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J Appl Physiol 101: 1356-1361, 2006. First published July 6, 2006; doi:10.1152/japplphysiol.01160.2005
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Muscle metabolic function and free-living physical activity

Gary R. Hunter,1,2 D. Enette Larson-Meyer,3 Bovorn Sirikul,2 and Bradley R. Newcomer4

Departments of 1Human Studies, 2Nutrition Sciences, 4Critical and Diagnostic Care, University of Alabama at Birmingham, Birmingham, Alabama; and 3University of Wyoming, Laramie, Wyoming

Submitted 15 September 2005 ; accepted in final form 26 June 2006


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
We have previously shown that muscle metabolic function measured during exercise is related to exercise performance and subsequent 1-yr weight gain. Because it is well established that physical activity is important in weight maintenance, we examined muscle function relationships with free-living energy expenditure and physical activity. Subjects were 71 premenopausal black and white women. Muscle metabolism was evaluated by 31P magnetic resonance spectroscopy during 90-s isometric plantar flexion contractions (45% maximum). Free-living energy expenditure (TEE) was measured using doubly labeled water, activity-related energy expenditure (AEE) was calculated as 0.9 x TEE – sleeping energy expenditure from room calorimetry, and free-living physical activity (ARTE) was calculated by dividing AEE by energy cost of standard physical activities. At the end of exercise, anaerobic glycolytic rate (ANGLY) and muscle concentration of phosphomonoesters (PME) were negatively related to TEE, AEE, and ARTE (P < 0.05). Multiple regression analysis showed that both PME (partial r = –0.29, <0.02) and ANGLY (partial r = –0.24, P < 0.04) were independently related to ARTE. PME, primarily glucose-6-phosphate and fructose-6-phosphate, was significantly related to ratings of perceived exertion (r = 0.21, P ≤ 0.05) during a maximal treadmill test. PME was not related to ARTE after inclusion of RPE in the multiple regression model, suggesting that PME may be obtaining its relationship with ARTE through an increased perception of effort during physical activity. In conclusion, physically inactive individuals tend to be more dependent on anaerobic glycolysis during exercise while relying on a glycolytic pathway that may not be functioning optimally.

anaerobic glycolysis; phosphomonoesters; activity-related energy expenditure

OBESITY CONTINUES TO BE A major concern in the United States with over 30% of the population now classified as obese (BMI > 30) and 6% classified as morbidly obese (BMI > 40) (8). Participation in free-living physical activity has been shown to be related to reduced rate of weight gain (29). Despite this, little is known concerning metabolic factors that predispose an individual to increased participation in physical activity.

Reduced measures of difficulty (measured by submaximal heart rate, ventilation, and perceived exertion) during activities such as walking and climbing stairs are related to free-living energy expenditure and physical activity (17). Maximal oxygen uptake (VO2 max) is also positively associated with decreased exercise difficulty (15). Previous studies from our laboratory have found that VO2 max and treadmill endurance time, as would be expected, are negatively related to weight gain over 1 yr in premenopausal women (18). In addition, women who maintain, rather than gain weight, over 1 yr were found to be stronger and have better muscle metabolic economy than those who gain weight. Multiple regression analysis reveals that muscle metabolic economy, VO2 max, and quadriceps strength all are independently related to rate of weight gain (model R = 0.48, P < 0.01) (18). We know of no other studies that have shown that muscle metabolic economy and leg strength are related to subsequent weight gain, although Borg et al. (2) have recently shown that weight-reduced obese men who participated in a resistance training program gained less body fat than nonexercisers and walkers during the 6 mo after a 2-mo dietary intervention that produced a 14.3-kg weight loss.

A limited amount of information exists to support the notion that the aerobic oxidative profile of skeletal muscle may contribute to weight maintenance by having some effect on energy expenditure. Studies have found that malate dehydrogenase (a marker of Krebs cycle activity) was 20% lower in men who have high amounts of subcutaneous fat compared with men with low amounts of subcutaneous fat (24), and oxoglutarate dehydrogenase (also a marker of Krebs cycle activity) was negatively related to weight gain during overfeeding in lean adults (25). In addition, oxoglutarate dehydrogenase activity was negatively related to 13-yr weight gain whereas cytochrome-c oxidase and citrate synthase activity were positively related to 24-h energy expenditure measured in a room calorimeter (7). Although it is difficult to determine what is cause and effect, these data suggest that muscle function may play some role in weight maintenance, possibly by affecting participation in physical activity.

