Exercise physiology is the study of the function of the human body during various acute and chronic exercise conditions.
These effects are significant during both short, high-intensity exercise, as well as with prolonged strenuous exercise such as done in endurance sports like marathons, ultramarathons, and road bicycle racing.
In exercise, the liver generates extra glucose, while increased cardiovascular activity by the heart, and respiration by the lungs, provides an increased supply of oxygen.
When exercise is very prolonged and strenuous, a decline, however, can occur in blood levels of glucose. In some individuals, this might even cause hypoglycemia and hypoxemia.
There can also be cognitive and physical impairments due to dehydration. Another risk is low plasma sodium blood levels.Prolonged exercise is made possible by the human thermoregulatory capacity to remove exercise waste heat by sweat evaporation.
This capacity evolved to enable early humans after many hours of persistence hunting to exhaust game animals that cannot remove so effectively exercise heat from their body.
Humans have a high capacity to expend energy for many hours doing sustained exercise. For example, one individual cycling at a speed of 26.4 km/h (16.4 mph) across 8,204 km (5,098 mi) on 50 consecutive days expended a total of 1,145 MJ (273,850 kcal) with an average power output of 182.5 W.
Skeletal muscle burns 90 mg (0.5 mmol) of glucose each minute in continuous activity (such as when repetitively extending the human knee), generating ?24 W of mechanical energy, and since muscle energy conversion is only 22-26% efficient, ?76 W of heat energy.
Resting skeletal muscle has a basal metabolic rate (resting energy consumption) of 0.63 W/kg making a 160 fold difference between the energy consumption of inactive and active muscles.
For short muscular exertion, energy expenditure can be far greater: an adult human male when jumping up from a squat mechanically generates 314 W/kg, and such rapid movement can generate twice this power in nonhuman animals such as bonobos, and in some small lizards.
This energy expenditure is very large compared to the resting metabolism basal metabolic rate of the adult human body. This varies somewhat with size, gender and age but is typically between 45 W and 85 W.
Total energy expenditure (TEE) due to muscular expended energy is very much higher and depends upon the average level of physical work and exercise done during a day.
Thus exercise, particularly if sustained for very long periods, dominates the energy metabolism of the body.
ATP recycled from ADP in mitochondria provides the energy needed for muscle contraction. The quickest generation of ATP comes from the splitting of already existing phosphocreatine (PCr).
This is then followed by the anaerobic (without oxygen) breakdown of the muscle’s stores of glycogen to produce lactic acid. This anaerobic metabolism quickly generates large amounts of ATP energy but is limited to providing energy for short exertion spurts.
A rapid switch occurs to aerobic ATP energy generation: by 75 seconds, anaerobic metabolism reduces to producing only half of a muscle’s ATP.
Initial aerobic energy substrates are plasma carried free fatty acids and lactate. However, plasma glucose also increasingly comes to be generated by the liver for muscle consumption.
In adults, active physical exertion by skeletal muscle extracts plasma glucose (after muscle glycogen stores are depleted) in a glucose concentration dependent manner.
This extraction of plasma glucose can be considerable, for instance, the muscle working repetitive knee extending draws 0.5 mmol kg?1 min?1. Hepatic (liver) output of glucose can increase to compensate in adults fivefold to make up for this exercise depletion.
This extra glucose usually results in a higher level of plasma glucose than at rest. However, this increase can be insufficient in intense exercise to keep up with prolonged glucose utilization from plasma (replacing only a third to two thirds).
As a result, strenuous prolonged exercise can dramatically reduce plasma glucose levels: for example, before starting ergometer cycling, this can be 4.3 mmol L-1, but after 3 hours, 2.5 mmol L-1.
That this is due to a limited capacity to replace glucose is demonstrated by the fact that there is no drop if cyclists take a glucose polymer supplement every 20 minutes.
Physical exercise in one part of the body can also compete with another, for example, the glucose extracted from plasma by knees doing extensions drops by 20% when arm cranking is added.
(Heart muscle, it should be noted, while able to use glucose, normally uses free fatty acids, as does skeletal muscle at rest.
Increased cardiac output and pulmonary activity occur during exercise to meet the metabolic needs of muscles (this is measured by VO2 max).
Also, like with the plasma levels of glucose, these initially increase but with prolonged strenuous exercise can decrease below resting blood levels.
Intense prolonged exercise produces metabolic waste heat, and this is removed by sweat based thermoregulation. A male marathon runner, loses each hour around 0.83 L in cool weather, and 1.2 L in warm (losses in females are about 68 to 73% lower).
