Limitations to VO2max
Introduction
Maximum oxygen uptake denoted as VO2 is defined as the highest rate of oxygen uptake by muscles at the highest intensity of exercise. It is one of the major factors used to denote an individual’s cardio-respiratory fitness in exercise physiology(Bassett & Howley, 2000),
Several factors influence a working muscle, and this affects their endurance capability, these factors include but are not, limited to the type of muscle fibres involved, duration and intensity of the exercise, the inherent characteristic of the muscle fibres metabolism involved and the cardiovascular support(Terjung et al., 1985)
Maximum oxygen uptake does not take into consideration the rate of oxygen delivery, therefore becomes a limiting factor to the usage of maximal oxygen uptake as an endurance test. This can be further supported by (Bassett & Howley, 2000) who proved alteration in maximal oxygen uptake by tweaking oxygen delivery by use of drugs or blood doping, increasing cardiac output from training and increased muscle perfusion during exercise that increases the muscle’s oxygen consumption.
Muscular adaptation to metabolic changes is also an influential factor for maximal endurance performance. Training alters mitochondrial activity by increasing enzymatic reactions which increase lipid oxidation and lower lactate accumulation, thereby improving muscular performance. (Di Prampero, 1985)
Limitations to VO2max
Atmospheric oxygen transition to a useful form in the mitochondria for energy production occurs in a cascade. Each of the steps in the cascade represents a potential limiting factor. The steps are broadly categorized into central and peripheral factors. The central factors include pulmonary diffusion, cardiac output and blood’s oxygen-carrying capacity; the peripheral factor is the character of the skeletal muscle involved. (Bassett & Howley, 2000)
The Pulmonary System
Maximal oxygen consumption increases relative to the amount of oxygen inspired(Di Prampero, 1985) As opposed to the cardiovascular system, the respiratory system of a healthy young individual is not a limiting factor to VO2max during high-intensity endurance exercise. This is supported by the fact that a healthy system can adequately support the ventilatory requirements in the body in strenuous exercise(Amann, 2012). During exercise, the lung vital capacity has the capability to raise the partial pressure of oxygen to supply the oxygen deficit, therefore maintaining a constant saturation of oxygen.
In some individuals, the metabolic demands associated with strenuous exercise require extreme ventilation and more gaseous exchange at the lungs(Alghannam, 2012) this could compromise their respiratory functional capacity and eventually deterioration of blood oxygenation and oxygen transportation. Compared to untrained individuals, trained athletes have a higher cardiac output. This leads to a decreased transition of red blood cells in the pulmonary vessels, also the time to saturate blood could be limited before the blood exits the pulmonary circulation(Powers et al., 1989).
It has been proven by (Alghannam, 2012) that increasing the oxygen concentration in the air being breathed, raises the maximum oxygen uptake. (Di Prampero, 1985) states that an increase in the partial pressure of oxygen proportionately increases with maximal oxygen consumption.
Empirically, healthy individuals can adequately compensate for their oxygen deficit at sea level. It is at high altitude and with chronic obstructive pulmonary diseases that the limitation becomes significant. To manage this limitation, increasing oxygen concentration, increases exercise ability; this is due to the increase in oxygen diffusion into the blood. This also proves the pulmonary limitation of VO2max. (Powers et al., 1989)
Maximum Cardiac Output
In the exercising human, the ability of the cardio-respiratory system to deliver oxygen to the exercising muscles limits the maximal oxygen uptake (VO2max). Three major factors prove this;
- alteration of oxygen delivery through doping, use of beta-blocker drugs to lower cardiac output and hypoxia.
- An increase in maximum oxygen uptake due to an increase in cardiac output from athlete training.
- Increased muscle’s capacity to uptake oxygen when a small mass of it is over-perfused during exercise. (Bassett & Howley, 2000)
It has been demonstrated that trained athletes have a higher cardiac output and superior pumping capacities. (Terjung et al., 1985). With a very slight variation in the heart rate between trained and untrained individuals, the VO2max variation is principally from the difference in the maximal stroke volume. Oxygen supplication to the exercising muscles is through the blood vessels perfusing the muscles. A comparison of the oxygen content between the arterial and venous supply of a muscle revealed a significant reduction in oxygen concentration. This proves that the best mechanism to increase maximum oxygen uptake is through increasing the blood supply. In connection to this, cardiovascular limitation of VO2max is estimated at 70-85%(Bassett & Howley, 2000).
It has been shown that exercising increases the cardiac output and therefore leads to an increase in maximal oxygen uptake by muscles. Beta blockade causes a reduction in cardiac output which causes a reduction in Vo2max, from diminished oxygen delivery and blood flow. This is proof of the significant limitation of the cardiovascular system in VO2max.
Oxygen Carrying Capacity
The oxygen content of blood is defined as the amount of oxygen carried per a 100ml of blood. Oxygen delivery is the amount of oxygen delivered to peripheral tissues which is a product of arterial oxygen content by the cardiac output. Oxygen returned is a product of mixed venous oxygen content by the cardiac output. In relation to this, oxygen uptake is the difference between oxygen returned to the lungs and oxygen delivery. The oxygen-carrying capacity of blood is defined as the maximum amount of oxygen that can be transported by blood (Amann, 2012). The haemoglobin levels define this.
Oxygen delivery to the exercising muscle is, therefore, highly dependent on blood’s oxygen-carrying capacity. This is evidenced by the alteration of oxygen delivery by interference with the haemoglobin levels. (Terjung et al., 1985) Alteration of haemoglobin levels can be attained by re transfusion or blood doping which increases the red blood cells concentration and therefore increased oxygen delivery to muscles which in return improves exercise endurance. According to (Bassett & Howley, 2000) re transfusion of 900ml to 1350ml of blood has the capability to raise VO2max by 4% to 9%. This is evidence enough to prove the effect and linkage of maximal oxygen delivery to exercise endurance which is a limiting factor not accounted for.
