Cardiovascular Drift in Heated and Neutral Conditions During Prolonged Exercise

SECTION I: INTRODUCTION

Cardiovascular drift is a phenomenon that reflects the progressive cardiovascular reactions during prolonged steady state exercise at moderate intensity.  Within about ten minutes of exercise, stroke volume drifts downward followed by an upward drift in heart rate.  This inverse relationship is the key component to cardiovascular drift which may occur in either a heated or thermo-neutral environment in order to maintain cardiac output (Coyle et al., 2001).  As physical activity duration progresses, various systematic responses occur in order to maintain cardiac output, core body temperature, and muscle contraction, including: shifts in cutaneous blood flow (CBF) and reductions in pulmonary and mean arterial pressure (MAP) (Wingo & Cureton, 2006; Coyle et al., 2001).  The functioning of the thermoregulatory, cardiovascular, metabolic, and nervous system is interrelated to the drift phenomenon and impacted by hydration level, workload intensity, training status, ambient and body temperature (ACSM 2007; Trinity et al., 2010). 

During exercise, metabolic heat is produced and transferred within the body from the working muscles to the blood, body core, skin, and then released into the environment through sweat glands (ACSM 2007).  Prolonged exercise in heated environmental conditions may increase the core temperature, sweating response, and heart rate due to sympathetic stimulation  (Trinity et al., 2010; Gonzalez-Alonso, Calbet & Nielsen, 1999).  Sweating is a regulatory response for evaporative cooling and in order to dissipate heat, blood flow redistributes to the peripheral, which causes cutaneous blood flow and cutaneous venous volume to increase (Trinity et al., 2010).  This fluid volume shift may alter nerve impulses, hormones, and autonomic regulation of the heart, causing an upward drift in exercise heart rate (Gonzalez-Alonso, Calbet & Nielsen, 1999).   As a result, the shift in blood volume to the skin will lead to reductions in central blood volume and central venous pressure.  This causes the cardiac ventricular filling pressure to decrease, which directly impacts the amount of preload cardiac filling volume, or end diastolic volume (EDV).  These systematic readjustments to circulating blood volume and exercise heart rate will ultimately lead to a reduction in stroke volume (Trinity et al., 2010).

The purpose of the study was to compare the effects of prolonged treadmill bouts of moderate intensity exercise (70-80% max heart rate reserve) on cardiovascular drift responses in two different environmental conditions.  Steady state exercise of 70-minutes was performed in the thermo-neutral condition, when hydration status was normal, and in the heated condition, when hydration status was below normal.  The effects of hydration status and ambient temperature variations were compared to the cardiovascular drift responses by measuring the following variables: oxygen consumption (VO2), heart rate, blood pressure, rating of perceived effort (RPE), plasma volume, and blood volume.   

SECTION II: METHODS & PROCEDURES

Participants

The participants were selected using a convenience sample of male and female volunteers recruited from Texas Woman’s University.  All participants were enrolled in the graduate level course Cardiovascular Response to Exercise, KINS 5613-01.  There were 10 participants recruited and the inclusion criteria was that the participants were: between 20-30 years old, low risk according to ACSM guideline for PAR-Q, healthy and capable of withstanding long exercise bouts, and not taking any prescribed medication or supplements that would deter from the findings.  All participants were informed of the procedure, testing protocol, and purpose of the study.   

Measurements & Procedure

In accordance with ACSM’s Guidelines for Exercise Testing and Prescription (2000), resting blood pressure, heart rate, height and weight were measured.  Resting blood pressure was measured in supine position three separate times and the first and fifth Korotoff sounds were recorded as systolic and diastolic blood pressure, respectively.  Blood pressure was measured using the standard of mercury (mmHg) with the 3M Littmann Master Cardiology Stethoscope and Omron Sphygmomanometer.  Resting heart rate (RHR) was measured in a supine position through a Polar RS300 heart rate monitor.  The Salter 200 Academy Mechan Scale measured weight (without shoes or heavy apparel) and height was recorded to the nearest 0.5 cm (without shoes). 

