Endurance and Adaptation

The three systems differ in speed and in size of tank. Muscle ATP (adenosine triphosphate) itself is a working balance, not a store — about 8 mmol per kilogram of muscle, held nearly constant even when demand rises a thousandfold, because falling ATP (adenosine triphosphate) is what fatigue protects against; the phosphagen system spends stored phosphocreatine to remake ATP (adenosine triphosphate) at the highest rate of the three, dominates the first 5–6 seconds of an all-out effort and is largely depleted within about 10 seconds; glycolysis breaks glucose from blood or glycogen into pyruvate and, at high rates, lactate, without needing oxygen, and reaches its maximal rate after 10–15 seconds; oxidation in the mitochondria burns carbohydrate and fat, with protein normally contributing 5–10 % of the energy at rest and during exercise, and it is the primary system for long-distance running.⁵¹ The older picture — one system handing over to the next — has been replaced by measurements showing glycolysis active almost immediately at the onset of a sprint and oxidation contributing even to a 30-second effort.⁵

Two facts about fuel make the marathon a distinct problem, and neither is a prescription. Fat is abundant: even the leanest athlete stores enough to fuel more than four marathons, if the working muscles could run on fat alone.⁶ Carbohydrate is scarce: for a 70-kg runner a marathon costs roughly 2,950 kcal, while a typical liver holds about 88 g of glycogen (about 350 kcal) and the leg muscles of a lean 70-kg man about 310 g (about 1,250 kcal), and the share of energy drawn from carbohydrate rises with the fraction of VO₂max at which a runner works.⁶ More than 40 % of marathoners report "hitting the wall" — the rapid onset of severe fatigue from near-complete depletion of carbohydrate in the leg muscles and liver — and one model puts that point at around mile 21 (about 34 km) for runners at 80–95 % of VO₂max (maximal oxygen uptake).⁶ Endurance training raises the muscle's capacity to store glycogen and its ability to use fat, sparing glycogen at a given pace, and in the best marathon runners slow-twitch fibres, which are rich in mitochondria and capillaries, can make up 90 % or more of the leg muscle.¹

The arithmetic behind the definition is the Fick relationship: oxygen uptake equals cardiac output — heart rate times stroke volume — multiplied by the difference between the oxygen content of arterial and mixed venous blood, which widens from roughly 4–5 mL per 100 mL at rest to 15–16 mL per 100 mL near maximal work.¹ Ventilation rises from about 10 L/min at rest to more than 100 L/min at maximal work in untrained adults and beyond 200 L/min in large, highly trained athletes, which is why the lungs are rarely the limit.¹ Three lines of evidence place the limit at delivery: alter the oxygen delivered — by altitude, by changing the blood's carrying capacity, or by slowing the heart — and VO₂max (maximal oxygen uptake) moves with it; training raises VO₂max (maximal oxygen uptake) mainly through maximal cardiac output; and a small muscle mass, when the whole heart's output is available to it, can consume oxygen at extraordinary rates.¹² The concept goes back to Hill and Lupton in 1923, and the plateau in a graded test remains the best evidence that a true maximum was reached, though it is not seen in every test.⁹

What training changes is mostly the pump. In an untrained person stroke volume rises with effort and then plateaus at roughly 40–60 % of VO₂max (maximal oxygen uptake), while in highly trained people it can keep rising to near-maximal work; endurance training raises stroke volume at rest and at every intensity, largely through a bigger plasma volume, more blood returning to the heart and a larger, stronger left ventricle, and this is the dominant reason maximal cardiac output rises.¹ Elite endurance athletes reach maximal cardiac outputs of roughly 30–40 L/min against about 20 L/min in sedentary men, and VO₂max (maximal oxygen uptake) values of about 70–85 against under 45 mL/kg/min.⁷ The reverse experiment shows the same thing: with complete bed rest, VO₂max (maximal oxygen uptake) falls about 15 % within 10 days and 27 % within 3 weeks, and the loss traces to a smaller stroke volume and cardiac output, with maximal heart rate and oxygen extraction unchanged.¹ Altitude removes oxygen from the other end of the chain: above about 1,500 m the lower pressure of oxygen in the air reduces the driving force that loads it into the blood, and VO₂max (maximal oxygen uptake) falls significantly.¹ Typical training gains are 15–20 % over six months for a previously sedentary adult, with wide individual variation — in one study of men and women aged 60–71 who trained for 9–12 months, from 0 to 43 % — and the HERITAGE study estimated that about half of the variation in its own participants' response was heritable.¹¹³

