7.3 The heart, energy and exercise
Controlling the heart
The heart is myogenic – it contracts and relaxes automatically without stimulation from nerves to pump blood around the body. It is specific and made of specialised tissue called cardiac muscle. Rhythmic contraction of the cardiac muscle is coordinated through electrical impulses passing through the cardiac tissue.
In the right atrium wall, muscle tissue is present called the sinoatrial node (SAN) which acts as a pacemaker. This has an intrinsic rate of contraction a bit higher than the rest of the heart muscle. As the SAN cells contract, they generate action potentials, sending a wave of depolarisation along the right atria wall, causing them to contract (atrial systole).
When the wave of depolarisation reaches the atroventricular node (AVN), it is delayed by 0.13 seconds to ensure the atria have finished contracting before the ventricles and the depolarisation then continues down between the ventricles, along fibres called the bundle of His and down the purkyne fibres, and up through the ventricle walls. This causes the ventricles to contract together from the bottom up (from the apex), slightly after the atria (ventricular systole). Blood is squeezed into the aorta and pulmonary artery.
There is then a short delay before the next wave of depolarisation in the SAN. During this time the heart muscles relax and repolarises, this is diastole.
Differences in resting heart rate are caused by different size, body size and genetic factors. A larger heart usually has a lower resting heart rate – it expels more blood with one beat so does not need to beat as frequently to keep blood circulation constant. Endurance training produces a lower heart rate because there is an increase in the heart size due to thickening of the muscle cell walls.
Electrocardiograms (ECG)
The electrical activity in a heart is monitored and recorded by an ECG which produces a trace. Electrodes are attached to a person’s chest and limbs to record the electrical currents produced during the cardiac cycle. When there is a change in polarisation of the cardiac muscle, there is a small electrical current that can be detected on the skin. An ECG is usually performed on a patient at rest.
- P wave = contraction (depolarisation) of the atria
- QRS complex = contraction (depolarisation) of the ventricles
- T wave – relaxation/recovery (repolarisation) of the ventricles
- PR interval – time for impulses to be conducted from SAN across the atria to the ventricles, through the AVN
You can work out the time for one complete cardiac cycle by multiplying the number of squares between the QRS complex by 0.2 then doing 60 divided by the answer.
Abnormal ECGs can be used to diagnose heart problems. Doctors compare patient’s ECGs with a normal trace to diagnose problems with the heart rhythm such as CVD.
For example:
- Tachycardia – increased heart rate of more than 100bpm – sign of heart failure – cannot pump blood efficiently – can increase risk of heart attack
- Bradycardia – heart rate of less than 60pbp
- Fibrillation – irregular heartbeat – atria and ventricles have lost their rhythm. Atrial fibrillation – chest pains, fainting and increased risk of stroke. Ventricular fibrillation – heart attack
- Ischaemia – heart muscle does not receive blood due to atherosclerosis causing blockage of coronary arteries – disrupts normal electrical activity and rhythm, arrhythmias is caused (irregular heart beat)
- A longer delay between the P and R waves – electrical impulses cannot pass easily from the atria to the ventricles – e.g. damage to the bundles of His
- A flat T wave – indicate lack of blood flow to cardiac muscle in the heart wall – no energy for contraction – could be an indication of CVD
- Problems with AVN – atria are contracting but ventricles are not – some P waves not followed by a QRS complex
So ECGs can provide information on irregular heartbeats, areas of damage and inadequate blood flow.
Homeostasis and responding to exercise
Homeostasis = The maintenance of a steady internal state in the body almost regardless of changes in either the external or internal conditions.
The core body temperature must be maintained in a narrow range at around 37oC for cells to function and stop enzymes becoming denatured. This is a dynamic equilibrium, matching the supply of oxygen and glucose to the changing demands, while removing carbon dioxide and maintaining an even temperature. Each condition has a norm value that the mechanism maintains.
