Larry A. Wolfe

Acute effects of exercise intensity on appetite in young men.

This study investigated the acute effects of two exercise intensities on three measures of appetite. Fifteen, 12-h-fasted, college-age males completed three experimental sessions in counterbalanced orders: no-exercise control; cycle exercise performed at 35% VO2max; and cycle exercise performed at 68% VO2max. Both exercise conditions involved a total energy expenditure of 4.1 kcal.kg-1 body weight. Dependent measures were intermittent hunger and sucrose palatability ratings, and food intake at a test meal given approximately 1 h post-exercise. Hunger was briefly suppressed in the high-intensity exercise condition compared to low-intensity exercise and control, while intake of liquid-source kilocalories and carbohydrates was higher after the exercise sessions. Total caloric intake remained stable. Sucrose palatability did not vary across sessions. Intensity is inferred to be an important variable mediating exercise effects on appetite. Relations between appetite measures are discussed, and validity of sucrose palatability ratings and common methods of measuring food intake questioned. Exercise, while not decreasing food intake, does not appear to increase it, and the benefits of exercise for body fat reduction are not immediately offset by compensatory caloric intake.

Canadian guidelines for exercise in pregnancy.

The need for guidelines for exercise during pregnancy and the postpartum period was stimulated during the early 1980s when active women of the “baby boom” generation became interested in whether it was safe to continue their active lifestyles during pregnancy. As a result of the strong demand for information, important questions were raised concerning the risk/benefit ratio of such exercise. Postulated risks included the possibility that the fetus may be forced to compete with contracting maternal skeletal muscle for oxygenated blood flow (leading to fetal hypoxia and distress), essential substrates (leading to fetal growth restriction), and heat dissipation (leading to fetal hyperthermia and potential teratogenic effects). Concern was also expressed that exercise may increase the chance of early miscarriage, spontaneous abortion, and premature labor, as well as chronic fatigue and musculoskeletal injury. Putative benefits included maintenance of prenatal aerobic and musculoskeletal fitness levels, prevention of excessive maternal weight gain, facilitation of labor and recovery from labor, promotion of good posture, prevention of gestational glucose intolerance and low back pain, and improved psychological adjustment to the changes of pregnancy. As a result of the conflict between these postulated benefits and risks, the idea that a dose-response relationship existed between the quantity and quality of exercise and maternal/fetal well-being quickly emerged (Fig. 1). The concept that exercise is safe for some pregnant women but not others also led to the need for absolute and relative medical contraindications to exercise and the need for medical screening by a qualified health care provider before engaging in fitness training after becoming pregnant. As a result of a lack of scientific information, early guidelines for exercise during pregnancy were necessarily conservative and based primarily on common sense and Note: A copy of the Physical Activity Readiness Medical Examination for Pregnancy can be obtained from the Internet at: www.csep.ca/forms.asp Correspondence: Larry A. Wolfe, PhD, School of Physical and Health Education, Queen’s University, Kingston, Ontario K7L 3N6, Canada. E-mail: wolfel@post. queensu.ca CLINICAL OBSTETRICS AND GYNECOLOGY Volume 46, Number 2, 488–495

Clinical Physiology of Exercise in Pregnancy: A Literature Review

OBJECTIVES To review the existing literature on the physiology of exercise in pregnancy as a basis for clinical practice guidelines for prenatal exercise prescription. METHODS MEDLINE search for English language abstracts and articles published between 1966 and 2003 related to physiological adaptations to pregnancy, effects of pregnancy on responses to acute exercise and aerobic conditioning, effects of acute maternal exercise on indexes of fetal well-being, impact of physical conditioning on birth weight and other pregnancy outcomes, and use of exercise to prevent or treat gestational diabetes mellitus and preeclampsia. RESULTS Maximal aerobic power (VO(2)max, L/min) is well-preserved in pregnant women who remain physically active, but anaerobic working capacity may be reduced in late gestation. The increase in resting heart rate, reduction in maximal heart rate, and resulting smaller heart rate reserve render heart rate a less precise way of estimating exercise intensity. As rating of perceived exertion (RPE) is not altered by pregnancy, the use of revised pulse rate target zones along with Borgs RPE scale is recommended to prescribe exercise intensity during pregnancy. Responses to prolonged submaximal exercise (>30 min) in late gestation include a moderate reduction in maternal blood glucose concentration, which may transiently reduce fetal glucose availability. The normal response to sustained submaximal exercise is an increase in fetal heart rate (FHR) baseline. Transient reductions in FHR reactivity, fetal breathing movements, and FHR variability may also occur in association with more strenuous exercise. Controlled prospective studies have demonstrated that moderate prenatal exercise during the second and third trimesters is useful to improve aerobic fitness and maternal-fetal physiological reserve without affecting fetal growth. CONCLUSIONS The Physical Activity Readiness Medical Examination for Pregnancy is recommended for use by physicians and midwives to provide medical clearance for prenatal exercise. Evidence-based prenatal exercise guidelines are needed to counsel healthy and fit pregnant women on the safety of involvement in more strenuous physical conditioning. Future study is also recommended to determine the usefulness of prenatal exercise in the prevention and treatment of gestational diabetes mellitus and preeclampsia.