Skeletal Muscle Limitations
Peripheral diffusion gradient
A study by (Connett et al., 1990) demonstrated that oxygen diffusion in peripheral muscles is a limiting factor for maximal oxygen uptake in muscles. According to the study, oxygen diffusion resistance occurs principally between the sarcolemma and red blood cell surfaces. A higher gradient between the two surfaces leads to higher uptake of oxygen, and the vice versa is true. According to (Connett et al., 1990) oxygen delivery is not a limiting factor as per se but rather the difference between cellular and blood oxygen concentration.
To create the oxygen gradient, the muscle must contract and cause oxygen utilization by mitochondria. This proved that without the rise of oxygen gradient in the periphery, oxygen uptake would not increase, and hence concluded that mitochondrial activity interaction with oxygen transport is the major limiting factors. The limitation to this conclusion, however, is that we can not deduce the exact difference or effect of the individual factors.
Enzymatic activity
The mitochondrial enzymatic activity has been a factor of interest when studying the limitations of VO2max. Empirically, doubling the number of mitochondria can double the oxygen uptake capacity and improve endurance. However, it ha been proven even for individuals with identical VO2max, the mitochondrial enzymes are highly variable (Holloszy & Coyle, 1984) Contrary, (KLAUSEN et al., 1981) proved that and increased in Mitochondria has a significant effect on VO2max where it causes a rise. What seems to agree is that an increase in muscular mitochondria increases the oxygen uptake. This agrees with the study by (Connett et al., 1990) who supported that increased Mitochondrial activity increases Oxygen gradient and therefore, the eventual rise in maximal oxygen uptake by muscles.
Conclusion
In conclusion, VO2max remains a classical test in endurance. All these limiting factors seem to be interdependent. Pulmonary limitation, though relative to the person health, significantly affects the oxygen diffusion capacity. The blood, on the other hand, limits VO2max by its oxygen binding capacity, higher haemoglobin concentration increases the oxygen binding capacity as seen in re transfusion. Once in the blood, oxygen delivery to the muscle is a major limiting factor; therefore, cardiac output plays a vital role. With increased cardiac contractility and reduced peripheral resistance that increases blood supply to the muscle, there is an increase in the amount of oxygen utilized by the muscles. Oxygen gradient between the extracellular and intracellular oxygen concentration also is a major factor. To increase the oxygen gradient, it has been proven that there should be an increase in mitochondrial activity. Increase in mitochondrial activity has been linked to an increase in mitochondrial enzymatic activity. These prove beyond doubt that the oxygen delivery cascade contributes greatly to the limitations of VO2max.
With the recent advancement from the studies as evidenced above, we get a clearer understanding of the dynamics that play in endurance exercises. Recently biopsies of muscle fibres have been used to relate their contractility to their metabolism and oxygen utilization. Through such studies, it has been proven possible to identify the exact factors that alter exercise endurance. Several factors influence a working muscle, and this affects their endurance capability (Terjung et al., 1985). However, there still is a need for more studies to bring a better understanding of maximal oxygen uptake.
Alghannam, A. F. (2012). Metabolic Limitations of Performance and Fatigue in Football. In Asian Journal of Sports Medicine (Vol. 3, Issue 2). www.tums.ac.ir
Amann, M. (2012). Symposium Report Symposium Report Pulmonary system limitations to endurance exercise performance in humans. Experimental Physiology Exp Physiol, 97(3), 311–318. https://doi.org/10.1113/expphysiol.2011.058800
Bassett, D. R., & Howley, E. T. (2000). Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine and Science in Sports and Exercise, 32(1), 70–84. https://doi.org/10.1097/00005768-200001000-00012
Connett, R. J., Honig, C. R., Gayeski, T. E. J., & Brooks, G. A. (1990). Defining hypoxia: A systems view of V̇O2, glycolysis, energetics, and intracellular PO2. In Journal of Applied Physiology (Vol. 68, Issue 3, pp. 833–842). https://doi.org/10.1152/jappl.1990.68.3.833
Di Prampero, P. E. (1985). METABOLIC AND CIRCULATORY LIMITATIONS TO AT THE WHOLE ANIMAL LEVEL. In J. exp. Biol (Vol. 115).
Holloszy, J. O., & Coyle, E. F. (1984). Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. In Journal of Applied Physiology Respiratory Environmental and Exercise Physiology (Vol. 56, Issue 4, pp. 831–838). https://doi.org/10.1152/jappl.1984.56.4.831
KLAUSEN, K., ANDERSEN, L. B., & PELLE, I. (1981). Adaptive changes in work capacity, skeletal muscle capillarization and enzyme levels during training and detraining. Acta Physiologica Scandinavica, 113(1), 9–16. https://doi.org/10.1111/j.1748-1716.1981.tb06854.x
Powers, S. K., Lawler, J., Dempsey, J. A., Dodd, S., & Landry, G. (1989). Effects of incomplete pulmonary gas exchange on V̇(O(2 max)). Journal of Applied Physiology, 66(6), 2491–2495. https://doi.org/10.1152/jappl.1989.66.6.2491
Terjung, R. L., Dudley, G. A., & Meyert, R. A. (1985). LIMITATIONS TO PERFORMANCE AND MALLEABILITY OF THE SYSTEM METABOLIC AND CIRCULATORY LIMITATIONS TO MUSCULAR PERFORMANCE AT THE ORGAN LEVEL. In J. exp. Biol (Vol. 115).