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Curtin University
School of Physiotherapy

To train or not to train during pregnancy: the cardiorespiratory factors.

Proposition for Debate - by Andrea Stanley

Contents

Statement of the Topic

To train or not to train during pregnancy: the cardiorespiratory factors.

Introduction

Exercise and training is becoming an integral way of life for many people. For both the elite and recreational athlete, any break in their training schedule due to illness or injury can have a marked detraining effect. Pollock et al (1998) state that "a significant reduction in cardiorespiratory fitness occurs after two weeks of detraining, with participants returning to near pretraining levels of fitness after 12 weeks to eight months. A loss of 50% of their initial improvement in maximum oxygen consumption has been shown after 4-12 weeks of detraining". For many women the desire to have a family but also maintain a high level of fitness creates a dilemma. The ability to continue to train throughout gestation is not debatable, what causes concern is the intensity at which pregnant woman can safely train.

Much research has been directed at the effects of exercise in the sedentary and highly trained individual and there is a base of knowledge regarding the effect of exercise on pregnant woman, however little research has focused on the effects of maintaining high level training regimes throughout pregnancy. The effects of such training on both the fetus and the mother have yet to be fully determined as has the level of training needed to maintain a prepregnancy fitness level through gestation.

It is the purpose of this debate therefore to address briefly the normal cardiorespiratory responses to pregnancy, exercise and the combination of the two. In particular, attention will focus on the body of knowledge available regarding the benefits of training throughout pregnancy.

Background Knowledge

Maximal Oxygen Uptake (VO2 max)

Maximal oxygen uptake (VO2 max) is defined as the "highest rate at which oxygen can be taken up and utilized by the body during severe exercise" (Basset and Howley 2000). Graphically, it is seen as the point at which O2 consumption plateaus and shows only minimal or no further increases with additional workload. It has also been referred to as the maximal oxygen uptake, maximal aerobic power or maximal oxygen consumption. It reflects a persons' capacity to aerobically resynthesize ATP and thus will vary between individuals (McArdle et al 1986).

It can be measured using continuous stepwise increments in exercise intensity or discontinuous increments. The continuous protocol appears to be the method of choice in the literature available.

It has been argued that in order to accept an oxygen uptake level as maximum several other criteria should also be met. It has been proposed that blood lactic acid levels should be greater than 8-9 mMol and the expiratory exchange ratio should exceed 1.15 (Basset and Howley 2000). Other authors have suggested age predicted maximum heart rate should also be reached (McArdle et al 1986).

It is interesting to note that differences in values have been obtained for the same individual when the different protocols have been used (McArdle et al 1986).

Maximal heart rate may also be used to predict VO2 max. This is an accepted method as there is a proven linear relationship between heart rate and oxygen consumption during aerobic work (McArdle et al 1996).

Oxygen consumption is also linearly related to energy expenditure, therefore when oxygen consumption is measured, an individual's maximal capacity to do work aerobically can be inferred. Thus, this value is used as an indicator of an individuals cardiorespiratory fitness and can be used in exercise prescription (Basset and Howley 2000).

Research suggests a linear relationship between oxygen consumption and cardiac output over a wide range of submaximal exercise (McArdle et al 1986). Basset and Howley (2000) estimate that 70-85% of the limitation in VO2 max is attributable to maximal cardiac output.

Anaerobic Threshold

The term Anaerobic Threshold has been used to describe the blood lactate response to exercise.  Other terms also used to describe this phenomenon include, Lactate Threshold (LT), Onset of Blood Lactate Accumulation (OBLA), Maximum Steady State and Individual Anaerobic Threshold, Lactate Breaking Point.

Lactate Threshold

Lactic acid is known to begin accumulating at about 55% of the healthy, untrained subjects maximum capacity for aerobic metabolism. This is due to the rate of lactic acid production exceeding the rate of its removal via oxidation in the Krebs cycle or its resynthesis back to glucose. (McArdle et al 1996)

Lactate Breaking Point

The lactic acid threshold, when defined as a breakpoint, refers to the highest VO2 that can be attained during incremental exercise before an elevation in blood lactate is observed. (Ivy et al 1980, Tanaka et al 1985)

Onset of Blood Lactate Accumulation (OBLA)

This has been described as the level of oxygen consumption (or exercise) at which blood lactate begins to rise above baseline and again occurs at about 55-65% of a persons maximal oxygen uptake (McKardle et al 1986).

