Introduction

At rest, the average adult takes 10 to 15 breaths per minute, with a volume of about 0.5 litres, producing a ‘minute ventilation’ (_E) of 7.5 l·min^− 1 (15 × 0.5). The volume of each breath (tidal volume: V_T) depends on body size and metabolic rate. Larger people have larger lungs and take larger breaths; they also require more energy and oxygen (O₂) to support their metabolism; accordingly, they require a larger _E.

During heavy exercise, breathing frequency (f_r) rises to around 40 to 50 breaths per minute. In a physically active young male, V_T rises to around 3 to 4 litres, generating a _E of 120 to 160 l·min^− 1. However, in Olympic-class male endurance athletes, V_T can be over 5 litres, resulting in a _E of 250 to 300 l·min^− 1.

Kilogram for kilogram, Olympic oarsmen can achieve a _E that is equivalent to that seen in thoroughbred racehorses! Take the rower Sir Matthew Pinsent as an example. In his 20s, this four-time Olympic gold medalist (1992, 1996, 2000, 2004) and 13-time senior world champion possessed the largest lungs of any British athlete; his forced vital capacity (FVC) was 8.25 litres. Sir Matthew stood just under 2 m (6 feet 5 inches) tall and weighed around 108 kg (240 pounds); a man of his size would normally have a FVC of about 6 litres, whilst the average man has a FVC closer to 5 litres. During a 2000-meter rowing race, Sir Matthew would generate a massive 460 watts of propulsive power for around 6 minutes, requiring a peak oxygen uptake (O_2peak) of around 8 l·min^− 1 and a _E of close to 300 l·min^− 1. The total volume of air that was moved into and out of his lungs during a race would have been close to 1700 litres, requiring a power output by his respiratory muscles of around 85 watts. These are truly staggering statistics, and they give some insight into what the human cardiorespiratory system is capable of achieving.

The respiratory pump during exercise

During exercise, the rate and depth of breathing are increased in order to deliver a higher _E and oxygen uptake (O₂); this response is known as the exercise hyperpnoea, and requires the respiratory muscles to contract more forcefully and to shorten more quickly. At rest, expiratory muscles make very little contribution to breathing, but during exercise they contribute to raising V_T and expiratory air-flow rate. However, at all intensities of exercise the majority of the work of breathing is undertaken by the inspiratory muscles; expiration is always assisted to some extent by the elastic energy that is stored in the expanded lungs and rib cage from the preceding inhalation. This elastic energy is ‘donated’ by the contraction of the inspiratory muscles as they stretched and expanded the chest during inhalation. Recent studies have estimated that, during maximal exercise, the work of the inspiratory respiratory muscles demands approximately 16% of the available oxygen (Harms & Dempsey, 1999), which puts into perspective how strenuous breathing can be in healthy young people.

The strategy that the respiratory controller adopts in order to deliver a given _E depends upon a number of factors, especially in the presence of disease. Chapter 1 described how the respiratory controller most likely regulates ventilation and breathing pattern so as to ‘keep the operating point of the blood at the optimum while using a minimum of energy’ (Priban & Fincham, 1965). Figure 2.1 illustrates how tidal volume changes as exercise intensity increases, placing it within the subdivisions of the lung volumes that are illustrated in Figure 2.1. Initially, during light exercise, V_T increases by the person exhaling more deeply, and utilizing the expiratory reserve volume, but this increase is quickly supplemented as a result of the deeper inhalation and utilization of the inspiratory reserve volume.

Eventually, V_T reaches a point where it does not increase any further, despite a continuing need to increase _E. This can be seen more clearly in Figure 2.2, which shows how _E, V_T, f_r and O₂ change during incremental cycling to the limit of tolerance in a well-trained athlete. Each point on the plot represents an individual breath, and there are two key features to note. Firstly, unlike the linear response of O₂ to incremental exercise, _E is non-linear, rising steeply at about 70% of maximal intensity. As a result, the _E required at 80% of maximum capacity is not twice the amount required at 40%; rather, it is more like four or five times greater. Secondly, as V_T levels off, f_r rises steeply to meet the need for an escalating _E.

