cohabiting”) theory. According to this theory, mitochondria may have originally been the remnants of early bacteria that were engulfed by ancient eukaryotic cells about 1 billion years ago. Over time, mitochondria gradually evolved to become the energy-yielding organelles now present in eukaryotic cells. Notably, in the early 1960s scientists discovered that mitochondria had their own DNA, the genetic instructions used in the development and functioning of all known living organisms.
As seen in Figure 1, a mitochondrion has two cell membranes. The outer membrane has distinct channels, which allow specific molecules to enter and exist. The inner membrane folds uniquely through the oval-shaped organelle. The inwardly directed folds of the inner membrane go toward the mitochondrion’s center (known as the matrix), and each of these folds is referred to as a crista (plural: cristae) membrane. The cristae membranes house the protein sectors that shuttle electrons, which arrive from the tricarboxylic acid cycle (TCA, also called the Krebs cycle) and contribute to the energy-yielding process. These electron shuttles are composed of distinct energy-transferring proteins, collectively referred to as the electron transport chain.
Mitochondria have their own independent DNA, thus allowing them to adapt by increasing in size and number. Thigh muscle cells have been shown to replicate 50% more mitochondria during 12 weeks of consistent, moderately intense aerobic exercise (Schardt 2008).
Mitochondria are often (and accurately) referred to as the “food-burning furnaces” in a person’s body cells (Schardt 2008). Within the mitochondria, as the chemical bonds in fat (in the form of triglycerides), carbohydrate (in the form of glucose and glycogen) and protein (in the form of amino acids) molecules are broken up though metabolism, they begin to lose electrons, a process called oxidation.
During the oxidation process, molecules release energy and heat. So the term fat burning, which is commonly used in the fitness and weight loss industry, is an appropriate analogy of what is actually happening to fat in a cell’s mitochondria. Since energy is neither created nor destroyed (the first law of thermodynamics), biologists like to suggest that within the mitochondria furnaces, the bonds in foodstuffs (i.e., triglycerides, glucose, amino acids) are broken apart, with the energy being released and transferred into the synthesis of adenosine triphosphate (ATP). ATP is the form of energy that is then delivered to other areas of the cell (such as muscle proteins) to carry out cell processes that promote growth and sustain life (Schardt 2008).
Mitochondria, in effect, coordinate the chemical energy released from the oxidation of foodstuffs in a section of their inner membrane (the electron transport chain) through a complex system of metabolic steps that result in the synthesis of ATP. The ATP-synthesizing process depends on a steady supply of oxygen, which is why this process is aptly nicknamed “aerobic metabolism” or “aerobic respiration.”
Perhaps one of the most important educational messages that exercise professionals can share with clients is that with regular endurance training, mitochondria adapt by metabolically using more fat and less carbohydrate for fuel during exercise (Hood et al. 2006). A coincident secondary effect is that there is a reduction in the amount of metabolic acidosis produced in the muscles, because they now rely less on carbohydrate for fuel (Hood et al. 2006). Thus the exercising body is able to do more work, experience less fatigue and burn more calories with each work bout.
This increase in fat-burning capacity from endurance exercise is referred to as mitochondrial biogenesis (Hood et al. 2006). In fact, Menshikova et al. (2007) showed that doing moderate-intensity physical activity (60%–75% maximal heart rate) four to six times a week (progressing from 30 to 40 minutes per session on a treadmill and cycle ergometer) for 16 weeks resulted in significant mitochondrial biogenesis adaptations in sedentary, obese men and women (BMI > 31 kg/m2; average age = 41 years), thus greatly enhancing their fat-burning capabilities. The obese subjects in this study were also placed on a 25% calorie reduction diet to help them achieve a 7% loss in body weight.
Menshikova and colleagues point out an intriguing aspect of the physiology of skeletal muscle: it has considerable metabolic plasticity, which means that with consistent aerobic exercise there is a dramatic increase in blood flow, oxygen consumption and rate of substrate utilization (cell use of foodstuffs for fuel) within the mitochondria of muscle.
The authors affirm that the opposite is also apparent: with sedentary behavior, skeletal muscle shows a drop in oxidative capacity and an increase in fat deposition—characteristics of insulin resistance and weight gain. Although most research demonstrating these prominent mitochondrial adaptations has been completed using aerobic exercise, Melov et al. (2007) state that resistance exercise may also show mitochondria-bolstering capabilities in older male and female populations.
Mitochondria are remarkably adaptable organelles within skeletal muscle. They can impressively boost a muscle’s capability to burn fat; improve insulin sensitivity (and thus help to manage or prevent prediabetes or diabetes); minimize fatigue; and enhance their own capacity to synthesize fuel for physical activity and exercise (Menshikova et al. 2007). The great news is that research shows these physiological changes occur in people of all ages. At any age, getting active is the stimulation that the marvelous mitochondria need to provide their health-giving benefits. Let’s get everyone moving.
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Melov, S., et al. 2007. Resistance exercise reverses aging in human skeletal muscle. PLoS ONE, 2 (5): e465. doi:10.1371/journal.pone.0000465.
Menshikova, E.V., et al. 2007. Characteristics of skeletal muscle mitochondrial biogenesis induced by moderate-intensity exercise and weight loss in obesity. Journal of Applied Physiology, 103, 21–27.
Sagan, L. 1967. On the origin of mitosing cells. Journal of Theoretical Biology, 14 (3), 225–74.
Schardt. D. 2008. Manipulating mitochondria. Nutrition Action Healthletter, 35 (10), 8–10.
Tonkonogi, M., & Sahlin, K. 2002. Physical exercise and mitochondrial function in human skeletal muscle. Exercise and Sport Sciences Reviews,
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