Maximum Steady State

Some authors have defined LT as a blood lactate concentration value of 1mMol/l above baseline. In this protocol, blood lactate concentration is monitored during incremental exercise and the value of VO2 which correlates with an increase in blood lactate concentration of 1 mMol/l above baseline is determined as the LT (Hagberg and Coyle 1983).

In addition to this, other researchers take LT as the point where blood lactate concentration reaches a value of 2.0 mMol/l, 2.5 mMol/l or 4.0mMol/l during incremental exercise. These absolute concentrations were chosen as they were thought to reflect a maximum balance between lactate production and elimination during continuous exercise (Weltman et al 1990).

Individual Anaerobic Threshold

More recently, researchers have recognized that the blood lactate concentration varies from individual to individual as does the ability to maintain a steady state blood lactate response during prolonged exercise. It is for this reason that the individual anaerobic threshold (IAT) has been argued to be the most accurate assessment for LT. This is again assessed during incremental exercise, followed by a passive recovery and usually results in blood lactate levels of between 2-7mMol/l (McLlennan, Cheung and Jacobs 1991).

Factors Affecting VO2 max

Several factors are known to limit an individuals VO2 max. These include pulmonary diffusion capacity, maximum cardiac output and the oxygen carrying capacity of the blood. In addition are factors relating to the skeletal muscle which include the capillary density, mitochondrial enzyme levels and the peripheral diffusion gradient (Basset and Howley 2000)

Cardiorespiratory Response to Pregnancy

The response of the cardiorespiratory system in a normal, healthy, untrained individual has been well documented and is designed to accommodate for the increased demands of the fetal-placental unit. It also allows the mother to cope with the extra weight associated with pregnancy, extra heat production and other waste products being eliminated from the fetus via the placenta into the mothers' circulatory system. These normal adaptations are outlined below.

Cardiovascular

The blood volume of the pregnant women increases by 40-50% by the end of the third trimester, with blood plasma volume increasing by 30-60% and red blood cell content by 20-30%. This disparity in increased plasma volume compared to red blood cell content leads to a relative physiological anemia during pregnancy (Ireland and Ott 2000, Spedding 1993). Maternal heart rate at rest is known to increase on average by 15-20 beats/min during pregnancy (Spedding 1993). Pregnancy is also associated with an increased cardiac output and stroke volume as well as dilatation of all four chambers in the heart, dilatation of the arteriolar resistance vessels, an increase in aortic diameter and an enlargement of the venous capacity vessels (Shephard 2000). This peripheral vasodilatation may lead to blood pooling in the extremities and is often associated with swelling of the hands and feet.

It must be acknowledged that there is a significant diversion of blood to the uterus during pregnancy to meet the demands of the fetal and placental unit. This diminishes the baseline supply to other maternal organs and is associated with some of the other observed symptoms of pregnancy such as cramps.

Pulmonary

As the uterus enlarges it displaces the diaphragm superiorly causing the subcostal angle to widen with the transverse diameter of the thoracic cage increasing by 2cm and the circumference by 6cm (Ireland and Ott 2000). The resultant effect is a decrease in residual lung volume, expiratory reserve volume and total lung volume (Shephard 2000). In addition there is an increase in tidal volume and respiratory minute volume with oxygen consumption increasing by 16%-32% during pregnancy (Ireland and Ott 2000, Shephard 2000). Increased oxygen consumption may be due to the combined effects of increased effort of movement, resulting from the increased body mass, and an increase in respiratory effort.

Cardiorespiratory Response to Exercise

The body also accommodates well to an increase in physical activity. The changes that occur function to provide adequate oxygen and fuel requirements to the exercising muscles, and to rid the body of the waste products of energy production. The usual response to an increase in physical activity is outlined below.

Cardiovascular

At the onset of an exercise effort cardiac output in know to increase. Cardiac output is a function of stroke volume and heart rate and may be measured using the Fick Equation:

Cardiac Output (ml/min) = O2 consumption (ml/min) x 100 / a-v O2 difference (ml/100ml blood)
(a-v O2 = difference in oxygen content between arteriole and mixed venous blood) McKardle et al 1986

Upon initiation and during moderate exercise, stroke volume increases as does heart rate. As the intensity of exercise increases stroke volume plays less of a role in the increased cardiac output, with an increase in heart rate accounting the majority of the response observed.