The 'athletic heart syndrome'. A critical review.

SummaryCardiological findings in athletes are often similar to those observed in clinical cases. Electrocardiographic and cardiac imaging abnormalities as well as physical findings may be the same in both of these groups. Bradycardia and rhythm disturbances are the most common abnormalities in athletes. Most athletes with abnormal electrocardiograms are asymptomatic and numerous investigators have failed to detect heart disease in association with such electrocardiograms. In contrast to cardiac dysfunction observed in clinical cases, enhanced or normal ventricular systolic and diastolic function have been reported in athletes. In endurance athletes, this is associated with very high values for maximal aerobic power (V̇O2max).Absolute and body size-normalised cardiac dimensions in most athletes do not approach values from chronic disease states, and may not exceed echocardiographic normal limits. In addition, pathological and physiological enlargement appear to be biochemically and functionally different. Myosin ATPase enzyme expression and calcium metabolism are different in rats with pathologically or physiologically induced enlargement. The reported biochemical differences underlie systolic and diastolic dysfunction in pathological enlargement. Conversely, trained rodents and humans have demonstrated enhanced systolic and diastolic function. It is important to note that cardiac enlargement observed in athletes is the result of normal adaptation to physical conditioning and/or hereditary influences. Conversely, pathological changes result from disease processes which can lead in turn to reduced function, morbidity and mortality.Since the mid 1970s echocardiography has been used to compare cardiac dimensions in male endurance- and resistance-trained athletes. A sport-specific profile of eccentric and concentric enlargement has been documented in endurance and resistance athletes, respectively. Subsequent studies of athletes have examined factors such as age, sex and degree of competitive success to determine their contribution to these sport-specific cardiac profiles. Unique athletic subgroups have also been analysed and have included ballet dancers, rowers, basketball players and triathletes. However, there is a paucity of data on cardiac dimensions in female athletes. Finally, physical conditioning studies have also examined echocardiographic dimensions before and after endurance and resistance training. Significant enlargement of internal dimensions, wall thickness or left ventricular mass have been reported but such increases are relatively small and by no means universal.Several conflicting explanations for enlarged cardiac dimensions appear in the literature. Chronic volume and pressure haemodynamic overloading during physical conditioning has been proposed to explain eccentric and concentric cardiac enlargement in endurance- and resistance-trained athletes respectively. However, twin studies suggest that hereditary factors may be important determinants of cardiac dimensions and/or the degree of cardiac adaptability to physical conditioning.Another body of research has suggested the possibility that endocrine effects related to normal growth and/or physical conditioning may stimulate cardiac enlargement. Thyroid hormone, catecholamines, growth hormone and testosterone can alter cardiac dimensions and their blood levels are elevated with exercise. However, their influence on myocardial structure in athletes has not yet been clarified. In this regard, blood testosterone levels increase transiently following acute exercise bouts in young men and may contribute to the process of skeletal muscle hypertrophy. Significant statistical associations have been reported between skeletal and cardiac muscularity. Therefore, a common influence of testosterone or other hormones on skeletal and cardiac muscle hypertrophy has been hypothesised and may account for hereditary and/or conditioning induced cardiac enlargement in athletes. Future investigations should reassess the role of haemodynamic stress and clarify the quantitative role of heredity and endocrine factors in determining cardiac dimensions. In this way a clearer indication may be deduced as to the mechanism(s) involved in the apparent moderate cardiac enlargement reported in athletes. Research should first describe the cardiac profile of a wide range of female athletes and then determine the cause of any potential gender-based differences in cardiac size and adaptation to exercise.

