Thermoregulatory Response Of The Human Body Physical Education Essay

Introduction

The human body relies upon the maintenance of a stable internal environment at reasonably consistent thermal conditions, ranging from 36-37Ëš Celsius, (Rhoades et al, 2003). Deviations from this narrow range can cause catastrophic and even debilitating conditions. This is important such as when the body is under cold stress. Thermoregulation is dependent on the integration of signals from peripheral thermoreceptors, conveying information about skin temperature; and central thermoreceptors which monitor core temperature. Both peripheral and central thermoreceptor afferents go to the posterior hypothalamus (Longstaff, 2005), where temperatures detected outside the thermoneutral range is initiated with appropriate physiological responses to return core body temperature to normal.

Key physiological mechanisms in response to the decrease in environmental temperature is to reroute blood flow from the periphery to the core organs that is, peripheral vasoconstriction to conserve body heat, shivering which increases muscular activity, tone and metabolic rate, and piloerection which is able to contribute to heat conservation.

The autonomic nervous system (ANS) is divided into two categories: the sympathetic nervous system, stimulating various effector organs, heart rate and force, and blood flow to the skin as well as to the skeletal muscles and brain, whereas the parasympathetic nervous system is primarily involved in conserving the body’s resources and maintaining organ functions during periods of physical inactivity such as slowing down heart rate and stimulating digestion (Brown et al, 2006).

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Temperature regulation can function to control the sympathetic activity to cutaneous vessels and subsequently peripheral blood flow. Thus cutaneous vessels are influenced by reflexes involved in both arterial pressure regulation and temperature regulation (Mohrman & Heller, 2006), such as, an increase in baroreceptors firing rate results in a decrease in sympathetic output and simultaneous increase in parasympathetic output.

Potential applications for this study may be applied to modern-day research in both the science and medical fields with regards to frostbite, hypothermia and trench foot. By gaining an insight to the underlying mechanisms involved, this may also be relevant to the development of drugs and prevention methods in reducing potential side effects to the human body with regards to conditions and illnesses brought on by hypothermia.

The idea of this study is to investigate the contribution of thermoreceptor activity in maintaining homeostasis not only during cold stress but also, overall temperature control mechanisms activated by the body, but also the main thermoreceptor activity the body gives precedence to in response to a conflicting thermal stimulus to the periphery while under cold stress. This will be achieved by observing the alterations of each parameter of oral and core temperatures as well as heart rate, blood pressure, skin temperatures, patella reflex, metabolic rate and respiratory rate from set point values each taken before the cooling period and relevant parameters during the extra testing.

Method

Subjects Studies were conducted upon 19 healthy subjects of which 10 were male and 9 female (age: 19.47 +/- 0.22 yr; height: 169.81 +/- 2.36 cm; weight: 68.31 +/- 3.00 kg). Subjects where selected voluntarily, were not taking medication(s) and where informed prior to experimentation about the objectives of the study and procedures involved. The experiments were conducted within the same day with participation from all subjects.

Protocol design and practice of measurements Consumption of food 30 minutes prior to testing was prohibited and bladders to be emptied immediately before experimentation. Subjects wearing shorts and a t-shirt were seated in a relaxed, sitting position on a chair for 40 minutes at room temperature of 22°C where the appropriate physiological data was recorded at 10 minute intervals – the control period. Within each 10 minute interval the core temperature, oral temperature and respiration rate were recorded once, blood pressure and patella reflex recorded twice; and heart rate and all skin temperatures were recorded three times. Upon completion of the control period that is, after 40 minutes, baseline values were established for each parameter. At time points 10, 20, 30 and 40 minutes, the following parameters were measured:

Core Temperature: To measure core temperature, a soft-thermistor was used, this entailed the ear to be cleaned before the subject slowly placed the thermistor into the auditory canal. A small amount of cotton wool was used to plug the canal which prevented both air from entering and the thermistor from falling out before it was heavily taped down. The core temperature is monitored for the length of the entire experiment (80 minutes) and measurements recorded once for every 10 minute interval during the cooling period.

Oral Temperature: A clinical thermometer was used to measure the oral temperature. The thermometer was placed beneath the tongue and held in this position for 2 minutes while lips were closed. Temperature was recorded once within each 10 minute interval of the control period.

