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Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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In this double-blinded study, 37 women with iron depletion without anemia (age 19-36 yr) were randomly assigned to receive either an iron supplement (135 mg/day) or a placebo. Endurance capacity was assessed during a 15-km simulated time trial (TT) on a cycle ergometer before and after the 8-wk treatment. After the treatment, although the iron-supplemented group did not have shorter time to finish the TT (time), it had 2.0 kJ/min lower energy expenditure and 5.1% lower fractional utilization of peak oxygen consumption during the TT compared with the placebo group, after controlling for work rate (P < 0.05). Time, fractional utilization of peak oxygen consumption, and plasma lactate concentration at the 5th km of the TT were all negatively associated with hemoglobin levels, after controlling for work rate (P < 0.05). In conclusion, repletion of iron stores to women with iron depletion without anemia increased their energetic efficiency, and oxygen transport capacity of the blood was found to be an important determinant of endurance capacity and energy metabolism in nonanemic women.
hemoglobin; endurance; lactate; glucose; energy efficiency
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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IN THE United States, the prevalence of iron-deficiency anemia in 18- to 44-yr-old women is only ~2.3%, but the prevalence of marginal iron deficiency, referring to both iron deficiency without anemia and depletion of iron store, is ~16% (6). In iron depletion without anemia, hemoglobin (Hb) concentration is above the cutoff for anemia, which is 120 g/l for women age 18-44, but serum ferritin (sFer) is below a cut-off concentration (16 µg/l) for iron depletion (11). Those young women who are physically active seem to have a higher risk of iron deficiency (20, 28).
Although the effect of iron deficiency without anemia on maximum
oxygen consumption
(
O2 peak) has been
extensively investigated (15, 23, 27, 35), little is known about the
effects of marginal iron deficiency on other aspects of physical
performance, such as endurance capacity. Different factors determine
O2 peak and endurance
capacity. Under normal conditions,
O2 peak is determined
mainly by oxygen supply (3, 32), whereas endurance capacity may be
affected by both oxygen supply and oxygen utilization capabilities of
the muscles (7). Only aerobic phosphorylation allows for prolonged
exercise because anaerobic energy production (glycolysis) may lead to
lactate accumulation and consequently to fatigue (13).
Although nonanemic individuals who are iron deficient have Hb concentrations above the cutoff for anemia, their oxygen-transport capacity may not have reached an optimal level and may still be a limiting factor of endurance capacity. In addition, oxygen-utilization capacity may also be impaired, causing further reduction of endurance capacity. Animal studies indicated that endurance capacity could be affected by iron deficiency per se, probably due to decreased iron-containing oxidative enzymes and respiratory proteins, which determine oxygen-utilization capability (7, 8, 12, 14, 24, 34).
Endurance capacity has not been found to be impaired because of iron deficiency without anemia in previous investigations (4, 15, 16, 23). This may be due to the limitations of the time-to-exhaustion protocol used to measure endurance capacity in these studies.
Endurance has been defined as the maximum length of time an individual
can sustain a given workload measured by fractional utilization of
O2 peak
(%O2 peak) (25).
%O2 peak is a better
measurement of workload than is the absolute work rate in individuals
with different values of
O2 peak, because
different body sizes are compared. Therefore, endurance should be
assessed by measuring the time to exhaustion at individualized
workloads that are at the same percentage of
O2 peak for all
subjects. However, it is often impossible to keep subjects at the same
%O2 peak during
a prolonged exercise test. In addition,
O2 peak might change
during a prospective study so that
%O2 peak at the same work intensity may change before and after iron treatment. In previously published studies, there was an ~5% variation in
%O2 peak during the
time-to-exhaustion test before and after iron treatment, but none of
these studies controlled for
%O2 peak when
analyzing the treatment effect on endurance time (4, 15, 16, 23). One
way to solve these problems is to control for
%O2 peak
statistically, as a covariate in multivariate regression analyses,
with time to exhaustion as the dependent variable. Although the time to exhaustion was not found by LaManca and Haymes (16) to be changed by
iron supplementation in iron-deficient mildly anemic subjects, they
found that the
%O2 peak
during the time-to-exhaustion test was significantly decreased by the
iron treatment. This finding suggests that the variation
in %O2 peak might have
negatively confounded the treatment effect on time to exhaustion.
