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ORIGINAL RESEARCH |
From the School of Physical and Health Education and the Departments of Obstetrics and Gynaecology, and Physiology, Queen’ University, Kingston, Ontario, Canada.
Address reprint requests to: Larry A. Wolfe, PhD Queen’s University School of Physical and Health Education Kingston, Ontario K7L 3N6 Canada E-mail: wolfel{at}post.queensu.ca
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Abstract |
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Methods: The pregnant (n = 14, mean gestational age 34.7 ± 0.4 weeks) and nonpregnant control group (n = 14) included healthy, physically active women. Groups were matched for age, height, parity, prepregnant body mass and body mass index (BMI), and aerobic fitness. Breath-by-breath gas exchange was measured at rest, during exercise, and 15 minutes after exercise. The minimum sample size to detect a statistically significant result for a reasonable difference (0.25 L/min) in the ventilatory threshold was calculated to be ten subjects per group; thus, 14 was considered adequate.
Results: Maximal oxygen uptake, the ventilatory threshold, the point of respiratory compensation, and calculated work efficiency did not differ significantly between groups. However, the respiratory exchange ratio at maximal exercise, peak postexercise lactate, and excess postexercise oxygen consumption were significantly lower in the pregnant group. Peak lactate was significantly correlated with the respiratory exchange ratio and excess postexercise oxygen consumption.
Conclusion: The capacity for weight-supported work is preserved in late gestation, and work efficiency is unchanged. However, carbohydrate utilization might be blunted at high levels of exertion. Blunted respiratory responses were attributed to reduced lactate production and/or dilution of lactate in an expanded blood volume.
Recently there has been a substantial increase in the involvement of young women in nontraditional activities that involve high levels of physical exertion (eg, military service, police work, fire fighting, construction work, and strenuous sports and recreational activities). When physically active women become pregnant, it is important for health care providers to understand the normal maternal and fetal responses to strenuous exercise in order to advise these women on appropriate physical activities at various stages of gestation.
Pregnancy is accompanied by significant changes in substrate utilization, cardiovascular and respiratory control, and acid-base regulation.1,2 Each of those variables has an important effect on the response to exercise. Therefore, tolerance for strenuous exercise might be altered in late gestation to accommodate the needs of the growing fetus.
There are few investigations of strenuous exertion in pregnancy, and they used simple conventional methodologies and examined a limited number of variables. There is very little information available on the effects of pregnancy on the ventilatory threshold3,4 and the point of respiratory compensation.4 Furthermore, those previous studies did not use breath-by-breath technology, which detects the ventilatory threshold and the point of respiratory compensation more precisely and facilitates analysis of more ventilatory variables for more precise characterization of ventilatory responses.
The ventilatory threshold is characterized during a progressive exercise test by an increase in minute ventilation that is disproportionate to the increase in oxygen uptake (
CO2) as well as a disproportionate increase in carbon dioxide output (CO2) plotted against CO2. The ventilatory threshold is an index of the onset of blood lactate accumulation and reflects the peak intensity that an individual can sustain without progressive accumulation of lactic acid and muscular fatigue. Thus, the ventilatory threshold reflects an individual’s capacity for prolonged exercise.
The point of respiratory compensation is indicated during a progressive exercise test by an increase in minute ventilation that is disproportionate to the increase in CO2 and by a second disproportionate increase in CO2 relative to O2. Respiratory compensation helps attenuate exercise-induced increases in blood pH by eliminating excess carbon dioxide (CO2) formed from the buffering of lactic acid.
Excess postexercise oxygen consumption refers to additional oxygen uptake (above resting levels) that occurs during recovery from a bout of exercise. The magnitude of excess postexercise oxygen consumption reflects the extent of the changes in body temperature, circulating catecholamines, calcium ions, and fatty acids brought about by that exercise bout as well as energy requirements to restore glycogen, adenosine triphosphate, and creatine phosphate stores.5 It has been reported that excess postexercise oxygen consumption is the same6 or greater7 during pregnancy compared with postpartum in response to steady-state exercise. However, reports of blunted blood catecholamine1 and lactate3,8,9 responses to strenuous exercise in late gestation suggest that excess postexercise oxygen consumption might be lower after strenuous exercise during pregnancy.
