Sports Med 2010; 40 (6): 449-457 0112-1642/10/0006-0449/$49.95/0
CURRENT OPINION
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Nullius in Verba A Call for the Incorporation of Evidence-Based Practice into the Discipline of Exercise Science William E. Amonette,1 Kirk L. English1 and Kenneth J. Ottenbacher 2 1 Preventive Medicine and Community Health, Division of Rehabilitation Sciences, University of Texas Medical Branch, Galveston, Texas, USA 2 Division of Rehabilitation Sciences, University of Texas Medical Branch, Galveston, Texas, USA
Abstract
Evidence-based practice (EBP) is a concept that was popularized in the early 1990s by several physicians who recognized that medical practice should be based on the best and most current available evidence. Although this concept seems self-evident, much of medical practice was based on outdated textbooks and oral tradition passed down in medical school. Currently, exercise science is in a similar situation. Due to a lack of regulation within the exercise community, the discipline of exercise science is particularly prone to bias and misinformation, as evidenced by the plethora of available programmes with efficacy supported by anecdote alone. In this review, we provide a description of the five steps in EBP: (i) develop a question; (ii) find evidence; (iii) evaluate the evidence; (iv) incorporate evidence into practice; and (v) re-evaluate the evidence. Although objections have been raised to the EBP process, we believe that its incorporation into exercise science will improve the credibility of our discipline and will keep exercise practitioners and academics on the cutting edge of the most current research findings.
Beneath all physiological phenomena lie causal mechanisms. The purpose of the scientific process as it relates to human physiology is to uncover these mechanisms. Unfortunately, knowledge of a phenomenon is often buried deep beneath many partially understood or even misunderstood mechanisms, rendering what we currently know incomplete. Ideally, with each research experiment, we gain a more complete understanding of a given phenomenon; thus, knowledge is dynamic and continually evolves. The evolution of knowledge creates a unique challenge; instructors and practitioners must teach and practice with incomplete knowledge. Despite their best efforts to incorporate the latest scientific evidence, by the time a lecture is deliv-
ered, it is likely that science has already uncovered more of the story. Usually, discovery simply adds to the information that was presented to students, but sometimes advances in knowledge radically change scientific thought. In the 1930s and 1940s it was believed that muscle contractions were the result of folding and unfolding of long protein filaments located within skeletal muscle sarcomeres.[1] With the invention of a new, more powerful light microscope,[2] Huxley and Hanson were able to see two proteins, actin and myosin, that appeared to slide over each other during the shortening and lengthening of a muscle.[3,4] Now, 55 years later, the sliding filament theory of muscle contraction is taught to all physiology students as the basis of
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muscular contraction. While the teachers of the 1940s taught to the best of their ability based on contemporary knowledge, Huxley and Hanson’s discovery rendered what was taught incomplete and inaccurate. Evidence-based medicine is a term coined in the early 1990s to describe a paradigm in which clinical decisions are based on the highest available levels of research knowledge or evidence.[5,6] Although this idea seemed obvious, it was a novel approach to clinical practice. In fact, in 2000 it was estimated that only 15–40% of clinical decisions were based on research evidence.[7,8] The medical community’s call to evidence-based practice (EBP) argued that knowledge is dynamic and that clinicians should incorporate the latest evidence into practice to optimize clinical outcomes. EBP has since spread from the field of medicine to other health fields. Much has been written about the incorporation of EBP into nursing,[9,10] physical therapy[11-13] and various medical disciplines including orthopaedics.[14-16] Exercise science is susceptible to misinformation and bogus claims – perhaps more than any other field. This is evident from a cursory knowledge of the personal training industry. While organizations such as the National Strength and Conditioning Association (NSCA) and the American College of Sports Medicine (ACSM) have done much to legitimize the credentials of exercise scientists, the field is still full of misinformation. This misinformation is due, in part, to the lack of standardization among agencies that certify instructors in exercise and sports science. Many exercise certifications require minimal academic training. In fact, the only requirements of some certification agencies are to attend a weekend-long workshop and pass a written multiple choice exam. The result of such certifications are under-qualified exercise professionals equipped with minimal theoretical knowledge of training physiology and little or no ability to access the latest scientific research pertinent to their profession. These certified exercise professionals often base their practice on a flawed set of theoretical knowledge, personal experience or anecdotal hearsay, and non-peer-reviewed publications. Inevitably, misinformation leaks into the field ª 2010 Adis Data Information BV. All rights reserved.
Amonette et al.
and exercise specialists are poorly equipped to evaluate the legitimacy of information, resulting in a plethora of devices, nutritional supplements and programme theories that have little or no scientific merit. The intention of academia and practice should be to constantly evolve with the literature in a quest to create highly effective exercise programmes that are based on current knowledge. We propose that EBP be taught in undergraduate exercise science programmes as the foundation of all exercise programming. The purpose of this paper is to introduce the structural framework of EBP as it relates to exercise science and to present the advantages and limitations of EBP in the discipline of exercise science. 1. The Mechanics of Evidence-Based Practice (EBP) Sackett et al.[17] have suggested that EBP is applicable in three distinct facets of medicine: prognosis, diagnosis and intervention. While it might be argued that there are diagnostic and prognostic components of exercise science, the primary application of EBP in exercise is at the intervention or programming level. Thus, we focus solely on the programming aspect. 1.1 Step One: Develop a Question
The evaluation and interpretation of client or patient data should lead to the development of a focused, practical question.[17-20] The question should include information about the subject population, exercise parameters (e.g. duration, frequency, intensity) and desired adaptations. Questions that are too broad will yield enormous amounts of information, making interpretation of the literature difficult. Narrowing the population will result in a smaller and more focused list of abstracts. When considering the population, at least five questions should be addressed: (i) is the scenario sex specific; (ii) are there underlying clinical issues; (iii) what is the training experience of the client; (iv) what is the chronological age of the client; and (v) what is the desired outcome of the programme (e.g. increased strength, power, Sports Med 2010; 40 (6)
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cardiovascular fitness)? Each of these questions may be useful in narrowing the search and providing better evidence to construct the programme. 1.2 Step Two: Search for Evidence
Acquiring appropriate, reputable evidence has become increasingly easier with the availability of peer-reviewed research on the internet. The definition of ‘evidence’ has been a source of debate as some have mistakenly assumed that advocates of EBP believe that research alone constitutes evidence. Others have argued strongly for the value of clinical intuition and experience as important contributors to evidence.[21,22] We believe that there are three primary sources of evidence: professional experience, academic preparation and research knowledge. 1.2.1 Sources of Evidence
When evaluating the three sources of evidence, it is important to understand that each element of knowledge is incomplete, open to interpretation and therefore potentially biased. First, professional experience can be a valuable source of evidence. Lessons learned through field experience can reinforce academic knowledge. However, it is vital to understand that knowledge gained through professional experience is the least objective and most influenced by bias. For instance, in prescribing medicine, doctors may be influenced by relationships with drug companies, the preference of their mentors, and the static set of knowledge taught in medical school. While this information is often valid, it is important to understand that it may not represent the best treatment scenario. Exercise science practitioners are prone to these same biases. It is difficult to deviate from methodologies taught by mentors and well respected colleagues. While many of these methodologies are valid and effective, mentors were, at best, working from the best evidence available at that point in time. Second, academic preparation provides a valuable source of evidence. The best professors strive to incorporate recent research findings into courses teaching foundational scientific principles. Academic courses typically utilize textbooks ª 2010 Adis Data Information BV. All rights reserved.