Skin Temperature: Using the “Ezi Scan” thermometer, skin temperature for the forehead, forearm and finger were measured. This was held without making contact, as close as possible to the target area, with all three skin temperature measurements recorded three times during each 10 minute interval.

Blood Pressure: An automatic blood pressure machine was used to record blood pressure. Systolic and diastolic blood pressure measurements were recorded twice for every 10 minute interval simultaneously. The machine was able to automatically record blood pressure as it had an electronic sensor that detected blood flow. Once the individual had placed the monitoring cuff around their arm, the cuff was inflated to a pressure greater than the systolic pressure. The monitor continued to measure pressure as the cuff deflated until it was lower than the diastolic pressure. The device then gave a digital readout of the systolic and diastolic pressures.

Heart Rate: To measure heart rate a heart rate monitor consisting of a transmitting belt and a receiving watch were utilised. Water was placed on the transmitting electrodes and attached on the chest. Measurements were taken three times for every 10 minute interval of the control period.

Patella Reflex: A patella reflex hammer was used to obtain patellar reflexes from the subject. The approximate angle of knee extension is recorded with a protractor twice during the 10 minute interval.

Respiration rate and Metabolic rate: Respiratory rate was calculated using the formula: f(number breaths)/3 minutes. This required the use of the Douglas bag method which collected the total volume of expired air over a three minute period while E and FEO2 were determined from the data collected from the gas analyser and gas meter.

Metabolic rate was determined from oxygen consumption under the assumption that expired volume is equal to inspired volume and that 20.1KJ of energy was produced with one litre of oxygen consumption. Oxygen consumption rate was determined using: O2 (l/min) = E (pulmonary ventilation per minute) x (0.2093- FEO2).

Lastly, metabolic rate was determined by: O2 (l/min) x 20.1(Kj/l) x 60/ Body surface area (m2), where the body surface area (m2): 0.00718 x (weight in kg^0.425) x (height in cm^0.725)

During the 40 minute cooling period immediately following the control period, the lower limbs of the subject, just over the knees were placed in cold water (10-12°C) and a large fan was placed to blow air over the back for the course of the cooling period. The data obtained for each parameter was recorded at 10 minute intervals at timepoints 10, 20, 30 and 40 minutes as per the method used in control period.

Extra Test The control period for the extra test commenced immediately after the completion of the cooling period during which relevant parameter values were recorded and baseline data was established, while the subjects’ legs were still immersed in water and the fan still blowing cold air. The initial set of control measurements, the core and oral temperatures, skin temperatures, blood pressure and heart rate were measured once as soon as the control for the extra test started. Upon obtaining baseline values, the extra test was conducted with the subject’s hand placed in a bucket of warm water while the fan was still on and the lower limbs still immersed in the cold water bath. This occurred for a five minute period and measurements of the parameter were taken at 30 second intervals. Core temperature and the three skin temperatures as well as heart rate were taken at every 30 second interval, whereas oral temperature was taken at every minute mark; 1, 2, 3, 4 and 5. However, blood pressure was measured at 1, 3 and 5 minutes. Extra test and cooling was stopped after the final measurements had been taken.

Statistical analysis

A paired t-test was used to compare two data sets, each control value with the previous control value and evaluate whether they were significantly different. Each control value was compared to the previous control value which would ensure that the subjects were in a relaxed, constant state. The different parameter for the cooling values were then compared with the final control time point, t=-10 minutes for each respective parameter. All intervals of the extra test were compared against the control for each extra test parameter. Differences were considered statistically significant if the p-value was less than 0.05.

Other statistical analyses were also included in the graphical representation. Error bars in both vertical directions which were used on the graphs to indicate the error in a reported measurement which provides a general idea of variability. The standard deviation was also calculated where it is used to measure the variability of a data set, but more importantly, the measure of confidence in statistical inferences whereas the standard error of mean represented the accuracy of the mean. The two are linked: SEM = SD/(square root of sample size).

