Effects of oral contraceptives on peak exercise capacity.

We examined the effects of menstrual cycle phase and oral contraceptive (OC) use on peak oxygen consumption (VO(2 peak)). Six moderately active, eumenorrheic women (25.5 +/- 1.5 yr) were studied before and after 4 mo of OC. Subjects were tested during the follicular and luteal phases before OC and the inactive and high-dose phases after OC. Before OC, there were no significant differences between the follicular and luteal phases in any of the variables studied. There were also no differences between the inactive and high-dose phases. Dietary composition, exercise patterns, and peak heart rate, minute ventilation, and respiratory exchange ratio did not change with OC use. However, OC use significantly (P 相似文献   

Substrate and hormonal responses to exercise in women using oral contraceptives

Hormone and substrate responses to mild and heavy treadmill exercise were compared in women who used oral contraceptives (OC group; n = 7) and in normally menstruating women (control group; n = 8). Venous blood samples were obtained before exercise (-5 min), during exercise (15, 30, 45, and 60 min), and 30 min after exercise. All samples were analyzed for glucose, lactate, free fatty acids (FFA), glycerol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), human growth hormone (hGH), cortisol, insulin, estradiol (E2), and progesterone (P). Substrate patterns during exercise were not altered by the phase of the menstrual cycle or OC usage. However, in the OC group the FFA concentrations were consistently higher during mild exercise and the glucose concentrations were lower at rest and during exercise than in the control group (P less than 0.05). No differences in lactate or glycerol responses were observed between the groups (P greater than 0.05). The responses of insulin and hGH to exercise were not related to the OC use per se but rather to the steroid status, either endogenous or exogenous. Specifically, during the steroid phases (OC use phase and luteal phase) 1) insulin concentrations were not quite as markedly reduced (i.e., 12% higher when luteal phase and OC usage phase data were combined; P less than 0.05), and 2) hGH concentrations at rest and during light exercise were higher in the OC group during the OC use phase (P less than 0.05). LH patterns were not affected by exercise (P greater than 0.05), but a slight decrease was found in FSH (P less than 0.05). Increments in P and E2 were observed in the control group in both the follicular and luteal phase (P less than 0.05), but much greater increments in P occurred in the luteal phase than in the follicular phase (P less than 0.05). In contrast to the control group, no increments in P, E2, or cortisol occurred in the OC users during exercise (P greater than 0.05). Therefore the new observations in this study are that 1) insulin and growth hormone respond in a complex manner during exercise with either the phase of the menstrual cycle or the phases of OC use and disuse and 2) the steroid concentrations (P, E2, cortisol) are increased in the controls but not in the OC users during exercise. The latter point suggests that normal steroid increments are due to an increased rate of secretion rather than a decrease in the hepatic clearance of these steroids.(ABSTRACT TRUNCATED AT 400 WORDS)     

Menstrual cycle phase dissociation of blood glucose homeostasis during exercise

The purpose of this investigation was to evaluate the effects of 24-h carbohydrate-poor diet on metabolic and hormonal responses induced by prolonged exercise in both follicular (FP) and luteal (LP) phases of the menstrual cycle. At mid-FP and at mid-LP, seven eumenorrheic young women [means +/- SE; chronological age, 21.1 +/- 0.6 yr; O2 uptake (VO2) peak, 43.7 +/- 2.0 ml X kg-1 X min-1; body fat, 19.2 +/- 2.0%] were subjected to a 90-min bicycle exercise period at an intensity representing 63% of their measured VO2 peak. Venous blood samples obtained before and during exercise were analyzed for levels of substrates (glucose, lactate, free fatty acids, glycerol) and hormones (luteinizing hormone, progesterone, estradiol, insulin, glucagon, cortisol, catecholamines). Contrary to FP, a significant (P less than 0.01) decrease in blood glucose concentration was observed after 70 and 90 min of exercise during LP. Significant phase differences were also observed for blood lactate (highest in FP), cortisol (highest in LP), and progesterone (highest in LP). Although not significantly different, tendencies for menstrual phase dissociations were noticed for some of the other measured variables. Hence, a menstrual phase dissociation in circulating glucose level, unmasked by a prolonged exercise performed after a 24-h carbohydrate-poor diet, suggests to the authors a specific metabolic involvement for gonadotrophic and/or gonadal hormones.     