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containing fundamental physiology knowledge that is needed to read scientific research. However, there are two inherent flaws to academic preparation: (i) the material delivered in academic lectures is often outdated by the time it is presented; and (ii) lecture material is subject to the personal bias and current knowledge of the professor. By the time a professor prepares and delivers a lecture, new evidence has already been added to the body of knowledge. It is estimated that by the time a new edition of a textbook is published, it is at least 1 year out of date;[23] similarly, with the time required to develop coursework, academic lectures are likely several months out of date by the time they are delivered – assuming they are updated each semester with the latest evidence. Like practitioners, instructors are prone to bias. There is a tendency for instructors to teach with a style similar to those who mentored them. Additionally, there is a propensity to teach the very material that one was taught. Thus, when information is presented to students it may be severely out of date; this underscores the need for the incorporation of less biased research evidence. Scientific research constitutes the level of evidence that is least prone to bias. The motto for the Royal Society of London is the Latin phrase ‘Nullius in verba’, which translates as ‘on no man’s word’. The best way to minimize bias is to remove the human element and let the data speak for itself. While the interpretation of research evidence can be biased, research evidence per se is less biased than personal experience, textbooks or academic lectures. It is our opinion that research evidence should provide the foundation for all practical programming decisions. Empirical data should exert the ultimate influence on exercise programming as it is a less biased form of evidence. 1.2.2 Gathering Evidence
In past generations, the collection of peerreviewed materials required travel to libraries, searching through card catalogues, retrieving materials from library shelves and extensive photocopying. Today, the internet enables easy access to quality resources including medical Sports Med 2010; 40 (6)
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databases and peer-reviewed journal articles online. Instead of travelling to the library, practitioners need only to search topics using publicly available databases such as PubMed and Google Scholar. The result is a vast availability of research, requiring minimal effort. 1.3 Step Three: Evaluate Evidence
The proponents of EBP argue that there is a hierarchy to evidence and that not all evidence (even scientific research) should be considered equal (table I).[20] The highest level of evidence is a systematic review of randomized controlled trials.[24] This type of research evidence is assigned a level 1a ranking, as it represents a series of replicated randomized controlled trials. Level 1b evidence is a single randomized controlled trial with narrow confidence intervals.[24] Systematic reviews of non-experimental studies (e.g. cohort studies), both single well designed cohort studies and poorly designed randomized controlled trials, and outcomes research are given rankings of 2a, 2b and 2c, respectively.[24] Systematic reviews of case-control studies (3a) and a single case-control study (3b) are given lower rankings
because of the greater potential for bias.[24] Finally, expert opinion, textbooks, decisions based on mechanistic research (basic science), and practical experience are given level 5 rankings.[24] In this system, the research that is least prone to bias, replicated randomized controlled trials (i.e. a systematic review), is recognized as the highest level of evidence while the information that is most prone to bias, expert opinion, is assigned the lowest level of evidence. This provides an impartial method of ranking evidence and determining its influence on practical decision making. 1.4 Step Four: Incorporate Evidence Into Practice
The highest available level of evidence should be used as the basis for exercise prescription. If practice is currently founded on reputable level 5 evidence, then it is likely that new evidence will only fine tune current exercise programmes. However, it is prudent for all individuals who prescribe exercise to understand the science upon which prescriptions are based. This may be especially important for exercise professionals who currently base their practice on non-peer-reviewed
Table I. Classic levels of evidence for rehabilitation practice (reproduced from Law and MacDermid,[24] with the permission of SLACK Inc.) Level
Classic ‘levels of evidence’ for therapy/prevention
Placement of additional types of clinical evidence
1a
Systematic review (with homogeneity) of RCTs
CPGs where recommendations are based on systematic reviews that contain multiple RCTs and the development includes supplemental data or expert opinion to make recommendations only where evidence is lacking
1b
Individual RCT (with narrow confidence interval)
1c
All or none
2a
Systematic review (with homogeneity) of cohort studies
2b
Individual cohort study (including low-quality RCT; e.g. 2 hours) exercise[12] or from dehydration (-2.8%) induced by passive heating or intermittent exercise[13] in well controlled settings. The increase in AVP appears to be intensity dependent, from the proportional movement of hypotonic fluid from the intravascular into the interstitial space.[14] The increase in AVP per unit rise in POsm during exercise, however, tends to be higher than the per unit rise in AVP seen after infusion of hypertonic saline, suggesting that other factors may be involved in the stimulation of AVP secretion during exercise.[14] 2. The Possible Effects of Non-Osmotic AVP Secretion on Fluid Regulation Non-osmotic or non-suppressed AVP secretion for a given level of hypo-osmolality at rest or during exercise may potentially lead to inappropriate fluid retention and hyponatraemia. The pathophysiological consequence of inappropriate AVP secretion at rest in clinical scenarios was first described in 1967 as the ‘‘syndrome of inappropriate anti-diuretic hormone secretion.’’[15] It is thereby hypothesized in this review that nonsuppressed exercise-induced AVP secretion may be one potential cause of hyponatraemia in exercise settings, primarily due to inappropriate fluid retention and secondarily to concomitant pressure natriuresis.[16-22] During exercise, especially long-distance competitive exercise, limited descriptive evidence Sports Med 2010; 40 (6)