Results

Figure 1 shows that core temperature declined significantly (p<0.05) at each timepoint during the cooling period when compared with t=-10min of the control period, t=10min p=0.0181, t=20min p=0.0067, t=30min p=0.0041, t=40min p=0.0130, (36.53±0.15, 36.39±0.16, 36.30±0.17 and 36.33±0.16 - ËšC respectively), however, control temperatures for core temperature were similar when compared with previous control. It also gives an indication of no significant values for oral temperatures were obtained in either period, oral temperature remained constant.

Figure 2 indicates the changes in skin temperature of the forehead, forearm and finger during a control period and cooling period. During the cooling period, all body temperatures decreased. Significant values to coincide with the decrease during the cooling period from t=-10min of the control period were obtained (p<0.05), for Forehead temperature: t=10min p=0.0001, t=20min p=0.0001, t=30min p=0.0000, t=40min p=0.0007, (32.06±0.49, 32.36±0.34, 32.19±0.35 and 32.50±0.36 - ËšC respectively); Forearm temperature: t=10min p=0.0000, t=20min p=0.0000, t=30min p=0.0000, t=40min p=0.0000, (30.52±0.36, 29.81±0.44, 29.51±0.43 and 29.13±0.45 - ËšC respectively); Finger temperature: t=10min p=0.0000, t=20min p=0.0000, t=30min p=0.0000, t=40min p=0.0000, (25.13±0.78, 24.75±0.71, 24.54±0.68 and 24.17±0.65 - ËšC respectively). Finger temperature also showed a significant decrease during the control period compared to the previous control time, t=-10min, p=0.0200, (30.45±0.76 - ËšC).

Figure 3 illustrates the changes in systolic and diastolic blood pressures as well as mean arterial pressure, during a 40min control period in which each control timepoint was compared with the pervious and 40min cooling period where values obtained were compared with t=-10min of the control period. It can be deduced that all blood pressures initially increased before reaching a relatively steady state during the cooling experiment. Significant values (p<0.05), obtained for Systolic blood pressure: t=-30min p=0.0177, t=10min p=0.0007, t=20min p=0.0350, (118.39±3.08, 128.28±3.63 and 125.97±2.98 - mmHg respectively); Diastolic blood pressure: t=-10min p=0.0246, t=10min p=0.0044, (77.03±2.57 and 88.23 ±2.00 - mmHg respectively); Mean arterial pressure: t=-10min p=0.0468, t=10min p=0.0008, t=30min p=0.0356, t=40min p=0.0439, (91.78±2.43, 98.26±2.40 and 81.78±2.86 - mmHg respectively).

Figure 4 indicates that heart rate declined throughout the control and cooling periods with significant values suggesting this decline as compared with previous control timepoints at t=-10min of the control period respectively (p<0.05). Significant values for heart rate were obtained at t=-20min p=0.0140, t=20min p=0.0196, t=30min p=0.0208, t=40min p=0.0001, (79.25±1.99, 76.49±1.66, 77.28±1.59 and 76.44±1.94 - beats/min respectively).

Figure 5 shows the changes in the angles obtained with the patella reflex. However, no significant values were obtained in either the control or cooling periods when compared with the previous control time or t=-10min of the control period respectively (p<0.05), therefore parameter did not alter significantly.

Figure 6 indicates the differences in respiratory rate during a control and cooling period. Although the rate remained constant, significant values (p<0.05) obtained during the cooling period when compared to t=-10min during the control period, respiratory rate showed an increase at t=10min p=0.0302, t=40min p=0.0285, (16.82±1.21 and 17.82±1.33 - breaths/min respectively).

Figure 7 shows the differences in litres of expired ventilation of the data set. However, no significant values were obtained in either the control or cooling periods, therefore parameter did not alter significantly upon comparisons with previous control or final 40min mark of control value respectively, (p<0.05).

Figure 8 illustrates the changes in the volume (litres) of oxygen consumption throughout the entire experiment, the control and cooling periods. However, no significant values were obtained in either period (p<0.05); therefore parameter did not alter significantly when compared with the previous control time or t=-10min of the control period respectively.

Figure 9 shows the differences in metabolic rate (kJ/m2/hr) during the control and cooling periods. However, no significant values were obtained throughout the experiment upon comparisons with previous control or final 40min mark of control value respectively; therefore parameter did not alter significantly (p<0.05).

