Oxygen Deficit and EPOC consumption during steady state exercise
Oxygen Deficit and EPOC consumption during steady state exercise
at low and high intensity.
Introduction:
Previous research has shown that in the transition from rest to light or moderate exercise, The body's oxygen requirements increase the moment exercise begins and reaches steady state within 1-4 mins, depending on factors such as intensity of the exercise and participants training status (Powers and Howley, 1994; Martin, 1974). Therefore because oxygen requirements and oxygen supply differ during the transition from rest to exercise, the body incurs an oxygen deficit. (Powers and Howley, 1994) described the term 'oxygen deficit' to apply to the delay in oxygen uptake at the beginning of exercise, and has been defined as the difference between oxygen uptake in the first few minutes of exercise and an equal time period after steady state has been obtained.
Figure 1. This table shows EPOC and Oxygen Deficit.
Krogh and Lindhard (1919) stated that the deficit at the beginning of exercise and recovery oxygen after exercise were essentially equal in size.
Hill and Lupton (1923), stated that during the initial minutes of recovery, even though your muscles are no longer actively working, oxygen demands do not immediately decrease. Instead, oxygen consumption remains elevated temporarily. This consumption, which exceeds that usually required when at rest, has traditionally been referred to as oxygen debt. Contemporary theory no longer uses this term. Instead, recovery oxygen uptake or excess post-exercise oxygen consumption (EPOC) defines the excess oxygen uptake above the resting level in recovery (Gaesser & Brooks, 1984). (Hill and Lupton 1923) concluded that EPOC occurred due to the oxidation of 20% of the lactate produced during the exercise to provide the ATP necessary to reconvert the remaining 80% lactate to glycogen. Two of the lactic acid removal post-exercise are oxidation to pyruvate and subsequent generation of ATP via the Krebs cycle (non-energy requiring process) or re-synthesis to glucose/glycogen (energy requiring process). Many studies involving steady-state exercise have identified exercise intensity as a primary factor that effects EPOC. Bahr & Segersted (1991) concluded that there is a relationship between exercise intensity and EPOC at intensities greater than 50% VO2max. Brehm and Gutin (1986), Gore and Withers (1990b) and Naughton and Smith, (1993) have reported similar results indicating that a threshold exists, between 50% and 75% VO2 max, where exercise begins to significantly increase the magnitude of EPOC. (Naughton & Smith, 1993) investigated the effects of intensity on EPOC in eight trained men and eight women. The men had significantly higher resting VO2 values being 0.31 (SEM 0.01) l.min-1 than did the women, 0.26 (SEM 0.01) l.min-1 (P < 0.05).
They concluded that the EPOC for both the men and women during the postexercise period when compared with resting levels was dependent upon the exercise intensity employed.
The aim of this investigation is to compare the oxygen deficit and EPOC during steady state exercise at two different intensities of low and high intensity exercise, and investigate those factors that may contribute to EPOC.
Alternative Hypothesis:
There will be a significant difference in oxygen deficit during steady state exercise at high intensity exercise compared to that of low intensity exercise.
There will be a significant difference in EPOC during steady state exercise at high intensity exercise compared to that of low intensity exercise.
Method
Experimental/ design procedure:
The practical sheet for this investigation can be found in the appendix.
Participant information:
8 participants volunteered to take part in the practical laboratory investigation at University College Worcester on Friday 31 October 2003, 9 of the volunteers carried out the exercise at low intensity and 9 at high intensity. The participants were sports studies students at University College Worcester of both males and female, who were various ages that were not recorded. Each participant completed an Informed consent form and health questionnaire (Look in appendix).
Mean Height
Mean Weight
Low Intensity
73.3cms (? 10.4)
68.6kg (? 9.9)
High Intensity
71.5cms (? 7.3)
72.8kg (? 10.4)
Participants Overall
72.4cms (? 8.8)
70.7kg (? 10.1)
Table 1. The mean (?SD) of height and weight of the participants taking part in the experiment
Environmental Data:
Before the experiments began Ambient Temperature (?C), Ambient Pressure (mmHg) and Relative Humidity (%) were recorded (look in appendix).
Statistical Analysis
All statistical tests were carried out using SPSS software. An independent samples-t test was used ...
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Mean Height
Mean Weight
Low Intensity
73.3cms (? 10.4)
68.6kg (? 9.9)
High Intensity
71.5cms (? 7.3)
72.8kg (? 10.4)
Participants Overall
72.4cms (? 8.8)
70.7kg (? 10.1)
Table 1. The mean (?SD) of height and weight of the participants taking part in the experiment
Environmental Data:
Before the experiments began Ambient Temperature (?C), Ambient Pressure (mmHg) and Relative Humidity (%) were recorded (look in appendix).