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suggests the possibility that non-osmotic stimuli to AVP secretion may override the osmotic regulation of AVP resulting in life-threatening fluid overload during vigorous physical activity.[17-22] Possible non-osmotic AVP stimuli during exercise include plasma volume contraction,[17,23,24] elevated body temperature,[25] nausea with or without vomiting,[26] hypoglycaemia[27,28] or other yet to be identified factors.[29] Circulating endocrine factors, which have recently been implicated as potential non-osmotic stimuli to AVP secretion in animals and humans during exercise, include interleukin (IL)-6,[30] angiotensin II,[31,32] corticosterone, oxytocin and brain natriuretic peptide.[17,33] It must be emphasized that plasma concentrations of AVP ([AVP]p) do not have to be abnormally high or even out of the ‘normal’ range to cause fluid dysregulation, morbidity or death.[18,20,34,35] AVP secretion that is simply inappropriate for the current state of plasma hypo-osmolality can lead to pathological fluid retention and dilutional hyponatraemia.[15,36] More simply described, if [Na+]p fall below 135 mmol/L (or below ~280 mOsmol/kg H2O for POsm), pituitary AVP secretion and the corresponding [AVP]p should be maximally suppressed (i.e. under the detectable range for the assay, which in most cases is 200 or resting diastolic blood pressure >110 mmHg should be evaluated on a case-by-case basis Orthostatic blood pressure drop of >20 mmHg with symptoms Critical aortic stenosis (peak systolic gradient of >20 mmHg with aortic valve orifice area 120 beats/min) Third-degree AV heart block (without pacemaker) Active pericarditis or myocarditis Recent embolism Thrombophlebitis Resting ST-segment displacement (>2 mm) Uncontrolled diabetes mellitus (resting blood glucose >400 mg/dL) Severe orthopaedics that would prohibit exercise Other metabolic problems, such as acute thyroiditis, hypo- or hyperkalaemia, hypovolaemia, etc. No
Yes Is immediate intervention indicated? Yes
Further cardiological consultation and medical assessment
No Prehabilitation Systemic exercise: if moderate or high intensity then GXT required
Localized exercise: no medical GXT required
Adverse symptoms during exercise? Examples of systemic exercise
n
tio
Duration: 30 min at target intensity or four sets at 20 min each (4 min rest between sets)
Endothelium Smooth muscle
nc
Intensity: 30−50% or maximal voluntary contraction or 70% maximal work at 30 contractions/min for 30 min
Fu
Duration: Start at 15 min at target exercise intensity, advance to 60 min (within patient tolerence)
Activities such as handgrip exercise 2−7 d/wk
Duration of training
Intensity: Exercise intensity below myocardial ischaemic threshold RPE 11−14, or 40−75% of HRpeak
Artery function and structure
Artery remodelling
Aerobic training: Activities such as walking/running, cycling and swimming 4−7 d/wk
Examples of localized exercise
Resistance (weight) training: Activities such as circuit weight training, theraband exercise and bodyweight exercise 2−3 d/wk Intensity: RPE 11−15 Six to 15 repetitions per set Commence at one set per exercise, progressing to up to three sets Four to eight different exercises for the major muscle groups
−ve
+ve
CABG or PTCA
Fig. 3. Risk stratification, examples of exercise training . and changes in vascular function with proposed ‘arterial prehabilitation’. Moderate exercise: 40–50% of maximal oxygen consumption (VO2max); 3–6 metabolic equivalents (METs); ‘‘an intensity well within the individuals . capacity, one which can be comfortably sustained for a prolonged period of time (~45 minutes).’’[92] High intensity exercise: >60% of VO2max; >6 METs; ‘‘exercise intensity enough to represent a substantial cardiorespiratory challenge.’’[92] Examples of systemic exercise[15,80,93-95] and localized[30,41,44] exercise in patient populations in the literature. ACSM = American College of Sports Medicine; AV = atrioventricular; CABG = coronary artery bypass graft; GXT = graded exercise test; HRpeak = peak heart rate; PTCA = percutaneous transluminal coronary angioplasty; RPE = rating of perceived exertion; ST = ECG derived ST segment; -ve = negative; +ve = positive.
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Sports Med 2010; 40 (6)
Prehabilitation: Exercise to Enhance CV Outcomes
small muscle group exercise and whole body exercise can enhance endothelial function, enlarge conduit arteries and modulate endothelial progenitor cell number and function. 5. Based on the above evidence, we propose ‘arterial prehabilitation’, the concept that interventions aimed at enhancing arterial function, remodelling and repair should be undertaken prior to cardiac catheterization, or artery harvest for bypass graft surgery, in order to optimize subsequent outcomes and minimize complications such as artery spasm and occlusion or graft patency post-bypass surgery. 6. Future research effort should focus directly on examination of the hypothesis that beneficial effects of exercise training may be evident prior to routine procedures and that ‘prehabilitation’ may serve as an effective strategy in reducing clinical complications of common interventional procedures.
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8.
9.
10.
11.
12.
13. 14.
15.
Acknowledgements 16.
Daniel Green was supported by the National Heart Foundation of Australia. Dick Thijssen was supported by the Netherlands Organisation for Scientific Research (NWOgrant 82507010) and is a recipient of the E. Dekker-stipend from the Dutch Heart Foundation. The authors have no conflicts of interest that are directly relevant to the content of this review.