31P magnetic resonance spectroscopy (31P-MRS) can be used to measure ATP generation from oxidative, glycolytic, and creatine kinase (CK) reactions during exercise (3). It is thus possible to examine how various measures of muscle metabolism relate to muscular strength, whole body aerobic capacity, and exercise performance, and finally how these measures of muscle function and fitness relate to physical activity and long-term weight maintenance. We have recently shown that quadriceps isometric strength and 31P-MRS muscle oxidative capacity (postexercise ADP recovery rate x volume of muscle ÷ body weight) are independently related to treadmill endurance time (18), suggesting that both strength and aerobic capacity independently influence walking endurance for a maximal graded exercise task lasting ~6–7 min.

The purpose of this study was to examine the relationship between in vivo submaximal exercise skeletal muscle function and free-living physical activity and free-living activity-related energy expenditure (AEE). We hypothesize that ability to resynthesize ATP from metabolic pathways during a submaximal exercise task (anaerobic glycolysis and oxidative phosphorylation) will be related to increased free-living physical activity and AEE.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Seventy-one normal-weight, healthy premenopausal women (23–47 yr old) participated in this study. The subjects were selected from a larger ongoing study designed to measure metabolic factors that predispose women to obesity. Thirty-six of the women were examined after undergoing dietary-induced weight loss of 12.7 ± 3.2 kg. Thirty-five of the women were never overweight. None were taking any medication known to affect body composition, energy expenditure, or exercise performance. The study was approved by the University of Alabama at Birmingham Institutional Review Board. All volunteers were screened and briefed about the experimental protocol, and informed consent was obtained before testing.

Women were weight stable for 1 mo before testing, which included a macronutrient-controlled diet for the 2 wk preceding testing. All testing was performed in the follicular phase of the menstrual cycle (within 10 days of the start of menses). Exercise sessions on the treadmill and for 31P-MRS analysis were separated by at least 2 days.

Dual-energy X-ray absorptiometry.   Percent fat was determined by dual-energy X-ray absorptiometry (DPX-L, Lunar Radiation, Madison, WI). The scans were analyzed using the Adult Software (version 1.33).

VO2 max.   In the morning and after an overnight fast, VO2 max was determined by indirect calorimetry on a treadmill using a modified Bruce protocol to exhaustion. Volumes of oxygen and carbon dioxide were measured continuously by open-circuit spirometry and analyzed with a Sensormedics metabolic measurement cart (model 2900, Yorba Linda, CA). Heart rate was monitored by a Polar Vantage XL heart rate monitor (Polar Beat, Port Washington, NY). Immediately after the test, rating of perceived exertion (RPE) was obtained by using the Borg 6–20 scale (26). The highest oxygen uptake (VO2), respiratory exchange ratio, and heart rate achieved within the last 2 min of exercise were recorded. Standard criteria for heart rate, respiratory quotient, and plateauing were used to ensure achievement of VO2 max (13).

Submaximal oxygen uptake and energy cost of exercise.   Submaximal VO2 was obtained in the steady-state, during the third and fourth minutes of five standardized exercise tasks. The five tasks, selected to reflect typical activities of adult women in free-living conditions, were level walking (0% grade, 3 mph, 4 min), grade walking (2.5% grade, 3 mph, 4 min), cycling (bicycle ergometer, 60 rpm, 50-W workload, 4 min), stair climbing (7-in. step, 60 steps/min, 4 min), and level walking carrying a loaded box (0% grade, 2 mph, 4 min). The weight of the box was equivalent to 30% of the subject's maximal isometric elbow flexion strength and was intended to simulate carrying a small load. A shoulder harness was worn to standardize shoulder position, and the elbow was maintained at 110° flexion throughout the test. Average VO2 for the tasks was converted to kilocalories per minute with the assumption of 5 kcal/l of oxygen consumed per minute, as previously described (16). Energy cost of exercise was determined by subtracting average resting energy expenditure from energy expended in the five tasks.

