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Training in Extreme Conditions

Paper Type: Free Essay Subject: Sports
Wordcount: 3085 words Published: 17th Oct 2016

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Training is the acquisition of knowledge, skills, and competencies as a result of the teaching of vocational or practical skills and knowledge that relate to specific useful competencies. Training has specific goals of improving one’s capability, capacity, productivity and performance. (Wales)

Body’s physiological response during exercise:

Physiological response to exercise depends on intensity, duration and frequency of exercise and also depends on environment surroundings. During exercise requirement of oxygen and substrates in skeletal muscle are increased simultaneously leads to increase removal of metabolites and carbon dioxide. Chemical, mechanical and thermal stimuli affect alterations in metabolic, cardiovascular and ventilator function in order to meet these increased demands (Stokes).

Adenosine triphosphate is a high-energy phosphate molecule that initiate muscle contraction, immediate source of energy supplies to muscle are initially provided by energy sources like ATP and Phosphocreatine before other aspects of metabolism are activated. Pulmonary ventilation increases as increase in respiratory rate to cope up increase in oxygen demand (Stokes)

Some enzymes (ATPase) are able to use the energy stored between ADP and Pi bond. Water is involved is called hydrolysis. Each molecule of ATP releases 7.3 k cal.(30.7 kj) Energy can also provided by acetylate kinase reaction where ATP is produced from the conversion of two molecules of adenosine diphosphate(ADP to adenosine monophosphate(Amp) and ATP. (Stokes)Phosphocreatine stored in the muscle is a high-energy source for skeletal muscle it contributes energy in first 10 seconds of high intensity activities such as sprinting and are rapidly depleted but they provide important energy source in first few seconds of exercise before other aspects of metabolism are activated. (Stokes)

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resynthesis of ATP from energy-dense substrates glycolysis is a pathway by which glycogen and glucose are converted to two pyruvate molecules in the presence of oxygen, pyruvate enters the Krebs cycle via acetyl coA. Each turn of the Krebs cycle produces hydrogen carriers that enter the electron transport chain (ETC) and ultimately donate H+ to oxygen to form water, allowing ETC to proceed, however, when oxygen is not present, ETC cannot proceed which prevents flux through the Krebs cycle and result in a build up of pyruvate(Stokes. If it was allowed to continue the glycolysis may stop and no further ATP would be synthesized. Fortunately, pyruvate can accept the hydrogen carrier, forming lactic acid yields only 3 moll ATP per molecule of glycogen, but this can occur in absence of oxygen. In contrast, complete breakdown of glycogen via glycolysis, the Krebs cycle and the ETC yields 39 ATP per molecule of glycogen. (Stokes) Fatty acids are more energy dense than glycogen and there are very large stores of fat in adipose tissue, all energy stored as fat is stored as glycogen, body mass would increase by 50 Kg. Fatty acids are catabolized and enter into the Krebs cycle and ETC. A fully oxidized fat yields 129 molecules of ATP. The rate of resynthesize of fat is too slow to be of great importance during high intensity training. During exercise ventilation might increase from values around 5-6 liters min to >100 liter min. in an average young male, resting oxygen consumption is about 250 ml min and in endurance athlete during internes exercise might reach 5000 ml min (Stokes).Changes which occur in arterial pH, PO2 and PCO2 values during exercise are usually small, the increased reliance on glycolysis results in increased accumulation of lactic acid, which initially leads to an increase in PaCO2. Ventilation increases abruptly in the initial stages of exercise and is then followed by a more gradual increase. (Stokes) Oxygen requirements of working skeletal muscles are dramatically elevated above resting requirements. Resting blood flow to muscle is usually 2–4 ml•100 g muscle−1 min−1, but might increase to nearly 100 ml•100 g muscle−1 min−1 during maximal exercise. The circulatory changes which occur are increase blood flow to muscle leads to increase in cardiac output which leads to increase oxygen consumption. (Stokes) In the body maximum efficiency for conversion of energy nutrients into muscular work is 20-25%, the remaining is released in non-usable form of heat which raises body temperature this heat is due to increase metabolism in the body during exercise and blood supply to skin is increased which in tern stimulates sweat glands which starts sweating which causes heat loss. (Stokes)

Training in Heat (Rg)

This report discuss the temperatures that are considered hot, how the physiology of a human body adjusts an increase in temperature, what the stages of illness that are caused by heat, along with precautions that should be taken while exercising in heat.