Afterwards, 70-80% max heart rate reserve was calculated to be used in future trials. The age predicted heart rate maximum (HRmax) was determined to be within +10 beats per minute of: 220-age.  HRmax minus resting heart rate (RHR) determined heart rate reserve (HRR), which was multiplied by the intensity percentage range of 70-80%.  The RHR was then added to the calculated %HRR to determine 70-80% max heart rate reserve.  The trial treadmill test during neutral conditions was designed increase elevation and walking pace until the desired heart rate range was maintained and recorded for use during the exercise tests. At the final 15-30 seconds of third minute stages, steady state heart rate, defined as two sequential HRs within + 5 bmp of each other, was determined by Polar RS300 monitor.  Following the exercise trial, resting blood pressure and heart rate was monitored until it returned to resting values.

Before and immediately after both heated and neutral treadmill bouts, blood samples were drawn and analyzed for hemoglobin (Hb) and hematocrit (Hct).  Initially, in order to warm up the hand and finger, warm water and/or a heated compressed was applied to the area.  Then, the warmed finger was sterilized using an alcohol swab and dried by the tester, who was wearing sterile gloves.  The SurgiLance safety lancet was readied, the red raised platform was positioned on the test site to puncture the fingertip, and it was properly discarded into a refuse container.  The blood was collected in four capillary tubes: two tubes for hematocrit (Hct) and two tubes for hemoglobin (Hb) analysis.  The capillary tubes for hematocrit measurement were plugged on one end with "crit-o-seal" sealing clay.  Next, the tubes were then placed in the correct position of the Micro Hematocrit Centrifuge Model MB by International Equipment Co. rotator grooves.  After securing the lid, the instrument was turned on for  two minutes, and the brake switch was used to decelerate the speed when the timer went off.  The centrifuged tube was placed vertically on the Micro Hematocrit Capillary Tube Reader by Veterinary Information Network (1991) chart with the bottom edge of the crit-o-seal touching the red line at 0%.  The tube was moved along the chart until the meniscus of the plasma intersected the 100% line. The height of the packed red cell column was measured directly as percent cell volume on the chart.  

In order to analyze hemoglobin, three test tubes were labeled: control, patient, and blank and then set aside.  Two tubes for hemoglobin were carefully evacuated into a 1.5mL micro-centrifuge tube and in each tube 2.0 μl of hemoglobin reagent was dispensed.  The test tubes were set-aside at room temperature for about three minutes.  In the blank, control, and patient labeled test tube, 0.01 µL of the following solutions were dispensed in this order: water, standard hemoglobin solution, and participant’s sample.  Then, each test tube was placed on the Fisher Branch Touch Vortex Mixer and mixed for about three seconds.  Using a transfer pipette, each sample was transferred into a clean cuvette that was wiped with a Kim-Wipe to ensure a smudge free surface.  The Hitachi U-2001 Spectrophotometer was turned on, set to 450 nm, and auto-zeroed.  Afterwards, the reagent blank was placed in the front spot where the reading was taken and recorded.  The blank was then moved to the back slot and zeroed out again for the other samples.  With the reagent blank in the back slot, the control was placed in the front slot where the reading was taken and recorded. The following procedure was repeated for the patient sample. 

In order to begin metabolic testing during heated and neutral conditions for the treadmill tests, the participants’ data (demographic measures: age, current weight, and height) and environmental conditions (relative humidity, room temperature, and barometric pressure) was measured, recorded and entered into the ParvoMedics metabolic cart.  Mouthpiece and headgear were positioned comfortably with a nose clip on to determine accurate airflow.  The metabolic cart was then calibrated with the 3-L syringe and paper towels were given to the participant for use during the test. 

On the treadmill test in the neutral conditions, the participants performed a 70-minute single-stage treadmill bout at room temperature. Thirty to forty minutes before exercise, the participant drank water at 5 ml/kg of body weight and did not eat for at least 2 hours before the start of the exercise bout.  Body weight was measured and blood samples were taken at baseline and analyzed for hemoglobin and hematocrit, as previously mentioned. Resting heart rate and blood pressure were recorded while standing on the treadmill belt.  The subject was asked to straddle the belt until the treadmill started at their designated walking intensity (speed and % grade).  The subject was instructed to begin walking and when comfortable and the test began.  Heart rate was monitored through a Polar RS300 and recorded at baseline, 5, 10, 20, 40, 60, and 70 minutes during exercise.   Rating of Perceived Exertion (RPE) was determined using the original Borg scale (6 to 20), as defined by Borg’s Perceived Exertion and Pain Scales (1998), and recorded at 10-minute intervals throughout exercise. The Bacharach Sling Psychrometer Relative Humidity Meter was the instrument used for dry bulb and wet bulb readings at baseline and then at 15-minute intervals during exercise. Blood pressure was taken every 15-minutes and Omega 450 ATH
Thermistor Thermometer measured oral temperature every 20-minutes.  Oxygen consumption (VO2) was recorded periodically at minute 5, 20, 40, and 60 minutes, as shown in Table 1. For both oral temperature and VO2 measurements, there was a 2-3 minute period of normalization before the readings were recorded. Blood samples were then taken afterwards and analyzed for hemoglobin and hematocrit, as previously described. Following the conclusion of the exercise trial, body weight was recorded, blood pressure and heart rate were monitored until values returned closed to resting.

