Introduction
While exercising at the same intensity (steady state) is known to enhance fitness levels, it evokes cardio-respiratory responses absent in interval training. The onset of steady state exercise maintains oxygen uptake (VO2), heart rate (HR), and blood pressure at optimal levels (Billman 2011). These cardio-respiratory changes constitute the body’s response to the needs of the aerobic exercise and are a product of neural cardiovascular mechanisms.
Several studies have investigated the cardio-respiratory responses to steady state training. The physiological responses occur in three stages. The first stage is a short phase I (about 15 s) characterized by cardio-respiratory response to anticipation. The second stage is a prolonged phase II (15 s – 3 min) in which the HR and VO2 uptake rises exponentially. The third stage or phase III occurs after 3 min and it involves changes in the variables in response to the work rate (Billman 2011). The effect of neural cardiovascular modulation on output variables, e.g., HR, relies on training intensity and mode (Yamashita et al. 2006). A comparison of cardio-respiratory response to steady state and dynamic training found a significant increase in “HR, systolic blood pressure (SBP), and diastolic blood pressure (DBP)” during dynamic workouts and minor increment in heart rate but a large increase in SBP during static exercising (Chapman & Elliott 2008: p.155). However, the observations did not compare the respiratory response to different exercise modes.
In contrast, Por et al. (2004) found a marked rise in HR during static leg press at steady state compared to dynamic exercise. Oxygen uptake (VO2) was significantly higher in the dynamic training than in the static mode, but heart rate was lower (Por et al. 2004). In addition, SBP and DBP for the static training exceeded the respective values for the dynamic training at steady state. A study comparing the HR variables while cycling judo randori versus ergometer at steady state found the mean HR to be above 180 beats x min-1 (Louhevaara et al. 2000). The researchers concluded that HR variability could distinguish isometric and ‘dynamic work’ performed at steady state.
The investigators used different experimental designs and variables, hence, the contradictory findings. The exercise mode, work rate, and duration were different. The studies also dwelt more on cardiovascular responses to exercise at steady state. In light of these limitations, the current study’s aim was to investigate the pattern of cardio-respiratory response to steady state exercise.
Method
Participants
The study involved one healthy male student aged 24 recruited by the investigator. The participant volunteered to take part in the study. The fitness level of the participant was measured using demographic data and self-reported weekly workouts. The subject refrained from strenuous work, alcoholic drinks, and caffeine for a day before the study.
Ethical Considerations
The researcher sought informed consent from the subject before the experiment. In addition, the physiologic data collected were not revealed to maintain the privacy and confidentiality of personal information. The researcher informed the participant that he would suffer no penalties if he decides to withdraw. The university’s ethics committee (University of Worcester) sanctioned this study upon a review of the ethical measures.
Procedure
Upon arrival at the laboratory, the participant’s weight and height were measured (Table 1). The experimental design involved four conditions. It started with a work rate (WR) of 30 for four minutes followed by WR 90 lasting five minutes. The subsequent phases were WR 120 lasting six minutes and WR 30 lasting 5 minutes. The subject’s HR, oxygen consumption (VO2), systolic pressure, and breathing frequency (dependent variables or DV) were measured.
Table 1: Participant characteristics.
Heart Rate
The participant’s HR response to different exercise modes was estimated with a ‘Polar HR’ monitor. The HR rate was measured from the onset for 20 consecutive minutes. The investigator recorded the HR in beats per minute for the initial work rate of 30, the subsequent rates of 90 and 120, and the final work rate of 30.
Blood Pressure
The measurement of SBP involved a stethoscope attached to a cuff wrapped to around the subject’s hand. The researcher recorded the systolic pressure shown on the gauge in mmHg during the exercise. The data (SBP) were collected at a two-minute interval over a period of 20 minutes.
Breathing Frequency
The subject’s breathing frequency was measured with a calibrated MedGraphic CardiO2 analyzer to monitor his ventilation rate. The frequency of breaths was measured at a one-minute interval during the experiment. In addition, the breathing rate at rest was measured before the exercise.
Oxygen Uptake (VO2)
The oxygen uptake during the test was measured using the MedGraphics CardiO2 analyzer calibrated to estimate oxygen consumption. The subject’s VO2 at rest was measured before the experiment. The investigator then measured the frequency of breaths at a one-minute interval.
Data Analysis
The study used the analysis of variance (ANOVA) to find out if the difference between the work rates is significant. Statistical significance was tested at p<0.05 or 95% confidence. Statistically significant results were compared to those of past studies.
Results
A summary of the cardio-respiratory responses to the four treatments/work rates, i.e., the initial rate of 30, the intermediate rates of 90 and 120, and the final rate of 30 are shown in Table 2. A higher work rate of 120 (treatment 3) produced the most VO2, HR, BF, and SBP in this experiment.
Table 2: Cardio-respiratory responses to different work rates (M ± SD).