The effect of exercise on blood pressure is dependant upon the type of exercise performed. McArdle et al (1986) suggested that during steady state submaximal exercise blood pressure was only minimally elevated, however isometric type exercise caused a significant increase in blood pressure.

The distribution of blood flow is obviously altered during exercise in order to meet the demands of the exercising muscles. Regional vascular constriction causes a decreased blood flow to the local tissue and thus blood can be diverted away from organs such as the kidneys and made available to the exercising muscles (McArdle et al 1986).

Pulmonary

Minute ventilation (V_ ) is the term used to describe the amount of air inspired per minute. It is commonly about 6L/min and is determined using the equation:

V_ = breathing rate X tidal volume

During moderate, steady state exercise, ventilation increases linearly with oxygen consumption and carbon dioxide production and is due to an increased tidal volume. At high intensities, breathing frequency accounts for most of the additional increase in minute ventilation.

Minute ventilation is affected by both the oxygen (O2) concentration of the inspired air and the plasma concentration of carbon dioxide and hydrogen ions. As the alveolar O2 concentration increases there is a decrease in V_. In contrast to this as the concentration of CO2 or hydrogen ions increases, there is a substantial increase in V_.

Cardiorespiratory Response to Aerobic Training

There are well documented physiological benefits of training and these adaptations are designed to allow the body to function more efficiently when placed under specific stress such as aerobic exercise. Outlined below are the known adaptations observed in aerobically trained individuals.

Cardiovascular

An increase in blood plasma volume and also haemoglobin is observed and this leads to an increase in blood volume. Resting heart rate is reduced and may be as low as 40-50bpm in highly trained endurance athletes. Cardiac output is maintained at a similar value to that observed in untrained normals by an increased stroke volume. Values for these changes are obviously individual sensitive as a certain amount of genetic predisposition impacts on the body's ability to adapt to exercise demands (McArdle et al 1986).

The left ventricle undergoes hypertrophy as a result of training and there is an increase in heart volume. Although there is an increased blood volume, and improved force production of the trained heart there does not appear to be any change in blood pressure in trained individuals.

Pulmonary

Resting values for lung functions are seen to be almost identical between untrained and trained individuals. The ability of the individual to extract oxygen from the blood is enhanced with training as reflected by an increased a-v O2 difference.

Effects of Exercise during Pregnancy

Pulmonary

Similar findings were revealed in the results of two longitudinal studies which compared the effects of exercise on sedentary and physically conditioned, pregnant women. Pivarnik et al (1993) and Ohtake and Wolfe (1998) found that physically conditioned, pregnant women demonstrated a smaller elevation in the ventilatory equivalent for oxygen (Ve/VO2), ventilatory equivalent for carbon dioxide (Ve/VCO2) and ventilation/perfusion ratios in response to submaximal exercise testing. Furthermore, the authors reported a slightly greater increase in maximal oxygen uptake (VO2 max), ventilation (Ve), tidal volume (Vt) and alveolar ventilation (Va) in these women during exercise.

Lotgering et al (1991) performed a longitudinal study of 33 women comparing their response to exercise during pregnancy and postpartum. Results suggested that there was no significant change in VO2 max between pregnancy and postpartum. The postpartum measurements were recorded at 8 weeks post delivery and may account for the lack of statistically significant results found, as another study did not observe any change in VO2 max until 12-20 weeks postpartum. However, because oxygen uptake (VO2) is increased at rest during pregnancy, the unchanged VO2 max during pregnancy suggests that there is a decrease in the amount of oxygen available for exercise at this time. Carbon dioxide production (VCO2) in response to exercise was found to be less during pregnancy. This, in combination with the unchanged VO2, caused a significant reduction in respiratory exchange ratios in the pregnant subjects.

