The effects of the menstrual cycle on cardiorespiratory variables, blood lactate, and performance were studied in exercising females. Nine healthy subjects, 20--24 yr of age, were investigated in midfollicular and midluteal phases of the menstrual cycle at 33, 66, and 90% of maximum power output (light, heavy, and exhaustive exercise). Occurrence of ovulation was confirmed in all subjects by measurement of progesterone, which increased from 0.6 +/- 0.1 (mean +/- SE) in the follicular to 8.9 +/- 2.2 ng/ml in the luteal phase. There was no difference in heart rate (HR), ventilation, O2 uptake, or CO2 output between the two phases during light and heavy exercise, and there was no difference in HR at exhaustion. Cardiac output measured midway through light and heavy exercise periods was not affected by the phase of testing. Time for which exhaustive exercise could be maintained increased from 1.57 +/- 0.32 in the follicular to 2.97 +/- 0.63 min in the luteal phase (P less than 0.02). Blood lactate was higher in the follicular phase after heavy exercise (6.62 +/- 0.8 vs. 4.92 +/- 0.5 mmol/l) (P less than 0.05) and at exhaustion (8.12 +/- 0.9 vs. 6.76 +/- 0.6 mmol/L) (P less than 0.01). A further study showed no effect of cycle phase on lactate disappearance during exercise. We conclude that while aerobic performance and the cardiorespiratory adaptations to exercise are not influenced by the phase of the menstrual cycle, performance of high-intensity exercise is improved, and lactate production appears to be decreased in the luteal phase when estradiol and progesterone levels are elevated.
To provide a description of the metabolic changes in muscle during maximal dynamic exercise, muscle biopsies were obtained in five healthy subjects before and after 30 s of isokinetic exercise at two pedaling frequencies (60 and 140 rpm) associated with contrasting fatigue characteristics. Higher peak power was attained at 140 rpm (1,473 + 185 W) (mean +/- SE) than at 60 rpm (1,122 +/- 70 W), but the decline in power during 30 s (fatigue index) was greater at 140 rpm (61.6 +/- 3.2 vs. 21.5 +/- 2.4%), total work in 30 s being similar (18.1 +/- 1.10 vs. 20.1 +/- 1.10 kJ). Changes in the concentration of muscle metabolites were similar; creatine phosphate concentration fell to approximately 50% of resting values, and the glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, and fructose 1,6-biphosphate increased up to 30-fold. Muscle lactate concentration ([La-]) was 29.0 +/- 3.98 and 31.0 +/- 4.31 mmol/kg wet wt immediately postexercise at 140 and 60 rpm, respectively. Even after only 10 s exercise (n = 2), large increases were measured in glycolytic intermediates and [La-]. In the two subjects, muscle [La-] increased to 17.2 and 15.1 mmol/kg at 140 rpm and to 14.3 and 14.2 mmol/kg at 60 rpm. In this type of exercise, glycogenolysis is activated very rapidly at both pedal speeds; the changes in glycolytic intermediates were consistent with rate-limiting steps at the phosphofructokinase and pyruvate dehydrogenase reactions. The greater fatigue at the higher speed is not accompanied by different biochemical changes than at 60 rpm.
Five healthy males performed four 30-s bouts of maximal isokinetic cycling with 4 min rest between each bout. Arterial and femoral venous blood was sampled during and for 90 min following exercise. During exercise, arterial erythrocyte [K+] increased from 117.0 +/- 6.6 mequiv./L at rest to 124.2 +/- 5.9 mequiv./L after the second exercise bout. Arterial erythrocyte [K+] returned to the resting values during the first 5 min of recovery. No significant change was observed in femoral venous erythrocyte [K+]. Arterial erythrocyte lactate concentration ([Lac-]) increased during exercise from 0.2 +/- 0.1 mequiv./L peaking at 9.5 +/- 1.5 mequiv./L at 5 min of recovery, after which the values returned to control. Femoral venous erythrocyte [Lac-] changed in a similar fashion. Arterial erythrocyte [Cl-] rose during exercise to 76 +/- 3 mequiv./L and returned to resting values (70 +/- 2 mequiv./L) by 25 min recovery. During exercise there was a net flux of Cl- into the erythrocyte. We conclude that erythrocytes are a sink for K+ ions leaving working muscles. Furthermore, erythrocytes function to transport Lac- from working muscle and reduce plasma acidosis by uptake of Cl-. The erythrocyte uptake of K+, Lac-, and Cl- helps to maintain a concentration difference between plasma and muscle, facilitating diffusion of Lac- and K+ from the interstitial space into femoral venous plasma.
Five male subjects performed two graded exercise studies, one during control conditions and the other after reduction of muscle glycogen content by repeated maximum exercise and a high fat-protein diet. Reduction in preexercise muscle glycogen from 59.1 to 17.1 mumol X g-1 (n = 3) was associated with a 14% reduction in maximum power output but no change in maximum O2 intake; at any given power output O2 intake, heart rate, and ventilation (VE) were significantly higher, CO2 output (VCO2) was similar, and the respiratory exchange ratio was lower during glycogen depletion compared with control. The higher VE during glycogen depletion was associated with a higher VE/VCO2 ratio, lower end-tidal and mixed venous CO2 partial pressures, and higher blood pH than in the control studies. Changes in exercise VE accompanying glycogen depletion were not explained by changes in CO2 flux to the lungs suggesting that other factors served to modulate VE in these experimental conditions.
This study compared plasma volume (PV) and ion regulation during prolonged exercise in control vs. glycogen-depleted (GD) conditions, with emphasis on the initial minutes of exercise. In two trials separated by 1-2 wk, four adult males cycled at 75% of peak oxygen consumption (VO2) until exhaustion (50 +/- 7 min for GD) or until the GD exhaustion time in the control trial. Blood was sampled from catheters placed in the brachial artery and retrograde in the femoral vein (fv). Arterial PV decreased rapidly and by 15 min PV was 83% (control) and 88% (GD) of initial. The decrease in PV was accompanied by a net osmotic flux of water from plasma and inactive tissues to contracting muscles. The significantly greater decrease in PV in control compared with GD was associated with a higher muscle lactate content (Lac-; 36 vs. 17 mumol/g dry wt, respectively). Increases in plasma [Cl-] and [Na+] were less than predicted from decreased PV, indicating net loss of these ions from the plasma compartment. Increases in arterial and fv [K+] were 50% greater than could be accounted for by decreased PV, corresponding with increased arterial and fv plasma K+ contents. The rapid net release of K+ and Lac- from contracting muscle during the first few minutes of exercise in both trials was abolished (control) or reversed (GD) within 15 min of beginning exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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