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Published in final edited form as: Biol Sport. 1994;11(4):241–248.

EFFECT OF THE MENSTRUAL CYCLE PHASE AND DIET ON BLOOD LACTATE RESPONSES TO EXERCISE

JZ Berend 1, MR Brammeier 1, NA Jones 1, SC Holliman 1, AC Hackney 1,2
PMCID: PMC7905774  NIHMSID: NIHMS1668674  PMID: 33642675

Abstract

Previous research has shown women on normal mixed diets have varied blood lactate (LA) responses to exercise across their menstrual cycle (MC) phases. This study examined the effect of diet on this finding. Eurmenonrheic women (n=10) completed a discontinuous exercise protocol consisting of 4 intervals of 6 min exercise, separated by 6 min rest, at 30, 50, 70 and 90% V̇O2max. The exercise was performed after a 3 day pen od under each of the following conditions: 1 - low carbohydrate (35% of total caloric intake) - mid-follicular phase (LCHO-FP), 2 - low carbohydrate - mid-luteal phase (LCHO-LP), 3 - high carbohydrate (75%) - mid-follicular phase (HCHO-FP), 4 - high carbohydrate - mid-luteal phase (HCHO-LP). Eucaloric status was maintained during the study. The MC phase was confirmed by blood hormonal levels. Significant (P<0.05) MC phase - diet interaction effects were found. LA was lower at 70% V̇O2max in the LCHO-LP (3.7±0.2 mmol·l−1) than at the other conditions (5.0±0.7 to 6.0±0.7 mmol·l−1; mean ±SEM). Also, LA during LCHO-LP at rest and all other exercise intensities tended to be lower than all other MC phase/diet conditions (P<0.06). LA responses at rest and during exercise in the HCHO-LP, HCHO-FP, and LCHO-FP conditions did not differ significantly. The present findings demonstrate that an “athletic type diet”, high in carbohydrates, negates the menstrual cycle phase difference in lactate responses to exercise previously reported in the literature; however, the menstrual phase differences do exist when a diet low in carbohydrates is consumed.

Keywords: Menstrual cycle, Diet, Exercise, Lactate

Introduction

The magnitude of changes in blood lactate in response to exercise has been suggested to be a sensitive metabolic marker of exercise intensity and an index quanifying training effects. Research has shown that there is a higher correlation between lactate response and performance than with some other physiological variables (e.g., heart rate, rating of perceived exertion) [5,9,18,29], For this reason, some sports have adopted lactate monitoring as a means of assessing the athlete’s physiological status.

In eurmenorheic women during the luteal phase of the menstrual cycle, when blood estrogen levels are elevated, there is a greater lipid than carbohydrate (CHO) usage as an energy substrate when compared to the follicular phase [4,11]. This shift in metabolism results in less lactate production in response to exercise during the luteal phase of the menstrual cycle [12]. Furthermore, research indicates muscle glycogen sparing when the levels of estradiol and progesterone are elevated, thus further increasing the reliance on lipids as an energy source in metabolism [10,13,16,24].

In men, the pre-exercise carbohydrate ingestion is know to influence glycogen stores and blood lactate response to exercise [1,14]. For example, the “carbohydrate loading” procedure can increase muscle glycogen stores to twice that found with a normal mixed (50 – 60% CHO) diet [6] and this procedure results in increased blood lactate responses to exercise [15,28]. On the contrary, men on a diet high in fat and protein have depleted muscle glycogen stores which can result in decreased blood lactate concentration after absolute and relative submaximal exercise intensities [2,15,21]. For women, the studies demonstrating that the lactate response to exercise varies across a menstrual cycle, have examined subjects who were consuming normal diets with approximately 50 – 60% of their caloric intake comprised of carbohydrate. Athletes, however, are known to typically consume more than 70% of their caloric intake in carbohydrates.

With this in mind, the purpose of this study was to examine the influence of a diet high in carbohydrates (“athletic type”), versus a low-carbohydrate diet, during the mid-follicular and mid-luteal phases of the menstrual cycle, on blood lactate concentration at rest and in response to increasing submaximal exercise intensities in eurmenorrheic women.

Material and Methods

Ten eumenorrheic, moderately active women with regular menstrual cycles for at least six consecutive months prior to the exercise testing, gave their written consent to be studied. The physical characteristics of the subjects were as follows (means ±SD):age, 26.7±3.2 years; height, 174.1±3.9 cm; weight, 68.2±9.3 kg and percent body fat, 20.9±6.0%.

Each subject completed a cycle ergometer (Monark 864, Sweden) VO2max test using a standard laboratory protocol (details reported elsewhere [22]). During the four subsequent experimental trials each subject performed a discontinuous submaximal exercise protocol (cycle ergometer) of 4 stages, involving alternating exercise (6min) and rest (6 min), at intensities of 30, 50, 70 and 90% VO2max. The workloads required to elicit the desired intensities were calculated from regression analysis of the VO2max test results. At each of the four submaximal exercise trials the workloads for each respective intensity were held constant.