Another problem with the time-to-exhaustion protocol is that measured time may be affected by both physiological and psychological factors that cannot be measured objectively. Although the effect of iron status on psychological response to strenuous exercise is unknown at the current time, the measured time to exhaustion may be confounded by motivational levels of the subjects.
In practice, endurance capacities of individuals are compared by their times to finish a given distance in a running or cycling test that requires maintenance of aerobic oxidative metabolism. A person who can finish the same distance in a shorter period of time is considered to have better endurance. Testing endurance by using a time-trial protocol has the advantage of providing an incentive to the subjects to finish the time trial as fast as possible, thus reducing the effect of the motivational factor.
The results from previous studies indicate that more research is needed to investigate the effects of iron depletion without anemia on endurance capacity. The purposes of this study were 1) to test the effect of iron depletion without anemia on endurance capacity as measured by performance in a 15-km simulated time trial; 2) to test the effects of iron depletion without anemia on metabolic responses during the time trial, including ventilation, gas exchange, and plasma lactate and glucose concentrations; and 3) to investigate the direct effects of iron-status indicators on endurance capacity and energy metabolism.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Subjects. One hundred seventy-two healthy, physically active, 19- to 36-yr-old women were recruited from the local community. After preliminary screening, 43 women were identified as iron depleted without anemia, with Hb concentrations >120 g/l and sFer levels <16 µg/l. After a physical examination by a physician, subjects were excluded for the following reasons: current pregnancy or pregnancy within the previous year, infectious illness in the past month or fever in the past week, hemolytic anemia, asthma, musculoskeletal problems, smoking, excess alcohol consumption, recent history of eating disorders, recent use of recreational drugs, and use of certain prescription medications that may interfere with dietary iron absorption.
Thirty-nine women qualified and were willing to participate in the study. Signed informed consent was obtained from each subject. This study was approved by the University Committee on Human Subjects at Cornell University.Study design. This study had a randomized and double-blinded design. Subjects were randomly assigned to two groups, receiving either an iron supplement or a placebo. Both the subjects and the investigators were blinded to the group assignment until the completion of data collection. Subjects took either iron supplement (45 mg elemental iron per capsule in the form of ferrous sulfate) or identical placebo capsules three times a day for 8 wk. These capsules were prepared by a local pharmacist. The mean (±SD) iron content of capsules was determined from a random sample of 20 capsules from each of two batches (45.1 ± 2.8 mg). The subjects were instructed to consume the capsules with a citrus juice and with meals to increase absorption and to reduce side effects. Compliance with the iron treatment was assessed by counting the capsules left over biweekly. For all the subjects, body composition and physical performance were measured immediately before and after the 8-wk treatment period. Thirty-seven women finished the entire research regimen. Two subjects, one from each group, dropped out of the study because of personal reasons or sickness unrelated to the study.
Prestudy habitual physical activity (PA) levels were assessed by a frequency questionnaire, which was analyzed by using the method described previously (35) to obtain a PA score for each subject. This was used to ensure that randomization resulted in equal PA between groups. To control for the potential effects of changes in PA level on physical performance, the subjects were asked to maintain the same exercise activity level during the entire study period. PA was monitored by daily PA records, which were also analyzed quantitatively by using the same method described previously (35). As part of the screening process, baseline dietary iron intake was assessed by a dietary record over 4 consecutive days including 1 weekend day. The dietary records were analyzed by using Nutritionist IV (Hearst, San Bruno, CA) to obtain daily dietary iron intake values. Subjects were instructed to avoid consumption of any other multivitamin and mineral supplements during the entire study period. Self-recordings of iron or placebo capsule compliance, consumption of medication, illness, menstrual status, gastrointestinal symptoms, PA, and musculoskeletal problems were collected daily.Physiological measurements.
Exercise tests were conducted on a mechanically braked and calibrated
bicycle ergometer (model 818E, Monark, Varberg, Sweden), by using a
computerized metabolic cart (Physiodyne, Quogue, NY) in the Human
Bioenergetics Laboratory at Cornell University. The ergometer was
equipped with a digital readout of cadence [revolutions per
minute (rpm)] or distance pedaled. Concentrations of oxygen and
carbon dioxide in expired air and volume of respiration were analyzed
with Ametek gas analyzers (Pittsburgh, PA) and a Fitco Micro Flow
respiratory pneumotachograph (Fitness Instrument Technologies, Farmingdale, NY) through a Hans Rudolph breathing valve (Kansas City,
MO). Data output from the instruments was directed to a IBM 386 computer for the breath by breath calculation of oxygen consumption (O2),
CO2 production
(CO2), and respiratory
exchange ratio (RER)
(CO2/O2),
and minute ventilation.