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74. Sinoway LI, Musch TI, Minotti JR, et al. Enhanced maximal metabolic vasodilatation in the dominant forearms of tennis players. J Appl Physiol 1986; 61 (2): 673-8 75. Martin 3rd WH, Kohrt WM, Malley MT, et al. Exercise training enhances leg vasodilatory capacity of 65-yr-old men and women. J Appl Physiol 1990; 69 (5): 1804-9 76. Green DJ, Cable NT, Fox C, et al. Modification of forearm resistance vessels by exercise training in young men. J Appl Physiol 1994; 77 (4): 1829-33 77. Dinenno FA, Tanaka H, Monahan KD, et al. Regular endurance exercise induces expansive arterial remodelling in the trained limbs of healthy men. J Physiol 2001; 534 (Pt 1): 287-95 78. Miyachi M, Tanaka H, Yamamoto K, et al. Effects of onelegged endurance training on femoral arterial and venous size in healthy humans. J Appl Physiol 2001; 90 (6): 2439-44 79. Miyachi M, Iemitsu M, Okutsu M, et al. Effects of endurance training on the size and blood flow of the arterial conductance vessels in humans. Acta Physiol Scand 1998; 163 (1): 13-6 80. Hambrecht R, Adams V, Erbs S, et al. Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase. Circulation 2003; 107 (25): 3152-8 81. Gielen S, Erbs S, Linke A, et al. Home-based versus hospital-based exercise programs in patients with coronary artery disease: effects on coronary vasomotion. Am Heart J 2003; 145 (1): E3 82. Higashi Y, Sasaki S, Kurisu S, et al. Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects: role of endothelium-derived nitric oxide. Circulation 1999; 100 (11): 1194-202 83. Higashi Y, Sasaki S, Sasaki N, et al. Daily aerobic exercise improves reactive hyperemia in patients with essential hypertension. Hypertension 1999; 33 (1 Pt 2): 591-7 84. Radegran G, Saltin B. Nitric oxide in the regulation of vasomotor tone in human skeletal muscle. Am J Physiol 1999; 276 (6 Pt 2): H1951-60 85. Laughlin MH, Overholser KA, Bhatte MJ. Exercise training increases coronary transport reserve in miniature swine. J Appl Physiol 1989; 67 (3): 1140-9 86. Laughlin MH, Rubin LJ, Rush JW, et al. Short-term training enhances endothelium-dependent dilation of coronary arteries, not arterioles. J Appl Physiol 2003; 94 (1): 234-44 87. Kingwell BA, Arnold PJ, Jennings GL, et al. Spontaneous running increases aortic compliance in Wistar-Kyoto rats. Cardiovasc Res 1997; 35 (1): 132-7 88. McAllister RM, Laughlin MH. Short-term exercise training alters responses of porcine femoral and brachial arteries. J Appl Physiol 1997; 82 (5): 1438-44 89. McAllister RM, Kimani JK, Webster JL, et al. Effects of exercise training on responses of peripheral and visceral arteries in swine. J Appl Physiol 1996; 80 (1): 216-25 90. Ruiz-Salmeron RJ, Mora R, Velez-Gimon M, et al. Radial artery spasm in transradial cardiac catheterization: assessment of factors related to its occurrence, and of its consequences during follow-up. Rev Espan Cardiol 2005; 58 (5): 504-11
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91. Fukuda N, Iwahara S, Harada A, et al. Vasospasms of the radial artery after the transradial approach for coronary angiography and angioplasty. Jpn Heart J 2004; 45 (5): 723-31 92. American College of Sports Medicine. ACSM’s guidelines for exercise testing and prescription. 6th ed. Philadelphia (PA): Lippincott Williams & Wilkins, 2000 93. Maiorana A, O’Driscoll G, Cheetham C, et al. Combined aerobic and resistance exercise training improves functional capacity and strength in CHF. J Appl Physiol 2000; 88 (5): 1565-70 94. Maiorana A, O’Driscoll G, Dembo L, et al. Effect of aerobic and resistance exercise training on vascular function in
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heart failure. Am J Physiol Heart Circ Physiol 2000; 279 (4): H1999-2005 95. Maiorana A, O’Driscoll G, Rankin S, et al. Effect of circuit weight training on functional capacity, strength and vascular function in patients with heart failure. Circulation 1998; 98: I-774
Correspondence: Dr Ellen A. Dawson, Research Fellow, Research Institute for Sport and Exercise Science, Liverpool John Moores University, Tom Reilly Building, Byrom Street, Liverpool L3 3AF, UK. E-mail:
[email protected] Sports Med 2010; 40 (6)
Sports Med 2010; 40 (6): 493-507 0112-1642/10/0006-0493/$49.95/0
REVIEW ARTICLE
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Physical Activity and Pregnancy Cardiovascular Adaptations, Recommendations and Pregnancy Outcomes Katarina Melzer,1,2 Yves Schutz,3 Michel Boulvain2 and Bengt Kayser1 1 Institute of Movement Sciences and Sports Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland 2 Department of Obstetrics and Gynaecology, University Hospitals of Geneva, Faculty of Medicine, University of Geneva, Geneva, Switzerland 3 Department of Physiology, University of Lausanne, Lausanne, Switzerland
Contents Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1. Cardiovascular Adaptations to Training and Detraining in Pregnant and Nonpregnant States . . . . 1.1 Cardiovascular Adaptations to Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2 Cardiovascular Adaptations to Detraining. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2. Cardiovascular Changes due to Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 Cardiovascular Changes during Labour and Delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Postpartum Cardiovascular Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3. Physical Activity and Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Submaximal Aerobic Capacity during Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2 Work Efficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.3 Maximum Aerobic Capacity during Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.4 Maximal Heart Rate during Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4. Physical Activity Recommendations during Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1 Recommended Heart Rate Target Zones for Aerobic Exercise in Pregnancy . . . . . . . . . . . . . . . . 5. Compliance with Physical Activity Recommendations during Pregnancy . . . . . . . . . . . . . . . . . . . . . . 6. Effects of Physical Activity on Pregnancy Outcomes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Abstract
493 495 495 495 496 496 497 497 497 498 498 498 498 500 500 501 503