Figure 10 indicates the changes in core and oral temperature during the extra testing period. Although significant values were obtained for core temperature, t=210sec p=0.0041, t=240sec p=0.0119, t=270sec p=0.0349, t=300sec p=0.0207, (36.16±0.17, 36.16±0.16, 36.17±0.16 and 36.16±0.16 – ËšC respectively); it remained constant whilst the subject’s hand was placed in warm water, and continuous cooling of lower limbs occurred simultaneously when compared to extra test control time, (p<0.05). No significant values were obtained for oral temperature throughout the 5min period of the extra test.

Figure 11 shows the changes in skin temperatures of the forehead, forearm and finger during the 5min period of the extra test. However, no significant values were obtained throughout the experiment upon comparison with extra test control time; therefore parameters did not alter significantly (p<0.05).

Figures 12, illustrates the changes in systolic and diastolic blood pressures as well as mean arterial pressure (mmHg), during the extra test with conflicting information relay from the peripheral and central thermoreceptors. No significant values were noted (p<0.05) when compared to extra test control time.

Figure 13 shows the differences in heart rate (beats/min) during extra test. No significant values were obtained throughout the experiment (p<0.05)t; therefore when compared with extra test control time, parameter did not alter significantly.

Figure 1. Core and oral temperature measurements in degree Celsius calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). All temperature measurements were calculated at ten minute intervals. Values for both core and oral temperatures are means ± SEM (n=19 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 2. Forehead, forearm and finger temperatures in degrees Celsius calculated three times each at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). All body temperature measurements were calculated at ten minute intervals. Values for skin temperatures are means ± SEM (n=19 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 3. Systolic and diastolic blood pressures in mmHg calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). Mean arterial pressure, MAP in mmHg was auto calculated on Microsoft Office Excel during both periods. Blood pressure (mmHg) was calculated at ten minute intervals by recording the systolic and diastolic blood pressure twice for each interval. MAP was calculated using the formula MAP= Diastolic pressure + 1/3 (systolic-diastolic pressure). Values for blood pressures are means ± SEM (n=18 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 4: Heart Rate in beats per minute calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). Values for heart rate are means ± SEM (n=19 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 5. Patella Reflex in degrees calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). Values for patella reflex are means ± SEM (n=19 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 6. Respiratory rate in breaths per minute calculated at 10 minute intervals during a 40 minute control (t=-40 to t=-10) and a 40 minute cooling period (t=10 to t=40). Respiratory rate was calculated at ten minute intervals by counting the number of breaths taken over a three minute period, and calculating the average number of breaths/minute by using the formula f(number breaths in total)/3 minutes. Values for respiratory rate are means ± SEM (n=18 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 7. Expired ventilation in litres calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). Expired ventilation was calculated a ten minute intervals by the formula: tidal volume [TV] (l/breath) x f (number of breaths in total). Values for expired ventilation are means ± SEM (n=18 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 8. Oxygen consumption in litres calculated at 10 minute intervals during a 40 minute control (t=10 to t=40) and a 40 minute cooling period (t=-40 to t=-10). Oxygen consumption was calculated a ten minute intervals by multiplying the difference between inspired oxygen and (FIO2, 20.93% or 0.2093) an expired oxygen (FEO2) by using the formula O2 (l/min) = E (pulmonary ventilation per minute) x (0.2093- FEO2). Values for oxygen consumption are means ± SEM (n=18 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Figure 9. Metabolic rate in kJ/m2/hr was auto calculated on Microsoft Office Excel at 10 minute intervals during a 40 minute control (t=-40 to t=-10) and a 40 minute cooling period (t=10 to t=40). Metabolic rate was calculated at ten minutes intervals with the equation: O2 (l/min) x 20.1(Kj/l) x 60/ Body surface area (m2). Values for metabolic rate are means ± SEM (n=18 subjects). Control: Significantly different from control time measured against pervious control time. Cooling: Significantly different from cooling value to 40min mark of control period. Significant values (p<0.05) are indicated by an asterisk (*).