Table 1: Testing & Time Frames Yellow indicates that testing was recorded for this measurement at these time increments during the treadmill tests

Time	HR (bpm)	BP (mmHg)	Oral Temp (°F)	VO2 (L/min)	Blood Samples	Dry/ Wet bulb (°F)	RPE
Resting
5 min
10 min
15 min
20 min
30 min
40 min
45 min
50 min
60 min
65 min
70 min
5 min post exercise

To standardize testing procedures, the same testing subjects in the neutral conditions were used in the thermal conditions.  For the second treadmill test in heated conditions, resting heart rate, blood pressure, body weight, and blood samples were taken at baseline.  The participants performed a 70-minute treadmill bout in an enclosed heat chamber with a heater, dehumidifier, and fan on low to provide airflow.  The heater was set to oscillate between 84-88 degrees Fahrenheit, which was checked by the Bacharach Sling Psychrometer, and the Soleus Air Dehumidifier was set at 40%.  Three subjects (two testers and one participant) were stationed in the sealed thermal chamber while other individuals remained outside of the chamber to record and monitor the oxygen consumption (VO2) data.  Thirty to forty minutes before exercise, the participant drank water at half the amount of water as previously specified (2.5 ml/kg of body weight) and did not eat for at least 2-hours before the start of the exercise bout.  Measurements and readings for heart rate, VO2, blood pressure, RPE, oral temperature, dry/wet bulb, and blood samples were taken and recorded at the same intervals as the neutral condition, and defined in Table 1. At the conclusion of the heated exercise trial, blood pressure and heart rate were monitored values returned to resting and body weight was recorded.

Once the test was completed, the parameters of interests, including VO2, HR, RPE, blood pressure were plotted and compared between the heated and normal conditions.  Plasma volume and blood volume change were calculated with the equations below and compared to findings (Dill & Costil 1974).

BV_A = BV_B (Hb_B / Hb_A)

CV_A = BV_A (Hct_A)

PV_A = BV_A - CV_A

Δ BV, % = 100 (BV_A – BV_B) / BV_B

Δ CV, % = 100 (CV_A – CV_B) / CV_B

Δ PV, % = 100 (PV_A – PV_B) / PV_B

Note: Subscripts _B and _A indicate before dehydration and after dehydration, respectively.

BV = blood volume; PV = plasma volume; CV = red cell volume (hematocrit); Hb = hemoglobin

BV_B = 100 (given).

SECTION III: RESULTS

The phenomenon of cardiovascular drift characterizes the cardiovascular changes that occur after about 10 minutes of exercise in a neutral or heat environment at moderate intensity (Coyle et al., 2001).  In order to correctly assess the differences between a heated and thermo-neutral environment during prolong treadmill bouts, the values before minute 10 were recorded, but not accounted for in cardiovascular drift analyses. All data presented are the arithmetic means of ten participants’ recorded values, unless otherwise noted.

            In the first 10 minutes of exercise in both thermo-neutral and heated conditions, heart rate increased, as depicted in Figure 1 and Table 2. After the first 10 minutes, heart rate continued to rise over the 70 minutes of exercise, with heart rate increasing slightly more in the heated condition than in the thermo-neutral condition. Figure 2 and Table 3 show the percent change that occurred in heart rate from the value recorded at 10 minutes of exercise. At the end of exercise, heart rate increased almost twice as much in the heated condition than in at neutral conditions.