O2 peak was measured
following a modification of the protocol described by McArdle and Magel
(22) for the cycle ergometer. Testing began with a 5-min
warm-up at 30 W and a pedaling cadence of 60 rpm. The workload was
increased by 30-W intervals every 2 min until the
O2 stopped increasing, as
observed from the computer monitor.
O2 peak was
determined as the O2 at the final workload achieved, if that workload did not result in a >150-ml
increase in O2 from the
previous workload. Heart rate was monitored throughout with an
electrocardiograph (Burdick, Milton, WI). Test-retest reliability of
this protocol was determined with a similar sample of women as used
this study, and it yielded a correlation coefficient
(r) of 0.91.
Endurance was tested by a 15-km simulated time trial administered 2 days after the
O2 peak test.
Subjects were asked to finish the time trial as fast as possible,
against a predetermined resistance. Standardized words of encouragement
were used by the investigator throughout the test. The level of the
resistance allowed the subject, if she pedaled at 60 rpm, to achieve
70% of
O2 peak, as
determined individually from the result of her pretreatment
O2 peak test. The
same resistance level was used at the posttreatment endurance test.
During the test, O2,
CO2, and heart rate were
continuously monitored. Test-retest reliability of this protocol
determined in our laboratory is r = 0.93 for average
O2 during the
time trial and is r = 0.99 for average work rate during the time trial.
Blood samples were taken from finger punctures immediately before and
after the time trial and twice during the time trial, when the subject
reached the 5th and 10th km. Blood samples were drawn into 100-µl
heparinized capillary tubes (Baxter Scientific Products, McGraw Park,
IL), sealed, and stored on ice. The capillary tubes were centrifuged
immediately after the test, and plasma samples were separated and
stored at 
20°C for the analysis of lactate and glucose
concentrations.
Lactate and glucose concentrations of the plasma samples obtained from
the endurance test were measured enzymatically (Sigma Diagnostics, St.
Louis, MO). Samples from the same subject before and after the iron
treatment were analyzed concurrently at the completion of the entire
study to control for variation in assay conditions.
Body size and composition were measured in the Body Composition
Laboratory of the Human Metabolic unit at Cornell University. Anthropometry (weight, height) was assessed by using standard procedures described in Lohman et al. (18). Body fat and fat-free mass
(FFM) were assessed by densitometry following the technique described
by Consolazio et al. (5). The Siri equation adapted for females was
used, assuming the density of FFM to be 1.096 g/ml (17).
Iron-status measurements. Iron status was assessed at screening and for those subjects enrolled into the study, before, in the middle of, and after iron treatment. To control for potential variation in assay conditions from batch to batch, samples from the same subject collected at the three different time points during the study were analyzed concurrently at the completion of the entire study.
Hb was determined by the cyanomethemoglobin method described by Van Assendelft and England (31a) (Sigma Diagnostics). Hematocrit was determined by the microhematocrit method. sFer was assessed by the ELISA method according to the method of Flowers et al. (9) (Ramco Laboratories, Houston, TX). Transferrin saturation (TS) was determined from the ratio of serum iron (sFe) to total iron-binding capacity (TIBC) by the method described by Persijn et al. (26) (Sigma Diagnostics). Serum transferrin receptor (sTfR) was determined by the enzyme-linked immunosorbent assay method described by Flowers et al. (10) (Ramco Laboratories, Houston, TX). To control for day-to-day variation and the effect of regression to the mean, the averages of two independent measurements of Hb and sFer levels, at screening and before the iron treatment, which were 3-7 days apart, were used as the pretreatment concentrations.Statistical analysis. All statistical analysis was done by using SYSTAT, Version 5.2 (Evanston, IL). Independent Student's t-test was used to analyze group difference at baseline. Analysis of variance with repeated measurements (MANOVA) with treatment group as a covariate was used to detect changes of iron status and physical activity during the study. Changes of these variables within each group were analyzed by paired t-test. Regression analysis with baseline measurements as covariates was used to analyze group difference in posttreatment iron status or physical performance. The effects of iron status on outcome variables were analyzed by multiple linear regression analysis, controlling for baseline levels and other potential confounding or mediating factors. P < 0.05 was used to indicate statistical significance. Because sFer, sFe, and TS had skewed distributions, normalized values through log transformation of these variables were used in all statistical analyses.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Mean age was 24.8 ± 4.2 (SD) yr for the placebo group and was 23.8 ± 4.8 yr for the iron-supplemented group. Mean height was 1.68 ± 0.07 (SD) m for both groups. Dietary iron intake before the study was 16.6 ± 7.8 mg/day for the placebo group and was 18.2 ± 13.0 mg/day for the iron-supplemented group. There was no significant group difference in age, height, and dietary iron intake before the study. Results of the body weight and body composition measurements at baseline and posttreatment are presented in Table 1. There was also no significant group difference before and after treatment in body size and body composition. Within each group, body weight and body composition did not change during the study.