The non-linear increase of _E results from the role that breathing plays in compensating for the escalating metabolic acidosis. Chapter 1 described how breathing plays an important role in regulating blood and tissue pH by manipulating the excretion of CO₂ at the lungs. At the lactate threshold (LaT), lactic acid (also known as lactate) production exceeds its degradation leading to accumulation of lactic acid in the muscles and blood (see ‘Cardiorespiratory fitness, Lactate threshold’ below). Above the LaT, _E exceeds that required to deliver O₂, and the primary role of the respiratory system is stabilizing pH by removal of CO₂ via the lungs. This process is known as a ventilatory compensation for a metabolic acidosis (see Ch. 1,‘Acid–base balance’). The steep increase in _E at the LaT is a response to stimulation of the peripheral chemoreceptors by the hydrogen ion component of lactic acid (see Ch. 1, ‘Chemical control of breathing’). This ventilatory response is central to the system that minimizes the acidification of the body and the negative influence of this upon muscle function and fatigue (Box 2.1). As will be described in the section ‘Lactate threshold’ below, the inflection of the response of _E can be used to estimate the exercise intensity at which blood lactate accumulation commences, i.e., the so-called ventilatory threshold. The LaT and ventilatory threshold are related to the same physiological phenomenon, and are often used synonymously. However, they are not identical: the ventilatory threshold lags behind the LaT slightly because it is a response to the elevated hydrogen ion concentration in the blood.

The increasing reliance upon f_r to raise _E at high intensities of exercise arises because it becomes too uncomfortable to continue to increase V_T; typically, this occurs when V_T is around 60% of FVC. As V_T increases, progressively greater inspiratory muscle force is required to overcome the elastance of the respiratory system. Higher inspiratory muscle force output increases effort and breathing discomfort (see Ch. 1, ‘Dyspnoea and breathing effort’). Eventually, the sensory feedback from the inspiratory muscles signals the respiratory centre to change the pattern of breathing, and to increase f_r more steeply instead of V_T. The respiratory centre has an exquisite system for minimizing breathing discomfort, which also optimizes efficiency. This drive to optimize is also observed in the breathing pattern derangements that are seen in the presence of disease (see Ch. 3).

The influence of the LaT upon the exercise hyperpnoea can also be observed during constant intensity exercise. Figure 2.3 illustrates the typical ventilatory responses to two intensities of exercise, one below and one above the LaT. In both intensity domains, the ‘on’ transient response of _E has three phases: phase I is an almost instantaneous increase, which is followed by the monoexponential increase of phase II, and finally phase III, which is either a plateau or a continued, slow increase. During light and moderate-intensity exercise, phase III is a plateau (steady state); in contrast, during heavy exercise phase III continues to show a gradual increase throughout exercise, never achieving a steady state. The absence of a steady state in phase III is due to the presence of a ventilatory compensation for the metabolic acidosis. Unfortunately, this compensation is imperfect, and does not offset the fall in pH completely; accordingly, exercise above the LaT is non-sustainable. At exercise cessation, the ‘off’ transient also displays an abrupt fall in _E, followed by exponential decline; the recovery of _E following heavy exercise takes much longer than that following light and moderate exercise because of a continued drive to breathe originating from the metabolic acidosis.

Introduction

At rest, the average adult heart beats at a frequency of around 65 beats per minute. With each beat, around 75 ml of blood are ejected from the heart (stroke volume: SV), providing a cardiac output () of around 5 l·min^− 1 (65 × 0.075 l). The SV depends upon body size, training status and metabolic rate. Larger and fitter people both have larger hearts, which eject a larger SV. In the case of fitter people, this may be around 100 ml, and the increase results in a lower resting heart rate (f_c) since resting is unchanged. In contrast, the larger SV of larger individuals is supporting a higher energy and oxygen (O₂) demand, which requires a higher ; thus their resting f_c is unchanged.

During maximal exercise, f_c rises to over 200 beats per minute in a healthy young person. Accompanying this increase in f_c is a rise in SV, to around 110 ml, such that reaches around 22 l·min^− 1 at maximal exercise. In Olympic-class endurance athletes, has been measured at 40 l·min^− 1, thanks to a SV that can be as high as 210 ml.

In contrast to the ‘trainability’ of stroke volume, maximal f_c tends to remain the same in a given individual, but does decline with advancing age. Accordingly, an approximate estimate of a maximal f_c (f_cMax) can be obtained by using equations such as:

In the previous section, Sir Matthew Pinsent’s phenomenal lung capacity and respiratory power output were described. Along with his extraordinary ability to deliver fresh air to his alveoli, was an equally astonishing ability of his cardiovascular system to collect oxygen from the lungs, and deliver it to the exercising muscles. Sir Matthew’s O_2peak of around 8 l·min^− 1 would have required a maximal cardiac output of around 40 l·min^− 1.

The cardiovascular system during exercise

During exercise, both f_c and SV increase progressively in order to deliver an appropriate to the pulmonary and peripheral circulations. As is the case with the increase in respiratory V_T during exercise, SV also displays a non-linear response, showing a plateau at around 40–50% of maximal exercise capacity. The reasons for this are complex, but include a number of mechanical limitations that arise from both the filling of the ventricle during diastole and the ability of the heart to eject blood during systole (Gonzalez-Alonso, 2012).