Reports of a lower respiratory exchange ratio (ie, the ratio of CO2 produced to oxygen [O2] consumed) at maximal or near maximal exercise10–12,13 in the pregnant state combined with the reports of lower lactate concentration3,8,9 also suggest that there might be less buffering of lactic acid during strenuous exertion in late gestation. However, the peak respiratory exchange ratio and lactate concentration have not been reported together in the few studies that have examined maximal exercise responses in the pregnant state.
Work efficiency during pregnancy has only been examined using a weight-bearing treadmill protocol, where work efficiency was inferred from changes in oxygen uptake in response to changes in treadmill grade during exercise at a constant speed.14 Work efficiency relates to the percentage of energy released in the body that appears as external work. Information on these variables would add significantly to our understanding of the effects of pregnancy on maternal and fetal exercise tolerance.
We used modern breath-by-breath gas analyses to study maternal metabolic, ventilatory, and gas exchange responses to a maximal cycle ergometer stress test in late gestation. We hypothesized that the respiratory exchange ratio at maximal exercise and peak postexercise lactate concentration would be lower in pregnant subjects compared with nonpregnant controls and that this would be associated with lower excess postexercise oxygen consumption in late pregnancy compared with the nonpregnant state. Fetal heart rate responses to this protocol were reported in detail previously.15
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Materials and Methods |
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Medical clearance for pregnant subjects was obtained from the physician or midwife monitoring their pregnancy by using a standard form published by the Canadian Society for Exercise Physiology and reviewed by the study obstetrician (GD).16 Nonpregnant subjects completed the Physical Activity Readiness Questionnaire. Written informed consent was obtained from all subjects before entry into the study. The study protocol and consent form were approved by the Research Ethics Board, Faculty of Medicine, Queen’s University and the United States Army Medical Research and Materiel Command, Human Subjects Protection Branch.
Basic physical measurements included body height, body mass, and resting blood pressure (BP). Body mass index (kg/m2) was calculated as body mass/body height.2 The pregnant group and control group were matched for mean age, height, prepregnant body mass and BMI, parity, and aerobic fitness (assessed by progressive maximal exercise test).
Subjects in both groups performed a progressive maximal exercise test on a constant work rate cycle ergometer (Model 800S; Sensor Medics, Yorba Linda, CA). Subjects consumed a standard meal (350 kcal, 40% carbohydrate, 40% fat, 20% protein) 1–2 hours before testing and avoided strenuous physical activity and caffeine intake on the day of testing. The protocol involved 5 minutes of resting data collection and a 4-minute warm-up at 20 W, followed by a progressive increase in work rate of 20 W/minute to volitional fatigue.4,11,17,18 After the maximal exercise test, data collection continued into the recovery period for 15 minutes.
Respiratory responses were measured on a breath-by-breath basis at rest, during, and after exercise using a computerized system (First Breath Inc., St. Agatha, Ontario, Canada) that incorporates a respiratory mass spectrometer (MGA 1100; Marquette Electronics Inc., Milwaukee, WI) with a low dead space, bidirectional volume turbine (VMM-2; Interface Associates, Aliso Viejo, CA) as described by Hughson et al.19 The mass spectrometer was calibrated with a precision-analyzed gas mixture, and the volume turbine was calibrated before each test using a syringe of known volume (3.004L). Respiratory gases (O2, CO2, and nitrogen [N2]) were sampled at the mouth at a flow rate of 60 mL/min. Electrical signals from the equipment were converted from analog to digital and stored on a microcomputer. Heart rate was monitored with both a Polar Vantage monitor (Polar Electro Inc., Woodbury, NY) and a Marquette Max-1 electrocardiograph (Marquette Electronics Inc.). Thirty seconds of data were averaged for each subject for between-group comparisons of sub-maximal and maximal exercise. Submaximal exercise was taken at O2 100 mL below the measured ventilatory threshold for each subject.