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Compliance with and response to iron treatment. On average, the placebo group consumed 144 ± 23 capsules (87.3 ± 9.5% of total prescription) and the iron-supplemented group consumed 145 ± 29 capsules (87.5 ± 16.5%). There was no group difference in the number of capsules consumed.
Results of the serial measurements of iron status variables are presented in Table 2. There was no significant group difference at baseline for any of the iron-status variables measured. After 8 wk of treatment, neither group experienced significant change in hematocrit, sFe, TIBC, and TS.
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Habitual PA levels during the study. At baseline, there was a marginal group difference in habitual PA level (P = 0.09, data not shown). There was no significant group difference in PA level for any of the 2-wk periods during the study. MANOVA did not reveal changes in PA throughout the study period for either group.
Physical performance.
Results of the physical performance measurements before and after iron
treatment are presented in Table
3. At baseline, there was
no group difference in any of these measurements. Both groups increased
O2 peak during the
treatment period, but there was no group difference in final
O2 peak after
controlling for baseline level. After the 8-wk treatment, both groups
significantly increased average
O2 and average oxygen pulse
(O2/heart rate) and
significantly decreased average RER during the time trial (Table 3).
Significant group difference existed in the posttreatment
%O2 peak and energy expenditure (kJ/min) during the time trial, after controlling for
baseline level.
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O2 and average nonprotein RER
during the time trial (Table 3) after McArdle et al. (21). A multiple
linear regression analysis was conducted to examine the effect of
treatment group on posttreatment energy expenditure, with average work
rate and pretreatment energy expenditure rate during the time trial as
covariates. This analysis revealed a significant group difference in
the rate of energy expenditure during the posttreatment time trial
(P < 0.05). The regression
coefficient was 2.0 kJ/min (P < 0.05) for the treatment group, indicating that the supplemented
group consumed 2.0 kJ/min less energy than did the placebo group at the
same work rate. On the basis of the mean time to finish in the time
trial of 30 min, iron supplementation decreased the total energy
expenditure by ~60 kJ during the posttreatment time trial in these
iron-depleted nonanemic women.
There was no significant group difference in the time to finish in the
15-km time trial, after controlling for the baseline time to finish,
and posttreatment
%O2 peak during the
time trial, which were significantly correlated with the time to
finish. Final Hb concentration was significantly and negatively
associated with posttreatment time to finish, after controlling for
baseline time and posttreatment
%O2 peak during the
time trial (P = 0.042, partial
r = 0.366). A 10 g/l increase in final
Hb resulted in 0.89-min decrease in time to finish the time trial.
Figure 1 illustrates this
negative relationship between posttreatment time to finish the time
trial and final Hb concentration.
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O2, and RER throughout
the time trial before and after iron treatment. Multiple linear
regression analysis, controlling for baseline levels and work rate, did
not reveal a significant treatment effect on average
O2, heart rate, and RER
during the time trial.
To further analyze the observed group difference in
posttreatment %O2 peak
during the time trial, multiple regression analysis was
conducted with posttreatment
%O2 peak as a
dependent variable, controlling forpotential confounders (Table
4). Because
%O2 peak during the
time trial was expected to be associated with work rate and fitness
level of the subject, absolute work rate during the time trial and
habitual PA level of the subjects during the treatment were tested as
potential confounders. Only work rate was found to be correlated with
%O2 peak during the
time trial, and it was included as a covariate in all models. To avoid
collinearity, baseline work rate during the time trial was not included
in the models. The group difference in final
%O2 peak
was still significant after controlling for baseline
%O2 peak and work rate
during the time trial (P = 0.016, model 1). The iron-treated group was consuming oxygen relative to
O2 peak at a 5.1%
lower rate than was the placebo group, after controlling for baseline
%O2 peak and
work rate.
