Home of Sports Medicine and Exercise Physiology

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)

During short, intense exercise bouts, blood glucose rises above preexercise levels because the autonomic nervous system stimulates hepatic glycogenolysis and in some cases, blood [glucose] actually rises in male athletes during hard exercise. However, the ability of the liver to maintain a high rate of glucose release over time is limited by the amount of glycogen stored and by the activities of the hepatic glycogenolytic and gluconeogenic enzymes. During prolonged exercise, glucose production may be limited to gluconeogenesis because of hepatic glycogen depletion; thus, glucose production may fall below the level required by working muscle and other essential tissues such as the brain. Also, in prolonged exercise leading to dehydration and hyperthermia, shunting of blood flow away from the liver and kidneys occurs. Thus, the levels of gluconeogenic precursors (lactate, pyruvate, alanine) rise, and hepatic glucose production falls. In this case of falling blood glucose, the exercise becomes subjectively more difficult because of CNS starvation and difficulty in oxidizing fats in muscle due to the absence of anaplerotic substrates

Glycogen deletion in skeletal muscle is associated with fatigue during prolonged sub-maximal exercise to exhaustion. In cycling, when the pedaling rate is moderate (i.e. 60 to 70 revolutions/min), glycogen appears to be depleted uniformly from the different fiber types. However, according to the work of Gollnick and associates (1973), when subjects perform at a given work rate, rapid cycling at 100 revolutions / min (low resistance) will result in selective recruitment and depletion of glycogen from the low-force-producing, slow-twitch fibers. Maintaining the same work rate at a slow, but high-force pedaling frequency (i.e., 50 revolutions / min) results in recruitment of high-force, fast-twitch fibers. Thus, it is possible for an athlete to exercise to exhaustion and fatigue because of glycogen depletion from specific muscle fibers, while glycogen remains in adjacent fibers within the tissue. These glycogen reserves can be mobilized if epinephrine levels rise, stimulating glycogenolysis, lactate production and release, and energy (lactate) exchange via the lactate shuttle.

But remember, it’s not advisable to depend on the glycogen reserves in the body. Therefore, within an hour after the exercise, it’s preferable to have high carbohydrate level meals along with high protein level meals to make up for the loses during exercise! Because working out to build body muscle requires output AND input of energy!

cycling at the gym, high or low rate, to burn glycogen.