Menstrual status and plasma vasopressin, renin activity, and aldosterone exercise responses

The effects of menstrual cycle phase (early follicular vs. midluteal) and menstrual status (eumenorrhea vs. amenorrhea) on plasma arginine vasopressin (AVP), renin activity (PRA), and aldosterone (ALDO) were studied before and after 40 min of submaximal running (80% maximal O2 uptake). Eumenorrheic runners were studied in the early follicular and midluteal phases determined by urinary luteinizing hormone and progesterone and plasma estradiol and progesterone assays; amenorrheic runners were studied once. Menstrual phase was associated with no significant differences in preexercise plasma AVP or PRA, but ALDO levels were significantly higher during the midluteal phase than the early follicular phase. Plasma AVP and PRA were significantly elevated at 4 min after the 40-min run in the eumenorrheic runners during both menstrual phases and returned to preexercise levels by 40 min after exercise. Plasma ALDO responses at 4 and 40 min after exercise were higher in the midluteal phase than the early follicular phase. Menstrual status was associated with no significant differences in preexercise AVP or PRA; however, ALDO levels were significantly higher in the amenorrheic runners. After exercise, responses in the amenorrheic runners were comparable with the eumenorrheic runners during the early follicular phase. Thus, submaximal exercise elicits significant increases in plasma AVP and PRA independent of menstrual phase and status. However, plasma ALDO is significantly elevated during the midluteal phase, exercise results in a greater response during this menstrual phase, and amenorrheic runners have elevated resting levels of ALDO.     

Exercise VE and physical performance at altitude are not affected by menstrual cycle phase.

We hypothesized that progesterone-mediated ventilatory stimulation during the midluteal phase of the menstrual cycle would increase exercise minute ventilation (VE; l/min) at sea level (SL) and with acute altitude (AA) exposure but would only increase arterial O2 saturation (SaO2, %) with AA exposure. We further hypothesized that an increased exercise SaO2 with AA exposure would enhance O2 transport and improve both peak O2 uptake (VO2 peak; ml x kg-1 x min-1) and submaximal exercise time to exhaustion (Exh; min) in the midluteal phase. Eight female lowlanders [33 +/- 3 (mean +/- SD) yr, 58 +/- 6 kg] completed a VO2 peak and Exh test at 70% of their altitude-specific VO2 peak at SL and with AA exposure to 4,300 m in a hypobaric chamber (446 mmHg) in their early follicular and midluteal phases. Progesterone levels increased (P < 0.05) approximately 20-fold from the early follicular to midluteal phase at SL and AA. Peak VE (101 +/- 17) and submaximal VE (55 +/- 9) were not affected by cycle phase or altitude. Submaximal SaO2 did not differ between cycle phases at SL, but it was 3% higher during the midluteal phase with AA exposure. Neither VO2 peak nor Exh time was affected by cycle phase at SL or AA. We conclude that, despite significantly increased progesterone levels in the midluteal phase, exercise VE is not increased at SL or AA. Moreover, neither maximal nor submaximal exercise performance is affected by menstrual cycle phase at SL or AA.     

Determination of maximal aerobic power during upper-body exercise

The purpose of this investigation was to evaluate four protocols for their effectiveness in eliciting maximal aerobic power (peak VO2) during arm-crank exercise. Comparisons were made 1) between a continuous (CON) and an intermittent (INT) protocol (both employed a crank rate of 50 rpm) and 2) among the CON protocols employing crank rates of 30, 50, or 70 rpm. For the first group of experiments no significant (P greater than 0.05) differences were found between the CON and INT protocols for peak VO2, maximal pulmonary ventilation (VEmax), maximal heart rate (HRmax), or maximal blood lactate (LAmax) responses. For the second group of experiments, the CON-50 was compared with the CON-30 and CON-70 protocols. In comparison to the CON-50, significantly higher peak VO2 (+10%) and VEmax (+14%) responses were elicited by the CON-70 protocol, whereas significantly lower peak VO2 (-11%), VEmax (-23%), HRmax (-8%), and LAmax (-29%) responses were elicited by the CON-30 protocol. Of the arm-crank protocols examined the combination of a continuous design and a crank rate of 70 rpm provided the most effective protocol to elicit peak VO2 values.     

Menstrual cycle phase affects temperature regulation during endurance exercise.

