Humans are homoeothermic, which means their internal body temperature of 36.1-37.8oC is kept relatively constant throughout life, with fluctuations of about 1oC. It is only during extreme environmental conditions of hot or cold, illness or prolonged exercise that the body will deviate from this range, with exercise often creating dangerously high internal temperatures of 40oC. At rest an individual will be able to dissipate heat by conduction and convection 20%), radiation (60%) and evaporation (20%). During exercise, evaporation contributes up to 80% of total heat loss. Environmental conditions play a major part in heat loss and a hot and humid climate (35.5oC and 60% relative humidity (RH) will limit heat loss and sweat evaporation.
During exercise at ambient temperatures (20oC) the heart rate (HR) rises from a resting level of about 60 beats per minute (bpm) to nearly 200 bpm, whilst stroke volume (SV) the volume of blood pumped per contraction, can rise from 80 ml/beat to 150 ml/beat. In combination these adjustments can increase cardiac output (Q = HR x SV) from 5 L/min to 30 L/min. the circulatory system. The increased Q causes the systolic blood pressure (SBP) to rise from 120 to 200 mm Hg at exhaustion, whilst the diastolic blood pressure (DBP) does not change (80 mm Hg). Blood volume tends to fall during exercise due to loss of plasma volume (PV), resulting from osmotic movement of water into the active muscle. PV is directly related to exercise intensity (VO2max), at 70% VO2max PV falls by 15% within few minutes of exercise and may be restored, depending on fluid consumption and sweat loss. This loss of PV results in an increase in concentration of red blood cells (RBC) and haemoglobin and therefore an increase in the oxygen carrying capacity of the blood.
Exercise in heat will increase the demand of blood flow and oxygen to the muscles at the same time increasing metabolic heat production. Heat is usually dissipated through the surface of the skin by blood flow and during exercise the blood flow to the skin needs to be increased, which creates competition between thermoregulation and cardiovascular demands of exercise.
During exercise in the heat the CV makes varying adjustments to maintain a constant cardiac output whilst shunting blood to the periphery. Redistribution of the blood reduces the volume returning to the heart, reducing the end diastolic volume, which in turn reduces the stroke volume (SV). The classic study by Rowell and colleagues (1966) showed a significantly lower Q, central blood volume and SV during exercise in a 43oC than in a 26oC environment at 63-73% VO2max. Reduced Q was due to larger reductions in SV compared with parallel increases in heart rate. Fink and colleagues (1975) have also demonstrated that in addition to increasing body temperature and heat rate when performing exercise in the heat, oxygen uptake is also increased. This results in the working muscles using more glycogen and producing more lactate compared to exercise in an ambient or cold environment.
Prolonged exercising or exposure in the heat can result in the CV thermoregulatory system being unable to dissipate metabolic heat quickly enough due to insufficient blood volume (which has decreased due to excessive fluid loss or mineral loss from sweating) to allow adequate distribution to the skin. This can result in an acute condition called hyperthermia where the internal body temperature rises uncontrollably > 40oC. At this stage it becomes a life threatening condition, sweating ceases, the skin becomes hot and dry, rapid pulse and respiration, hypertension, confusion and eventually unconsciousness leading to coma or death if untreated.
The proposed experiment aims to manipulate the rate of heat storage in subjects and observe the effect this has on CV responses whilst performing a maximal incremental test to exhaustion in a hot and humid environment.
Twelve healthy University athletes aged 21-25 years old (12 males) agreed to participate in this study. All subjects gave written consent for participation and completed an activity questionnaire outlining their specific sports, training schedules, injury incidents over past two years, and personal bests prior to inclusion in the study. Consent forms were also completed specifically for blood sampling. The study was approved by the University Ethics Committee and was performed in accordance with the ethical standards laid down in the Declaration of Helsinki.
All testing was conducted in the Sport and Exercise Performance Laboratory at The University of Birmingham.
The subjects visited the laboratory on three separate occasions and on the first visit the subjects performed a maximal incremental test on the cycle ergometer wearing normal gym wear at ambient room temperature (21oC), the second was a repeat of the first but in an environmental chamber set at 35oC and 20% relative humidity, and the third occasion required the subjects to be subjected to a hyperthermic situation and this was manipulated in two different ways 1) six of the subjects wore a full wetsuit to produce a hyperthermic environment during exercise, 2) whilst the other six subjects wore a liquid conditioning garment (with water at 40oC running through it) that passively heated them while they performed the test.
Both the second and third visit tests were conducted in an environmental chamber set at 35oC (20% relative humidity)
Maximal incremental exercise test
The test implemented was an incremental exercise to exhaustion on a cycle ergometer (Monark type 818E, Stockholm, Sweden). Previous studies and protocols (ACSM) suggest a starting work rate of 25 watts (Watts = weight (0.5 kg) x revolutions per minute (rpm) (50 rpm)) but previous protocols in our laboratory on sports science students (unpublished data) would indicate a starting point of 30 watts (0.5 kg x 60 rpm).
Prior to the exercise the cycle ergometer was calibrated and adjusted for each subject to the appropriate saddle height (enabling the leg to be almost straight at the bottom of the pedalling stroke). The subject had 1-2 minute warm-up on the bike and then testing commenced. The starting workload was 30 watts and the subject exercised at this workload for 3 minutes and then had a 0.5 minute rest. After this time the work rate was increased by 30 watts for a further 3 minutes and 0.5 minute rest and these incremental stages were continued until test termination at the point of volitional fatigue or the test was considered maximal when at least two of the following criteria were achieved: 1) failure to maintain the work rate, 2) respiratory exchange ratio >1.10, 3) maximal HR > 95% age-predicted, 4) Rectal temperature exceeded 39.5oC, and 4) an increase in work rate with no further increase in VO2. If two or more of these criteria were not met, a second maximal test was performed.