Regular physical activity is associated with improved physiological, metabolic and psychological parameters, and with reduced risk of morbidity and mortality. Current recommendations aimed at improving the health and wellbeing of nonpregnant subjects advise that an accumulation of ‡30 minutes of moderate physical activity should occur on most, if not all, days of the week. Regardless of the specific physiological changes induced by pregnancy, which are primarily developed to meet the increased metabolic demands of mother and fetus, pregnant women benefit from regular physical activity the same way as nonpregnant subjects. . Changes in submaximal oxygen uptake (VO2) during pregnancy depend on the type of exercise performed. During maternal rest or submaximal weight-bearing exercise (e.g. walking, stepping, treadmill exercise), absolute
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. maternal VO2 is significantly increased compared with the nonpregnant state. The magnitude of change is approximately proportional to maternal weight gain. When pregnant women perform submaximal weight-supported exercise on land (e.g. level cycling), the findings are . contradictory. Some studies remany others reported ported significantly increased absolute VO2, while . unchanged or only slightly increased absolute VO2 compared with the nonpregnant state. The latter findings may be explained by the fact that the metabolic demand of cycle exercise .is largely independent of the maternal body mass, resulting in no absolute VO2 alteration. . . Few studies that directly measured changes . in maternal maximal VO2 (VO2max) showed no difference in the absolute VO2max between pregnant and nonpregnant subjects in cycling, swimming or weight-bearing exercise. Efficiency of work during exercise appears to be unchanged during pregnancy in non-weight-bearing exercise. During weight-bearing exercise, the work efficiency was shown to be improved in athletic women who continue exercising and those who stop exercising during pregnancy. When adjusted for weight gain, the increased efficiency is maintained throughout the pregnancy, with the improvement being greater in exercising women. Regular physical activity has been proven to result in marked benefits for mother and fetus. Maternal benefits include improved cardiovascular function, limited pregnancy weight gain, decreased musculoskeletal discomfort, reduced incidence of muscle cramps and lower limb oedema, mood stability, attenuation of gestational diabetes mellitus and gestational hypertension. Fetal benefits include decreased fat mass, improved stress tolerance, and advanced neurobehavioural maturation. In addition, few studies that have directly examined the effects of physical activity on labour and delivery indicate that, for women with normal pregnancies, physical activity is accompanied with shorter labour and decreased incidence of operative delivery. However, a substantial proportion of women stop exercising after they discover they are pregnant, and only few begin participating in exercise activities during pregnancy. The adoption or continuation of a sedentary lifestyle during pregnancy may contribute to the development of certain disorders such as hypertension, maternal and childhood obesity, gestational diabetes, dyspnoea, and pre-eclampsia. In view of the global epidemic of sedentary behaviour and obesity-related pathology, prenatal physical activity was shown to be useful for the prevention and treatment of these conditions. Further studies with larger sample sizes are required to confirm the association between physical activity and outcomes of labour and delivery.
Regular physical activity is associated with improved physiological, metabolic and psychological parameters, and with reduced risk of morbidity and mortality from diseases such as cardiovascular disease, hypertension, diabetes mellitus, obesity, osteoporosis, sarcopenia, cognitive disorders and some forms of cancer.[1] Current recommendations aimed at improving ª 2010 Adis Data Information BV. All rights reserved.
the health and well-being of nonpregnant subjects advise that an accumulation of 30 minutes or more of moderate physical activity should occur on most, if not all, days of the week.[2] Regardless of the specific physiological changes induced by pregnancy, which are primarily developed to meet increased metabolic demands of mother and fetus, pregnant women benefit Sports Med 2010; 40 (6)
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from regular physical activity the same way as nonpregnant subjects.[3] However, a substantial proportion of women stop exercising and decrease their general physical activity level after they discover they are pregnant, and only few begin participating in exercise or sport activities during pregnancy.[4] The adoption or continuation of a sedentary lifestyle during pregnancy may contribute to development of certain disorders such as hypertension, maternal and childhood obesity, gestational diabetes, dyspnoea and pre-eclampsia.[3] In view of the global epidemic of sedentary behaviour and obesity-related pathology, prenatal physical activity has been shown to be useful for the prevention and treatment of these conditions.[5] A systematic literature review was conducted on physical activity and pregnancy. The search included articles published in MEDLINE and ISI Web of Science databases. Keywords used were: ‘physical activity’ OR ‘physical exercise’, ‘pregnancy’ OR ‘gestation’, ‘pregnancy outcomes’, ‘labour’, ‘cardiovascular adaptations’, ‘heart rate’, ‘training’, ‘detraining’, ‘physical activity recommendations’ AND ‘pregnancy’. In a first round, there were no restrictions to certain years of publication. In a second round, publications published between 2007 and 2009 were specifically reviewed to assure inclusion of any relevant new publication. The aim of this article was to review the current state of knowledge on (i) the cardiovascular adaptations to physical activity in the pregnant and nonpregnant states; (ii) the compliance of pregnant women with current physical activity recommendations; and (iii) the effects of physical activity on pregnancy outcomes. 1. Cardiovascular Adaptations to Training and Detraining in Pregnant and Nonpregnant States 1.1 Cardiovascular Adaptations to Training
Repeated episodes of physical activity performed over a longer period (i.e. training) cause adaptations in the respiratory, cardiovascular and neuromuscular systems that enable physiª 2010 Adis Data Information BV. All rights reserved.
