Abstract
This chapter is mainly devoted to an analysis of the exercise transients, along the paths traced by Margaria in 1933. The oxygen deficit contracted during light exercise at the expense of anaerobic alactic metabolism (obligatory component of the oxygen deficit), the role of oxygen stores and early lactate in the oxygen deficit, especially at higher work loads, the metabolic control of muscle oxygen consumption during exercise and the slow component of its kinetics at the onset of exercise are discussed. A more detailed description of anaerobic metabolisms is carried out in the second part. Blood lactate accumulation in submaximal exercise, the energy equivalent of lactate and the maximal lactate power are analyzed. The maximal explosive power and the power and capacity of anaerobic alactic power are then discussed. In the appendix, a detailed analysis of the concept of anaerobic threshold is proposed along the energetic way of thinking of the School of Milano.
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Notes
- 1.
The terminology and the language used in the present discussion is typical of the way of expressing the concepts about the energetics of muscular exercise in the 1970s and 1980s. Terminology meanwhile has evolved, more in form than in substance. A representative case concerns the currently accepted taxonomy of exercise intensities: light (between rest and the lactate threshold), moderate (between the lactate threshold and the critical power), and intense (between the critical power and the maximal aerobic power) (see e.g. Poole and Jones 2012). If the third of these taxonomic categories is sound, the separation of a light and a moderate exercise domain by the lactate threshold looks conceptually weak. Notwithstanding the doubtful meaning of the lactate threshold concept, a steady state for oxygen uptake and for blood lactate concentration, implying no lactate accumulation after completion of the exercise transient, and thus no incurring anaerobic lactic metabolism, means that in both cases, after attainment of the steady state, the metabolism is entirely aerobic. The only difference is that in the light exercise domain, the steady blood lactate concentration corresponds closely to that at rest, whereas in the moderate exercise intensity, the steady blood lactate concentration is higher than at rest, because of “early” lactate accumulation during the exercise transient. We nevertheless acknowledge that the terminology used in more ancient times was somewhat lax.
- 2.
At steady state, the oxygen consumption (above resting), as measured at the upper airways level, is equal to that of the active muscles. However, during the metabolic transients at the onset and offset of the exercise, the muscle oxygen consumption is not necessarily equal to that measured at the upper airways, because of the “buffering” effect of the body oxygen stores.
- 3.
The symbol P/O2, as utilised in this section, refers to the overall ratio between ATP resynthesized and oxygen utilised. As such, the biochemical details concerning ATP resynthesis at the subcellular level will not be dealt with.
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Appendix
Appendix
3.1.1 The Anaerobic Threshold
This appendix is devoted to a critical analysis of the anaerobic threshold concept, to show that it cannot be seen as an index of the metabolic intensity above which the exercise becomes partially anaerobic.
To this aim, let us first consider a group of muscle fibers, all “aerobically” active in a homogeneous way. Under these conditions, graphically represented in Fig. 3.13A, each muscle fiber oxidizes completely the pyruvate produced by glycolysis, and the number of moles of ATP resynthesized per glycosidic unit (162 grams of glycogen) amounts to 3 + 34 = 37. In turn, this requires the consumption of 6 moles of oxygen, thus leading to a P/O2 ratio of 37/6 = 6.17.Footnote 3
Let us now consider a group of muscle fibers all active “anaerobically” in a homogeneous way, as represented graphically in Fig. 3.13B. Assume further that under these conditions, which should be more appropriately defined “hypo-aerobic,” each muscle fiber oxidizes only half the amount of pyruvate derived from glycolysis. Of course, the remaining pyruvate that cannot be oxidized at the mitochondrial level via the Krebs’ cycle, is anaerobically transformed into lactate in the cytosol, thus leading to an overall resynthesis of 37 + 3 = 40 moles of ATP. As a consequence, since the amount of oxygen required is the same as indicated in Fig. 3.13A, the P/O2 ratio is greater, in this specific example amounting to 40/6 = 6.67.
Let us finally consider a third group of muscle fibers all active in a homogeneous way in transforming lactate taken up from the extracellular space into pyruvate, which is then oxidized completely to carbon dioxide and water in the Krebs’ cycle (Fig. 3.13C). In this case, the number of moles of ATP resynthesized from the oxidation of this pyruvate, which is not formed in the glycolytic pathway within the muscle fibers at stake, is less than indicated in Fig. 3.13A or B. Thus, also the P/O2 ratio of these specific fibers turns out reduced, amounting to 34/6 = 5.67. This type of fiber can be defined “hyper-aerobic” to highlight their lower “efficacy” in terms of ATP resynthesis at the expense of the oxidative processes. Combining an appropriate number of “hypo-aerobic” and “hyper-aerobic” fibers (Fig. 3.14), it is possible to obtain an entirely aerobic system, in which the P/O2 ratio is (6 + 34 + 34)/12 = 6.17, as in a typically aerobic fiber (Figure 3.13A). Such a combination of “hyper-” and “hypo-” aerobic fibers can be defined a heterogeneously aerobic system.
Let us now attempt to interpret qualitatively experimental data on the anaerobic threshold, in the frame of the above-outlined theoretical considerations.