During each of the submaximal exercise trials the following physiological variables were monitored: heart rate (via ECG), minute ventilation, oxygen consumption (VO2), and carbon dioxide produced (VCO2). The latter data have been reported elsewhere in relation to another aspect of our study [3].

Each submaximal exercise trial was conducted under a different combination of menstrual cycle and diet treatments (administered in a random order) which were as follows: low carbohydrate (~35% of total caloric intake)/mid-follicular (LCHO-FP), high carbohydrate (~75% of total caloric intake)/mid-follicular (HCHO-FP), low carbohydrate/mid-luteal (LCHO-LP) and high carbohydrate/mid-luteal (HCHO-LP). All dietary treatments were applied for the 3 days preceding the exercise trials in each menstrual cycle phase. In all situations, the variation of the diets was within 3% of the desired macronutrient intake mean. Total energy intake (kcal/day) varied slightly, but was not significantly different across the four exercise trials. The dietary intake data appear in Table 1.

Table 1.

Percent composition of the diet of the three-day manipulation before each exercise test in the follicular (FP) and luteal (LP) phases (means ± SD)

High Carbohydrate Diet Low Carbohydrate Diet
FP LP FP LP
CHO 74.7±4.9 72.4±9.8 32.4±3.0 35.8±3.7
Fat 14.8±3.5 18.1±6.7 52.1±2.0 49.3±7.0
Protein 11.1±0.7 11.0±1.6 15.6±4.8 14.8±3.7
Kcal 2524.4±545.7 2535.6±511.5 2389.2±479.5 2426.8±415.6

Diet was controlled by using self-reporting by five subjects who prepared own meals, while the remaining five subjects used a controlled setting in which their meals were prepared in the UNC Research Kitchen at the University Hospital. Prior to and at the time of the study the menstrual cycle phase was monitored by oral temperature records (for about 3 months) and urinary hormone levels, and later confirmed by resting blood estrogen and progesterone levels at the time of submaximal exercise trials. During the submaximal exercise tests blood was drawn from intravenous catheters placed in the antecubital vein. Blood samples were taken at rest (45 min after catheter placement) and during the last 45 s of each of the 6 min rest periods following the exercise bouts. Resting and exercise blood samples were assayed for lactate (assay kits from Kodak Ektachem, Rochester, NY, USA), hemoglobin, and hematocrit. Estrogen and progesterone were measured only in the resting blood by standard radioimmunoassay procedures (assay kits from DPC, Los Angeles, CA, USA).

Statistical analysis was performed with a 2 (diet) × 2 (cycle phase) × 5 (sampling time) repeated measurements ANOVA, the level of P= 0.05 being considered significant. The Fisher LSD post-hoc test was used to determine the nature of the significance. All lactate data are reported as means ± SEM.

Results

The blood hormone concentrations confirm that the subjects were in the desired phase of the menstrual cycle (estrogens: LCHO-FP − 45±61; HCHO-FP − 52±74; LCHO-LP − 276±180; HCHO-LP − 295±150 pg·ml−1; progesterone: LCHO-FP – 22±30; HCHO-FP − 31±46; LCHO-LP – 903±51; HCHO-LP − 1056±598 ng·ml−1).

Significant main effects for diet and for the menstrual phase were found (P<0.05). The low-CHO diet was found to result in lower blood lactate levels at rest and in response to exercise as compared to the high-CHO diet. Furthermore, luteal phase of the cycle was associated with lower resting and post-exercise lactate levels than the follicular phase.

The most important statistical finding relative to the purpose of this study was a significant (P<0.04) interaction of the menstrual cycle phase and the diet. Lactate was significantly lower at 70% V̇O2max in the LCHO-LP than in other combinations (i.e. LCHO-FP, HCHO-LP and HCHO-FP at 70% V̇O2max). Also, lactate in LCHO-LP at rest and at all exercise intensities tended to be lower than in other menstrual cycle phase-diet conditions (P<0.06). However, lactate responses at rest and during exercise in the HCHO-LP, HCHO-FP, and LCHO-FP conditions did not differ from one another. These results are shown in Table 2.

Table 2.

