Biochemical Foundations of Human Vital Activity - Volkov, N.I., Nesen, E.N. 2000

Biochemistry of Sports
Biochemical Changes in the Body During Exercise of Various Intensity and Duration
Oxygen Transport to Working Muscles and Its Consumption During Muscular Activity

Oxygen Delivery to Muscles

The rate of oxygen delivery to Tissues is one of the most critical factors influencing Muscle energy supply. This is because the rate of ATP resynthesis in Skeletal Muscle Cell/35.html">Mitochondria—where roughly 90% of all required energy is generated—depends closely on the concentration or partial pressure of oxygen within The Cell. Figure 140 illustrates how the rate of ATP resynthesis, driven by various Energy Sources, varies with intracellular oxygen tension. At a low metabolic rate, such as in a resting muscle, Changes in the rate of O₂ delivery to tissues do not affect the rate of ATP resynthesis (the saturation plateau). However, when the oxygen tension (pO₂) in the cell drops below a certain critical threshold, maintaining the rate of ATP resynthesis becomes possible only through adaptive shifts in intracellular METABOLISM. This inevitably requires an increase in the rate of O₂ delivery to the muscles and its uptake by the mitochondria. The maximum rate of O₂ consumption by skeletal muscle mitochondria can be sustained only down to a specific critical intracellular pO₂ value ranging from 0.5 to 3.5 mmHg. If the metabolic activity During Muscle contraction exceeds the maximum possible enhancement of aerobic ATP resynthesis, the escalating energy demand can be compensated for by anaerobic ATP resynthesis. Nevertheless, the range of anaerobic metabolic compensation is quite narrow, and any further increase in the rate of ATP resynthesis in the working muscle—as well as normal Muscle Function—becomes impossible. Metabolic activity ranges wherein O₂ delivery is insufficient to sustain the necessary level of ATP resynthesis are generally referred to as hypoxic states (i.e., states of oxygen deficiency) of varying severity.

To maintain mitochondrial O₂ tension above the critical threshold that preserves the conditions for adaptive Regulation of cellular metabolism, the O₂ tension at the outer cell membrane must be at least 15—20 mmHg. To maintain this level and ensure normal muscle function, the oxygen tension in arterioles supplying Blood directly to working muscles should be approximately 40 mmHg, while in major Arteries it should reach 80—90 mmHg. In the pulmonary alveoli, where gas exchange occurs between the blood and atmospheric air, O₂ tension is roughly 110 mmHg, and in inspired air, it is 150 mmHg. As seen in Figure 141, which depicts the critical O₂ tension values at various stages of Oxygen transport within the body as a series of descending steps with progressively lower pO₂ levels and O₂ delivery rates to tissues, the "oxygen cascade" ensures a continuous influx of O₂ into working tissues matching their metabolic demand. Maintaining the critical oxygen tension at each designated stage of oxygen transport to tissues is achieved through the combined activity of various physiological systems of the body.

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Fig. 140 Changes in the rate of aerobic and anaerobic ATP resynthesis as a function of intracellular oxygen tension

Fig. 141 The body's "oxygen cascade":

1 — inspired air; 2 — respiratory tract; 3 — Lungs (alveoli); 4 — arterial blood; 5 — mixed venous blood; 6 — at the outer cell membrane; 7 — in skeletal muscle mitochondria

Oxygen contained in inspired air diffuses into the blood through the walls of the pulmonary alveoli and blood capillaries driven by the gradient of O₂ partial pressure between alveolar air and blood. Only a small fraction of the oxygen entering the blood dissolves in the plasma (about 0.3 ml of O₂ per 100 ml of blood); the vast majority binds to Hemoglobin in erythrocytes. Under normal conditions, each gram of blood hemoglobin can bind 1.34 ml of O₂. Since 100 ml of blood in an adult contains approximately 14—16 g of hemoglobin, the oxygen capacity of blood—meaning the total amount of oxygen it binds at full hemoglobin saturation—can reach 21—22 ml of O₂ per 100 ml of blood.