The activation of a heterogeneously aerobic system, as described in Fig. 3.14, requires an appropriate concentration gradient allowing lactate diffusion from the “hypo-aerobic” fibers, where it is produced, to the “hyper-aerobic” ones, where it is re-transformed into pyruvate and oxidized. The establishment of such a gradient takes some time from work onset, during which the extracellular lactate concentration increases: this appears during the exercise transient as “early lactate” accumulation. The “hypo-” and “hyper-aerobic” fibers can be identified, as a first approximation, with the type II white glycolytic and the type I red oxidative fibers, respectively. Lactate diffusion from the intra- to the extracellular space and vice-versa is facilitated by, but does not need passive transporters, the number of which increases with training, mainly at the level of the cell membrane of the type I fibers. Finally, the lactate-producing fibers (“hypo-aerobic”) deplete their glycogen stores at a faster rate than the “hyper-aerobic” ones that do utilize lactate. The “hypo-aerobic” fibers may then constitute the factor limiting the exhaustion time and/or the maximal exercise intensity.
The above line of thinking suggests to define “aerobic threshold” as the workload below which all, or at least the great majority of the active fibers are in a homogenously aerobic condition (P/O2 = 6.17). Hence, in the range of exercise intensities below the aerobic threshold the blood lactate concentration ([La]b) does not exceed the values prevailing at rest: [La]b ≤ 2 mM. In a large range of exercise intensities, the [La]b does not change substantially, as compared to the resting values. When muscle fiber metabolism is homogeneously aerobic, each muscle fiber (or group thereof) oxidizes all, and only, the pyruvate that it produces from glycogen (Fig. 3.13A).
At exercise intensities greater than the aerobic threshold, as defined here above, an aerobic status can still be achieved thanks to the appropriately combined activity of hypo- and hyper-aerobic fibers, to yield a “heterogeneously aerobic” condition, in which hyper-aerobic fibers oxidize the excess lactate produced by the hypo-aerobic ones (Fig. 3.14). This condition requires an initial increase in Lab (early lactate) to prime the system. All work intensities in which, after the initial ≈ 5 min, [La]b attains a constant level, higher than resting, belong to this exercise category, regardless of the absolute lactate level. It is interesting to note that this analysis bears an analogy with Brooks' theory of the lactate shuttle (Brooks 1985, 1986, 2000, 2009).
The constant value that [La]b attains after work onset in a heterogeneously aerobic condition, is greater the higher the exercise intensity. The highest exercise intensity compatible with a constant [La]b, MLSS (Beneke 2003), represents the maximal power that can be sustained by the whole body oxidative processes, albeit heterogeneously distributed. Above the work intensity corresponding to the MLSS, lactate keeps increasing with time, thus leading to a corresponding continuous increase of [La]b. The MLSS is attained at a power, which is probably higher than the critical power. Throughout the whole range of the aerobic work intensities, regardless of the fact that the aerobic metabolism sustaining them be homogeneously or heterogeneously distributed, after the initial 5 min of exercise (classical duration of the exercises transient, during which early lactate may be accumulated, Cerretelli et al. 1979), whole body oxygen consumption is a correct quantitative measure of the overall rate of energy expenditure, as long as the terms \( b\ \dot{La} \) and \( a\ \overset{\rightharpoonup }{\dot{PCr}} \) of the general equation of the energetics of muscular exercise (Eq. 3.16) are nil.
From an energetic viewpoint, it seems legitimate to ask whether the maximal aerobic power, at which \( \dot{E}=\dot{V}{O}_2 \)max, does, or does not, coincide with the power corresponding to the MLSS. According to Busso and Chatagnon (2006), there exists a range of workloads close to, but lower than,\( \dot{V}{O}_2 \)max, in which [La]b keeps increasing with time. This being so, the maximal aerobic power would be higher than that corresponding to the MLSS. This is coherent with the data reported in Fig. 3.10, showing that, at least in cycling and swimming, [La]b starts increasing continuously at intensities below \( \dot{V}{O}_2 \)max, specifically at 85 and 78% thereof, respectively (Eqs. 3.10, 3.11, and 3.12).
It should finally be noted that the power at which [La]b keeps increasing continuously even after the initial phase, is crucially dependent not only on the intensity and type of exercise but also on the subject’s training level. At even higher exercise intensity, the activity and/or number of the “hypo-aerobic” fibers exceeds the capacity of the “hyper-aerobic” ones to oxidize lactate. Thus, [La]b keeps increasing also beyond the initial minutes of exercise. This exercise intensity level constitutes the true whole-body anaerobic threshold. It represents the exercise intensity above which the oxygen consumption is not sufficient to cover the total energy requirement and is generally attained at workloads closer to \( \dot{V}{O}_2 \)max: it definitely does not correspond to the traditional anaerobic threshold set at a conventional [La]b of 4 mM. For a schematic representation of these three levels of exercise intensities, see Fig. 3.15. Concerning the relation of early lactate to oxygen delivery, see Chap. 4.
After this analysis, we are confident to conclude that the conventional anaerobic threshold is neither a “threshold,” in so far as it does not represent a net transition between two different conditions, nor “anaerobic” (at least if the whole body is considered), in so far as, under constant blood lactate concentration, regardless of its absolute value, the whole organism is always in aerobic conditions. It follows from this conclusion that the widespread use of the conventional anaerobic threshold concept has introduced a strong bias in the interpretation of the energetics of muscular exercise, especially as far as the meaning of anaerobic lactic metabolism is concerned. Only the School of Milano has been fighting fiercely against the shadow cast by this bias, unfortunately with less success than it would have deserved.
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di Prampero, P.E., Ferretti, G. (2023). Margaria’s Concept of Oxygen Debt. In: Ferretti, G. (eds) Exercise, Respiratory and Environmental Physiology. Perspectives in Physiology. Springer, Cham. https://doi.org/10.1007/978-3-031-19197-8_3
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