Table 2 shows that a work rate of 30 following an intense exercise produces significantly different HR and SBP responses from the initial work rate (treatment 1 vs. treatment 4). Other cardio-respiratory variables are not significantly different between treatments 1 and 4. The results show that a higher work rate elicits significant cardiovascular responses to steady-state exercise compared to a lower work rate.
Discussion
The rise of the subject’s VO2 at intense steady-state exercise (treatment 3) was caused by high Q (cardiac output) levels according to the Fick equation, i.e., VO2 = Q*avO2 diff (Brooks et al. 2000). The increase in SBP shows that intense training elevates the ventricular contractions, leading to elevated blood pressure. Heart contractions may be a response to the activation of sympathetic nerve or the secretion of the adrenal catecholamine hormone (Simpson and Karageorghis 2006). Since HR and SBP rose during the experiment, the ventricular contractions could be attributed to the sympathetic nervous system that often increases the heart rate.
Elevated activity of the skeletal muscles has been linked to a rise in VO2 (Simpson and Karageorghis 2006). During intense steady-state exercise, more blood flows to the skeletal muscles per second, hence, the high VO2 in treatment 3. When slowing down, the volume of blood delivered to the tissues declines, which explains why VO2 was higher in treatment one than in treatment 2 (1.73±.14 vs. 1.4±.7) despite the same work rate. This observation may result from the decline in the O2 demand by the muscles during the recovery period.
The elevated VO2 and HR are consistent with the Billman’s (2011) findings, which indicated that these cardio-respiratory variables peak at phase II. Chapman and Elliot (2008) also found a significant increase in SBP and DBP during dynamic training at steady state. They investigators also found minimal increment in HR during static exercise. This finding differs from the high HR observed in this study at the greatest work rate (treatment 3). The inconsistency may be attributed to differences in the exercise protocols and measurements.
The breathing frequency increased with the intensity of the exercise peaking at a steady-state work rate of 120. The high VO2 requirement by the muscles might have increased the demand for ventilation, leading to frequent breaths. However, after the maximum work rate, the demand for ventilation drops significantly, which explains the minimal difference in breathing frequency between treatment 2 and treatment 4 (18±2.8 vs. 18.7±3.1).
The higher HR and SBP can be attributed to the gradual increase in Q as the exercise intensity rises. Since both HR and SBP were greatest during intense exercising (treatment 3), the cardiac muscular reached optimal contractions to achieve higher VO2 levels, which is a favourable outcome physiologically to endurance athletes (McArdle et al. 2007). The respiratory responses may be the result of the stimulation of organs such as the lungs. Although VO2 increased in treatment 3, the number of breaths remained the same (25), which is an indication of an improvement in pulmonary efficiency.
Given that the optimal cardio-respiratory response is experienced at the highest work rate, maximum steady-state exercises could be critical in influencing physiological response in endurance athletes. All the variables, including VO2, HR, SBP, and BF, reached maximum values at the highest work rate of 120. The current study has some limitations. First, the use of data drawn from a single subject may reduce the external validity and reproducibility of the results. Second, the failure to compare the cardio-respiratory response between trained and untrained states may cause the variables to differ widely between the two conditions. Nevertheless, the study has established that cardio-respiratory response is optimal at the maximal steady-state endurance level.
Conclusion
The results of the experiment show that the highest cardio-respiratory response occurs at the optimal work rate. The VO2, SBP, BF, and HR are highest at the elevated work rate in a steady state. In this study, the difference in breathing frequency before and after attaining the highest work rate was not significant, indicating an improvement in pulmonary efficiency. Therefore, exercising at the highest steady-state work rate has a positive influence on cardiac and respiratory efficiency.
References
Billman, G. (2011) Heart rate variability—a historical perspective. Front Physiology, 2 (8), 112-127.
Brooks, G., Fahey, T., White, T. & Baldwin, K. (2000) Exercise Physiology: Human Bioenergetics And Its Applications. Mountain View, CA, Mayfield Publishing Company.
Chapman, J.H. & Elliott, P.W. (2008) Cardiovascular effects of static and dynamic exercise. European Journal of Applied Occupational Physiology, 58, 152-157.
Louhevaara, V., Smolander, J., Aminoff, T., Korhonen, O. & Shen, N.Y. (2000) Cardiorespiratory responses to fatiguing dynamic and isometric hand-grip exercise. European Journal of Applied Physiology, 82 (1), 340-344.
McArdle, W.D., Katch, F.I. & Katch, V.L. (2007) Exercise Physiology: Energy, Nutrition, & Human Performance. Philadelphia, Lippincott Williams & Wilkins.
Por, A., Kijima, M., Arimoto, S. & Muramatsu, E. (2004) Cardiorespiratory response to dynamic and static leg press. Occupational Physiology, 5 (1), 395-408.
Simpson, S.D. & Karageorghis, C.I. (2006) The effects of synchronous music on 400-m sprint performance. Journal of Sports Science, 24 (10), 1095-1103.
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