In contrast to this, Clapp and Capeless (1991) reported a significant increase in the VO2 max of their experimental group compared to the control group at final evaluation. They found that despite the fact that the pregnant women's overall exercise performance fell during pregnancy and the immediate postpartum period, their absolute VO2 max was not significantly changed 6-8 weeks postpartum. In addition, they stated that although these women's exercise performance did not return to preconception levels, there was an increase in their VO2 max of 2-14% at the 12-20 week postpartum evaluation. The reason for the delay in VO2 max response remains unclear and was not addressed by the authors.

Different forms of exercise were analysed by Spinnewijn et al (1996) to determine the differences that occurred not only as a result of pregnancy but also between two different forms of exercise. These authors compared the response of individuals to swimming and cycling to determine whether pregnancy affected peak oxygen uptake (VO2 peak). They concluded that in both swimming and cycling V_ increased during gestation as a result of increased tidal volume as there was no change in respiratory rate. They also observed a decrease in the lactic acid concentration during recovery in pregnant subjects for both exercise groups. In swimming, it was noted that peak carbon dioxide production (VCO2 peak) was significantly lower during pregnancy and, as no difference in VO2 peak was found, the respiratory exchange ratio was also lower.

The differences that were noted between the two forms of exercise were that VO2 peak, VCO2 peak and V_ peak were all lower during swimming in both pregnancy and postpartum.

Lotgering et al (1995) examined the effects of high intensity exercise on a number of variables to determine why the observed differences in VCO2 peak compared to VO2 peak may occur during pregnancy. They concluded that the reduction in the VCO2 peak, relative to VO2 peak which occurred during pregnancy, was a result of a shallower slope of VCO2 vs VO2 above the anaerobic threshold. This was not seen postpartum and the authors hypothesized that this may reflect a reduction in the buffering of lactic acid by bicarbonate during pregnancy.

Cardiovascular

Pivarnik et al (1993) reported that the physically active individuals in their study demonstrated a significantly greater stroke volume and therefore cardiac output in response to exercise than did their sedentary counterparts. These authors, as well as Ohtake and Wolfe (1998), found a decrease in heart rate response to exercise in the physically active women.

Both exercise and pregnancy lead to an increase in plasma volume. It has been observed that the combined effect is additive, with physically active pregnant women having blood volumes up to 20% greater than their sedentary counterparts (Clapp 2000). This author also noted changes in end-diastolic volume and stroke volume which were 10% greater in the women who continued to exercise. The authors concluded that this led to an increase in cardiac output at rest of 40% above that of the sedentary controls. In addition it was found that these changes persisted postpartum and were accentuated by a subsequent pregnancy. In exercising women, 12 months postpartum, Clapp (2000) reported that total peripheral resistance was still 11% below and cardiac output 11% above those values obtained prepregnancy.

Problems

Most of the studies that utilized VO2 max as their criteria for cardiovascular endurance did not directly measure it but instead inferred its value from submaximal exercise testing. McMurray et al (1993) in a review article stated "Predicting VO2 max from submaximal heart rate X work rate relationships using conventional tests (eg. Astrand nomogram) is probably not a valid procedure during pregnancy due to violation of basic assumptions on which these tests are based. Specifically, oxygen cost of work is slightly increased, the slope of heart rate X power output regression line is flattened and maximal heart rate may be reduced during pregnancy and will introduce significant error if these tests, which have only been validated on nonpregnant subjects are used".

In addition to questionable measuring procedures, there is a paucity of literature addressing the issue of trained women maintaining fitness levels during pregnancy. Many of the studies compare sedentary and active individuals but few, if any have investigated those trained women who continue to exercise throughout pregnancy and those that do not. Further to this, the methods used to collect data on activity levels are far from accurate. Most rely on questionnaires or daily recordings of activity levels which are both difficult to estimate and generally provide less than accurate estimations.

Clinical Implications

As far as the clinician is concerned, the literature supports the benefits of exercise throughout gestation. To date there has been no evidence to suggest that a healthy individual with no pregnancy complications should not continue an exercise program under medical supervision.

In terms of the level of exercise required to maintain prepregnancy aerobic fitness levels, insufficient studies have been conducted to enable an accurate prediction. It would seem however, that it is possible to reduce the intensity of training both during and in the immediate postpartum period whilst still maintaining, and possibly improving aerobic fitness as measured by VO2 max.

References

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Exercise Physiology Educational Resources 2001