Generally the human body tries to maintain a certain body temperature range. This helps it function within its optimal levels. The normal human body temperature is 37°C. Increases in body temperature of 2°C to 3°C generally do not result in causing ill effects. However, increases in body temperature above 40°C to 41°C can be associated with a variety of heat-related problems (Astrand.P, 1986). During exercise, constant heat is produced as a bi-product of metabolism and muscular contraction. This heat increases the core temperature of the body, which alarms its thermoregulatory mechanism, returning the body back to a homeostatic state. There are two important functions contributing to this mechanism are increase in blood flow to the skin, facilitating cooling and increasing sweating. This sweat helps evaporate the heat and lowers the core temperature.

The result of the aforementioned mechanism leads to cardiovascular strain due to the increase in blood flow to skin, blood flowing to the muscles and the decrease of blood plasma volume, due to sweat loss. This leads to a cardiovascular drift. Cardiovascular drift is due to the competition of the blood flow toward the skin and muscles. This leads to a decrease in stroke volume, meaning in order to maintain cardiac output we would have to increase heart rate. Increasing heart rate helps provide proper blood supply to skin and working muscles.

C:UsersBOBBYDesktopthermoregulation feedback.jpg The process of the body’s core temperature increasing occurs when the blood perforates the hypothalamus. The hypothalamus then signals the rest of the body to reduce its exercise intensity (Phil wallace, 2013) . Exercising in hot climates without proper acclimatization can lead to a severe consequence called “Heat illness.” This illness is categorized into different stages based on the pathological events occurring at that time.

(wordPress, 2012)

Figure taken from (Ali Al-Nawaiseh, 2013)

The different stages of heat illness are:

  1. Heat Cramps: It is thought to be due to the ingesting water with no salt during restitution from thermal dehydration.

Clinical Feature – Defined by a painful muscle cramp.

  1. Heat exhaustion: It is caused by sweat loss that results from exposure to high environmental heat or hard work.

Clinical Feature – Defined by clinical symptoms that involve a high body core temperature and signs of cerebral ischemia such as weakness, fatigue, discomfort, anxiety, dizziness, and headache.

  1. Heat syncope: It reflects cardiovascular failure caused by reduced venous return to the heart due to excessive seat loss.

Clinical features – Includes dizziness, fainting, and pale face.

  1. Heat stroke: It is the most severe heat-related disturbance and can be fatal.

Clinical Feature – Core temperatures greater than 40°C accompanied by hot and dry skin, indicative of impaired thermoregulation. It is also associated with delirium, convulsions or coma, indicating, impaired central nervous system function.

Figure taken from (Yamazaki, 2012)

Heat Acclimatization: – Heat acclimatization is a process which body adapts to temperature change. It happens for the first 10-15 days of initial change, but major change occurs for the first 3 to 4 days. Heat acclimation improves endurance exercise performance in the heat, and thermal comfort at a given exercise rate. The primary adaptations that occur during heat acclimation are: Increased plasma volume by 10% – 12%, earlier onset of sweating, higher sweat rate, reduced salt loss in sweat, reduced blood flow to skin and increased synthesis of heat shock proteins

There are many precautions that need to be taken while exercising in hot environments few of them are “obtain players or exercisers history of previous heat illnesses. Allow a period of seven to the ten days for acclimatization. Instruct players to wear appropriate clothing during the acclimatization period. Take regular measurements of the WBGT index. Encourage players to adequately replace fluids. Record body weight of players before and after, during practice and matches. Identify susceptible players. Constantly be vigilant and monitor players for signs of heat illness. Players must have unlimited access to water”. (International Hockey Federation (FIH), 2010)

Training in Cold Conditions (Tyler)

Exercising in cold temperatures is a complex idea. There are many factors and variables that need to be taken into account before contemplating or beginning to exercise in a cold environment or during a cold season. There are four major topics that we will be discussing: A) Metabolic changes B) Cardiovascular changes C) Thermal aspects and D) Adaptations.