Measurement of sleeping energy expenditure.   Subjects spent 23 h in a whole-room respiration calorimeter (3.38 m long, 2.11 m wide, and 2.58 m high). The calorimeter design characteristics and calibration have been previously described (28). Oxygen consumption and carbon dioxide production were continuously measured by magnetopneumatic differential oxygen analyzer (Magnos 4G) and the NDIR industrial photometer differential carbon dioxide analyzer (Uras 3G, both Hartmann & Braun, Frankfort, Germany). The calorimeter was calibrated before each subject entered the chamber. The zero calibration was carried out simultaneously for both analyzers. The full scale was set for 0–1% for the carbon dioxide analyzer and for 0–2% for the oxygen analyzer.

Each subject entered the calorimeter at 8 AM. Although metabolic data were collected throughout the 23-h stay, only sleeping metabolic data are reported here. The onset of sleep was determined when the lights were turned off, between 9:30 and 11:00 PM in all cases. Sleep may have included some resting awake time while the subject was falling asleep. Radar motion sensors used to detect spontaneous physical activity indicated the subjects were inactive during the sleep period. The subject was awakened at 6:30 AM on the second morning in the calorimeter. Energy expenditure was calculated by the Weir equation (6).

Measurement of total energy expenditure.   Free-living total energy expenditure (TEE) was measured over 14 days of controlled diet and energy-balance conditions by the doubly labeled water technique. The previously described protocol (9) has a theoretical error of <5%. Samples were analyzed in triplicate for H218O and 2H2O by isotope ratio mass spectrometry at the University of Alabama at Birmingham as previously described (10). When all samples for deuterium and oxygen-18 were reanalyzed in seven subjects, values of TEE were in close agreement (coefficient of variation = 4.3%), as previously described (10). Carbon dioxide production rates were determined using a fixed assumption for the dilution space ratio (1.0427) by using Eq. R2 of Speakman et al. (27), and energy expenditure was calculated using Eq. 12 of de Weir (6) using a mean value for the dietary food quotient of 0.88 obtained from the foods provided.

Assessment of AEE.   Physical AEE was estimated by subtracting sleeping energy expenditure (SEE) from TEE after reducing total energy expenditure by 10% to account for the thermic response to meals. SEE was used instead of resting energy expenditure to estimate AEE, because SEE encompassed a much longer period of assessment and had a 45% lower standard deviation than resting energy expenditure.

Free-living ARTE.   Free-living physical activity (min/day) was derived from AEE by using the activity-related time equivalent (ARTE) index, which we developed previously (30).

Formula
The ARTE index is therefore an index of the portion of the day the subject spends in free-living physical activities comparable with the five tasks performed in the laboratory. The ARTE index provides a practical measure of physical activity because it adjusts AEE for each subject's exercise economy by using energy cost of exercise. This is important because exercise economy varies as much as 42% in women (30) and, as previously reported (23), enables comparisons of duration of physical activity between subjects who vary on the cost of movement because of differences in body weight and economy of exercise.

31P-MRS.   1H-magnetic resonance images (MRI) and 31P-MRS were collected on the right calf muscle by using a 4.1-T whole body imaging and spectroscopy system. Subjects were studied on 2 separate days. A series of resting calf muscle MRIs were collected on the first day to measure maximal cross-sectional area of the gastrocnemius and soleus muscles. The images were collected by using a torroid coil with the following protocol: repetition time = 1,000 ms, echo time = 14.5 ms, 256-mm field of view, and 5-mm slice thickness with a slice separation of 10 mm. The cross-sectional area of the gastrocnemius and soleus muscle group was determined by manually drawing the area around both muscles from the MRIs of each slice. The coefficient of variation for maximal cross-sectional area in our laboratory is 3.9% (20). The maximal cross-sectional area was subsequently used to normalize force output between individuals. In addition, the subjects practiced performing isometric plantar flexion. Maximal isometric plantar flexion was measured three different times across 2 days with the highest force defined as maximal plantar flexion force output. The coefficient of variation for maximal isometric plantar flexion in our laboratory is 4.9% (19).

