Five numbers that change the moment you start, and one that changes before you do

Heart rate rises from a resting value of roughly 60 to 80 beats per minute towards a maximum of around 200 in an adolescent, and it does so in a sequence that has three distinct parts.

Before exercise: the anticipatory rise. This answers Card 01. Adrenaline released by the adrenal glands, together with increased sympathetic nervous stimulation, raises heart rate before the first movement. It is triggered by the expectation of exercise, not by a metabolic demand, which is why a swimmer's heart rate is elevated on the block and why the effect is larger before a race than before a training swim. It is useful rather than wasteful: it shortens the oxygen deficit met in Lesson 10, because circulation is already elevated when the first muscle contraction occurs.

At the onset of exercise: a rapid rise. Heart rate climbs steeply in the first seconds as sympathetic stimulation increases and parasympathetic inhibition is withdrawn, then continues to rise in proportion to the intensity of the work.

During sustained sub-maximal exercise: a plateau. At a constant sub-maximal workload heart rate levels off at the steady state, where oxygen supply matches demand. If the work continues for a long time in the heat, heart rate then drifts slowly upward even at unchanged intensity — cardiovascular drift, caused by the fall in plasma volume from sweating that Lesson 11 described, which reduces stroke volume and must be compensated for by more beats.

Ventilation rate is the volume of air moved per minute, and it is the product of two things: how often you breathe and how deeply. At rest an adolescent moves roughly 6 to 8 litres per minute, from about 12 to 15 breaths of around 500 millilitres each. During maximal exercise that can exceed 100 litres per minute.

Both factors rise, but not equally, and the order matters. At low and moderate intensities most of the increase comes from tidal volume — deeper breaths rather than faster ones, which is more efficient because a larger share of each breath reaches the alveoli rather than sitting in the airways. As intensity rises further, tidal volume approaches its limit and further increases come almost entirely from breathing frequency. That is why hard exercise feels like panting and moderate exercise does not: the shift from depth to rate is a real physiological change, not a change in effort.

There is an anticipatory rise in ventilation too, from the same nervous and endocrine origin as the heart rate one, and for the same benefit.

These two are handled together because they are not independent. Cardiac output is the product of the other two responses, and writing that relationship down settles most of the questions this dot point produces:

Stroke volume is the blood ejected by the left ventricle in one beat: roughly 70 to 80 millilitres at rest in an untrained adolescent, rising to around 100 to 120 during exercise. It rises for one main reason, and it is worth stating properly: venous return increases. The muscle pump — contracting skeletal muscle squeezing the veins — and the respiratory pump return more blood to the heart, so the ventricle fills more completely, stretches further, and contracts more forcefully in response. A more forcefully contracting ventricle also empties more completely, so both the filling and the emptying improve.

In most people, stroke volume then stops rising, at roughly 40 to 60 per cent of maximum effort, and this is the answer to the second Card 01 question. Beyond that intensity the heart is beating so rapidly that the filling time between beats becomes the limiting factor: the ventricle simply has less time to fill, which cancels out the greater venous return. Stroke volume plateaus, and in some people at very high intensities it declines slightly. That is the pattern in untrained and moderately trained people, and the model this lesson works with. Highly trained endurance athletes are the exception: their larger, more compliant ventricles keep filling even at high heart rates, and their stroke volume can go on rising towards maximum. Describing that continuing rise for an elite endurance athlete is not an error.

Cardiac output nonetheless keeps rising all the way to maximum, and the equation shows exactly how. Once stroke volume plateaus, every further increase in output must come from heart rate alone. The numbers make it concrete:

Notice the third row against the second. Stroke volume is identical, and cardiac output has risen by half. That is the plateau and the equation working together, and being able to point at those two rows is worth more than any amount of description.

Lactate is produced continuously by the glycolytic system, even at rest, and is continuously removed — taken up by the heart, by the liver and by less active muscle, where it is either oxidised for energy or converted back to glucose. Blood lactate concentration is therefore a balance between production and removal, not a measure of production alone, and that single sentence explains everything that follows.

At rest and at low intensities, removal keeps pace with production and blood lactate stays near its resting value of about 1 to 2 millimoles per litre. As intensity rises, production rises faster than removal can match, and at a certain point the concentration begins to climb steeply. That point is the lactate threshold, and it typically occurs around 50 to 60 per cent of maximum in an untrained person and 80 to 85 per cent or higher in a trained endurance athlete.

The threshold is the single most useful number in this lesson, because it predicts what an athlete can sustain. Below it, an athlete can continue for a long time. Above it, lactate and the hydrogen ions accompanying it accumulate, muscle pH falls, enzyme activity is impaired and the effort must end within minutes. A race is in large part the management of that boundary, which is why an athlete who starts too fast pays for it for the rest of the event.

The dot point lists five responses, which invites five separate paragraphs. They are better understood as one coordinated answer to one demand, and an answer built that way reads as physiology rather than as recall.

The demand is this: the working muscle needs more oxygen delivered and more carbon dioxide removed, immediately.

Read item 5 again, because it is the organising idea. The first four are the body's attempt to meet the demand. Lactate is the read-out on whether the attempt worked. Below the threshold, delivery is winning. Above it, it is not, and the clock has started. That is why lactate is the response a coach would measure to set training intensities, and the other four are the responses that explain why the threshold sits where it does.

You can measure three of the five directly with nothing but a clock. Write your predictions down before you collect anything — a prediction recorded after the data is not a prediction, and the disagreements are where the learning is.

Finish by comparing prediction with measurement. Name the single largest disagreement and explain it physiologically rather than dismissing it as measurement error — and if you do think it was measurement error, say precisely which step introduced it.

Each scenario gives you measurements rather than a description. For each: state what is happening physiologically, name which of the five responses explains it, and say what you would advise.

Scenario 2 is the one to spend time on. Both cyclists are producing the same power, so what differs is not the work — it is where that work sits relative to each rider's own threshold. Say what that predicts about the next twenty minutes for each of them.