The curve has two landmarks and many names. The first is where lactate leaves resting level, because production has begun to outrun the removal that muscle and heart perform by burning lactate as fuel; the second, the maximal lactate steady state, was defined by Heck and colleagues as the highest constant workload at which blood lactate rises by no more than 1 mmol per litre over the last 20 minutes of a roughly 30-minute run — a gold-standard test that needs several separate runs.⁸ Because that test is impractical, laboratories estimate the landmarks from a single graded test by different rules — the first visible rise, a rise of 1 mmol per litre above baseline, a fixed 4 mmol per litre, the point of maximal distance from a straight line, and others — and in a study of 48 well-trained male cyclists eight such rules were all repeatable and all predicted a time trial and a mountain road race, while placing the threshold at different powers.¹¹ The rules disagree; the physiology they estimate does not.

Naming is a live dispute, stated here as positions rather than adjudicated: the maximal lactate steady state is also called the "anaerobic threshold", and Heck and Wackerhage report that Mader and colleagues used "anaerobic" only to name glycolysis as a pathway that needs no oxygen — never to claim that the muscle lacks oxygen, since lactate is produced without any lack of it, a fact known since Warburg's experiments on cells — while Baker and colleagues object to labelling glycolysis by the presence or absence of oxygen at all; the wider controversy over the term has its own fifty-year review.⁸⁵¹⁷ Ventilation offers a second window on the same transition: at higher intensities rising carbon dioxide and hydrogen ions drive further increases in breathing, and ventilatory thresholds, read from breathing rather than blood, are used like the lactate ones to mark the boundaries between training zones.¹⁷

Why the threshold matters for a marathon: distance runners in a 1979 study set their race pace at or slightly above the lactate threshold, and highly trained endurance athletes reach their thresholds at a much higher fraction of VO₂max (maximal oxygen uptake) than untrained people, which is what lets them race faster at the same ceiling.¹ The speed at the threshold integrates VO₂max (maximal oxygen uptake), the fraction of it held and running economy, and is the best single physiological predictor of distance-running performance.¹² Training moves it through the muscle: more and larger mitochondria and more oxidative enzymes, more capillaries, more glycogen stored and more fat burned at a given pace, so that less lactate accumulates at the same oxygen uptake.¹¹²

Economy is expressed either as oxygen per kilogram per minute at a stated speed or as oxygen per kilogram per kilometre, and it is measured over 3 to 15 minutes at a steady speed below the threshold, because above it oxygen uptake keeps drifting upward and no steady state exists.³ Radcliffe's laboratory values illustrate the scale of an elite economy: 44 mL/kg/min at 16 km/h against a VO₂max (maximal oxygen uptake) of 75 mL/kg/min in one test.³ Its determinants are several at once — metabolic (fibre types and mitochondrial capacity), cardiorespiratory (the oxygen spent on breathing and on the heart's own work), biomechanical (stride length, which runners choose close to their own optimum, and joint and tendon behaviour) and neuromuscular (how efficiently force is produced and muscles are recruited); high training volumes and years of running experience have been suggested to matter, and several studies show that strength, power and plyometric training two or three times a week can improve economy in long-distance runners.³⁴ Radcliffe's vertical jump rose from 29 to 38 cm between 1996 and 2003, the period over which her economy and marathon performance improved.⁴ The Breaking2 attempt itself was run on 6 May 2017 at the Monza motor-racing circuit, where Eliud Kipchoge finished in 2:00:25 — not an official record, because pacers joined the race midway.¹⁹