We investigated whether menstrual cycle phase would affect temperature regulation during an endurance exercise bout performed at room temperature (Ta) of 22 degrees C and 60% relative humidity. Nine eumenorrheic women [age 27.2 +/- 3.7 yr, peak O2 uptake (VO2) 2.52 +/- 0.35 l/min] performed 60 min of cycle exercise at 65% of peak VO2. Subjects were tested in both midfollicular (F) and midluteal (L) phases, although one woman did not show a rise in serum progesterone (P4) that is typically evident 1 wk after ovulation. VO2, rectal (Tre) and skin (Tsk) temperatures, heart rates (HR), and ratings of perceived exertion (RPE) were measured throughout exercise. Sweat loss (SL) was estimated from pre- and postexercise body weight differences. VO2, SL, and Tsk were not affected by menstrual cycle phase. Preexercise Tre was 0.3 degrees C higher during L than during F conditions, and this difference increased to 0.6 degrees C by the end of exercise (P less than 0.01). Compared with F, HRs during L were approximately 10 beats/min greater (P less than 0.001) at all times, whereas RPE responses were significantly greater (P less than 0.01) by 50 min of cycling. No differences in any measured values were found in the subject whose P4 was low in both test conditions. Results indicate that thermoregulation (specifically, regulation of Tre), as well as cardiovascular strain and perception of exercise, was adversely affected during the L phase.     

Influence of gender, menstrual phase, and oral contraceptive use on immunological changes in response to prolonged cycling.

This study determined the influence of gender, menstrual phase (MP), and oral contraceptive (OC) use on immunological changes in response to endurance exercise. Twelve women and 11 men similar in age, aerobic power, and activity level cycled for 90 min at 65% maximal aerobic power. Women were OC users (n = 6) or nonusers (NOC) and cycled during the follicular (Fol) and the luteal (Lut) phases. Venous blood was collected before and after exercise to determine leukocyte counts, IL-6 concentrations, and cortisol. Higher resting levels of neutrophils (approximately 1.5-fold) and cortisol (approximately 2.5-fold) were found in OC vs. NOC and men. Exercise-induced immune cell count and IL-6 changes were similar between men and NOC, except for an approximately 38% greater lymphocyte response in NOC vs. men (P = 0.07). Neutrophil, monocyte, and lymphocyte responses to exercise during Lut in OC were greater than during Fol and also greater than the responses in men (P < or = 0.003). Changes in immune cell counts were consistently greater during Lut in OC vs. NOC, regardless of MP, but only neutrophil responses reached statistical significance (P = 0.01). The exercise-induced change in IL-6 was approximately 80% greater in NOC vs. OC during Fol (P = 0.06), but it was similar between these groups during Lut. Cortisol changes with exercise were not different between groups or MP. These results highlight the necessity to control for gender, and in particular OC use, when designing studies evaluating exercise and immunology.     

Rigorous running increases growth hormone and insulin-like growth factor-I without altering ghrelin

It has been suggested that ghrelin may play a role in growth hormone (GH) responses to exercise. The present study was designed to determine whether ghrelin, GH, insulin-like growth factor-I (IGF-I), and IGF-binding protein-3 (IGFBP-3) were altered by a progressively intense running protocol. Six well-trained male volunteers completed a progressively intense intermittent exercise trial on a treadmill that included four exercise intensities: 60%, 75%, 90%, and 100% of Vo2max. Blood samples were collected before exercise, after each exercise intensity, and at 15 and 30 mins following the exercise protocol. Subjects also completed a separate control trial at the same time of day that excluded exercise. GH changed significantly over time, and GH area under the curve (AUC) was significantly higher in the exercise trial than the control trial. Area under the curve IGF-I levels for the exercise trial were significantly higher than the control trial. There was no difference in the ghrelin and IGFBP-3 responses to the exercise and control trials. Pearson correlation coefficients revealed significant relationships between ghrelin and both IGF-I and IGFBP-3; however, no relationship between ghrelin and GH was found. In conclusion, intense running produces increases in total IGF-I concentrations, which differs from findings in previous studies using less rigorous running protocols and less frequent blood sampling regimens. Moreover, running exercise that produces substantial increases in GH does not affect peripheral ghrelin levels; however, significant relationships between ghrelin and both IGF-I and IGFBP-3 exist during intense intermittent running and recovery, which warrants further investigation.     

Influence of estrogen on markers of muscle tissue damage following eccentric exercise.

