Home of Sports Medicine and Exercise Physiology

Potential oxidative energy sources for muscle include sugars, carbohydrates, fats, and particular amino acids. As just noted, muscle tissue in healthy, fed individuals has significant reserves of glycogen. This fuel source can be supplemented by glucose supplied from the blood; liver glycogen, which can be broken down to glucose and delivered to muscle through the circulation; and fats and amino acids, which exist in muscle as well as in other depots around the body. Further, Continue reading.

Our lives depend on conversions of chemical energy to other forms of energy. These conversions, or transductions, of energy are limited by the two laws of thermodynamics, which apply to physical as well as biological energy transductions.Continue Reading

Speed-power activities such as 400-m sprinting, and court and field games such as basketball and football, are energetically driven by the combination of immediate and nonoxidative energy sources. However, the importance of nonoxidative, glycolytic energy sources described in this section extend far beyond a role in sustaining activities lasting a few minutes or less. Continue reading.

During short-term, high-intensity exercise, lactate accumulates as the result of lactic acid production being greater than its removal. At a physiological pH, lactic acid, a strong organic acid, dissociates a proton (H+). It is the H+ rather than the lactate ion that causes pH to decrease. Although lactate accumulation in blood is directly related to H+ accmnulation in blood because the muscle cell membrane exports into blood both lactate anions and protons, in muscle the cause of acidosis is different. All the glycolytic intermediates of glycolysis are weak organic acids and dissociate protons. Further, as pointed out by Cevers (1977), the degradation of ATP results in H+ formation. Thus, lactate accumulation is associated with acidosis for more than one reason, but it is important to recognize that it is unbuffered protons (i.e., H+), not lactate anions, that pose difficulties for the performer.
The H+ accumulation resulting from glycolysis and ATP catabolism as the result of lactic acid production can have several negative effects. Within the muscle, the lower pH may inhibit phosphofructokinase (FFK) and slow glycolysis. In addition, H + may act to displace Ca 2+ from Troponin, thereby interfering with muscle contraction. Further, the low pH may stimulate pain receptors.
Hydrogen ion liberated into the blood and reacting in the brain causes severe side effects, including pain, nausea, and disorientation. Within the blood itself, H+ inhibits the combination of O2 with hemoglobin in the lungs. Some species actually run themselves to the point where O2 delivery is reduced by lactic acid formation and the blocking of oxyhemoglobin fonnation. High circulating H+ levels also thwart the action of hormone-sensitive lipase activity in adipose tissue by stimulating phosphodiesterase and the reesterification of fatty acids to triglycerides. The net result is a limiting of the release of free fatty acids (FFA) into the circulation. Fat oxidation in muscle is directly dependent on circulating FFA levels.
As debilitating as high levels of H + from lactic acid dissociation may be in the muscles and blood, it is uncertain whether the pH decrement actually stops exercise. Because of a muscle’s gross and microanatomy, muscle biopsies actually yield little information on the pH at critical sites of metabolism. Many active sites on enzymes are hydrophobic, and the environment pH has minimal effect. In theory, a lowered cytoplasmic pH should benefit mitochondrial function. Recent studies utilizing nuclear magnetic resonance (NMR) technique to look within muscles noninvasively during exercise and recovery suggest that fatigue is due to CF depletion, as noted, rather than to lactic acid accumulation.
Muscle and blood lactate accumulation during exercise are symptomatic of more than muscle and blood acidosis. Lactate accumulation means that the mechanisms of lactate disposal and clearance have been exceeded. Thus, the overall system is failing to cope with metabolic demands. Further, lactate accumulation is indicative of glycogen depletion, as noted.

Source: McGraw Hill, Brooks, Fahey, Baldwin – Exercise Physiology, Human Bioenergetics and Its applications – Fourth Ed(book)

Not long ago, the story of muscle fatigue was easy for scientists, textbook authors, and students to explain. The explanation went like this: When exercise was too difficult, an athlete went into “O2 debt.” The athlete then built up lactic acid, which caused fatigue. During recovery, the “O2 debt” was repaid, and lactate was reconverted to glycogen. Unfortunately, the lactic acid explanation is not now universally accepted as an explanation of either the “O2 debt” or fatigue. Most of the data concerning lactic acid and fatigue reveal that the relationship is circumstantial at best. Certainly during prolonged exercise, glucose, glycogen, and lactate levels are low. Today, one popular sports drink (CYTOMAXR) even contains organic and inorganic lactate salts as a major component. In addition, injected lactate actually enhances the performance of people with genetic defects in the glycolytic pathway. More likely than the lactate anion, it is the accumulation of the associated hydrogen ion that is detrimental to performance.

Source: McGraw Hill, Brooks, Fahey, Baldwin – Exercise Physiology, Human Bioenergetics and Its applications – Fourth Ed(book)