Table 2: Heart Rate Response During Prolonged Exercise
	Heart Rate (bpm)
Time (min)	Thermo-neutral	Heat
Rest	63	60
5	140	139
10	147	145
20	153	155
40	156	162
60	157	165

Table 3: Heart Rate Percent Change During Prolonged Exercise
	Percent Change From 10 Min Value (%)
Time (min)	Thermo-neutral	Heat
10	0	0
20	+4.08	+6.9
40	+6.12	+11.72
60	+6.80	+13.79

            Systolic and diastolic blood pressure values had similar fluctuations in the thermo-neutral and heated trials, as shown in Figure 3 and Table 4.  After the first 15 minutes of exercise, systolic blood pressure slightly rose in both conditions but after 30-minutes in the heat chamber, there was a plateau in systolic blood pressure.  Overall, exercise in the heated environment produced slightly lower systolic blood pressure values than the thermo-neutral environment.  Diastolic pressure decreased slightly in the first 10 minutes and then remained relatively consistent for the rest of exercise in both conditions. There were no noticeable differences between the two conditions based on diastolic blood pressure readings.

Table 4: Blood Pressure Response During Prolonged Exercise
	Blood Pressure (mmHg)
Time (min)	Thermo-neutral	Heat
Rest	115/71	114/71
15	133/68	132/67
30	140/67	138/67
60	145/66	138/67

            Mean arterial blood pressure (MAP) was calculated by the following equation: diastolic pressure (mmHg) + ⅓ [systolic pressure (mmHg) – diastolic pressure (mmHg)].  MAP values showed a slightly different trend between the two environmental conditions. Both conditions had an increase in MAP after the first 15-minutes of exercise. As shown in Figure 4 and Table 5, after 30 minutes of exercise, MAP continued to rise during the thermo-neutral condition, but plateaued in the heated condition.

Figure 5 and Table 6 depict the 3% increase in MAP at 60 minutes of exercise during the thermo-neutral trial and no change in MAP from 30 to 60 minutes in the heated trial, evening out at 2.25% increase from the 10 minute MAP value.

Table 5: Mean Arterial Blood Pressure Response During Prolonged Exercise
	MAP (mmHg)
Time (min)	Thermo-neutral	Heat
Rest	86	85
15	90	89
30	91	91
60	93	91

Table 6: Mean Arterial Blood Pressure Percent Change After 15 Min of Exercise
	Percent Change From 15 Min Value (%)
Time (min)	Thermo-neutral	Heat
15	0	0
30	+1.11	+2.25
60	+3.33	+2.25

            Figure 6 and Table 7 reveal opposite trends in core temperature readings during the exercise trials. In both conditions, the resting core temperature was similar.  During the first 20 minutes of exercise in the thermo-neutral environment, core temperature showed a negative relationship with time, decreasing 0.64% at 40 minutes and a slight increase at 60 minutes of exercise, for a percent change of -0.61% (Table 8). While in the heated trial, core temperature showed a positive relationship, increasing 0.53% during exercise.

Table 7: Core Temperature Response During Prolonged Exercise
	Core Temperature (°F)
Time (min)	Thermo-neutral	Heat
Rest	97.52	97.53
20	96.79	97.99
40	96.17	98.29
60	96.20	98.51

Table 8: Core Temperature Percent Change After 20 Min of Exercise
	Percent Change From 20 Min Value (%)
Time (min)	Thermo-neutral	Heat
20	0	0
40	-0.64	+0.31
60	-0.61	+0.53

            In both trials, after 10 minutes of exercise, relative oxygen consumption (VO2) increased with time and then dropped at 60-minutes, as shown in Figure 7 and Table 9. Although VO2 during the heated trial was higher at every time interval (omitting the 5-minute value), VO2 during the thermo-neutral trial had a greater increase (4%) from 20 to 40 minutes. Even though both exercise conditions produced a VO2 decrease toward the end of exercise, the heated trial elicited a greater drop in VO2 (3%) than the thermo-neutral condition. These percent changes are shown in Table 10.

Table 9: Oxygen Consumption During Prolonged Exercise
	VO2 (mL/kg/min)
Time (min)	Thermo-neutral	Heat
5	29.09	28.26
20	29.52	31.02
40	30.66	31.56
60	28.80	30.16

Table 10: Oxygen Consumption Percent Change after 20 Min of Exercise
	Percent Change From 20 Min Value (%)
Time (min)	Thermo-neutral	Heat
20	0	0
40	+3.86	+1.74
60	-2.44	-2.77

            Figure 8 and Table 11 depict mean hematocrit levels before and after exercise for nine participants’ samples. In both conditions, hematocrit increased from pre-exercise values. Hematocrit levels were higher before and increased more after heated exercise than in thermo-neutral conditions, as seen in the 7% increase shown in Table 11.