Breath-by-breath alveolar gas exchange was calculated using the algorithm of Beaver et al.20 Arterial carbon dioxide tension (PaCO2) was calculated from end-tidal CO2 tension (PETCO2) and tidal volume (VT) using the following equation: PaCO2 = 5.5 – 0.90 PETCO2 - 0.0021 VT.21 The ventilatory threshold was identified using the V-slope method,22 which involves a two-segment linear regression (constrained at one point) that is fit on the CO2 and O2 pairs within the region of interest. This is done to provide an unbiased estimate of the O2 where the CO2 compared with O2 relationship breaks from linearity.
The point of respiratory compensation was identified by using a modified version of the V-slope method, where the lower limit for the analysis was placed slightly above the ventilatory threshold and the upper limit was placed near maximal exercise. The break from linearity calculated in this way was also inspected visually by two investigators (APH and LAW) to verify correct identification of respiratory compensation. Excess postexercise oxygen consumption was calculated by subtracting mean resting O2 from the mean recovery O2 of the 15-minute recovery period and then multiplying by 15 minutes.5
Work efficiency was calculated as described by Davis et al23 using the following equation:efficiency = [(
work rate x 2.39 x 10-4 x 60)/(O2 x 4.985)] x 100, where units for work rate, CO2, and the constant 2.39 x 10-4 and 60 are watts, L/minute, kilocalories per second per watt, and seconds per minute, respectively; 4.985 corresponds to the kilocalories expended per liter of oxygen consumed per minute for the best estimate of the substrate mixture utilized.23
An indwelling venous catheter was inserted before the test, and venous blood samples were obtained at rest and 1, 3, and 5 minutes after exercise. Blood samples were centrifuged for 10 minutes at 2500 rpm and the plasma was frozen at -80C for later analysis. Plasma lactate concentration was determined using an automated analyzer (model 2300; Yellow Springs Instruments, Yellow Springs, OH). The analyzer was calibrated before analysis and at regular intervals during the analysis using 5 and 15 mmol/L standards. All measurements were made in duplicate and averaged. The test-retest reliability of lactate measurements was described and confirmed in an earlier publication by our laboratory.3
A sample size calculation (two-sided independent samples formula) for adequate statistical power (80%) was done for oxygen uptake (O2) at the ventilatory threshold, an important variable to assess pregnancy-induced effects on working capacity that have not been well documented in pregnancy. This calculation assumes a reasonable and substantive mean difference of 0.25 ± 0.18 L/minute based on unpublished data (S.J. McAuley, MSc thesis, Queen’s University, 1998) from this laboratory dealing with significant changes in the ventilatory threshold. The minimum sample size to yield a statistically significant (P < .05) result was calculated to be ten subjects in each group, so 14 subjects in each group was considered an adequate sample.
Student t statistics for independent samples were used for simple between-group comparisons of physical characteristics, ventilatory threshold, point of respiratory compensation, excess postexercise oxygen consumption, and work efficiency. One-tailed tests were used to compare excess postexercise oxygen consumption and peak postexercise lactate between groups, because we hypothesized that values would be lower in the pregnant compared with the control group. Similarly, a one-tailed test was used to test the hypothesis that peak lactate concentration would be correlated positively with the respiratory exchange ratio3 and excess postexercise oxygen consumption using the Pearson product-moment correlation coefficient.
Data from rest and submaximal and maximal exercise time points were compared within and between subjects using a two-way analysis of variance with repeated measures on the second factor to determine significant between-group main effects, group x time interactions, and within-subject main effects. Planned comparisons were conducted between groups at rest and at submaximal and maximal exercise to identify significant differences using separate independent Student t statistics (two-tailed). The statistical package SPSS version 7.5 (SPSS Inc., Chicago, IL) was used. Statistical tests were considered significant if P < .05. Because comparisons between groups were planned and only three comparisons were made in each case, the critical alpha level for significance was maintained at P < .05.24
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Results |
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). As expected, the body mass and BMI of the pregnant group were significantly greater than those of the control group. However, the prepregnant body mass and BMI of the pregnant group were similar to those of the control group.
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Heart rate was significantly higher in the pregnant group than the control group at rest, but that difference decreased with increasing exercise intensity and was not found at maximal exercise (Table 2). Oxygen uptake and CO2 were significantly different between groups at rest but not at either exercise intensity (Table 2). The only significant difference in respiratory exchange ratio between groups occurred at maximal exercise, where the respiratory exchange ratio was significantly greater in the control group than in the pregnant group (Table 2). Work rate at maximal exercise was not significantly different between groups (pregnant group, 190 ± 7 W compared with control group, 202 ± 6 W).