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill running bout at approximately 60% VO2max. The OC completed the exercise during the mid-luteal phase (day 22.9 +/- 1.5; high estrogen) while the EU did their exercise in the mid-follicular phase (day 9.6 +/- 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed pre-exercise, immediately post-, 24, 48 and 72 h post-exercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p < 0.001), and the interaction of group x time was significantly different (p < 0.01). The OC group had lower CK at 72 h post-exercise than did the EU group. Pre-exercise estrogen levels correlated with the overall mean CK (r = -0.43, p < 0.05) and 72 h (r = -0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p < 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear but may be related to the anti-oxidant characteristics and membrane stability properties associated with estrogen and its derivatives.     

Control of sweating during the human menstrual cycle

Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4-7) phase and during the luteal (L, days 19-22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (Tes), mean skin temperature (Tsk), oxygen uptake and forearm sweating (ms) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at approximately 80% VO2 peak during which the environmental chamber was controlled at Ta = 50.0 degrees C, rh = 14% (Pw = 1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at approximately 85% VO2 peak at Ta = 35 degrees C and rh = 25% (Pw = 1.4 kPa). The normal L increase in resting Tes (approximately 0.3 degrees C) occurred in all seven subjects. Tsk was higher during L than F in all experiments conducted at 50 degrees C. During exercise and passive heat exposure, the Tes threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of ms to Tes between menstrual cycle phases. This rightward or upward shift in Tes threshold for initiation of sweating averaged 0.5 degrees C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

Leukocyte, lymphocyte and platelet response to dynamic exercise. Duration or intensity effect?

The influence of work intensity and duration on the white blood cell (WBC), lymphocyte (L) and platelet (P) count response to exercise was studied in 16 trained subjects (22 +/- 5.4 years, means +/- SD). They performed three cyclo-ergospirometric protocols: A) 10 min at 150 W followed by a progressive test (30 W/3 min) till exhaustion; B) constant maximal work (VO2max); C) a 45 min Square-Wave Endurance Exercise Test (SWEET), (n = 5). Arterial blood samples were taken: at rest, submaximal and maximal exercise in A; maximal exercise in B; 15th, 30th and 45th min in the SWEET. Lactate, [H+], PaCO2, PaO2, [Hct], Hb, cortisol, ACTH, total platelet volume (TPV), total blood red cell (RBC), WBC, L and P were measured. At 150 W, WBC, L, P, and TPV increased. VO2max did not differ between A and B, but a difference was found in total exercise time (A = 25 +/- 3 min; B = 7 +/- 2 min, p less than 0.001). In A, at VO2max, the increase was very small for Hct, [Hb], and RBC (10%), in contrast with large changes for WBC (+93%), L (+137%), P (+32%), TPV (+35%), [H+] (+39%), lactate (+715%), and ACTH (+95%). At VO2max there were no differences in these variables between A and B. During the SWEET: WBC, L, P, TPV and ACTH increased at the 15th min as much as in VO2max, but no difference was observed between the 15th, 30th and 45th min, except for ACTH which continued to rise; the lactate increase during the SWEET was about half (+341%) the value observed at VO2max, and [H+] did not vary with respect to values at rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Growth hormone treatment in growth hormone-deficient adults. II. Effects on exercise performance

Growth hormone (GH) treatment in adults with GH deficiency increases lean body mass and thigh muscle cross-sectional area. The functional significance of this was examined by incremental cycle ergometry in 24 GH-deficient adults treated in a double-blind placebo-controlled trial with recombinant DNA human GH (rhGH) for 6 mo (0.07 U/kg body wt daily). Compared with placebo, the rhGH group increased mean maximal O2 uptake (VO2max) (+406 +/- 71 vs. +133 +/- 84 ml/min; P = 0.016) and maximal power output (+24.6 +/- 4.3 vs. +9.7 +/- 4.8 W; P = 0.047), without differences in maximal heart rate or ventilation. Forced expiratory volume in 1 s, vital capacity, and corrected CO gas transfer were within normal limits and did not change with treatment. Mean predicted VO2max, based on height and age, increased from 78.9 to 96.0% in the rhGH group (compared with 78.5 and 85.0% for placebo; P = 0.036). The anaerobic ventilatory threshold increased in the rhGH group (+159 +/- 39 vs. +1 +/- 51 ml/min; P = 0.02). The improvement in VO2max was noted when expressed per kilogram body weight but not lean body mass or thigh muscle area. We conclude that rhGH treatment in adults with GH deficiency improves and normalizes maximal exercise performance and improves submaximal exercise performance and that these changes are related to increases in lean body mass and muscle mass. Improved cardiac output may also contribute to the effect of rhGH on exercise performance.     