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cally trained persons to exercise for longer at a given absolute exercise intensity, or to exercise at a higher exercise intensity for a given duration.[6] The adaptations in metabolic and physiological systems depend on the type of exercise overload imposed. Short duration activities demanding high levels of anaerobic metabolism favour the adaptation of the immediate and short-term energy systems, with limited impact on the aerobic system. Regular endurance training, on the other hand, improves overall aerobic capacity.[7-9] For public health concerns and in contrast to training for sports-specific improvement, current interest in physical activity participation arises largely from a desire to improve health-related fitness components, primarily cardiorespiratory fitness.[10] Aerobic training produces significant changes to the cardiovascular system: enlarged left ventricular cavity of the heart; enhanced blood and stroke volume; increased maximum ˙ ); and decreased resting and subcardiac output (Q maximal exercise heart rate.[6] The lower resting and sub-maximum exercise heart rate generally reflect an improved submaximal and maximal . oxygen uptake (VO2max) and a correspondingly higher level of cardiovascular fitness. 1.2 Cardiovascular Adaptations to Detraining
While regular physical activity is accompanied by better cardiovascular fitness, a reduction or cessation of physical activity leads to partial or complete reversal of the physiological adaptations. Inactivity is accompanied by a rapid . decline in VO2max and blood volume. Consequently, submaximal exercise heart rate increases but insufficiently to counterbalance decreased stroke volume, thus resulting in a reduction of ˙ .[11] Measurable alterations in physiomaximal Q logical functions take place after only a week or two of detraining.[8] Total loss of training improvements occurs within several months.[8] As a result, any sudden physical effort imposed on the detrained subjects leads to physiological and metabolic stress, as they are not able to respond to imposed physical exertion as efficiently as trained subjects. Sports Med 2010; 40 (6)
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2. Cardiovascular Changes due to Pregnancy Regardless of training status, women who become pregnant undergo profound cardiovascular system alterations (figure 1). The first haemodynamic change during pregnancy is a rise in heart rate, both at rest and during submaximal workout. It starts between 2 and 5 weeks of pregnancy and continues well into the third trimester.[12] On average, the resting heart rate raises 8 beats/min by the eighth week, and reaches an increase of 16 beats/min by the end of pregnancy.[13] The effect is less evident in supine or lateral positions and more evident during sitting.[14] The mechanism of the increased heart rate is not yet clearly identified. It may be attributed to chorionic gonadotropin, or to sympathetic reflex adjustments to maintain arterial blood pressure despite reduced peripheral vascular resistance.[15] Between 10 and 20 weeks of pregnancy, a notable increase in blood volume takes place due to an increase in both plasma and erythrocytes.[16,17] This represents a rise of approximately 1500 mL,[16] of which 1000 mL is plasma volume and 500 mL is erythrocytes.[18] Since plasma volume amplifies more than red blood cell volume, a relative dilutional anaemia occurs.[19] Blood volume expansion may be even greater in multifetal gestations.[18] ˙ is increased as early as the fifth week Resting Q of pregnancy as a result of the increased heart
Increase in. resting and sub-VO2max
Descrease in blood pressure
rate, stroke volume and blood volume.[12,17,20] ˙ increases by 1 L/min at 8 weeks of gestResting Q ation, which represents >50% of the overall change in pregnancy.[20] During the third trime˙ increases only minimally, primarster, resting Q ily because of the increase in heart rate as term approaches.[21] In multifetal pregnancies, resting ˙ is greater by approximately 20% maternal Q ˙ is also compared with singleton pregnancies.[19] Q affected by the positional changes of the women.[14] After 20 weeks of gestation, the gravid uterus may obstruct the aorta and inferior vena cava, causing a decrease in uteroplacental blood flow and venous return to the heart,[9] especially when the woman is in the supine position. The left lateral position quickly relieves compression of the inferior vena cava.[21] Left uterine displacement also tends to prevent aortocaval compression, although it is less optimal than the left lateral position.[19] Blood pressure is not increased in normal pregnancy due to decreased peripheral vascular resistance.[19] In fact, systolic pressure remains quite stable, whereas diastolic pressure decreases up to 15 mmHg in mid-pregnancy.[22] 2.1 Cardiovascular Changes during Labour and Delivery
˙ remains relatively constant in the Although Q latter half of pregnancy, there is a significant
Increase in resting and sub-maximal heart rate
Pregnancy-induced cardiovascular changes
. Increase in Q
Increase in plasma and red blood cell mass
Increase in blood volume Increase in stroke volume
. ˙ = cardiac output; VO2max = maximal oxygen uptake. Fig. 1. Pregnancy-induced cardiovascular changes. Q
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increase during active labour and immediately after delivery. A study[12] of normal labour in women without epidural anaesthesia reported an increase ˙ of 12% and 34% between contractions and at in Q ˙ full dilatation, respectively. The increase in Q seems to be caused by an increase in heart rate and stroke volume. Such changes are thought to be sympathetically mediated and are likely due to the combined effects of pain, increased metabolic demand and increased venous return during uterine contractions.[23] Circulating blood volume also increases during contractions by an additional 300–500 mL due to blood autotransfusion from the placenta.[24] The physical effort of normal labour does not impose high energy demands on the parturient. The energy requirement is affected more by the frequency and duration of uterine contractions than by the total duration of labour.[25] Katz et al. measured energy expenditure of la[25] bour in 23 healthy . women. The results showed oxygen uptake (VO2) of 0.255 L/min during uterine relaxation (at 4 cm dilatation), 0.338 L/min during contractions (at 4 cm dilatation), and . 0.510 L/min at delivery. Thus, the VO2, which increases ~20% during normal pregnancy, may increase an additional 60% during the contractions, but remains rather low when compared with the increase observed during physical activity (walking, running, cycling). It is higher in multiparous women than in nulliparous women and is highest in those women with the shortest labour.[25] If the process of expulsion is prolonged (>30 minutes), the increased demand for oxygen is partially met by anaerobic metabolism causing an increase in maternal blood lactate levels.[25] The haemodynamic changes seen during labour and delivery are influenced by anaesthetic and analgesic techniques.[21] Lumbar epidural anaesthesia during labour reduces maternal [26] and decreases adrenaline (epinephrine) levels, . the work of breathing, VO2,[27,28] fetal heart ˙ and blood pressure.[30-32] The rate,[29] maternal Q haemodynamic changes are also influenced by the ˙ and position of the parturient. For example, Q stroke volume are significantly decreased in the supine, compared with the lateral, position.[33] ª 2010 Adis Data Information BV. All rights reserved.