Statistical Analysis
All statistical tests were carried out using SPSS software. An independent samples-t test was used to present and evaluate the difference of mean and standard deviation of oxygen deficit and EPOC in exercise at both high and low intensity exercise. All of the data are shown as the mean (?SD) and statistical significance is set at P<0.05. The raw data is shown in the 'appendix' section of this report, and the tests and results are shown in the 'results' section of this report.
Results
Figure 2. Shows the difference between VO2 (l/min) at both high and low intensity exercise. There is a increase in VO2 levels at certain points throughout the experiment for high intensity exercise, compared to that of low intensity exercise. Minute 3 showed a significant difference of P<0.04, minute 15 a significant difference of P<0.05, minute 16.1 also showed a significant difference of P<0.009, and finally minute 20 showed a significant difference of P<0.029. This therefore shows that high intensity exercise has a significant effect on VO2 consumed compared to that of low intensity exercise.
Figure 2. Group means VO2 values for low and high intensity exercise.
Figure 3. Shows the difference between Heart Rate (HR) at both high and low intensity exercise. There is an increase in HR during exercise regardless of exercise intensity. There are however a significant difference of P<0.00 for HR during exercise, and there is a significant difference of P<0.01 for HR during HR recovery. Therefore the results displayed in the figure 3 show there is a significant increase in Heart rate at high intensity exercise compared to that of low intensity exercise.
Figure 3. Mean Value of Heart Rate for High and Low Intensity Exercise
Figure 4. Shows the difference between Temperature (?C) at both high and low intensity exercise. There is an increase in temperature for all the participants during exercise regardless of exercise intensity. There is however no significant difference for temperature. However the temperature increases prominently during the high intensity exercise, and tends to show the higher deviation post exercise and post recovery.
Figure 4. Mean Values for Body Temperature during High and Low intensity exercise
Figure 5. Shows the difference between O2 Deficit and EPOC consumption at low and high intensity exercise. There is an increase in both O2 deficit and EPOC at high intensity exercise compared to that of low intensity exercise. From the results in this study O2 deficit (3.8litres ?2.2) was greater than EPOC (2.7litres ?1.0) when at high intensity exercise, however at low intensity exercise EPOC (2.3litres ?1.4) was greater than O2 (1.6litres ?0.5) deficit when at low intensity exercise. There is no consistence in relationship between O2 deficit and EPOC. There is a significant difference of P<0.024 for O2 deficit during exercise, however there is no significant difference for EPOC (P<0.414).
Figure 5. Mean values of Oxygen Deficit and EPOC consumption at Low and High intensity exercise.
Discussion:
Results from this study suggest that O2 deficit, EPOC, body temperature, VO2 consumption all increase with high intensity exercise compared to that of low intensity exercise. O2 deficit at low intensity had a group mean of 1.59litres(?0.45) whereas high intensity exercise has a group mean of 3.78 litres (?2.17). The O2 deficit had a significant difference of P<0.009528508, this deficit increased during exercise due to the increased demand exerted on the body. Previous research supports the data collected for O2 deficit, (Powers and Howley, 1994; Martin, 1974; Katch, et al 2001) stated oxygen requirements increase the moment exercise begins, and reaches steady state depending on intensity and the participants personal fitness. High intensity exercise would mean the body's oxygen requirements would increase significantly the moment exercise began, moderate-to-heavy aerobic exercise requires a larger time to reach steady rate, which creates a larger oxygen deficit than less-intense exercise.
EPOC at low intensity had a group mean of 2.3litres (? 1.4) whereas high intensity exercise has a group mean of 2.7 litres (? 1.0). The EPOC had no significant difference (P<0.423716921). The increase of EPOC at high intensity was greater than that of the low intensity due to the body's increased oxygen requirements and the oxidation of lactate. EPOC occurs after exercise, it is the amount of oxygen consumed during recovery, when exercising at low intensity exercise the body's oxygen requirements are lower than that of high intensity exercise. The body would require more oxygen at the high intensity exercise to maintain exerted demands placed upon it. The results show the EPOC demands increase with high intensity exercise (2.7litres ? 1.0) compared to that of low intensity exercise (2.3litres ? 1.4).