If rectal temperature reached 39.5oC then subjects were cooled back down to their original temperature by running 8oC fluid through the LCG jacket
Measurements taken on both test occasions
Prior to the start of the exercise each subject had resting measures for BP, HR, RPE, VO2, minute ventilation rate, and lactate taken in a supine position and sitting on the cycle prior to the start of the test.
Subjects had been instructed refrain from exercise 24 hours before the test procedure and to fast overnight. Upon arrival at the laboratory, body mass of each of the subjects was measured to the nearest 25 g, following which a thermistor was inserted 10 cm beyond the anal sphincter for measurement of rectal temperature. Thermistors were also attached to the skin of the chest, triceps, thigh and calf on the right hand side of the body to measure skin temperature.
Arteriol systolic (SP) and diastolic (DP) pressures were measured with automatic oscillometric equipment (Omron HEM-705CP, Tokyo, Japan) on the left arm at the level of the heart.
RPE was recorded during the final 15-s of each stage using either the 6-20 or 0-10 scale (Borg, 1982)
Blood samples were obtained at rest and at the end of the exercise to determine glucose, measurement of haemoglobin and packed cell volume and from this plasma volume changes could be calculated.
Blood samples were obtained prior to testing, during the 30-s rest period at each stage, at test completion, 1, 2, 5, 7 and 10 min post-exercise from the earlobe or fingertip to measure blood lactate, using the Lactate Pro Portable Lactate Analyzer (California, USA).
Measurements of oxygen uptake (VO2), CO2 production (VCO2), minute ventilation (VE), and heart rate (HR), were collected using a portable telemetric system, Quarkb2 Pulmonary Gas Exchange System (Quak Cosmed, Rome, Italy).
Subject appearance and symptoms were monitored and recorded regularly
Significant differences between measures of maximal oxygen consumption (VO2max), Q, SV, HR, BP, RPE, lactate, glucose, packed cell volume, skin temperature and rectal fatigue were determined using paired sample t-tests with the null hypothesis of no significant differences in means at 20oC versus 35oC. A paired sample t-test also explored significant differences between the two hyperthermic induced environments.
A number of previous studies that have investigated the influence of heat stress on CV function during exercise have compared responses in hot (36-44oC) vs ambient (18-25oC) conditions (Nadel et al, 1979; Nielsen et al, 1990 & Rowell et al, 1966), or using perfusion suits to elicit hot and cold situations (Rowell, 1986 & Gonzalez-Alonso et al, 1999), eliciting responses of increased skin temperatures and increased core temperatures. The majority of these studies have observed highly trained endurance athletes at exercise intensities of 60-70% VO2max.
The purpose of this study was to observe a population of university athletes averaging 60-90 minutes of hard intensity (60-84% VO2max) physical activity at least 5 times a week and ascertain their responses to an enforced hot environment and manipulation of heat rate storage. The data collected will enable a greater understanding of how moderately active athletes react to extremes during maximal exercise.
During the first visit baseline measures of maximal oxygen consumption (VO2max), Q, SV, HR, BP, RPE, lactate, glucose, packed cell volume, skin temperature and rectal fatigue temperature were ascertained for a maximal incremental exercise test at ambient temperature of 21oC.
During the baseline condition the HR increased linearly with workload and VO2 reaching 95% of maximal predicted HR (185-189 bpm). SV increased to about 150 ml/beat and Q to 30 l/min. Lactate was measured throughout the test and 1, 2, 5, 7, & 10 min post-exercise with maximal lactate concentrations of 10-13 mmol/l being recorded for the subjects.
Comparison of the ambient and hot environment demonstrated the typical adaptations observed in other studies (Rowell et al, 1966; Gonzalez-Alonso et al, 1999; Nadel et al, 1979; Nielsen et al, 1990), that the CV system makes in order to maintain the body in the heat. This consisted of an increase in HR due to exercise and heat stress caused to the body, a decrease in SV in the hot environment due to redistribution of the blood to the skin to dissipate the heat, which also impacts on Q.
Comparison of the two hyperthermic inducing events saw time to exhaustion dramatically decreased in the subjects wearing the full neoprene wet suit and this was largely due to the fact as the subjects increased work load, demand of blood to the periphery was significantly increased to dissipate the heat but due to the 5-8mm thickness of the wetsuit, heat was not able to dissipate, resulting in a rapid increase in the skin temperature and concurrent increase in core body temperature. Plasma volume was significantly greater in the full wetsuit condition compared to the liquid conditioning garment, due to the earlier increases in temperature and thus increases in sweating. Blood lactate levels were similar in both hyperthermic events and all subjects fatigued at the same rectal temperature (40.1 – 40.2oC), and CV strain (HR = 196-198 bpm, Q = 19.9-20.8 l/min), which corroborates work by Gonzalez-Alonso and colleagues (1999).
The relevance of this study was to try and understand the CV response to heat stress of normal recreational athletes during a maximal exercise test and compare this to the main body of published data that has focussed on highly trained endurance athletes. Further work could now concentrate on manipulating the two hyperthermic situations discussed here using recreational athletes, by increasing temperatures, relative humidity, varying VO2max, and using ECG measures and observing the various responses.