Homeostasis involves coordination and control. Changes in the body are detected by a sensor/receptor. This sends a message to an effector which reverses or increases the change. Negative feedback systems provide a way of maintaining a condition – a change is registered by receptors and effectors are stimulated to restore the equilibrium. In a positive feedback system, effectors increase the effect which triggered the response.
The communication in a feedback system can be hormones (chemical messengers) or by nerve impulses (electrical messengers). Homeostasis plays a role in exercise when conditions change rapidly and demands are high.
Nervous control:
Heart rate is controlled by the cardiovascular control centre in the medulla of the brain. Chemical and stretch receptors in the blood vessels and heart chambers send nerve impulses to the cardiovascular centre. Two types of nerves of the autonomic system then carry impulses to the heart, controlling its rate:
- Sympathetic nervous system: Usually excitatory – speeds heart rate – releases adrenaline and noradrenaline when stimulated
- Parasympathetic nervous system: Usually inhibitory – slows heart rate – releases acetylcholine when stimulated
Nerve impulses travelling down the sympathetic nerve from the cardiovascular centre stimulate the SAN. This increases the frequency of the signals from the pacemaker region so the heart rate increases. In contrast nerve impulses in the parasympathetic nerve inhibit the SAN and slow the heart down.
Hormonal control:
Adrenaline is secreted from the adrenal glands above the kidneys during fear, shock or excitement, stimulating the SAN to increase its rate of contraction. This speeds the frequency of excitation, supplying extra oxygen and glucose for the muscles and brain in a fight or flight response. Adrenaline also causes dilation of the arterioles supplying skeletal muscles and constriction of arterioles going to the digestive system and other non-essential organs. This maximises blood flow to the active muscles. Adrenaline also causes an anticipatory increase in heart rate before exercise.
Responding to exercise
As the atria fill with blood at the start of the cardiac cycle, stretch receptors in the muscle walls of the heart send nerve impulses to the cardiovascular control centre. This sends more impulses along the sympathetic nerve to the SAN, increasing the heart rate. The increased stretching of the heart atrial muscle also makes the muscles contract harder, increasing the volume of blood expelled at each stroke.
Baroreceptors (sensitive to pressure) in the aorta and carotid arteries are stretched as blood pressure increases after exercise. They send nerve impulses to the parasympathetic system to slow the heart rate and cause vasodilation. This lowers the blood pressure.
The reverse happens when exercise starts – the blood vessels dilate in response to adrenaline and blood pressure falls, reducing the stretch of the baroreceptors. When the baroreceptors do not stimulate the cardiovascular control centre it sends signals along the sympathetic nerve to stimulate the heart rate and increase blood pressure.
Increased heart rate caused by:
- Increase in carbon dioxide
- Decrease in oxygen
- Decrease in blood pH
- Increase in temperature
Breathing rhythms: Components of lung volume
Ventilation rate is the volume of air breathed in or out in a minute
Ventilation rate = tidal volume x breathing rate
- Tidal volume is the volume of air in a normal breath (about 0.4dm3)
- Breathing rate is how many breaths are taken in a minute
Cardiac output is the total volume of blood pumped by the left ventricle every minute.
Cardiac output increases during exercise because heart rate and stroke volume both increase as the heart pumps faster and harder.
Cardiac output (cm3/min) = stroke volume (cm3) x heart rate (bpm)
- Stroke volume is the volume of blood pumped by the left ventricle each time it contracts
Cardiac output can be increased by:
- Increasing strength of contraction which increases the rate oxygen enters the blood in the lungs and carbon dioxide leaves it
- Increasing heart rate which increases the rate blood moves through the vessels, delivering oxygen to muscle tissues and removing carbon dioxide and lactate from them.
Vital capacity is the maximum volume of air we can inhale and exhale
Aerobic capacity is the ability to take in, transport and use oxygen
Long periods of strenuous exercise depends on maintaining a constant ATP supply, this depends on aerobic capacity.
- VO2 is the volume of oxygen we consume per minute
- VO2 max is the maximum amount of oxygen we can consume per minute
During exercise, there are greater muscle contractions so more blood returns to the heart (venous return) – in diastole the heart fills with a larger volume of blood – the heart muscle is stretched more, increasing stroke volume and cardiac output.