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O2 peak during time
trial, after controlling for baseline
%O2 peak and average
work rate during the time trial (P = 0.004, partial r = 0.493). Figure
2 illustrates this
significant relationship between posttreatment
%O2 peak during the
time trial and change in Hb concentration. The interaction between change in Hb and iron treatment on
%O2 peak was not found
to be significant.
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O2 peak
(O2/O2 peak)
assumes a linear relationship between the numerator and the denominator
with an intercept of zero (31), multiple regression analysis was also
conducted by using average O2
during the time trial as the dependent variable, controlling for
O2 peak and work rate.
The results were essentially the same as using %O2 peak as a
dependent variable (results not shown).
Table 5 presents the mean
plasma glucose and lactate concentrations measured during the time
trial. There was some variation in the glucose
concentration during the time trial within each group, but there was no
significant group difference before and after treatment. At
pretreatment, there was no significant group difference for all the
lactate concentrations measured. As expected, the preexercise lactate
concentrations were significantly lower than those during the time
trial (P < 0.05).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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After 8 wk of iron treatment, iron-depleted subjects were able to replenish their body iron stores as indicated by increased mean sFer concentration, and to decrease tissue iron deficiency as indicated by decreased mean sTf R concentration. This improvement in iron status occurred without an increase in mean Hb concentration, indicating that these subjects as a group were not anemic at the beginning of the study. On the other hand, the iron supplementation prevented a further deterioration of iron status, as evidenced by the decrease in mean Hb concentration in the placebo group.
Endurance capacity and cardiorespiratory responses during the time
trial.
Although the time to finish the time trial was not affected by iron
treatment, iron supplementation resulted in a 2.0 kJ/min lower energy
expenditure and a 5.1% lower
%O2 peak compared with
the placebo group, after controlling for work rate during the 15-km
time trial. This means that after 8 wk of supplementation, the
iron-supplemented group was able to exercise at the same intensity as
did the placebo group with a lower level of physical exertion and
became more energetically efficient. They consumed ~60 kJ less total
energy than did the placebo group, to complete the 15 km in the same
time and with the same work rate. These findings are consistent with
the smaller 3% decrease in
%O2 peak during a
time-to-exhaustion test observed by LaManca and Haymes (16) in mildly
anemic subjects who received a similar 8-wk iron-treatment regimen.
O2 peak should not
have been due to difference in motivation between iron-supplemented and
placebo groups, unless iron treatment affects motivation. To our
knowledge, no evidence exists to indicate such an effect.
The negative associations between Hb concentration and posttreatment
time to finish the time trial or
%O2 peak
observed in the present study suggest that oxygen transport capacity of the blood may be one of the mechanisms that determine endurance capacity and energetic efficiency in these nonanemic women. In the
study by LaManca and Haymes (16), the group difference in %O2 peak was
accompanied by an increase in Hb concentration of the iron-supplemented
group, suggesting that the treatment effect on
%O2 peak was probably
associated with change in Hb concentration. Unfortunately, those
authors did not report the association between
%O2 peak and Hb
concentration.
Reduced oxygen transport capacity has been demonstrated to be the major
cause of reduced endurance capacity in anemia. Celsing et al. (4) have
shown that time to exhaustion was decreased in an anemic state induced
by repeated venesections, and the time to exhaustion could be increased
dramatically in a few days after blood transfusion. The negative
relationship between Hb and time to finish the time trial observed in
the present study further indicates that even in iron deficiency
without anemia, oxygen transport capacity is still an important
determinant of endurance capacity.