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). A significant group x time interaction was found for tidal volume, as the pregnant group started higher at rest but was slightly lower (P > .05) at maximal exercise compared with the control group.
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). End-tidal oxygen tension (PETO2) was not significantly different between groups. End-tidal CO2 tension and predicted PaCO2 were significantly lower in the pregnant group than the control group at rest and submaximal exercise.
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). Plasma lactate concentration was not different between groups at rest, but peak lactate concentration was significantly lower in the pregnant group compared with the control group (Table 5). Excess postexercise oxygen consumption was significantly higher in the control group than in the pregnant group (Table 5). Peak lactate concentration was significantly correlated with both respiratory exchange ratio (r = .39) and excess postexercise oxygen consumption (r = .35) within the pooled data of the two groups. Work efficiency was not different between groups (Table 5).
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Discussion |
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The lack of difference in the maximum O2 of pregnant and nonpregnant subjects is consistent with results of studies that examined maximal or peak O2 using the same women in the pregnant and postpartum state.11–13,25,26 The physiologic changes of pregnancy do not seem to affect maximal aerobic power, provided women remain physically active. However, the higher resting O2 of pregnant women could contribute to a small, nonsignificant reduction in peak power output because more oxygen is devoted to resting maternal and fetal metabolism and less is available to perform external work.
The mean peak power output of the pregnant subjects in this study (190 ± 7 W) was nearly identical (±3 W) to that of other reports11,18 of the peak power output of pregnant women during maximal cycling exercise and was only slightly lower (P = .20) than that of the nonpregnant controls (202 ± 6 W). The mean heart rate (178 ± 2 beats per minute) and O2 (2.25 ± 0.10 L/minute) at maximal exercise of pregnant subjects were also in the upper range of reported values (171–181 beats per minute and 1.94–2.36 L/minute, respectively) for maximal cycling exercise.11,13,18,26
The ventilatory threshold was also similar in the pregnant and control groups. This confirms, using modern breath-by-breath technology, the findings of two previous studies3,4 that examined the ventilatory threshold in women tested during pregnancy and postpartum using conventional open-circuit methods. Because the ventilatory threshold reflects the peak intensity that an individual can sustain without progressive accumulation of lactic acid, it appears that pregnancy does not affect the capacity for prolonged weight-supported work. Our finding of the same point of respiratory compensation between the pregnant and control groups also agrees with that of Lotgering et al,4 who used conventional open-circuit measurement methods.
Increased respiratory sensitivity, beginning in the first trimester, has been well documented.2 In the present study, evidence for augmented respiratory sensitivity included significantly increased pulmonary ventilation and the ratio of tidal volume to inspiratory time at rest, increased ventilatory equivalents for oxygen and carbon dioxide during submaximal exercise, and altered gas tensions (reduced PET CO2 and PaCO2) at rest and during submaximal exercise. These effects previously have been attributed to augmented circulating levels of progesterone, a known respiratory stimulant, and an estrogen-mediated increase in hypothalamic progesterone receptors.2 As described in detail in recent reviews,2,27 studies of laboratory animals also confirmed the involvement of variables such as plasma osmolality, the strong ion difference (sum of strong cations minus the sum of strong anions), and circulating levels of angiotensin II and arginine vasopressin in the chemical control of ventilation. Because all of those factors that would stimulate breathing are changed in human pregnancy, we hypothesized that they are involved in pregnancy-induced increases in respiratory sensitivity in addition to the well-accepted effects of progesterone.2
The present study results also help to explain the earlier findings of Lotgering et al,4 who used conventional open-circuit gas analysis technology and the same maximal cycle ergometer testing protocol to examine the exercise responses of healthy women at 16, 25, and 35 weeks’ gestation and approximately 7 weeks postpartum. As in the present study, there was no significant effect of pregnancy on oxygen uptake at the ventilatory threshold or the point of respiratory compensation for metabolic acidosis. Also consistent with the present findings, those authors reported reduced CO2 output (and respiratory exchange ratio) at peak exercise throughout pregnancy compared with the non-pregnant state. In this regard, the slope of the CO2 versus O2 relationship measured between the ventilatory threshold and point of respiratory compensation was attenuated throughout pregnancy, and the slope of that relationship above the point of respiratory compensation was reduced in late gestation compared with the nonpregnant state. Accordingly, those results were attributed to reduced buffering of lactic acid during exercise above the ventilatory threshold. The blunted peak postexercise lactate levels observed in late gestation and the significant correlation between the respiratory exchange ratio and peak postexercise lactate levels in the present study support that hypothesis.