On the second day women performed 90-s unilateral, isometric plantar flexion exercises at 45% of maximal voluntary contraction. The theoretical maximal voluntary contraction force was determined from maximal cross-sectional areas of the gastrocnemius and soleus muscle groups as determined by the MRI images (3). A 7-cm 1H/31P surface coil, fastened to the underbelly of the calf muscle, was used to collect 2-s time-resolved 31P-MRS data during 60 s of rest, 90 s of exercise, and 7.5 min of recovery. The 31P-MRS data were collected by using a repetition time of 2,000 ms, four dummy pulses, one signal average, and a half-passage adiabatic excitation pulse. This adiabatic pulse produced a uniform 90° excitation pulse over the sensitive volume of the coil and increased the signal-to-noise ratio of our acquisitions. An example of the 31P-MRS data collected with these parameters in our laboratory has previously been published (19). Peak areas and positions of the phosphate metabolites were found by time domain fitting, using Fitmasters (Phillips Medical Systems, Shelton, CT) as previously described (4). The exercise bench and force collection devices in our laboratory are also described elsewhere (19).

31P-MRS was commonly used to measure the intracellular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), and ATP. The intracellular pH was also calculated from the chemical shift difference between PCr and Pi. These pieces of information were used to quantitatively study the energetics of skeletal muscle during exercise and recovery (4, 21). A detailed description of the methods and model used for calculating ATP production rates from time resolved 31P magnetic resonance spectra has been previously published (21). Briefly, PCr's rate of depletion during exercise was used to measure the ATP production rate from the CK reaction (4, 21). AMP concentration was calculated from the adenylate kinase equilibrium (21), and ADP concentration was calculated from the equilibrium equation of the CK reaction (19). The rate of ATP production from anaerobic glycolysis (ANGLY) was calculated from the time courses of pH, PCr, and Pi by assuming a H+ stoichiometry of the ATP producing reactions and a buffering capacity of muscle (4). The rate of PCr increase during the first 14 s of recovery was used to estimate the ATP production rate from oxidative phosphorylation (OXPH) (4). Muscle metabolic economy (ME) was calculated as average force across the last 14 s of force production divided by ATP production rate from the sum of the CK reaction, ANGLY, and OXPH. As Fig. 1 illustrates, force did not change during the 90 s of 45% maximal isometric contractions. In addition, Boska (4) has previously shown that ME does not change during 120 s of isometric contractions whether the intensity was submaximal or 100% of maximum, suggesting that the last 14 s of exercise is representative of the ME for the entire 90-s task. The sum of these three production rates was defined as the total ATP production rate in this study. As previously reported (22), the test-retest R2 was 0.88 for ANGLY, 0.87 for the CK reaction, 0.95 for OXPH, and 0.99 for ME for 45% plantar flexion tested twice in seven subjects.


Figure 1
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  		Fig. 1. Average time course of force output (A), intramuscular pH (B), Pi (C), and phosphocreatine (PCr; D) during 60 s of rest, 90 s of exercise at 45% maximal isometric plantar flexion, and 7.5 min of recovery. The data are plotted every 2 s as means ± SE. Every third data point is displayed for clarity.

 
Statistics.   Relationships between AEE and ARTE with submaximal muscle metabolic and whole body aerobic capacity variables were determined by Pearson product zero-order correlations. Multiple regression was used to determine independent relationships between muscle metabolic variables and AEE and ARTE. Alpha was set at 0.05 for all analyses.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Descriptive characteristics are contained in Table 1. The women were young, normal body mass index, and relatively low aerobic fitness. Table 2 contains simple Pearson product correlations between AEE and ARTE and submaximal exercise metabolic variables. ANGLY and PME were significantly negatively related to both AEE and ARTE (r –0.24 to –0.31, P all < 0.04, Fig. 2 contains the PME-ARTE graph). OXPH, ADP, AMP, difference between average force and end force, ME, and maximal RPE were not significantly related to either AEE or ARTE, although the correlation for ME (0.22, P < 0.08) approached significance. The only variables significantly related to PME were ME (r = –0.25, P < 0.04) and RPE during the maximal treadmill test (r = 0.21, P < 0.05). Maximal RPE was not significantly related to either maximal heart rate (r = 0.03, P = 0.82) or maximal respiratory exchange ratio (r = 0.07, P = 0.59), suggesting that low effort in those with low perceived exertion was not affecting the perceived exertion-PME relationship.