Table 11: Hematocrit Levels Before and After Prolonged Exercise & Percent Change
	Thermo-neutral			Heated
	Before	After	%Change	Before	After	%Change
Hematocrit (%)	41.28	43.89	+6.32	43.06	45.94	+6.69

            As seen in hematocrit levels, hemoglobin levels increased after exercise in both thermo-neutral and heated conditions, presented in Figure 9. Pre-exercise values for hemoglobin were higher for the heated trial and increased 4% after exercise, as compared to a 3.25% increase in the thermo-neutral trial (Table 12). Only seven participants’ data were used when calculating the arithmetic mean for hemoglobin levels.

Table 12: Hemoglobin Levels Before and After Prolonged Exercise & Percent Change
	Thermo-neutral			Heated
	Before	After	%Change	Before	After	%Change
Hemoglobin (g/dL)	13.63	14.28	+3.25	14.40	14.98	+4.03

            After exercising in both conditions, seven participants experienced plasma volume loss, as indicated in Figure 10. There was a greater plasma volume loss after heated exercise than exercise in thermo-neutral conditions.

Table 13: Plasma Volume Change After Prolonged Exercise
Plasma Volume Change (%)
Thermo-neutral	Heat
-7.01	-9.06

SECTION IV: DISCUSSION

The classic model of cardiovascular drift has been well documented and is characterized by a progressive increase in heart rate and core temperature, with a decrease in stroke volume, mean arterial and pulmonary pressures.  These cardiovascular responses occur while cardiac output remains constant after about 10 minutes of prolonged, moderate-intensity exercise (Ekelund & Holmgren, 1964; Fitzsche, Switzer, Hodgkinson, & Coyle, 1999; Rowell, 1993).  There are two main theories to explain the changes associated with cardiovascular drift that occur and most notably studied by Rowell (Rowell, 1993; Rowell, 1974; Rowell, Marx, Bruce, Conn, & Kusumi, 1966) and Coyle (Coyle & Gonzalez-Alonso, 2001).  Since this study did not measure stroke volume or cardiac output, explanations for cardiovascular and hemodynamic responses can only be postulated from previous literature.  Cardiovascular drift responses become exaggerated during heat stress and in the present study the following responses supported this relationship, increases in: core temperature, heart rate, Hct, Hb, plasma volume change and slightly lower MAP values than the thermo-neutral condition (Gonzalez-Alonso, Crandall, & Johnson, 2008; Mora-Rodriguez, 2012; Trinity, Pahnke, Lee, & Coyle, 2010).  

Classic cardiovascular drift occurred in this experiment as seen in the core temperature response in the heated condition and heart rate adjustments in both ambient temperatures.  It was not reflected in the core temperature readings or the MAP values in the thermo-neutral condition.  The core temperature increases during prolonged exercise under thermal stress (Gonzalez-Alonso, Crandall, & Johnson, 2008; Mora-Rodriguez, 2012; Trinity, Pahnke, Lee, & Coyle, 2010).  It is hypothesized that due to a rise in core temperature, blood flow is shifted away from the core and working skeletal muscles through vasodilation of peripheral blood vessels, therefore increasing cutaneous blood flow (Ekelund & Holmgren, 1964; Johnson & Rowell, 1975; Rowell, 1993). This drop in central blood volume and central venous pressure causes the cardiac ventricular filling pressure to decrease, that ultimately impacts the preload cardiac filling volume or end diastolic volume (EDV) (Trinity et al., 2010).  As a result, this leads to the decline in stroke volume. The increase in heart rate observable in both ambient temperature conditions, according to Rowell (1966; 1974; 1993), is in response to the falling stroke volume in order to maintain cardiac output.  If stroke volume and cardiac output had been measured in this experiment, there would more than likely have been a decrease in stroke volume and a constant cardiac output.  This is a characteristic of cardiovascular drift due to shift in blood flow with rising core temperatures (Ekelund & Holmgren, 1964; Johnson & Rowell, 1975; Rowell, 1993). This relationship should have been present in the thermo-neutral condition, and further exaggerated in the heated trial.