Previous research supports the data collected for EPOC, Bahr & Segersted (1991) concluded that there is a relationship between exercise intensity and EPOC at intensities >50% VO2max. In addition, Brehm and Gutin (1986), Gore & Withers 7(1990b) and Naughton & Smith, (1993) have reported similar results indicating that a threshold exists, between 50% and 75% VO2 max, where exercise begins to significantly increase the magnitude of EPOC. Although this study was different from that of the previous research due to the fact this study did not work with each participant's VO2 max, but rather with workloads (90W, 60W, 120W and 180W), the findings are similar to that of the previous research. The higher the intensity, the higher increase in EPOC. The difference in EPOC between the low and high intensity exercise is due to HR and Breathing, they remain elevated above resting levels for several minutes following exercise therefore requiring additional oxygen. The amount of body heat gained, total PC depleted and Blood lactate levels also have an effect on EPOC at different intensities (Katch et al, 2001).
Previously, there has been disagreements concerning the relationship between EPOC and O2 deficit. Krogh & Lindhard (1919) concluded that the two were approximately equal and some subsequent investigators agreed; (Furusawa et al, 1924 and Wasserman et al, 1967). However, Bonde-Petersen et al (1974) and Girandola and Henry, (1974) have confirmed that the EPOC always exceeds the deficit. Alpert (1965) and Kubica et al, (1985) have shown that EPOC can be greater or less than O2 deficit and that there is no consistence in relationship between them. From the results in this study O2 deficit (3.8litres ?2.2) was greater than EPOC (2.7litres ?1.0) when at high intensity exercise, however at low intensity exercise EPOC (2.3litres ?1.4) was greater than O2 (1.6litres ?0.5) deficit when at low intensity exercise.
Therefore these results are associated with Alpert (1965) and Kubica et al, (1985) theory that EPOC can be greater or less than O2 deficit and that there is no consistence in relationship between them. It is therefore misleading to identify how EPOC is used to repay O2 deficit. There are factors effecting, such as intensity, duration and total work performed because EPOC is proportionally more affected by these factors than is the O2 deficit (Gore and Withers 1989).
There are some limitations to the data presented. The participants were volunteers of mixed age and gender. No specific level of fitness was made throughout the group, to make the results more accurate it could have been of single sex, a closed age range and could have been trained or untrained participants.
Trained and untrained individuals have roughly the same steady-rate consumption values. An endurance trained individual however, reaches steady-rate more rapidly with a smaller oxygen deficit than that of an untrained or sprint-power athletes. Consequently the aerobically trained person consumes a greater amount of total oxygen during steady-rate exercise (Katch et al, 2001).
There are other factors that can effect results, especially EPOC results. Body temperature can rise about 3?C during long bouts of intense exercise, and can remain elevated for several hours in recovery. Elevated body temperature stimulates metabolism to increase recovery oxygen consumption (Katch et al, 2001).
A ventilation volume increases in intense exercise up to 10 times than that of resting requirements, this can equal 10% of the EPOC (Katch et al, 2001). The heart works harder and requires a greater oxygen supply during recovery. All aspects of physiological systems in exercise increase their own needs for oxygen, which can all have an effect of EPOC (Katch 2001).
Conclusion:
The original aim has been met, the results show oxygen deficit and EPOC at both high and low intensity exercises, the results were as to be expected from previous research. VO2 increased at high intensity exercise compared to that of low intensity exercise. Heart Rate increased from rest to during exercise regardless of intensity, however predominantly increased in high intensity exercise.
The Temperature of the participants increased for both high and low intensity exercises, the higher intensity has the greater temperature throughout the exercise. The oxygen deficit and EPOC showed correlation, both increasing with intensity, showing large increases with high intensity exercise. However there was no consistent relationship between them. The hypothesis presented at the beginning of the report has been proved to be accurate from the results found.
APPENDIX
Discussion (continued)
The temperature of the participant will be greater in the high intensity therefore greater body heat will be gained. The results show that body temperature increased markedly on the high intensity exercise compared to that of the low, however there was no significant difference. This is supported by Brooks et al. (1971) reported that increased muscle and core temperatures due to exercise have a significant impact on post-exercise consumption.
The VO2 consumption requirements of the participant will be greater in the high intensity due to the body requiring more oxygen. The results show that VO2 increased markedly on the high intensity exercise compared to that of the low, with significant differences at certain points of the exercise (please refer to results). This is supported by Bahr & Segersted (1991), Brehm & Gutin (1986), Gore and Withers (1990b) and Naughton & Smith (1993) who reported that a threshold exists, between 50% and 75% VO2 max, where exercise begins to significantly increase EPOC.