Plasma lactate and glucose concentrations during the time trial. In the present study, we observed a significant and negative association between posttreatment Hb concentration and lactate concentration at the end of the first 5 km of the time trial, after controlling for work rate and pretreatment level of lactate, indicating that plasma lactate concentration is inversely related to oxygen transport capacity of the blood. Plasma lactate concentration is the function of lactate production and removal rates. In humans, lactate is primarily produced by glycolysis and is removed during exercise by aerobic oxidation in exercising and nonexercising muscles (2, 30). An increase in oxygen-transport capacity may increase aerobic oxidative capacity, causing either a decrease in lactate production or an increase in lactate oxidation, or both. This mechanism may explain the decreased lactate concentration after iron supplementation in iron-deficient mildly anemic subjects (16, 19, 29), because the reduction in lactate concentration in these previous studies was accompanied by an increase in Hb concentration. However, the association between the decreased lactate concentration and the increase in Hb concentration was not reported by any of these authors. The inverse relationship between plasma lactate and Hb concentrations observed in the present study strongly supports a role of oxygen transport capacity on lactate metabolism, even in marginal iron deficiency.
The lack of treatment effect on lactate concentration measured at the later stages of the time trial may be due to a ceiling effect. Toward the end of the time trial, lactate concentration was reaching a plateau, indicating that lactate metabolism had progressed toward a steady state. Therefore, the margin remaining for improvement by iron treatment was probably inadequate to allow the influence of iron status to be observed beyond the 5th km. We did not observe a treatment effect on glucose concentration. This result should be expected, because euglycemia is well maintained in normal healthy people until glycogen stores are depleted (33). Therefore, glucose concentration is unlikely to be affected by iron status and the exercise test in these subjects, who were not starved and should have adequate glycogen stores at the time of the testing. Whether the maintenance of euglycemia may be affected by iron deficiency after glycogen depletion needs further investigation. In summary, Hb concentration is found to be associated with three major physical performance variables in this study: time to finish the time trial, %O2 peak during
the time trial, and plasma lactate concentration at 5th km of the time
trial. This association was not observed before treatment, probably due
to the small variation in Hb concentration at baseline. After the 8-wk
study, the placebo group decreased their mean Hb concentration, causing
a broader range of final Hb concentration, which possibly enabled us to
observe the effect of Hb on physical performance. At the end of the
study, the placebo group was probably borderline anemic and became
energetically less efficient than the iron-supplemented group, even
though the mean final Hb concentration of the placebo group was still
much higher than the clinical cutoff for anemia. In other words,
individuals with Hb as high as 132 g/l may still be functionally
anemic, having a Hb concentration that is not sufficient for optimal
physical performance in stressful situations such as a 15-km time
trial.
The negative association between Hb concentration and physical
performance in nonanemic subjects observed in the present study also
indicates that the Hb effect is continuous rather than threshold bound.
The conventional use of a cutoff to identify anemia assumes a threshold
effect of Hb on functional outcomes and thereby results in
misclassification. In addition, these data indicate that a cutoff value
of Hb concentration for functional anemia may be much higher than 120 g/l for premenopausal women when their oxygen delivery system is
stressed.
In conclusion, within the limitations of the present study, iron
depletion without anemia was not found to affect endurance capacity as
measured by the time to finish in a 15-km time trial on a cycle
ergometer. However, after iron supplementation, the rate of energy
expenditure and the
%O2 peak during the
time trial were lower in the iron-supplemented group compared with the
placebo group, after controlling for absolute work rate. This indicates
that iron depletion without anemia could increase the level of exertion
and energy cost to achieve the same work rate. In addition, Hb
concentration was found to be negatively associated with time to
finish in the time trial,
%O2 peak during the
time trial and lactate concentration at the early stage of the time trial. Therefore, oxygen transport capacity was found to play an
important role in determining endurance capacity, energetic efficiency,
fractional utilization of
O2 peak, and lactate
metabolism, even in marginally iron-deficient women who are not
considered to be anemic by classic criteria.
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ACKNOWLEDGEMENTS |
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The authors acknowledge the help of Linda H. Bennett and Dr. Wesley K. Canfield.
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FOOTNOTES |
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This study was supported by US Department of Agriculture Grant 9500850 and by a Graduate Research Grant from the Division of Nutritional Sciences, Cornell University.
Present address of Y. I. Zhu: College of Physicians and Surgeons of Columbia University, Box 324, 630 W. 168th Street, New York, NY 10032 (E-mail yiz1{at}columbia.edu).
Address for correspondence: J. D. Haas, 211 Savage Hall, Cornell University, Ithaca, NY 14853 (E-mail jdh12{at}cornell.edu).
Received 23 June 1997; accepted in final form 21 January 1998.
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REFERENCES |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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, Placebo group; 
,
iron-supplemented group.