The oxygen-binding capacity of hemoglobin is influenced by blood Temperature and hydrogen ion concentration: the lower the temperature and the higher the pH, the more oxygen hemoglobin can bind. The release of CO₂ from the blood into exhaled air promotes blood alkalinization and hemoglobin oxygen saturation. Each hemoglobin molecule contains four heme groups capable of binding four O₂ molecules, with the binding of the first oxygen molecule increasing hemoglobin's affinity for oxygen and accelerating the uptake of subsequent O₂ molecules.

Oxygen-enriched blood enters the systemic Circulation. At rest, The Heart pumps 5—6 liters of blood per minute, thereby transporting 250—300 milliliters of oxygen per minute from the lungs to the tissues. During exercise, Cardiac Output increases to 30—40 L·min^-1, and The amount of oxygen transported by the blood rises to 5—6 L·min^-1.

The concentration of free oxygen in tissue capillaries is higher than in the intracellular space, prompting the release of oxygen from hemoglobin and its diffusion into the Cells. An elevated concentration of CO₂ and acidic metabolic byproducts, alongside a local increase in blood temperature within tissue capillaries, enhance oxyhemoglobin dissociation and oxygen release.

In muscle cells, oxygen metabolism is mediated by Myoglobin, a protein structurally similar to hemoglobin. Myoglobin transports oxygen to the mitochondria—the sites of oxidative processes—and partially stores it. It possesses a higher chemical affinity for oxygen than hemoglobin (Fig. 142), ensuring a more complete utilization of blood-delivered oxygen by the muscles.

Fig. 142 Hemoglobin and myoglobin dissociation curves

Muscle Oxygen Consumption

Transitioning from rest to intense muscular activity causes a multifold increase in oxygen demand, which cannot be met instantaneously. Time is required for the respiratory and circulatory systems to ramp up their activity and for oxygenated blood to reach the working muscles. As these systems scale up their activity, oxygen consumption in the working muscles gradually rises. If heart rate (HR) exceeds 150 bpm during exercise, the rate of O₂ consumption increases until a true steady state of metabolic processes is established, wherein current O₂ consumption precisely matches the body's physiological demand.

The level of O₂ consumption in a steady state depends on the power output of the exercise performed (Fig. 143). During intense exercise exceeding 200 W in power (HR of 150—180 bpm), a steady state is not achieved, and O₂ consumption may continue to rise until the end of the exercise bout or until the maximal possible level is reached. In the latter scenario, a "false steady state" may occur, where O₂ consumption remains at its maximum level for a short period (6—10 min)—not because the body's oxygen demand is fully met, but because The Cardiovascular system has exhausted its capacity to deliver oxygen to tissues. This system significantly limits O₂ delivery to muscles. However, the primary limiting factor at the muscle fiber level is the ability of mitochondria to utilize oxygen and the capacity of oxidative Enzymes to use it within the working muscles. The maximal rate of O₂ consumption cannot be sustained indefinitely; during prolonged exercise, it declines due to fatigue.

Fig. 143 Oxygen consumption during exercises of varying intensity and duration

Fig. 144 MAIN MECHANISMS OF energy production (a), oxygen intake and oxygen deficit (b), and blood lactate accumulation (c) during short-term maximal-intensity exercise: 1 — O₂ deficit; 2 — O₂ consumption (intake); 3 — O₂ demand; 4 — O₂ consumption during exercise; 5 — O₂ consumption during recovery

The amount of oxygen required by the body to fully meet its energy demands through aerobic processes is termed the oxygen demand of the exercise. During intense exercise, actual oxygen consumption—the oxygen intake—constitutes only a fraction of this oxygen demand. The difference between the exercise oxygen demand and the actual oxygen consumed represents the body's oxygen deficit. Under conditions of oxygen deficit, anaerobic pathways of ATP resynthesis are activated, leading to the accumulation of incompletely oxidized anaerobic breakdown products in the body (Fig. 144).