No effect of menstrual cycle phase and oral contraceptive use on endurance performance in rowers

The aim of this study was to examine whether variables commonly used in aerobic exercise testing are influenced by menstrual cycle phases and use of oral contraceptive (OC) in female rowers. Twenty-four eumenorrheic female rowers distinguished on the basis of both menstrual status and athleticism participated in this study and were divided into competitive cyclic athletes (n = 8), recreationally trained cyclic athletes (n = 7), and recreationally trained athletes taking OC pills (ROC; n = 9). Rowers performed 2 incremental tests to voluntary exhaustion on a rowing ergometer during 2 different phases of the menstrual cycle: the follicular phase (FP) and the luteal phase (LP). The study variables were power output (Pa), heart rate (HR), oxygen consumption (VO2), carbon dioxide production (VCO2), minute ventilation (VE), the mean respiratory exchange ratio, and ventilatory equivalents of O2 (VE/VO2)) and CO2 (VE/VCO2), which were measured at maximal and at the aerobic-anaerobic transition intensities. In addition, maximal blood lactate (La) values after the test were obtained. When comparing Pa, &OV0312;o2, HR, and La values, no significant differences (p > 0.05) between FP and LP at maximal load and at threshold intensity were found in all 3 groups of the rowers studied. However, we observed higher values (p < 0.05) for VE/VCO2 at both intensities in LP compared with FP in the ROC group. In conclusion, sport-specific endurance performance was not influenced by the phase of the normal menstrual cycle and the synthetic menstrual cycle of the OC users in the rowers studied. Therefore, normally menstruating female rowers and female rowers taking OC pills should not be concerned about the timing of their menstrual cycle with regard to optimized sport-specific endurance performance.     

Effects of human menstrual cycle on thermoregulatory vasodilation during exercise

To investigate the effects of the menstrual cycle and of exercise intensity on the relationship between finger blood flow (FBF) and esophageal temperature (Tes), we studied four women, aged 20-32 years. Subjects exercised at 40% and 70% VO2max in the semi-supine posture at an ambient temperature of 20 degrees C. Resting Tes was higher during the luteal phase than the follicular phase (P less than 0.01). There were no significant differences between the two phases in FBF, oxygen consumption, carbon dioxide production, heart rate or minute ventilation at rest and during exercise, respectively. Each regression line of the FBF-Tes relationship consists of two distinct segments of FBF change to Tes (slope 1 and 2). FBF increased at a threshold Tes for vasodilation ([Tes 0]) and the rate of FBF rise became greater at ([Tes 0]) and the rate of FBF rise became greater at another Tes above this threshold ([Tes 0']). For both levels of exercise, [Tes 0] and [Tes 0'] were shifted upward during the luteal phase, but the slopes of the FBF-Tes relationship were almost the same in the two phases of the menstrual cycle. Increasing exercise intensity induced a significant decrease in slope 1 of the FBF-Tes relationship during the follicular (P less than 0.01) and the luteal phases (P less than 0.02), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of exercise to rest ratio on plasma lactate concentration at work rates above and below maximum oxygen uptake

The metabolic and physiological responses to different exercise to rest ratios (E:R) (2:1, 1:1, 1:2) of eight subjects exercising at work rates approximately 10% above and below maximum oxygen uptake (VO2max) were assessed. Each of the six protocols consisted of 15 1-min-long E:R intervals. Total work (kJ), oxygen uptake (VO2), heart rate (fc) and plasma lactate concentrations were monitored. With increases in either E:R or work rate, VO2 and fc increased (P < 0.05). The average (15 min) VO2 and fc ranged from 40 to 81%, and from 62 to 91% of maximum, respectively. Plasma lactate concentrations nearly doubled at each E:R when work rate was increased from 90 to 110% of VO2max and ranged from a low of 1.8 mmol.l-1 (1:2-90) to a high of 10.7 mmol.l-1 (2:1-110). The 2:1-110 protocol elicited plasma lactate concentrations which were approximately 15 times greater than that of rest. These data suggest that plasma lactate concentrations during intermittent exercise are very sensitive to both work rate and exercise duration.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.     

