One day at the gym, I was warming up on a bike when two guys on the adjacent bikes were talking about training while seemingly pushing themselves through a brutal bike workout. One of them said to the other, "How do you choose what intensity to bike at each day?", while the other replied, "I always just put it on the hardest gear and cycle as fast as possible while I'm on the bike." He proceded to give an example, "Like, if I've been cycling for 30 minutes and don't think I can go any further, I just turn the gear up, pedal faster than before, and push through the pain for at least another 10 minutes." While there is so much wrong with this guy's theory of being able to "push through the pain" of cycling at his max, the main question to ask is truely, what exactly would cause this guy to not be able to cycle ANY longer or harder?
Prepare for a bit of a sciency article. If this stuff is not your background, here's the best way to describe what I'm explaining in the words below. When you're at the gym, on your favorite piece of cardio machine, doing a hard long workout, or short brief sprints at your personal max, what is limiting you? If you've ever done a test with a personal trainer or physiologist, they may have shown you a Borg scale, Dyspnea scale, or something similar, asking you, "How does this feel out of 10.... on your legs, breathing, or overall?" Such questions give us indications on what is personally limiting you from pushing any harder, but the science on the physiological mechanisms preventing you from going any "harder" during cardiovascular training are actually quite interesting:
Whether an athlete performs to their best ability with technical excellence at speed, under pressure and when fatigued (Goldsmith, 2003), is dependent on a multitude of factors. As exercise physiologists, we are concerned most with an athlete’s physiology and how it can improve or hinder performance. In endurance sports especially, the athlete’s VO2max is of interest as it relates to performance1. VO2max is a product of the athlete’s cardiovascular output and arteriole-venous difference in oxygen content 1–4.
Two factors that limit cardiac output (Q) are heart rate (HR) and strove volume (SV). The HR is limited by age and one’s individual ability to reach their maximum heart rate, but this factor does not change with training5. Stroke volume is limited by the amount the ventricles can fill (end-diastolic filling) which is both determined by a reduction in pericardial resistance, and an increase in blood volume5,6 found in elite trained athletes. SV is also limited by the ejection volume possible by the ventricles which can be explained by the Frank-Starling mechanism in which a reduction in pericardial resistance would provide more filling, and greater contractility to increase the ejection volume6. Increased heart size would also explain the increase in SV with elite trained athletes due to chronic and prolonged training leading to increased ventricular wall size6. Thus, with proper training, stroke volume appears to be the main limiting central factor that if improved, can greatly increase cardiac output and consequently, VO2max.
Two factors that limit cardiac output peripherally are the peripheral circulation of blood to the working muscles and the diffusion and perfusion of oxygen at the lungs and at the muscle2. Peripheral adaptations to training include capillary density, hemoglobin content, and total blood volume, as well as a conversion of type IIb muscle fibers to type IIa resulting in increased mitochondrial respiratory enzymes5. Basset and Howley (1999) support the presence of a peripheral limitations to VO2max during exercise, because with endurance training, adaptations such as mitochondrial density, type of metabolism used to metabolize lactic acid, and thresholds determined by this metabolism, are factors affecting VO2 via peripheral mechanisms. It was previously thought that during exercise, a healthy individual only experiences a 2-3% desaturation of the blood at maximal exercise, however there may be greater than 9% desaturation that actually occurs due to fall in PaO2 and a right shift in the oxyhemoglobin dissociation curve (due to increase in lactic acid and body temperature during exercise)7. However, strong research supports the notion that central factors remain the main limiting factor to performance1,2. This is because with training, maximal cardiac output occurs, rather than increases in a-vO2 difference, and because muscle has an extremely high capacity for consuming oxygen 1,2.
In conclusion, the research supports the fact that cardiac output, a central limitation in trained athletes, is the primary limiting factor to maximal oxygen uptake. This is despite the fact that at VO2max, athletes may demonstrate a decrease in the a-vO2 difference, perhaps due to very high blood flow limiting the full oxyhemoglobin saturation 7. Consistent across many research findings 1,3–6, oxygen delivery is the primary limiting factor for VO2.
1. Basset, D.R., Howley ET. Limiting factors for maximum oxygen uptake and determinants of endurance performance. J. Med. Sci. Sport. Exerc. 1999;32(1):70-84.
2. Ferretti G. Maximal oxygen consumption in healthy humans: theories and facts. Eur. J. Appl. Physiol. 2014;114(10):2007-36. doi:10.1007/s00421-014-2911-0.
3. Hill A V., Lupton H. Muscular Exercise, Lactic Acid, and the Supply and Utilization of Oxygen. Q. J. Mediting 1923;(62):135-171. doi:10.1093/qjmed/os-16.62.135.
4. Astrand, P-O., Saltin B. Maximal oxygen uptake and heart various types of muscular activity. J. Appl. Physiol. 1961;16(6):977-981.
5. Spina RJ, Ogawa T, Kohrt WM, Martin WH, Holloszy JO, Ehsani a a. Differences in cardiovascular adaptations to endurance exercise training between older men and women. J. Appl. Physiol. 1993;75(2):849-55. Available at: http://www.ncbi.nlm.nih.gov/pubmed/8226490.
6. Zhou BEN, Conlee RK, Jensen R, Fellingham GW, George JD, Fisher AG. Stroke volume does not plateau during graded exercise in elite male distance runners. J. Med. Sci. Sport. Exerc. 2001;33(11):1849-1854.
7. Powers SK, Dodd S, Lawler J, Landry G, Kirtley M, Mcknight T. h ologs Incidence of exercise induced hypoxemia in elite endurance athletes at sea level. J. Appl. Physiol. 1988;58:298-302.
8. Goldsmith (2003).