Phasic menstrual cycle effects on the control of breathing in healthy women

This study examined the effects of menstrual cycle phase on ventilatory control. Fourteen eumenorrheic women were studied in the early follicular (FP; 1-6 days) and mid-luteal (LP; 20-24 days) phase of the menstrual cycle. Blood for the determination of arterial PCO(2) (PaCO(2)) , plasma strong ion difference ([SID]), progesterone ([P(4)]), and 17beta-estradiol ([E(2)]) concentrations were obtained at rest. Subjects performed a CO(2) rebreathing procedure that included prior hyperventilation and maintenance of iso-oxia to evaluate central and peripheral chemoreflex, and nonchemoreflex drives to breathe. Resting PaCO(2) and [SID] were lower; minute ventilation (V (E)), [P(4)] and [E(2)] were higher in the LP versus FP. Within the LP, significant correlations were observed for PaCO(2) with [P(4)], [E(2)] and [SID]. Menstrual cycle phase had no effect on the threshold or sensitivity of the central and/or peripheral ventilatory chemoreflex response to CO(2). Both (V (E)) and the ventilatory response to hypocapnia (representing nonchemoreflex drives to breathe) were approximately 1L/min greater in the LP versus FP accounting for the reduction in PaCO(2) . These data support the hypothesis that phasic menstrual cycle changes in PaCO(2) may be due, at least in part, to the stimulatory effects of [P(4)], [E(2)] and [SID] on ventilatory drive.

Prescription of Aerobic Exercise During Pregnancy

SummaryAvailable evidence supports the existence of both risks and benefits of aerobic conditioning during human pregnancy. During intensive exertion, maternal skeletal muscle and the fetus may compete for blood flow, oxygen delivery and essential fuel substrates. Hence, the most important hypothetical risks include acute fetal hypoxia, hyperthermia and malnutrition. If exercise is repeated on a chronic basis, teratogenic effects, fetal growth retardation or altered fetal development may result if maternal/fetal adaptive reserve is exceeded. A dose-response relationship for such effects has been demonstrated in laboratory animals, but specific findings may have limited applicability to voluntary exercise in pregnant women.Although further investigation is needed, the majority of published studies suggest that fitness-type conditioning does not jeopardise fetal well-being in healthy well-nourished women. Benefits of such exercise appear to include increases in maximal aerobic power (V̇O2 max, L/min) and enhanced cardiopulmonary reserve. It has also been proposed that exercise prevents accumulation of excess body fat, promotes psychological well-being, helps to prevent gestational diabetes and low back pain and may facilitate labour. However, these benefits remain to be confirmed by objective scientific study.Due primarily to a lack of scientific data, existing medical guidelines for exercise during pregnancy are conservative and follow a common sense approach. Good agreement exists on the need for preparticipation medical screening and continuing surveillance to verify the existence of maternal/fetal adaptive reserve. Women are advised to select safe, non-ballistic exercise modalities and to avoid thermal or hyperbaric environmental stress during exercise. Exercise in the supine position is also prudent to avoid, particularly in late gestation. The usefulness of heart rate in prescribing and monitoring exercise intensity has been questioned, with use of conventional perception of exertion scales being the most logical alternative. Prediction of maximal aerobic power (V̇O2max) from submaximal work rate/heart rate relationships is also problematic during pregnancy. Other areas of debate include the advisability of initiating a new exercise programme during pregnancy, methods for prevention of fetal hyperthermia, the safety of weight-training/isometric exercise and optimal methods for training of pre/postnatal fitness instructors.

Acid-base regulation and control of ventilation in human pregnancy.

The purposes of this review were twofold: to apply modern physicochemical principles to explain changes in acid-base regulation and the control of ventilation in human pregnancy; and to demonstrate the value of pregnancy as a model for the study of endocrine effects on physiological control systems. Application of P.A. Stewarts approach (P.A. Stewart. Can. J. Physiol. Pharmacol. 61: 1444-1461, 1983) shows that lower values of plasma hydrogen ion concentration ([H+]) observed at rest and in association with exercise in pregnancy are the result of lower values for carbon dioxide tension (Pco2) and total weak acid ([A(tot)]). This effect is partly offset by a lower strong ion difference ([SID]). The ability to predict plasma [H+] at rest and following strenuous exercise in pregnancy (J.G. Kemp, F.A. Greer, and L.A. Wolfe. J. Appl. Physiol. 83: 644-651, 1997) supports the validity of Stewarts approach. Jennings and associates (D.B. Jennings. Can. J. Physiol. Pharmacol. 72: 1499-1512, 1994) have further demonstrated in animal models the involvement of plasma osmolality and circulating levels of angiotensin II (ANG II) and arginine vasopressin (AVP) in the chemical control of ventilation. We hypothesize that pregnancy-induced increases in respiratory sensitivity to carbon dioxide are the combined result of reduced plasma osmolality, reduced cerebrospinal fluid [SID], and augmented circulating levels of progesterone, ANG II, and AVP.

Physical conditioning effects on fetal heart rate responses to graded maternal exercise.