Fig. 145 Main mechanisms of energy production (a), oxygen intake and oxygen deficit (b), and blood lactate accumulation (c) during prolonged exercise. Designations are the same as in Fig. 144

During steady-state work, a portion of anaerobic metabolites may be oxidized due to enhanced aerobic reactions during exercise, while another portion is removed post-exercise. When a steady state is not established, or during a "false" steady state, the amount of under-oxidized products continuously increases and they are eliminated only during the recovery period (Fig. 145). Restoring energy sources and oxidizing under-oxidized products requires an additional amount of oxygen; therefore, for some time after exercise cessation, oxygen consumption remains elevated compared to the resting level. This surplus oxygen consumption during the recovery period is termed "oxygen debt". Oxygen debt always exceeds the oxygen deficit, and the greater the intensity and duration of the work, the more significant this difference becomes (Fig. 146).

Fig. 146 Oxygen intake, oxygen deficit, and oxygen debt during work of varying intensity — light (a), heavy (b), exhausting (c); fast (1) and slow (2) Components of the O₂ debt

During the recovery period following muscular work, when the body contains a sufficient amount of Biological Oxidation substrates and oxygen supply to cellular mitochondria is not limited, the rate of oxygen consumption depends on the amount of free ATP that drives Respiratory Control in the mitochondria. The substrates for oxidative energy transformations are the anaerobic metabolites accumulated during work: lactic acid, succinic acid, a-glycerophosphate, glucose, and, at later stages of recovery, Fatty acids. The source of ADP consists of energy-consuming processes, primarily the resynthesis of CrP from creatine, the restoration of Glycogen and glucose stores, the repair of Cell Membrane Structures disrupted during exercise, and the functioning of the respiratory and cardiovascular systems, whose activity remains elevated for some time after work.

Part of the oxygen consumed during the rest period is used to replenish Myoglobin and hemoglobin reserves. During fatigue-inducing work, the efficiency of oxygen utilization decreases due to the partial uncoupling of energy substrate oxidation and ATP production. This uncoupling may persist even after exercise, leading to increased oxygen consumption compared to the resting level.

Oxygen debt during work of varying intensity can be caused by different factors. For instance, in short-term high-intensity exercise, the depletion of CrP and ATP reserves plays a decisive role in forming the oxygen debt, whereas in prolonged work, it is driven by glycogen depletion and shifts in acid-base balance. Following work performed at a steady state, the oxygen debt is half-repaid within just 30 s and fully repaid within 3—5 min. After intense exercise, the "repayment" of the oxygen debt occurs in two phases: initially a rapid return, followed by a slow, protracted return to the pre-work oxygen consumption level (see Fig. 146).

The fast component of the O₂ debt (alactacid component) comprises the amount of oxygen required for the resynthesis of ATP and CrP. It characterizes THE CONTRIBUTION OF the creatine phosphate mechanism to the Energy supply of exercise. The slow component of the O₂ debt (lactacid component) includes the amount of oxygen needed to oxidize the lactic acid produced during exercise. Its magnitude reflects the involvement of the glycolytic mechanism in the energy supply of muscular work, and during prolonged exercise, also other processes whose share is difficult to evaluate. The slow component of the O₂ debt is half-replenished in 15—25 min and fully eliminated within 1.5—2 h.

Determining The values of oxygen intake during exercise, as well as oxygen demand and oxygen debt, makes it possible to assess the relative power of the performed exercise. For this purpose, Energy Expenditure is calculated in units of maximum metabolic rate (MMR). This value represents The ratio of the oxygen demand rate (RO₂ = (EVO₂ + O₂D) / T_ex) to individual VO_2max:

MMR = (EVO₂ + O₂D) / VO_2max⋅ T_ex.