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  		Table 1. Descriptive characteristics of 71 pre-menopausal black and white women participating in the study

 

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  		Table 2. Pearson product simple correlations

 

Figure 2
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  		Fig. 2. Relationship between free-living physical activity (calculated from doubly labeled water) and phosphor-monoester concentration in plantar flexors at the end of a 90 s 45% maximal isometric plantar flexion task (r = –0.27, P = 0.02). MVC, maximum voluntary contraction.

 
Because PME primarily consists of glycolytic pathway intermediary substrates (glucose-6-phosphate and fructose-6-phosphate), it is possible that the relationship between PME and ARTE was mediated by high anaerobic glycolytic flux. Therefore, to determine whether PME and ANGLY are independently related to ARTE, a multiple regression was employed to determine the independence of the relationships of PME and ANGLY with ARTE (Table 3). Both PME (partial r = –0.24, P < 0.04) and ANGLY (partial = –0.29, P < 0.02) were independently related to ARTE. To ensure that group (either never overweight or postoverweight) was not affecting the PME-ARTE or ANGLY-ARTE relationship, group was also used as an adjusting variable in estimation of ARTE. Both PME (partial r = –0.25, P < 0.04) and ANGLY (partial r = –0.28, P < 0.02) remained independently correlated with ARTE, whereas group was not a significant correlate (partial r = –0.06, P > 0.64) in the model. When perceived exertion during the maximal treadmill test was added to the model (Table 4), PME (partial r = –0.19 P > 0.14) was no longer independently related to ARTE, whereas ANGLY (partial r = –0.37, P < 0.01) remained significantly related to ARTE.


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  		Table 3. Multiple regression model for estimating ARTE using phosphomonoester accumulation and anaerobic glycolytic rate from a 90-s 45% maximal isometric plantar flexion (n = 71)

 

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  		Table 4. Multiple regression model for estimating ARTE using RPE, PME accumulation and anaerobic glycolytic rate from a 90-s 45% maximal isometric plantar flexion (n = 64)

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The primary finding of this investigation was that increased participation in free-living physical activity and AEE are associated with decreased dependence on muscle anaerobic glycolysis and decreased accumulation of PME in skeletal muscle during submaximal isometric contractions. Because PME are made up of primarily glucose-6-phosphate and fructose-6-phosphate [two substrates directly downstream from the rate-limiting phosphofructokinase (PFK) step], increased PME would be expected with increased glycolytic rate due to an increase in mass action. However, anaerobic glycolysis and PME were independently related to ARTE and AEE, suggesting that those who tend to be physically inactive tend to be dependent on anaerobic glycolysis while also relying on a glycolytic pathway that may not be functioning optimally.

The PME generated during exercise are hexose phosphates, particularly glucose-6-phosphate and fructose-6-phosphate (5, 11, 14). ATP is "consumed" (ATP required phosphorylation of glucose) when glucose-6-phosphate is formed during the hexokinase reaction. However, an accumulation of PME indicates that the ATP was not regenerated by glycolysis because ATP generation occurs downstream from fructose-6-phosphate in glycolysis. Therefore, an accumulation of PME might be expected to be associated with decreased ATP and increased fatigue. No relationship was found between PME and either ADP or AMP concentrations. In addition, no relationship was found between the ability to maintain the 45% maximal force for 90 s and PME, suggesting that fatigue was not more prevalent in the individuals who had elevated PME. Similarly, Argov et al. (1) have found that PME accumulation in PFK-deficient patients was not associated with decreased exercise tolerance during submaximal muscle contractions.

Interestingly, in the present study there was a significant positive relationship between RPE during the VO2 max test and accumulation of PME during the submaximal isometric plantar flexion task, suggesting that individuals who are more prone to increase PME may perceive physical activity as more difficult. This correlation occurred despite maximal perceived exertion being unrelated to either maximal respiratory quotient or maximal heart rate, indicating perceived exertion scores were not related to level of effort on the maximal test, i.e., individuals were giving an equal amount of effort regardless of their perception of effort. Unfortunately we did not obtain RPE after the submaximal plantar flexion test. However, we have previously reported that high PME accumulation is accompanied by increased perceptions of fatigue (21). These results suggest that it is conceivable that individuals who accumulate large amounts of PME during exercise may perceive the exercise as more difficult, thus decreasing the likelihood of participation in free-living physical activity. The disappearance of a significant relationship of PME with free-living physical activity when RPE are included in the model suggests this may be the case.