Commensurate with this plateau in SV is a plateau in . As was mentioned above, SV is very amenable to training, and provides the only mechanism by which maximal can be increased; this will be described in the section ‘Principles of cardiorespiratory training, Training adaptations’ (below).

In the acute response to exercise, SV is enhanced by two main mechanisms: (1) an intrinsic mechanism whereby an elevation in the volume of blood returning to the heart (venous return) stimulates a more forceful ventricular contraction, and (2) an increase in the force of ventricular contraction due to neurohumoral influences (sympathetic drive to the heart and circulating catecholamine levels). Venous return is enhanced by both the pumping action of the exercising muscles (see below) and the more negative intrathoracic pressure swings that arise from increased V_T and inspiratory flow rate. The muscle pump ‘pushes’ blood towards the heart, whilst the thoracic pump ‘sucks’ it towards the heart. The result is an increased pre-load during diastole, which stretches the myocardial wall stimulating it to contract more forcefully. This response is possible because stretching of the myocardial muscle fibres leads to a pre-stretch that stores elastic energy within the fibres. This energy is released during contraction, leading to an increase in the force of myocardial contraction. The increase in force expels a greater proportion of the ventricular end-diastolic volume, as well as the additional blood that had caused the myocardial stretch. The result is an increase in SV, a reduction in the end-diastolic volume (EDV; akin to RV of the lungs) and an increase in the ejection fraction (proportion of EDV that is ejected). This mechanical response of the heart was first described in the early 1900s by Otto Frank and Ernst Starling, and is known as the Frank–Starling law of the heart. This intrinsic mechanism for enhancing SV is enhanced by the effects of the sympathetic neural and hormonal influences upon the myocardium, which also enhance the contractility of the myocardial wall.

As well as increasing during exercise, the integrated response of the cardiovascular system must also distribute blood to the parts of the body where it is needed most. So far as exercising muscle blood flow is concerned, this regulation takes place with exquisite precision such that muscle O₂ demand and supply are regulated tightly. However, if this increase were to take place without a compensatory restriction of blood flow elsewhere in the peripheral circulation, arterial blood pressure would be in jeopardy. Accordingly, the integrated response of the cardiovascular system during exercise includes redistribution of blood flow such that it is directed to areas of urgent O₂ demand, at the expense of areas such as the splanchnic circulations. For example, renal blood flow falls by about 75% during maximal exercise.

The control of exercising muscle blood flow is complex, and the factors responsible change as exercise progresses (Hussain & Comtois, 2005). At the immediate onset of exercise, rhythmic contraction of exercising muscles facilitates unidirectional ejection of blood through the venules and deep veins (backflow is prevented by venous valves); during relaxation, venous pressure drops, facilitating the inflow of blood via the arterial circulation. This pumping action also stimulates an increase in muscle blood flow via the release of local vessel endothelial factors that respond to ‘shear stress’ inside the arterioles; in other words, the physical stress exerted on the vessel endothelium by flowing blood stimulates the vessel to relax and dilate. As exercise progresses, muscle metabolism leads to an increase in local metabolites such as CO₂, lactic acid, adenosine, potassium ions and osmolarity, as well as a decline in O₂. This vasodilator stimulus supplements that from endothelial factors to produce a full-blown exercise hyperaemia (Hussain & Comtois, 2005).

The maximal capacity of the exercising muscles to accommodate blood flow far exceeds the ability of the to supply it. Accordingly, blood flow to exercising muscles, as well as non-exercising tissues, must be regulated by the sympathetic nervous system, whose job it is to defend arterial blood pressure (ABP). Without this regulatory restraint by the sympathetic nervous system, ABP would fall precipitously. One important component of the mechanism(s) contributing to this restraint is feedback from muscle metaboreceptors (Sinoway & Prophet, 1990). The afferent arm of the resulting reflex response (metaboreflex) is mediated by simple group III and IV afferents residing within skeletal muscles. These afferents sense both mechanical and metabolic stimuli during exercise, and, amongst other things, induce sympathetically mediated, active vasoconstriction in all tissues, including exercising muscles. In tissues with low metabolism this output stimulates powerful vasoconstriction, whist in exercising muscles the resultant vasoconstriction is a balance between the local vasodilatory influence and the neural vasoconstrictor influence.

In Chapter 3 (section ‘Respiratory muscle involvement in exercise limitation, Healthy people’) we will consider the ramifications of activation of the metaboreflex originating from exercising respiratory muscles.

1. Excitatory input to the motor cortex

2. Excitatory drive to lower motoneurons

3. Motorneuron excitability

4. Neuromuscular transmission

5. Sarcolemma excitability

6. Excitation–contraction coupling

7. Contractile machinery

8. Metabolic energy supply.