Plasma lacate concentrations (mmol·l−1) at rest and following exercise at 30, 50, 70 and 90% of V̇O2max in women at different diet-menstrual cycle phase combinations

Diet and menstrual phase V̇O2max (%)
Rest 30 50 70 90
LCHO-LP 1.1±0.1 1.2±0.1 1.6±0.1 3.7±0.1 10.5±0.5
HCHO-LP 1.2±0.1 1.4±0.1 2.0±0.2 5.0±0.7 9.7±1.2
LCHO-FP 1.3±0.1 1.5±0.1 2.2±0.1 6.0±0.7 10.8±0.9
HCHO-FP 1.2±0.1 1.4±0.1 2.1±0.2 5.1±0.7 10.4±0.9

LCHO-LP – Luteal phase-low carbohydrate diet; HCHO-LP – Luteal phase-high carbohydrate diet; LCHO-FP – Follicular phase-low carbohydrate diet; HCHO-FP – Follicular phase-high carbohydrate diet

The results of hematocrit and hemoglobin appear in Table 3. An expected hemoconcentration of the blood (P<0.001) occurred through the progression from rest to exercise at 90% V̇O2max in all experimental exercise trials [8]. However, no significant differences between the hematocrit and hemoglobin responses were observed due to the menstrual cycle phase or diet conditions.

Table 3.

Mean (±SD) values of hematocrit (HCT) and hemoglobin (HGB; g·dl−1) at rest and following exercise at 30, 50, 70 and 90% of V̇O2max in women at different diet-menstrual cycle phase combinations

Diet-cycle % V̇O2max
phase Variable Rest 30 50 70 90
FP
 HCHO HCT 38.8±1.0 38.9±0.8 39.5±0.8 41.1±1.1 42.0±0.9
HGB 12.5±0.2 12.3±0.3 12.6±0.6 13.5±0.6 13.6±0.6
 LCHO HCT 38.6±1.4 39.1±0.6 38.8±1.6 39.1±2.5 42.2±0.6
HGB 13.1±0.5 13.5±0.2 13.3±0.7 13.4±0.6 14.1±0.4
LP
 HCHO HCT 39.5±0.8 39.8±0.2 39.9±0.3 41.9±1.1 42.8±1.2
HGB 12.4±0.6 12.6±0.3 12.7±0.4 13.5±0.7 13.6±0.6
 LCHO HCT 39.0±1.6 39.6±0.5 40.6±0.6 41.2±1.8 43.2±0.8
HGB 12.6±0.9 13.1±0.6 12.9±0.8 13.5±0.6 13.9±0.9

For explanation of symbols see Table 2

Discussion

For the low-CHO diet/luteal phase trial after the exercise at 70% V̇O2max, blood lactate levels were found to be significantly lower than at the other three menstrual cycle phase/diet conditions. The observed differences in lactate concentrations at 70% V̇O2max did not seem to be a function of differences in hemoconcentration, as exercise-induced changes in hemo-globin and hematocrit were comparable regardless of menstrual cycle phase/diet conditions. We speculate that the effect of the higher estradiol levels during the luteal phase in combination with higher lipid availability (produced by the low-CHO diet manipulation), worked together to produce the decreased blood lactate levels after the 70% V̇O2max exercise. The present findings demonstrate that an “athletic type diet” high in carbohydrates negates the menstrual cycle phase difference in lactate responses to exercise previously reported [12]; however, the menstrual phase differences do exist when a diet low in carbohydrates is consumed.

Research indicates elevated estrogen levels stimulate an increase in lipolytic activity both directly (activation of lipase) and indirectly (via augmenting growth hormone release [4]) and seems to facilitate an enhanced lipid mobilization and utilization over that of carbohydrate [4,11,16,19,20]. Therefore, less glucoṡe and glycogen are converted to lactate. In the present data this hypothesis is supported by the respiratory exchange ratio (RER) results which showed that during the LCHO-LP, 70% VO2max exercise trial, the RER tended to be lower than in other conditions (LCHO-LP − 0.89±0.01 vs. 0.90±0.01, 0.93±0.01 and 0.91±0.02 for HCHO-LP, HCHO-FP, and LCHO-FP, respectively). These data have been reported elsewhere [3].

The present lactate findings are in disagreement with the study of De Souza et al. [7] who found no difference in lactate responses to exercise in the follicular and luteal phases. However, in that study no control for pre-exercise diet occurred, and the blood sampling and the protocol for exercise intensity - duration varied from that of the present study. Thus, a direct comparison with the present findings of this study is difficult.

In summary, both menstrual cycle phase (i.e. hormonal status) and dietary carbohydrate consumption seem to influence substrate utilization and thus blood lactate responses in women. However, the high-CHO diet seemed to override the hormonal phases differences in the blood lactate concentration that was observed. The implication of this finding is extremely important since in the lactate profiling procedure of athletes (to monitor exercise intensity), blood lactate concentrations at intensities at or around the anaerobic threshold (~65–90% V̇O2max [26]) are critical with respect to determining an optimal training load [5,9,17,23,25,27,29]. Fortunately, the findings from the present study also indicate that when eumenorrheic women consume a high-CHO diet, the hormonal phase effect on lactate concentration is not significant at 70% V̇O2max. Therefore, if physically active women consume a high-CHO diet, lactate measurements seem to be a valid standard for measuring training status and for accurately monitoring performance intensity.

Acknowledgments:

This research was supported in part by NIH grant RR00046 and by Tambrands Inc., Lake Success, NY.

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