Blunted blood lactate responses to strenuous exercise in late gestation have been reported by several laboratories,3,8,9 but the underlying mechanism(s) for this effect are not certain. Postulated causes include dilution of lactate because of expanded maternal blood volume,9 fetal and/or placental utilization of lactate as a metabolic fuel,28 reduced capacity of contracting maternal skeletal muscle to utilize carbohydrate and produce lactate,3 or a combination of these factors. Arguments in favor of reduced ability to metabolize carbohydrate and produce lactate center on the availability of glucose from the maternal blood glucose pool. In this regard, other laboratories have reported hypoglycemic responses to strenuous exercise in late gestation,1,8 which must be the result of increased maternal (which is unlikely) or fetal (which does occur) glucose uptake, or impaired glucostatic function of the liver. Reduced liver glycogen storage has been reported in pregnant rats,29 and blunted sympathoadrenal responses, as observed in association with strenuous exercise in pregnant women,1 could contribute to reduced exercise-induced liver glycogenolysis. Unpublished experiments from our laboratory also suggest that the level of GLUT 4 glucose transporters in maternal skeletal muscle is reduced in late gestation; therefore, glucose entry into contracting maternal skeletal muscle also could be reduced. This might help to protect fetal access to the maternal blood glucose pool.
Previous studies have examined excess postexercise oxygen consumption after steady-state exercise in pregnancy and have reported no change6 or a greater excess postexercise oxygen consumption7 in pregnancy compared with postpartum. However, the present study, which used a progressive maximal exercise test protocol, resulted in lower values in late pregnancy compared with the nonpregnant state. This finding suggests that smaller changes in temperature, catecholamines, calcium ions, fatty acids, or restoration of glycogen, adenosine triphosphate, and creatine phosphate stores5 contributed to lower excess postexercise oxygen consumption after strenuous exercise in pregnancy. Indeed, blunted catecholamine1 and body temperature8 responses to strenuous exercise have been reported in late gestation. The lower peak postexercise plasma lactate values in the pregnant group also suggest that the energy costs of lactate removal during recovery from strenuous exercise could be less and might contribute to lower excess postexercise oxygen consumption in late gestation compared with the nonpregnant state. This conclusion is also supported by the significant positive correlation between peak postexercise lactate concentration and excess postexercise oxygen consumption.
In contrast to an earlier study14 that used a weight-bearing treadmill protocol and reported that the caloric cost of exercise was reduced in the second trimester compared with postpartum (possible mechanisms responsible unidentified), we did not find any change in work efficiency using our non–weight bearing cycling protocol in late gestation. Nevertheless, this result supports the idea that pregnancy does not adversely affect a woman’s working capacity.
The lower peak postexercise lactate values and respiratory exchange ratio at peak exercise indicate blunting of carbohydrate utilization above the point of respiratory compensation, which might be a protective mechanism to spare glucose for the fetus or placenta. In addition, the maintenance of a lower [H+] during pregnancy at rest and in response to strenuous exercise17 protects the fetus from changes in pH. Although the physiologic effects of pregnancy do not affect a woman’s overall capacity for weight-supported work, alterations in energy metabolism and acid-base regulation appear to aid in the maintenance of fetal well-being during strenuous exercise.
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Footnotes |
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Received March 13, 2000. Received in revised form July 14, 2000. Accepted July 20, 2000.
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2. Wolfe LA, Kemp JG, Heenan AP, Preston RJ, Ohtake PJ. Acid-base regulation and control of ventilation in human pregnancy. Can J Physiol Pharmacol 1998;76:815–27.[Medline]
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