Choosing the correct diet for exercising in the cold can be tricky. After researching the subject there has shown to be no one significantly superior style of diet, whether it is carbohydrate, fat or protein dominant. However, one study did show that more work was achieved after a 3-day high carbohydrate diet (600g/day) as opposed to a 3-day normal diet (300g/day) [Thorp et al. 1990]. This would indicate an important relationship between exercise performance in a cold environment and carbohydrate intake. A study conducted by “Doubt and Hsieh in 1991 and Jacobs et al in 1984, 1985” shows us that venous lactate concentrations are higher with exercise in cold temperatures, which is due to the inverse relationship between muscle temperature and glycolysis. Lactate values have shown to be higher in colder temperature (-2°C), these values also seemed to increase at a slower rate than they did at warmer temperature (+24°C); indicating that there may be a temperature-related delay in lactate release. Samples were taken at the end of each incremental increase in workload throughout the study, leading to these results (Therminarias et al. 1989).

Ventilation experiences an increase when the body is exposed to a colder environment. However, the differences between ventilation in a cold environment and that of warmer environment diminish as we increase our exercise workload (Therminarias et al. 1989). As we know, during respiration our lungs work to bring in oxygen and expel carbon dioxide. However, if there is an increase in ventilation, this could result in the reduction of end-tidal carbon dioxide. Maintaining higher levels of CO2 within the body could eventually lead toward impaired mental function in persons working in a cold environment (Cooper et al. 1976). When we introduce our body into a cold environment, our body reacts. This is usually in the form of the cutaneous thermal receptors sending distress signals to our central nervous system via afferent signalling.

The body uses two mechanisms to account for higher VO2 during exercise in a cold environment. 1) A flux in our total body heat occurs (Nadel 1984; Park et al. 1984; Rennie 1988; Sagawa et al. 1988) 2) Our net mechanical efficiency is decreased (Pendergast 1988). If a flux in total body heat occurs, the body responds via negative feedback. First the body’s thermal receptors detect an unwanted change in body temperature at the skin. These receptors send a message via afferent messaging to the central nervous system which determines the best way to return the body back to its homeostatic state. A signal then is sent from the brain, to the hypothalamus which responds by sending its own message to our muscles forcing them to repeatedly contract at an express pace, this is commonly referred to as “shivering.” The more the body shivers, the more heat that is produced which in turn raises the body’s core temperature. After a homeostatic balance is regained, we begin to stop shivering as the “heat-promoting” portion of the hypothalamus begins to shut down. When considering the efficiency of our body to perform specific actions, we need to take into account how the cold temperature will affect us. Cold muscles tend to have a reduced contractile force, regardless of whether or not the kinetic energy requirement has been altered. This means that the body may have to try and recruit additional motor units to meet the required work output (Blomstrand et al. 1986). Exposure to a cold climate causes significant peripheral vasoconstriction, resulting in elevation of blood pressure. Cold temperature has the ability to affect cardiac output through an increase in intrathoracic blood volume, which is secondary to peripheral vasoconstriction (Pendergast 1988). The increase in intrathoracic volume is indicated through larger increases in stroke volume (McArdle et al 1976) or total body insulation (Rennie 1988). Increasing the intrathoracic blood volume has shown to increase both left ventricular end-diastolic and end-systolic dimensions at rest and during exercise (Sheldahl et al. 1984).

Exposure to cold temperatures during exercise can sometimes lead to injury, such as a non-freezing cold injury or frostbite. This can be seen early throughout the distal extremities. The distal extremities depend on blood flow to maintain a suitable local temperature because their intrinsic capacity to generate heat in limited (Doubt & Francis 1989). Our peripheral systems utilize a negative feedback technique to regain a suitable local temperature by alternating vasoconstriction and vasodilation (Rusch et al. 1981).


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