People doing heavy exercise may lose two and half times as much fluid in sweat as urine. This can have profound physiological effects.
Cycling for 2 hours in the heat (35 °C) with minimal fluid intake causes body mass declined by 3 to 5%, blood volume by 3 to 6%, body temperature to rise constantly, and compared to those with proper fluid intake, they have higher heart rates, lower stroke volumes and cardiac outputs, reduced skin blood flow, and higher systemic vascular resistance.
These effects are largely eliminated by replacing 50 to 80% of the fluid lost in sweat.
* Plasma catecholamine concentrations increase 10 fold in whole body exercise.
* Ammonia is produced by exercised skeletal muscles from ADP (the precursor of ATP) by purine nucleotide deamination and amino acid catabolism of myofibrils.
* interleukin-6 (IL-6) increases in blood circulation due to its release from working skeletal muscles. This release is reduced if glucose is taken, suggesting it links to energy related stresses.
* Sodium absorption is affected by the release of interleukin-6 as this can cause the secretion of arginine vasopressin which, in turn, can led to exercise-associated hyponatremia (dangerously low sodium levels).
This loss of sodium in blood plasma can result in encephalopathy (caused by swelling of the brain). This can be prevented by awareness of the risk of drinking excessive amounts of fluids during prolonged exercise.
At rest, the human brain receives 15% of total cardiac output, and uses 20% of the body’s energy consumption. The brain is normally dependent for its high energy expenditure upon aerobic metabolism.
The brain as a result is highly sensitive to failure of its oxygen supply with loss of consciousness occurring within six to seven seconds, with its EEG going flat in 23 seconds.
The metabolic demands of exercise if it effected the oxygen and glucose supply to the brain could therefore quickly disrupt its functioning.
Protecting the brain from even minor disruption is important since exercise depends upon motor control, and particularly, because humans are bipeds, the motor control needed for keeping balance.
Indeed, for this reason, brain energy consumption is increased during intense physical exercise due to the demands in the motor cognition needed to control the body.
Cerebral autoregulation usually ensures the brain has priority to cardiac output, though this is impaired slightly by exhaustive exercise. During submaximal exercise, cardiac output increases and cerebral blood flow increases beyond the brain’s oxygen needs.
However, this is not the case for continuous maximal exertion: “Maximal exercise is, despite the increase in capillary oxygenation [in the brain], associated with a reduced mitochondrial O2 content during whole body exercise” The auto regulation of the brain’s blood supply is impaired particularly in warm environments
In adults, exercise depletes the plasma glucose available to the brain: short intense exercise (35 min ergometer cycling) can reduce brain glucose uptake by 32%.
At rest, energy for the adult brain is normally provided by glucose but the brain has a compensatory capacity to replace some of this with lactate.
Research suggests that this can be raised, when a person rests in a brain scanner, to about 17%, with a higher percentage of 25% occurring during hypoglycemia.
In intense exercise, lactate has been estimated to provide a third of the brain’s energy needs.
There is evidence that the brain might, however, in spite of these alternative sources of energy, still suffer an energy crisis since IL-6 (a sign of metabolic stress) is released during exercise from the brain.
Humans use sweat thermoregulation for body heat clearance, particularly to remove the heat produced during exercise. Mild dehydration as a consequence of exercise and heat is reported to impair cognition.
These impairments can start after body mass lost that is greater than 1%. Cognitive impairment, particularly due to heat and exercise is likely to be due to loss of integrity to the blood brain barrier.
Hyperthermia also can lower cerebral blood flow, and raise brain temperature.
Exercised skeletal muscles produces ammonia. This ammonia is taken up by the brain in proportion to its arterial concentration. Since perceived effort links to such ammonia accumulation, this could be a factor in the sensation of fatigue.
These metabolic consequences of exercise can exacerbate each other’s negative neurological effects.
For example, the uptake of ammonia by the brain is greater with glucose depletion (CSF ammonia levels: rest, below 2 ?mol min?1 detection level; following 3 hours exercise with glucose supplementation, 5.3 ?mol min?1, without glucose supplementation, 16.1 ?mol min?1). The effects of dehydration are greater and happen at a lower threshold in hot environments.
Researchers once attributed fatigue to a build-up of lactic acid in muscles. However, this is no longer believed. Indeed, lactate may stop muscle fatigue by keeping muscles fully responding to nerve signals.
Instead, providing available oxygen and energy supply, disturbances of muscle ion homeostasis are the main factor determining exercise performance, at least during brief very intense exercise.