Because PFK is considered to be a rate-limiting enzyme in glycolysis and is responsible for catalyzing the conversion of fructose-6-phosphate to fructose-1,6-biphosphate, variation in its activity certainly can affect the concentration of PME. PME levels continuously rise during even light exercise in PFK-deficient subjects (1), supporting at least the possibility that PFK inhibition could play a role in PME accumulation. Although it is unknown whether it is PFK alone or in combination with another rate-determining enzyme in glycolysis that is affecting PME concentrations, it is possible that the less active women in this study were dependent on a metabolic enzyme system that was not functioning optimally while being more dependent on this same system (anaerobic glycolysis) for ATP production.

It was somewhat surprising that neither oxidative regeneration of ATP after the submaximal task nor whole body VO2 max were related to ARTE and AEE, especially because we have previously shown a positive relationship between VO2 max and physical activity (17). One possible difference in this comparison with our previous study is that the subjects in this study were relatively sedentary (mean VO2 max less than 32 ml O2·kg–1·min–1) with only one subject reporting as much as 50 min/wk of exercise above 8 METs and only three reporting as much as 50 min/wk of exercise above 6 METs. Therefore little variation in the submaximal ATP oxidation rate occurred after the exercise (the standard deviation was only 0.06 mM/s in this group) compared with samples that included more active subjects (the standard deviation was 0.12 mM/s) (22). In addition, because the women in this study were relatively sedentary, most of the activities they participated in were relatively low intensity and/or of short duration. Anaerobic metabolic pathways are likely to be relatively more important than aerobic pathways in activities of short duration (12) (the activity will be over before the oxidative processes can be fully activated). The subjects from our previous paper were also relatively sedentary (17); however, the data were collected 1 yr after any loss of weight. In fact, some of the women in that study had undergone weight gain during the previous year (mean weight gain of 3.8 ± 5.1 kg, range –5 to 17.2 kg). Even though the subjects in both this study and the previous study had been in energy balance for at least 4 wk before the evaluations of aerobic fitness and free-living physical activity, it might be possible that differences in energy balance during the month before the energy balance may have affected the relationship between free-living physical activity and aerobic fitness. It is therefore possible that ATP regeneration from aerobic pathways would be significantly correlated with physical activity and AEE in a more diverse group of active and inactive subjects that did not include subjects who had undergone recent weight loss. It is important to note that inclusion of group (either never overweight or postoverweight) as an adjusting variable did not affect the independent relationship between PME and ARTE (partial r = –0.25, P < 0.04) and anaerobic glycolysis and ARTE (partial r = –0.28, P < 0.02).

In conclusion, this study shows for the first time that individuals who tend to be physically inactive tend to be dependent on anaerobic glycolysis while also relying on a glycolytic pathway that may not be functioning optimally. Future studies should determine whether PME accumulation is mediated by impaired PFK activity. In addition, it is important to determine what role gene expression and exercise training have on the glycolytic pathway and participation in free-living physical activity.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
ACKNOWLEDGMENTS
 REFERENCES
 
This research was supported by National Institute of Diabetes and Digestive and Kidney Diseases Grants R01 DK-49779 and R01 DK-51684, DRR General Clinical Research Center Grant M01 RR-00032 from the National Center for Research Resources, and Clinical Nutrition Research Unit Grant P30-DK 56336. Stouffer's Lean Cuisine entrees, Nestle Food, Solon, OH and Weight Watchers Smart Ones, HJ Heinz Foods, Pittsburgh, PA kindly provided food for dietary control.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
REFERENCES
 
We thank Roland Weinsier, Harry Vaughn, Betty Darnell, Paul Zuckerman, David Fields, Robert Petri, and Nancy Davis for invaluable assistance.


   FOOTNOTES
 

Address for reprint requests and other correspondence: G. R. Hunter, Rm. 205 Education Bldg., 901 13th St. South, Univ. of Alabama at Birmingham, Birmingham, AL 35294-1250 (e-mail: ghunter{at}uab.edu)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 

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