In contrast, the core temperature actually decreased with prolonged exercise in thermo-neutral condition.   This unexpected response in the thermo-neutral condition does not coincide with the classic cardiovascular drift model characteristics and was most likely due to human error during measurement and other cofounding variables. These lower temperatures may be accounted for by: improper placement of the thermistor thermometer in the mouth or possibly not having the mouth completely closed for the entire measurement duration.  Also, if there was not a normalization period of about 2-3 minutes before the measurement, then the values may not have been accurately recorded.  The core body temperature was estimated at the mouth rather than rectally, as is common in many studies.  True internal core body temperature was unable to be achieved due to privacy concerns.  Other external factors that may have contributed to varying body temperature findings include sleep patterns and time of day for the exercise bouts, both of which may impact circadian rhythms.                  

During exercise, arterial blood pressure is regulated and balanced by dilating and constricting arterials.  Typically, systolic blood pressure rises with work while diastolic blood pressure remains either unchanged or decreases with exercise; these trends were evident in the treadmill trials.  The thermo-neutral environment elicited a slightly higher systole value, while the heated environment had slightly lower values that eventually began to plateau.  According to research, MAP should have progressively decreased overtime during exercise due to increased vasodilation and decreased total peripheral resistance (Raven & Stevens, 1988; Rowell, 1993).  This would be reflected by a decrease of systolic and diastolic blood pressure. Overall, this was not seen in either environmental condition and the rise in MAP may be due to testing error including: improper blood pressure technique, difficulty hearing the first and fifth Korotoff sounds due to treadmill exercise, or other variables.  In addition, a longer duration of exercise may have been more effective to be able to further investigate the effects of MAP. 

Coyle and Gonzalez-Alonso (2001) give a different justification for the expected decrease in stroke volume, which is the primary feature of cardiovascular drift. Coyle and Gonzalez-Alonso (2001) propose that the progressive decline of stroke volume is due to the increase in heart rate with increasing core temperature over the course of exercise, rather than shifts in blood flow. The increase in heart rate would decrease ventricular filling time and end-diastolic volume causing the lowered stroke volume in order to keep cardiac output constant (Coyle & Gonzalez-Alonso, 2001). A study by Fritzsche, Switzer, Hodgkinson, and Coyle (1999) used a β1-adrenoceptor blocker (atenolol) to blunt heart rate response during prolonged exercise. Surprisingly, with no rise in heart rate, there was no decrease in stroke volume, indicating that the characteristic decrease in stroke volume during prolonged exercise is due to the increased heart rate (Fritzsche, Switzer, Hodgkinson, & Coyle, 1999). Fritzsche, Switzer, Hodgkinson, and Coyle (1999) also found a strong correlation (r² = 0.95) between increases in core temperature and a rise in heart rate during cardiovascular drift. A rise in sympathetic nervous system activity may also be a cause for the increased heart rate (Fritzsche, Switzer, Hodgkinson, & Coyle, 1999). It is entirely possible that mechanisms presented in both theories may be at work to influence the shifts present in cardiovascular drift. It is difficult to pinpoint a single hypothesis to explain all the changes involved in cardiovascular drift, especially in this study where stroke volume and cardiac output were not measured.

During skeletal muscle contraction, the delivery of oxygenated blood to working muscles is required to sustain metabolism and oxygen consumption (VO2) is directly related to exercise.  VO2 max is not a cause or classic characteristic of cardiovascular drift, but a slight decrease of VO2 max has been associated with periods of cardiovascular drift (Lafrenz, Wingo, Ganio, & Cureton, 2008; Raven & Stevens, 1988; Wingo, Lafrenz, & Ganio, 2005). Because stroke volume is a determining factor of VO2, a decrease in VO2 could be linked to the decline in stroke volume during cardiovascular drift. Recent studies have tried to support a causal relationship between VO2 max and cardiovascular drift by measuring VO2 max during the same time interval as cardiovascular drift measurements (Lafrenz, Wingo, Ganio, & Cureton, 2008; Wingo & Cureton, 2006; Wingo, Lafrenz, & Ganio, 2005). Although more research needs to be done to confirm a causal link between cardiovascular drift and VO2 max, studies have shown that decreases in VO2 max occur at the same time as cardiovascular drift and are accentuated in heated conditions (Lafrenz, Wingo, Ganio, & Cureton, 2008; Wingo & Cureton, 2006; Wingo, Lafrenz, & Ganio, 2005).  According this study’s findings, a decrease in VO2 only occurred in the last 30-minutes of exercise in both the thermo-neutral and heated conditions.  This detrimental drop in oxygen consumption may be associated with dehydration, in which only a 2% change in the body weight caused by dehydration is critical (ACSM 2007; Gonzalez-Alonso, Calbet & Nielsen, 1999).  During the present study, a VO2 max measurement was not taken, so it is difficult to confirm if VO2 max indeed decreased after prolonged sub maximal exercise consistent with cardiovascular drift.