Core and Oral temperatures EXTRA TEST

Figure 10. Extra test measurements for core and oral temperatures in degrees Celsius calculated at 30 second intervals and at 1 minute intervals respectively during a 5 minute heating period. Subject was exposed to conflicting environmental temperatures. Values for both core and oral temperatures in extra test are means ± SEM (n=19 subjects). Extra test: Significantly different from extra test control time measured against extra test time. Significant values (p<0.05) are indicated by an asterisk (*).

Skin temperatures EXTRA TEST

Figure 11. Extra test measurements for skin temperatures in degrees Celsius for forehead, forearm and finger calculated at 30 second intervals during a 5 minute heating period.

Subject was exposed to conflicting environmental temperatures. Values for skin temperatures in extra test are means ± SEM (n=19 subjects). Extra test: Significantly different from extra test control time measured against extra test time. Significant values (p<0.05) are indicated by an asterisk (*).

Blood pressures EXTRA TEST

Figure 12. Extra test measurements for systolic and diastolic blood pressures (mmHg) calculated at 1, 3 and 5 minute intervals during a 5 minute heating period. MAP in mmHg was auto calculated on Microsoft Office Excel during both periods. MAP was calculated using the formula MAP= Diastolic pressure + 1/3 (systolic-diastolic pressure). Subject was exposed to conflicting environmental temperatures. Values for blood pressures in extra test are means ± SEM (n=18 subjects). Extra test: Significantly different from extra test control time measured against extra test time. Significant values (p<0.05) are indicated by an asterisk (*).

Heart rate EXTRA TEST

Figure 13. Extra test measurements for heart rate in beats per minute calculated at 30 second intervals during a 5 minute heating period. Subject was exposed to conflicting environmental temperatures. Values for heart rate in extra test are means ± SEM (n=19 subjects). Extra test: Significantly different from extra test control time measured against extra test time. Significant values (p<0.05) are indicated by an asterisk (*).

Discussion

Past research concerning thermoregulation of humans has publicised that the human body temperature is largely coordinated by the hypothalamus, receiving constant thermosensory input from the body regarding the fluctuations of internal and external temperature levels, from central and peripheral thermoreceptors, respectively (Rhoades et al, 2006). In contrast, previous studies have not specifically demonstrated the physiological mechanisms stimulated upon temperature deviations such as during cold stress or the primary thermoreceptor activity in the regulation of core temperature stability particularly when conflicting thermosensitive information is relayed to the hypothalamus. In an effort to observe these, cold stress was induced via cooling of the subject’s environment to approximately 10-12 degrees Celsius. By keeping lower limbs of subjects in iced cold water and placing a fan blowing cold air on the subject’s back, experimental error was reduced in an attempt to increase the degree of heat lost mainly via convection currents but also other such mechanisms. The experimental design provided various findings in relation to the changes in physiological mechanisms involving the body under cold stress or when receiving opposing thermosensory input.

The regulation of core temperature is mainly achieved through two induced homeostatic mechanisms: firstly, as external temperature decreases, there is a gradual and continual increase in muscle tone. If this is insufficient in maintaining body temperature, shivering occurs which is mediated peripherally by the somatic not the autonomic nervous system (Longstaff, 2005), increases internal heat production whilst heat is retained through peripheral vasoconstriction. Hence, the deviation from the thermoneural range in the hypothalamus results in shivering – in humans it is a series of rapid muscular tremors that can enhance heat production several fold in a few minutes. This starts in the jaw muscles and spread to the trunk and proximal limb muscles and when under cold stress (Longstaff, 2005), often increases the degree of movement at joints. However, this was not reflected in our study in which there was to be an expected increase in such parameters as the angle of patella reflex during the cooling period which instead remained constant, seen in Figure 5. This may correlate to previous research highlighting that shivering is a last resort response, as it is metabolically inefficient. Furthermore, due to the lower legs being immersed in iced cold water, shivering is even less effective than may be expected to increase metabolic rate as much of the heat is generated by the large muscles in the legs (Sessler, 2009). A further heat-gaining mechanism, non-shivering thermogenesis is caused by an increased sympathetic activity to brown adipose tissue. The mechanism of action is thought to be from released noradrenaline acting on beta-3-adrenoreceptors to stimulate a rise in cAMP, which activates lipolysis, ultimately generating heat (Lesna et al, 1998). However, this is not yet proven in adults and is thought to be more evident in neonates and children.