Each muscle contraction involves an action potential that activates voltage sensors, and so releases Ca2+ ions from the muscle fibre’s sarcoplasmic reticulum.
The action potentials causing this require also ion changes: Na influxes during the depolarization phase and K effluxes for the repolarization phase. Cl- ions also diffuse into the sarcoplasm to aid the repolarization phase.
During intense muscle contraction the ion pumps that maintain homeostasis of these ions are inactivated and this (with other ion related disruption) causes ionic disturbances. This causes cellular membrane depolarization, in excitability, and so muscle weakness.
Ca2+ leakage from type 1 ryanodine receptor) channels has also been identified with fatigue.Dorando Pietri about to collapse at the Marathon finish at the 1908 London Olympic Games
After intense prolonged exercise, there can be a collapse in body homeostasis. Some famous examples include:
* Dorando Pietri in the 1908 Summer Olympic men’s marathon ran the wrong way and collapsed several times.
* Jim Peters in the marathon of the 1954 Commonwealth Games staggered and collapsed several times, and though he had a five-kilometre (three-mile) lead, failed to finish. Though it was formerly believed that this was due to severe dehydration, more recent research suggests it was the combined effects upon the brain of hyperthermia, hypertonic hyponatremia associated with dehydration, and possibly hypoglycaemia.
* Gabriela Andersen-Schiess in the woman’s marathon at the Los Angeles 1984 Summer Olympics in the race’s final 400 meters, stopping occasionally and shown signs of heat exhaustion. Though she fell across the finish line, she was released from medical care only two hours later.
Tim Noakes based on an earlier idea by the 1922 Nobel Prize in Physiology or Medicine winner Archibald Hill has proposed the existence of a central governor. In this, the brain continuously adjusts the power output by muscles during exercise in regard to a safe level of exertion.
These neural calculations factor in prior length of strenuous exercise, the planning duration of further exertion, and the present metabolic state of the body. This adjusts the number of activated skeletal muscle motor units, and is subjectively experienced as fatigue and exhaustion.
The idea of a central governor rejects the earlier idea that fatigue is only caused by mechanical failure of the exercising muscles (“peripheral fatigue”).
Instead, the brain models the metabolic limits of the body to ensure that whole body homeostasis is protected, in particular that the heart is stopped from developing myocardial ischemia, and an emergency reserve is always maintained.
The idea of the central governor has been questioned since ‘physiological catastrophes’ can and do occur suggesting athletes (such as Dorando Pietri, Jim Peters and Gabriela Andersen-Schiess) can over-ride the ‘‘central governor’.
The exercise fatigue has also been suggested to be affected by:
* brain hyperthermia
* glycogen depletion in brain cells
* reactive oxygen species impairing skeletal muscle function
* reduced level of glutamate secondary to uptake of ammonia in the brain
* Fatigue in diaphragm and abdominal respiratory muscles limiting breathing
* Impaired oxygen supply to muscles
* Ammonia effects upon the brain
* Serotonin pathways in the brain
Prolonged exercise such as marathons can increase cardiac biomarkers such as troponin, B-type natriuretic peptide (BNP), and ischemia-modified albumin. This can be misinterpreted by medical personnel as signs of myocardial ischemia, or cardiac dysfunction.
In these clinical conditions, such cardiac biomarkers are produced by irreversible injury of muscles.
In contrast, the processes that create them after strenuous exertion in endurance sports are reversible, with their levels returning to normal within 24-hours (further research, however, is still needed).
Humans are specifically adapted to engage in prolonged strenuous muscular activity (such as efficient long distance bipedal running). This capacity for endurance running evolved to allow the running down of game animals by persistent slow but constant chase over many hours.
Central to the success of this is the ability of the human body, unlike that of the animals they hunt, to effectively remove muscle heat waste. In most animals, this is stored by allowing a temporary increase in body temperature.
This allows them to escape from animals that quickly speed after them for a short duration (the way nearly all predators catch their prey).
Humans unlike other animals that catch prey remove heat with a specialized thermore gulation based on sweat evaporation. One gram of sweat can remove 2,598 J of heat energy.
Another mechanism is increased skin blood flow during exercise that allows for greater convective heat loss that is aided by the upright posture.
This skin based cooling has involved humans in acquiring an increased number of sweat glands, combined with a lack of body fur that would otherwise stop air circulation and efficient evaporation.
Because humans can remove exercise heat, they can avoid the fatigue from heat exhaustion that affects animals chased in persistence hunting, and so eventually catch them when they fatigued from heat exhaustion due to being forced to constantly move.