No effect of menstrual cycle phase on glucose kinetics and fuel oxidation during moderate-intensity exercise

Resting and exercise fuel metabolism was assessed in three different phases of the menstrual cycle, characterized by different levels of estrogen relative to progesterone: early follicular (EF, low estrogen and progesterone), midfollicular (MF, elevated estrogen, low progesterone), and midluteal (ML, elevated estrogen and progesterone). It was hypothesized that exercise glucose utilization and whole body carbohydrate oxidation would decrease sequentially from the EF to the MF to the ML phase. Normal-weight healthy females, experiencing a regular menstrual cycle, were recruited. Subjects were moderately active but not highly trained. Testing occurred after 3 days of diet control and after an overnight fast (12-13 h). Resting (2 h) and exercise (50% maximal O(2) uptake, 90 min) measurements of whole body substrate oxidation, tracer-determined glucose flux, and substrate and hormone concentrations were made. No significant difference was observed in whole body fuel oxidation during exercise in the three phases (nonprotein respiratory exchange ratio: EF 0.84 +/- 0.01, MF 0.85 +/- 0.01, ML 0.85 +/- 0.01) or in rates of glucose appearance or disappearance. There were, however, significantly higher glucose (P < 0.05) and insulin (P < 0.001) concentrations during the first 45 min of exercise in the ML phase vs. EF and MF phases. In conclusion, whole body substrate oxidation and glucose utilization did not vary significantly across the menstrual cycle in moderately active women, either at rest or during 90 min of moderate-intensity exercise. During the ML phase, however, this similar pattern of substrate utilization was associated with greater glucose and insulin concentrations. Both estrogen and progesterone are elevated during the ML phase of the menstrual cycle, suggesting that one or both of these sex steroids may play a role in this response.     

Acute exercise has no effect on ghrelin plasma concentrations.

Exercise is a potent, dose-dependent stimulus of growth hormone (GH) secretion. The hypothalamic peptides, GH-releasing hormone (GHRH) and somatostatin are regarded as major regulators of this stimulation. The role of the stomach-derived peptide ghrelin, which has been shown to exert strong GH releasing effects, has not been fully characterized yet. We therefore studied GH and ghrelin plasma concentrations in response to graded levels of exercise in eight healthy young volunteers. After determination of their individual maximal exercise capacity, all individuals underwent a treadmill exercise at 50 %, 70 %, and 90 % of maximum oxygen consumption (VO (2)max) on different days. Maximal GH response to exercise was observed after 40 minutes at 50 % VO (2)max and after 20 minutes at 70 and 90 % VO (2max). GH serum concentrations increased significantly at all three exercise intensities (GH peak concentrations were 5.8 +/- 2.3 ng/ml, 12.0 +/- 3.2 ng/ml, and 9.8 +/- 4.7 ng/ml, respectively). In contrast, ghrelin plasma concentrations remained unchanged at all three workloads. Assuming that the sensitivity of the GH neuroendocrine/metabolic regulation of GH is unaltered, ghrelin does not participate in the regulation of the GH response to exercise in healthy males.     

Effects of the menstrual cycle and sex on postexercise hemodynamics

Factors associated with the menstrual cycle, such as the endogenous hormones estrogen and progesterone, have dramatic effects on cardiovascular regulation. It is unknown how this affects postexercise hemodynamics. Therefore, we examined the effects of the menstrual cycle and sex on postexercise hemodynamics. We studied 14 normally menstruating women [24.0 (4.2) yr; SD] and 14 men [22.5 (3.5) yr] before and through 90 min after cycling at 60% .VO2(peak) for 60 min. Women were studied during their early follicular, ovulatory, and mid-luteal phases; men were studied once. In men and women during all phases studied, mean arterial pressure was decreased after exercise throughout 60 min (P < 0.001) postexercise and returned to preexercise values at 90 min (P = 0.089) postexercise. Systemic vascular conductance was increased following exercise in both sexes throughout 60 min (P = 0.005) postexercise and tended to be elevated at 90 min postexercise (P = 0.052), and femoral vascular conductance was increased following exercise throughout 90 min (P < 0.001) postexercise. Menstrual phase and sex had no effect on the percent reduction in arterial pressure (P = 0.360), the percent rise in systemic vascular conductance (P = 0.573), and the percent rise in femoral vascular conductance (P = 0.828) from before to after exercise, nor did the pattern of these responses differ across recovery with phase or sex. This suggests that postexercise hemodynamics are largely unaffected by sex or factors associated with the menstrual cycle.