Practical – using a spirometer to investigate ventilation rate
Spirometers can be used to measure tidal volume and breathing rate and can also be used to investigate the effects of exercise. A spirometer is a machine with an enclosed chamber containing oxygen, lying over water.
- A person breathes through a mouthpiece/tube
- As they breathe in, the lid moves As they breathe out, it moves up
- These movements are recorded by a pen attached to the chamber lid, drawing on a rotating drum, creating a spirometer trace
- The soda lime in the tube absorbs carbon dioxide breathes out during respiration – only oxygen is in the chamber to inhale from – total volume decreases.
By counting the number of traces over a known period of time, breaths per minute can be calculated.
Control and regulation
The medulla controls breathing rate. Rhythmic patterns of nerve impulses are sent from the ventilation centre in the medulla to the muscles in the diaphragm and intercostal muscles, which respond by contracting rhythmically. There are two ventilation centres:
- Inspiratory centre – controls breathing in – sends nerve impulses to intercostal and diaphragm muscles to make them contract – increases volume and decreases pressure in lungs. These impulses inhibit action of the expiratory centre. As the lungs inflate, stretch receptors are stimulated and send nerve impulses back to the medulla, inhibiting the action of the inspiratory centre.
- Expiratory centre – controls breathing out – no longer inhibited, sends nerve impulses to the diaphragm and intercostal muscles to relax – lungs deflate, expelling air. The stretch receptors become inactive then the cycle repeats
Homeostasis
During exercise, there is an increase in carbon dioxide in the blood and a decrease in blood pH. This is detected by chemoreceptors in the medulla, aorta and carotid bodies which then send nerve impulses to the respiratory/ventilation centre. Impulses are sent to the breathing muscles (effectors) – intercostal muscles and diaphragm to change the breathing rate in a negative feedback system, removing the extra carbon dioxide and increasing oxygen uptake. The muscles contract harder and faster, increasing the rate and depth of breathing.
Temperature control and exercise
When energy is transferred, some is lost as heat, so respiration and muscle contraction produce heat. During vigorous exercise, heat is generated in muscles, causing the blood temperature to rise. Thermoregulation is an important aspect of homeostasis to prevent enzymes becoming denatured and ensuring that normal metabolic reactions can take place.
Human temperature regulation
Changes in core temperature are detected by thermoreceptors in the skin and sent to the hypothalamus in the brain. The hypothalamus then sends nerve impulses to effectors which respond:
When temperature rises:
- Vasodilation: Smooth muscle in the arteriole walls delivering blood to the skin dilate so a greater volume of blood flows into the surface capillaries – allows heat to be lost by radiation from the blood through the skin surface
- Sweat glands activate: Sweat flows up the sweat ducts onto the skin surface, where the water in it evaporates – takes heat from the skin
- Erector pili muscles attached to hairs relax to let hairs lie flat so they do not trap a layer of insulating air.
When temperature falls:
- Vasoconstriction: Arterioles constrict so less heat is lost from the skin surface, blood is diverted beneath the insulating fat layer beneath the skin
- Sweat glands secrete little or no sweat
- Erector pili muscles contract, pilling hairs up – traps a layer of insulating air next to the skin
- Certain muscles contract and relax rapidly (shivering), generating heat which increases blood temperature
| Heat gain process | Heat loss process |
| Vasoconstriction – arterioles in skin constrict | Vasodilation – inhibits arteriole contraction |
| Hair erector muscles contract | Hair erector muscles relax |
| Sweat glands are inhibited | Sweat glands are stimulated |
| Liver secretes hormones – increases metabolic rate | Liver – decreases metabolic rate |
| Skeletal muscles contract – shivering, increased respiration | Skeletal muscles relax – no shivering |
This is negative feedback – a receptor detects a change in the normal state of a system – triggers events to reverse the change. However temperature does fluctuate because of the lag time between the sensory (hypothalamus) detecting the change and the effectors respond to it.