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2.2 Postpartum Cardiovascular Changes
Within the first 15–20 minutes after delivery of the fetus and placenta there is a substantial ˙ , as the blood is no longer diverted increase in Q to the uteroplacental vascular bed, but rather redirected to the maternal circulation.[21] By ˙ is no longer signifi24 hours after delivery, Q cantly different from pre-labour values,[34] and fully returns to pre-pregnant values by 2 weeks after delivery. Stroke volume also decreases within 2 weeks, although there is a further small reduction up to 6 months after delivery.[12] 3. Physical Activity and Pregnancy ˙, Although pregnancy induces an increase in Q stroke volume and heart rate, women who continue aerobic exercise training during pregnancy have lower resting heart rate and higher stroke volume than matched sedentary controls.[35,36]. In addition, aerobically fit women have greater VO2 response at a given heart rate compared with their sedentary counterparts.[36] 3.1 Submaximal Aerobic Capacity during Pregnancy
. Changes in submaximal VO2 during pregnancy depend on the type of exercise performed. During maternal rest or submaximal weightbearing exercise (e.g. walking,. stepping, treadmill exercise), absolute maternal VO2 (L/min) is significantly increased compared with the nonpregnant state.[37,38] The magnitude of change is approximately proportional to maternal weight gain. At the same speed . or grade of walking or running, the values for VO2 expressed in mL/kg/min are thus similar or only slightly higher during pregnancy compared with the nonpregnant state.[37,39-41] When pregnant women perform submaximal weight-supported exercise on land (e.g. level cycling), where the energy cost of locomotion is not altered by maternal morphological changes, the findings are contradictory. Some studies . reported significantly increased absolute VO2,[37,40,42] while many others[15,35,38,40,43-47] reported .unchanged or only slightly increased absolute VO2 Sports Med 2010; 40 (6)
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compared with the nonpregnant state. The latter findings may be explained by the fact that the metabolic demand of cycle exercise is largely independent of the . maternal body mass, resulting in no absolute VO2 alteration. 3.2 Work Efficiency
Net efficiency of work during exercise, i.e. the . slope of the relationship between VO2 and work rate, appears to be unchanged during pregnancy in non-weight-bearing exercise (e.g. cycle ergometer testing).[38,44,48] The efficiency of weightbearing exercise (e.g. treadmill testing), on the other hand, was shown to be improved in early pregnancy in athletic women who continue exercising and those who stop exercising during pregnancy.[49,50] The increase in exercise efficiency is obscured after the fifteenth week of pregnancy by pregnancy-associated increases in maternal weight. When adjusted for weight gain, the increased efficiency is maintained throughout the pregnancy, with the improvement being greater in women who continue exercising during pregnancy.[49] 3.3 Maximum Aerobic Capacity during Pregnancy
. VO2max, as a criterion measure of cardiovascular fitness, is . poorly documented in pregnancy. Measuring VO2max during gestation holds a theoretical risk of inducing fetal stress due to blood distribution favouring maternal skeletal muscle at the expense of uterine blood flow. For ethical reasons, most studies report estimated values obtained by extrapolating individual sub. maximal heart rate-VO2 curves rather than actual measured values at peak exercise intensity. The few studies (table I). that directly measured changes in .maternal VO2max showed no difference in the VO2max (L/min) between pregnant and nonpregnant subjects in cycling,[44-47,50-53] swimming or weight-bearing exercise.[47,50,51,54] Well conditioned women or athletes who maintain a moderate to high level of exercise during and after pregnancy have even shown a small but . significant increase in VO2max following pregnancy.[53,54] Thus, pregnancy may have an added ª 2010 Adis Data Information BV. All rights reserved.
training effect in well conditioned, recreational sports women. 3.4 Maximal Heart Rate during Pregnancy
. Although the VO2max values do not seem to differ significantly in the pregnant compared with the nonpregnant state, maximal heart rate was reported to be approximately 4 beats/min lower in pregnancy compared with post partum.[50] The blunted heart rate responses to maximal exercise may be due to reduced sympathoadrenal responses to heavy exertion during pregnancy.[43] As a result of the increased resting heart rate and decreased maximal heart rate, heart rate reserve is reduced and . heart rate rises to a lesser extent with increasing VO 2, lowering the slope of the heart rate. VO2 relationship during pregnancy compared with the nonpregnant state.[15,51] However, with the exception . of resting heart rate, the change in the heart rate-VO2 relationship appears not to be affected significantly by a woman’s habitual exercise behaviour throughout pregnancy.[55] 4. Physical Activity Recommendations during Pregnancy In the past, recommendations for physical activity were based on cultural and traditional mores rather than scientific evidence. In the 1950s, continuation of household chores and a 1.6 km (1 mile) walk per day, preferably divided into several short sessions, was advised, whereas sports and exercise were discouraged.[5] In 1985, the American College of Obstetricians and Gynecologists (ACOG) formulated one of the first recommendations for exercising during pregnancy. It was advised that the intensity of exercise should not induce an increase in heart rate above 140 beats/min and that strenuous exercise should not last more than 15 minutes.[5] Since then, evidence has accumulated on the type, intensity, duration and frequency of exercise beneficial for mother and offspring,[56] leading to the revision of the guidelines. Present ACOG recommendations,[57] and those jointly published by the Society of Obstetricians and Gynecologists of Canada (SOGC) and the Sports Med 2010; 40 (6)
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. Table I. Studies reporting actual measured maximal oxygen uptake (VO2max) in pregnant women Study (year)
No. of subjects
Heenan et al.[44] (2001)
14
Lotgering et al.[50,51] (1991, 1992)
33
McMurray et al.[52] (1991)
10
Sady et al.[45] (1988)
45
Sady et al.[46] (1989)
45
Spinnewijn et al.[47] (1996)
11
. VO2 = oxygen uptake.