In addition, core body temperature was not predicted to change as it is maintained within a narrow temperature range (Rhoades et al, 2003). Any variation from this range are integrated and rectified by the control centre in the hypothalamus, initiating appropriate physiological responses. Our results shown in Figure 1 provides significant decreases in degrees Celsius throughout the 20minute cooling period, yet is still within the body’s regulated range. This is vital in terms of thermoregulation as large deviations from the set point may induce dire health risks, particularly frostbite and hypothermia with the potential to affect other important physiological mechanisms.

Secondly, accompanying this increase of muscle tone is peripheral vasoconstriction that shunts the blood away from the skin to conserve body heat and prevent loss of heat through convection and conduction – which during cold stress is induced via the activation of sympathetic outflow. Furthermore, the effect of peripheral vasoconstriction was also apparent in some of the body temperature parameters. All skin temperature observed significant change throughout the cooling experimentation, as shown in Figure 2, suggesting that in order to inhibit further heat loss, peripheral vasoconstriction and convection occurred as blood was redirected internally in maintaining core and vital organ temperature. This resultant decrease in diameter of blood vessels is expected to produce a consequent increase in the total peripheral resistance (TPR) and an initial rise in blood pressure, evident in Figure 3, which can be deduced from the equation:

Mean Arteriole Pressure (MAP) = Cardiac Output, CO (Heart Rate x Stroke Volume) x Total Peripheral Resistance, TPR.

The ANS is crucial for the short-term regulation of mean arterial pressure (MAP), which at rest, is maintained by negative feedback. This is detected by baroreceptors which are sensory nerve endings located within blood vessels which constantly monitor the stretching of vessel walls and respond via regulation of the blood vessels and contraction rate of heart (Rhoades, et al, 2003). The results in Figure 3 in regards to the rise in MAP can be correlated with the increase in blood pressure as it is ultimately regulated by cardiac output (CO), TPR and blood volume. The rise in MAP triggers the aortic arch and particularly the carotid sinus baroreceptors to increase firing rate and subsequently the cardiovascular centre responds by decreasing sympathetic innervation and increasing parasympathetic innervation to the heart reducing its rate and force of contraction where blood pressure will begin to plateau as evident in Figure 3. However, it can also be assumed that a large decrease in CO overtime was unable to counteract such a significant increase in TPR, ultimately increasing MAP and also blood pressure. The relationship of heart rate can be observed in the equation:

Heart Rate = CO x Stroke Volume.

Additionally, the decrease in CO predicted, supports the decrease in heart rate, shown in Figure 4. Cardiac output is a product of stroke volume, and is determined by the contractile force of the heart, and heart rate. In human hearts, sympathetic activity raises both force and rate, whereas parasympathetic activity lowers rate, but has little effect on force since few parasympathetic fibres innervate the ventricles (Longstaff, 2005). Thus, in Figure 4, parasympathetic innervation increased simultaneous to a decrease in sympathetic activation, thus a decrease in heart rate while changes in stroke volume are not known.

From external cold stress, the activation of various mechanisms and the fall in protein and enzymatic activity resulted. Our study showed metabolic rate remained constant as indicated in Figure 9, although was predicted to increase. This may be due to experimental error affecting the data as no significant changes were illustrated. Theoretically, the metabolic rate and respiratory rate were expected to rise with an increased metabolic waste, heat production and carbon dioxide as the by-product from raised metabolic activity in order to remove excess CO2 from the blood through expired ventilation. As noted, in Figure 6, a significant increase in respiratory rate was only evident at the final timepoint of the cooling period, t=40 minutes instead of throughout the experiment. On the contrary, no significantly values were obtained from the oxygen consumption and expired ventilation in Figures 7 and 8 – may be due to adequate gas exchange already occurring in the removal of CO2 but may also be due to experimental errors involving leakages from the Douglas bag during the air collection process.

Throughout the extra test, no significant values (p<0.05) were noted upon placing a hand in wa