PURPOSE This study examined the effects of advancing gestational age and maternal aerobic conditioning (stationary cycling) on fetal heart rate (FHR) responses to strenuous non-steady-state maternal exercise. METHODS Subjects chose to participate in either an exercise group (EG) or control group (CG). Fourteen healthy, previously sedentary pregnant women participated in the exercise group, and six pregnant controls remained sedentary. Stationary cycling (heart rate target: 145 beats x min(-1)) was performed 3 d x wk(-1) by the exercised group. Exercise duration was increased from 14 to 25 min x session(-1) during the second trimester and was maintained at 25 min x session(-1) throughout the third trimester. FHR was monitored before, during, and after a progressive submaximal cycle ergometer test (peak heart rate = 170 beats x min(-1)) performed at approximately 27 and 37 wk gestation. RESULTS Mean FHR increased significantly (P < 0.05) during exercise, followed by a modest suppression and then a delayed rise during the recovery period at both observation times. Fetal bradycardia was not observed in any of the exercise tests. Effects of advancing gestational age included a lower FHR baseline both at rest and in response to maternal exercise and a lower incidence of exercise-induced tachycardia. Maternal physical conditioning did not significantly alter FHR response to maternal exercise. CONCLUSION Our results support the hypothesis that FHR responses to strenuous exercise are altered by advancing gestational age and a brief progressive exercise test terminated at a maternal heart rate of 170 beats x min(-1) does not induce fetal distress during a healthy pregnancy.

Physiological mechanisms of hyperventilation during human pregnancy

This study examined the role of pregnancy-induced changes in wakefulness (or non-chemoreflex) and central chemoreflex drives to breathe, acid-base balance and female sex hormones in the hyperventilation of human pregnancy. Thirty-five healthy women were studied in the third trimester (TM(3); 36.3+/-1.0 weeks gestation; mean+/-S.D.) and again 20.2+/-7.8 weeks post-partum (PP). An iso-oxic hyperoxic rebreathing procedure was used to evaluate wakefulness and central chemoreflex drives to breathe. At rest, arterialized venous blood was obtained for the estimation of arterial PCO(2) (PaCO(2)) and [H(+)]. Blood for the determination of plasma strong ion difference ([SID]), albumin ([Alb]), as well as serum progesterone ([P(4)]) and 17beta-estradiol ([E(2)]) concentrations was also obtained at rest. Wakefulness and central chemoreflex drives to breathe, [P(4)] and [E(2)], ventilation and V CO(2) increased, whereas PaCO(2) and the central chemoreflex ventilatory recruitment threshold for PCO(2) (VRTCO(2)) decreased from PP to TM(3) (all p<0.01). The reductions in PaCO(2) were not related to the increases in [P(4)] and [E(2)]. The alkalinizing effects of reductions in PaCO(2) and [Alb] were partly offset by the acidifying effects of a reduced [SID], such that arterial [H(+)] was still reduced in TM(3) vs. PP (all p<0.001). A mathematical model of ventilatory control demonstrated that pregnancy-induced changes in wakefulness and central chemoreflex drives to breathe, acid-base balance, V CO(2) and cerebral blood flow account for the reductions in PaCO(2), [H(+)] and VRTCO(2). This is the first study to demonstrate that the hyperventilation and attendant hypocapnia/alkalosis of human pregnancy results from a complex interaction of pregnancy-induced changes in wakefulness and central chemoreflex drives to breathe, acid-base balance, metabolic rate and cerebral blood flow.

Electrocardiographic and echocardiographic characteristics of female athletes.

This study examined electrocardiographic and echocardiographic characteristics of endurance- and resistance-trained female athletes. The subjects were 10 varsity caliber endurance-trained athletes, 10 resistance-trained athletes, and 10 nonathletes. Data collection included anthropometric measurements, VO2max, standard 12-lead ECGs and left ventricular dimensions measured by M-mode and two-dimensional echocardiography. For endurance-trained athletes, absolute left ventricular end-diastolic volume and values normalized for lean body mass were significantly greater than in nonathletes. An interstudy comparison of female vs male endurance-trained athletes from the same population also revealed significantly lower values for M-mode left ventricular mass expressed per kilogram of lean body mass in the former. Absolute and normalized wall thicknesses were not significantly greater in resistance-trained athletes compared to the other two groups. Wall thickness indexed for lean body mass was similar for the three groups. Sinus bradycardia was observed in all endurance athletes and in four resistance-trained athletes. ECG criteria were unreliable for the prediction of left ventricular enlargement. It appears that both female resistance- and endurance-trained athletes exhibit a lesser degree of enlargement of left ventricular wall thickness and mass than male athletes. A close relationship between skeletal and cardiac muscularity in resistance-trained athletes of both genders also was supported.