The principles have plain names. Overload is physical stress greater in amount or intensity than usual, to which the body's structures and functions respond and adapt; progression is the continued small increase of that overload as the body adapts, and small steps are what let it adapt while keeping the risk of injury low; specificity is the rule that the benefit goes to the systems that did the work — walking largely benefits the legs and the cardiovascular system, push-ups the chest, shoulders and arms.² The risk of injury to bones, muscles and joints is related to the size of the gap between a person's usual level of activity and the new one — the amount of overload — and creating a small overload and waiting for the body to adapt and recover is what keeps that risk down.² Overload can be counted as volume (how much), intensity (how hard) and frequency (how often), and the same session can be described by its external load — the work done — or its internal load — the strain it imposed, which the same external work can raise or lower depending on how recovered the athlete is.⁷¹⁶

At the cellular level the picture is the same one drawn at the whole-body level. Training adaptation begins with a disturbance of the body's steady state; during recovery, repair mechanisms do more than return it to baseline — they overshoot, ideally in a supercompensatory way — and in the absence of a further stimulus that overshoot dissipates.⁷ Many of the changes that underpin endurance adaptation are the transient effect of repeated single bouts: the transcription of many mitochondrial genes rises briefly after one endurance session and returns to baseline, and only when the stimulus is repeated over weeks and months do those transient bursts accumulate into new steady-state levels of protein — more and larger mitochondria, more oxidative enzymes, more capillaries, more stored glycogen, more fat burned at a given pace, and a heart with a larger stroke volume.⁷¹ Different tissues and processes adapt on different timescales, so no single curve describes the whole body.⁷ Reversibility runs the same path backwards: declines in maximal and submaximal responses appear within the first 7–21 days of inactivity and level off after about two months.⁷

The vocabulary is layered: coaches build a season (the macrocycle) from mesocycles of about 3–8 weeks and microcycles of about 7–21 days, each targeting particular qualities and culminating in a competition peak.⁷ Since Arthur Lydiard introduced his system in the late 1950s, leading distance coaches have divided the year into ordered phases with the explicit goal of peaking for the main competitions; the general preparation period builds an aerobic foundation through high volume, and from the specific period onward the focus shifts toward more running at race-pace intensity, a pattern that bears some resemblance to Matveyev's model drawn from Soviet athletes of the 1950s and 1960s.⁴ Because injuries are attributed above all to rapid, excessive increases in load, world-class runners open the season at roughly 40–60 % of peak weekly volume and add about 5–15 km a week until the peak is reached; they keep at least 80 % of their running at low intensity throughout the year, and elite marathoners' weekly volumes in mid-preparation are typically 160–220 km, reached by adding sessions first and lengthening them later.⁴ The taper's mechanism is the fitness–fatigue balance from the previous unit: fatigue drains within days while adaptation fades over weeks, so cutting volume for a short period while keeping intensity leaves fitness largely intact and fatigue much reduced; most elite runners do not cut volume substantially until the last 7–10 days, and strong performances have been recorded across a three-month season with only a 4–5 day reduction before each race.⁴

Whether periodization theory rests on the foundations claimed for it is a live dispute, recorded here as positions. Haugen and colleagues describe the phased year as results-proven practice and note that the mechanisms behind any one periodization model's superiority remain unclear, with no direct evidence comparing outcomes across models.⁴ Kiely argues that periodization theory borrowed its justification from Selye's general adaptation syndrome, that the science of stress has since moved away from that model, and that no universally best template exists because people respond to the same training along different trajectories.¹⁰ Furrer and colleagues describe the periodized structure as what elite athletes and their coaches actually do while noting the individual variation in response.⁷ The three agree on the part this chapter teaches — load must be arranged over time — and none claims that a named template has been shown to beat the others.