During exercise, the average sweat rate is between 0.5 and 2.0 L/h and the magnitude of fluid loss is influenced by ambient temperature and individual characteristics, such as body weight, training status, and gender (ACSM 2007; ADA & ACSM, 2000).  Additionally, wearing heavy equipment and clothing may elicit high sweating rates. The type of clothing worn by participants was not standardized and the gender effect was not accounted for in the study.  Also, heat acclimation is associated with lower sodium concentration for a given sweat volume, thereby enhancing the sweat rate (ACSM 2007).  Training status was not a component that was accounted for in the study and these variations may be impacted the sweating response and the body’s ability to adapt to physiological stress.        

A plasma volume loss was to be expected after prolonged exercise in both thermo-neutral and heated conditions, especially during dehydration (Dill & Costill, 1974; Raven & Stevens, 1988). Participants in this experiment should have been hydrated before the thermo-neutral trial, but dehydration may have occurred over the 70-minutes of exercise due to no fluid consumption and the need for sweating to dissipate heat. Dehydration was accentuated in the heated condition due to a partially dehydrated status to prior to the heated trial, in addition to the lack of fluid consumption during the 70-minutes of exercise, accompanied by the increased sweating in order to dissipate heat. Dill and Costill (1974) supported the notion of plasma volume loss after dehydration. Since hemoglobin, the oxygen carrying protein in red blood cells, cannot pass through the cell or the blood, protein concentration would be higher due to the loss of plasma volume (Dill & Costill, 1974). Both hemoglobin and hematocrit levels were consistent with Dill and Costill’s (1974) findings, showing an increase after exercise, which was even higher in a more dehydrated state after the heated trial. A similar trend was found for plasma volume in both conditions, where there was a greater plasma volume loss in the heated condition. However, hematocrit levels for one participant were thrown out because the heat data showed a decrease in hematocrit. This could have been because of sampling error or an error in any step of the hematocrit measurement and analysis procedures, outlined previously. Only seven participants’ data was included for hemoglobin and plasma volume changes possibly due to sampling error or incorrect data measurement or analysis procedures, also outlined previously. Incorrect data could have also been due to improper hydration before each trial. 

In the present study, cardiovascular drift responses were impacted by the ambient temperature and the current hydration status during steady state prolonged treadmill bouts at moderate intensity.  The heated environment elicited greater responses than the thermo-neutral condition with increases in: core temperature, heart rate, Hct, Hb, plasma volume change and slightly lower MAP values than the thermo-neutral condition (Gonzalez-Alonso, Crandall, & Johnson, 2008; Mora-Rodriguez, 2012; Trinity, Pahnke, Lee, & Coyle, 2010).  When heat gain exceeds heat loss into the warm and humid environment, the core body temperature rises, blood flow redistributes to the peripheral and cutaneous venous volume increases (Trinity et al., 2010).  Sweating is a regulatory response for evaporative cooling that helps to maintain thermoregulation. This fluid volume shift may also alter nerve impulses, hormones, and autonomic regulation of the heart, causing an upward drift in exercise heart rate (Gonzalez-Alonso, Calbet & Nielsen, 1999).  However, dehydration suppresses heat dissipation and the sweating response, which overtime raises the body temperature and may eventually cause heat stroke (Gonzalez-Alonso, Calbet & Nielsen, 1999).  Exercise in cooler environments restricts blood flow to working muscle but dehydration in the heated environment impacts the body differently in the cooler environment.  In either environmental condition, after ten minutes of exercise, cardiovascular drift responses are observed during prolonged steady state exercise at moderate intensity.  Heart rate drifts upward in response to a decrease in stroke volume in order to maintain cardiac output (Coyle et al., 2001).  As physical activity duration progresses, various systematic responses occur in order to maintain cardiac output, core body temperature, and muscle contraction, including: shifts in cutaneous blood flow (CBF) and reductions in pulmonary and mean arterial pressure (MAP) (Wingo & Cureton, 2006; Coyle et al., 2001).  The functioning of the thermoregulatory, cardiovascular, metabolic, and nervous system is interrelated to the drift phenomenon and impacted by hydration level, workload intensity, training status, ambient and body temperature (ACSM 2007; Trinity et al., 2010). 

SECTION V:

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