The HR of the participants will be greater in the high intensity due to the body requiring more oxygen via the blood. In this study HR had significant difference of P<0.00 for HR during exercise, and there is a significant difference of P<0.01 for HR during recovery. The results show that HR increased on both intensities, but significantly on the high intensity.
Results (continued)
Rest
During Exercise
Post Recovery
Heart Rate (bpm)
(Low Intensity)
85.5 (?9.3)
23.9 (?12.7)
92.4 (?14.3)
Heart Rate (bpm)
(High Intensity)
85.8 (?8.8)
65.8 (?7.8)
16.1 (?11.8)
Table 2. The mean (?SD) of Heart Rate at Low and High intensity exercise.
Rest
Post Exercise
Post Recovery
Temperature ?C
(Low Intensity)
36.3 (?0.7)
36.8 (?0.8)
36.4 (?1.0)
Temperature ?C
(High Intensity)
36.6 (?0.4)
36.9 (?1.1)
36.7 (?1.1)
Table 3. The mean (?SD) of Body temperature at Low and High intensity exercise.
Oxygen Deficit (litres)
EPOC (litres)
Low Intensity
.6 (? 0.5)
2.3 (? 1.4)
High Intensity
3.8 (? 2.2)
2.7 (? 1.0)
Table 4. The mean (?SD) of Oxygen Deficit and EPOC consumption at Low and High intensity exercise.
References:
Bahr,R. (1992). Excess postexercise oxygen consumption: magnitude, mechanisms, and practical implications. Act Physiology. Scand, 144, 605.
Bahr, R. and Sejersted, O. (1991). Effect of feeding and fasting on excess postexercise oxygen consumption. Journal of Applied Physiology, 71, 2088-2093.
Bahr, R., Ingnes, I., Vaage, O., Sejersted, O., and Newsholme, E. (1987). Effect of duration of exercise on excess postexercise O2 consumption. Journal of Applied Physiology, 62, 485-490.
Berger, R.A. (1982). Applied Exercise Physiology, pp. 4 - 85 . Philadelphia, USA.
Brehm, B., and Gutin, B. (1986). Recovery energy expenditure for steady state exercise in runners and nonexercisers. Medicine and Science in Sport and Exercise, 18, 205-210.
Brooks, G., Hittelman, K., Faulkner, J., and Beyer, R. (1971). Temperature, skeletal muscle mitochondrial functions, and oxygen debt. American Journal of Physiology, 220, 1053-1059.
Chad, K., and Wenger, H. (1988). The effect of exercise duration on the exercise and post-exercise oxygen consumption. Canadian Journal of Applied Sport Science, 13, 204-207.
Costill, D.L. and Wilmore, J.H. (1999). Physiology of Sport and Exercise: second edition. Human Kinetics, UK.
Gaesser, G. and Brooks, G. (1984). Metabolic bases of excess postexercise oxygen consumption. Medicine and Science in Sport and Exercise, 16, 29-43.
Gore, C.J. and Withers, R.T. (1990a). The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption. European Journal of Applied Physiology, 60, 169 - 174.
Hill, A.V. and H. Lupton. (1923). Muscular exercise, lactic acid, and the supply and utilisation of oxygen. Q. J. Med. 16, 135 -171.
Katch, F.I., Katch, V.L. and McArdle, W.D. (2001). Exercise Physiology: fifth edition. Lippencott Williams & Wilkins, USA.
Krough, A. and J. Lindhard. (1920). The changes in respiration at the transition from work to rest. J. Physiology Lond. 53, 431 - 437.
Maehlum, S., Grandmontagne, M., Newsholme, E., & Sejersted, O. (1986). Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism, 35, 425-429.
Martin, T.P. (1974). Oxygen Deficit, oxygen debt relationship at submaximal exercise. Journal of Sports Medicine, 14, 252 - 253.
McNaughton, L. and Smith, J. (1993). The effects of intensity of exercise on excess postexercise oxygen consumption and energy expenditure in moderately trained men and women. European Journal of Applied Physiology, 67, 420 - 425.
Powers, S.K. and Howley, E.T. (1994). Exercise Physiology (2nd edition). Boston, Massachusetts: WCB McGraw-Hill.
Sedlock, D.A., Fissinger, J.A. and Melby, C.A. (1989). Effect of exercise intensity and duration on postexercise energy expenditure. Medicine and Science in Sports and Exercise, 21, 662 - 666.
Wilmore, J.H. and Costill, D.L. (1999). Physiology of Sports and Exercise (2nd edition). Champaign, illinois: Human Kinetics.