Measurements
Findings
. VO2 (L/min) measurements in pregnant women (35 – 0.4 wk) and age-matched nonpregnant control group (n = 14) while cycling maximally. Low agespecific aerobic capacity levels . VO2 measurements (L/min) at 16, 25 and 35 wk of pregnancy and 7 wk post partum at increasing levels of cycling and treadmill exercise until maximum aerobic power was reached. Average age-specific aerobic capacity levels . VO2 measurements (L/min) at 25–35 wk of pregnancy and 9–11 wk post partum during cycling and swimming maximally. Average age-specific aerobic capacity levels . VO2 (L/min) measurements in pregnant women (26 – 3 wk) and a nonpregnant control group (n = 10) while cycling maximally. Low age-specific aerobic capacity levels . VO2 (L/min) measurements at 26 – 3 wk of pregnancy and 8 – 2 wk post partum while cycling maximally. Low age-specific aerobic capacity levels . VO2 measurements (L/min) at 30–34 wk of pregnancy and 8–12 wk post partum during cycling and swimming maximally. Average age-specific aerobic capacity levels
. No significant differences in VO2max in pregnant vs control group
Canadian Society of Exercise Physiology (CSEP),[58] advise that pregnant women who are free of medical or obstetric complications follow the American College of Sports Medicine– Centers of Disease Control and Prevention (ACSM-CDC) guidelines for physical activity and exercise. According to these guidelines, pregnant women may safely engage in ‡30 minutes of moderate physical activity on most, if not all, days of the week.[57] Moderate physical activity is defined as an activity performed at an intensity of three to six metabolic equivalents (METs), which corresponds to brisk walking at ~5–7 km/h (3–4 mph).[59] Previously sedentary women should start with 15 minutes of continuous exercise three times a week, increasing gradually to 30-minute sessions four times a week.[58] The aim of exercising during pregnancy is to maintain a good condition without trying to reach a peak fitness level.[58] Because of the potential risk of certain activities, healthcare professionals should adapt the exercise prescriptions accordingly, prescribing ª 2010 Adis Data Information BV. All rights reserved.
. No significant differences in VO2max in pregnancy period vs post partum during cycling and treadmill exercise
. No significant differences in VO2max in pregnancy period vs post partum during cycling. . The swim VO2max was significantly greater post partum than in the 35th swim trials . No significant differences in VO2max in pregnant vs control group
. No significant differences in VO2max in pregnancy period vs post partum . No significant differences in VO2max in pregnancy period vs post partum during bicycle and swimming
activities such as walking, swimming, stationary cycling and aquafit rather than gymnastics, horseback riding, skiing, racquet sports or contact sports. The risks of injury associated with falling are increased in latter activities due to increased levels of oestrogen and relaxin, which augment ligamentous laxity and hypermobility.[54,60] Pelvic support belts and core stability exercise can be used to enable women to remain active in spite of these changes. In addition, muscle conditioning (light weight-lifting in moderate repetitions) is suggested to maintain flexibility and muscle tone, prevent gestational lower back pain, and promote general conditioning.[61] Abdominal strengthening is difficult to perform due to the development of diastasis recti and associated abdominal muscle weakness.[58] For that reason, pregnant women should avoid exercising in the supine position after ~16 weeks of gestation. Scuba diving is also to be avoided throughout pregnancy, as the fetus is not protected from decompression sickness and gas embolism.[58] Sports Med 2010; 40 (6)
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Exertion at altitudes above 2500 m (8250 feet) is advised only after 4–5 days of exposure and acclimatization to such high altitudes.[62] Metabolic responses during exercise in pregnancy are related to the duration and intensity of exercise. Blood glucose of pregnant women decreases at a faster rate and to a significantly lower level post-exercise than in nonpregnant women.[63] This decrease does not seem to cause hypoglycaemia, even after 40 minutes of moderate walking or aerobic dancing.[64,65] However, consuming adequate calories and limiting exercise sessions to 55% VO2max
Control group had heavier babies than those born to exercise group women (3.64 – 0.05 vs 3.44 – 0.1 kg; p = 0.01)
Clapp et al.[113] (2000)
22 exercise group; 24 control group
Weight-bearing exercise (treadmill, step aerobics or stair stepper) from the 8th wk of pregnancy, 20 min, 3–5·/wk at . 55–60% pre-pregnancy VO2max
Exercising mothers had heavier babies than those born to control women (3.75 – 0.8 vs 3.49 – 0.7 kg; p = 0.05)
Clapp et al.[114] (2002)
26 L-H; 24 M-M; 25 H-L
From the 8th wk of pregnancy, at . 55–60% VO2max: L-H, 20 min, 5·/wk through wk 20, increasing to 60 min 5·/wk by wk 24 and maintaining that level until delivery; M-M, 40 min, 5·/wk; H-L, 60 min, 5·/wk through wk 20, decreasing to 20 min, 5·/wk by wk 24 and maintaining that level until delivery
H-L group had heavier babies compared with the M-M and H-L groups (3.90 – 0.1 vs 3.44 – 0.1 vs 3.34 – 0.1 kg; p < 0.001)
Collings et al.[107] (1983)
20 exercise group; 12 control group
During the 2nd and 3rd trimester of pregnancy: aerobic exercise 3·/wk, . >25 min, 65–70% VO2max
Exercise group had no significantly heavier babies from those born to control group women (3.60 – 0.4 vs 3.35 – 0.4 kg)
Hall and Kaufmann[103] (1987)
393 control group (average 0.8 sessions); 82 low level exercise group (15 sessions); 309 medium level exercise group (32 sessions); 61 high level exercise group (64 sessions)
Throughout pregnancy, exercise session consisted of 3 components: warm-up (5 min treadmill at 5–6 km/h, or 5 min bicycle at 50 W) + 5·/wk, 45 min weightlifting + bicycle ergometer (~85% of maximal HR but
