Control of sweating during the human menstrual cycle

Summary 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 (T _es), mean skin temperature ( ), oxygen uptake and forearm sweating ( ) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at ∼80% peak during which the environmental chamber was controlled atT _a=50.0° C, rh=14% (P _w=1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at ∼85% peak atT _a=35° C and rh=25% (P _w=1.4 kPa). The normal L increase in restingT _es (≈0.3° C) occurred in all seven subjects. was higher during L than F in all experiments conducted at 50° C. During exercise and passive heat exposure, theT _es threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of toT _es between menstrual cycle phases. This rightward or upward shift inT _es threshold for initiation of sweating averaged 0.5° 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.     

Plasma volume during heat stress and exercise in women

Summary Five women were studied during exercise and passive heating to determine whether PV dynamics were affected by the menstrual cycle. The exercise bout (80% peak) on a modified cycle ergometer and the passive heat stress were done in a hot environment (T_a=50°C, P_w=1.61kPa) during the follicular and luteal phase. Esophageal temperature (T_es) was measured continuously. Blood samples were drawn after each 0.2° C increase in T_es and was measured at that time. Initial PV was estimated at rest during the follicular phase. PV changes from rest were calculated at each T_es from Hb and Hct. During passive heating, PV decreased by a mean volume of 156 (±80) ml to 2.83 (±0.09)l in the follicular phase. During the luteal phase, there was a larger volume reduction (300±100 ml) during passive heating, and the final PV was lower than in the follicular phase and averaged 2.47±0.181. During exercise, PV decreased 463 (±90) ml to 2.50 (±0.11) l in the follicular and 381 (±70) ml to 2.50 (±0.23) l in the luteal phase. These data indicate that there is a menstrual cycle effect on PV dynamics during passive heating such that more fluid is shifted out of the vasculature during the luteal phase. During severe exercise there is a greater fluid loss during the follicular phase, yet the final PV is not different between phases.     

Finger vasodilation correlates better with tympanic than esophageal temperature

Summary The relationship of finger blood flow (FBF) measured by venous occlusion plethysmography to tympanic temperature (T_ty) was compared with that of FBF to esophageal temperature (T_es) during exercise at 50% for 40 min at an ambient temperature of 25°C. The relationship of FBF to T_es showed an inflexion as T_es increased during exercise. The slope of the regression line showing the relationship between FBF and T_es was initially moderate, and then suddenly became steeper at the inflexion point. The relationship of FBF to T_ty, however, was linear, without an inflexion. The results suggest that finger vasodilation during moderate exercise correlates better with tympanic than esophageal temperature.     

Influence of the menstrual cycle and oral contraceptives on thermoregulatory responses to exercise in young women

Summary Thermoregulatory responses to exercise in relation to the phase of the menstrual cycle were studied in ten women taking oral contraceptives (P) and in ten women not taking oral contraceptives (NP). Each subject was tested for maximal aerobic capacity ( ) and for 50% exercise in the follicular (F) and luteal (L) phases of the menstrual cycle. Since the oral contraceptives would have prevented ovulation a quasi-follicular phase (q-F) and a quasi-luteal phase (q-L) of the menstrual cycle were assumed for P subjects. Exercise was performed on a cycle ergometer at an ambient temperature of 24° C and relative air humidity of 50%. Rectal (T _re), mean skin ( ), mean body ( ) temperatures and heart rate (f _c) were measured. Sweat rate was estimated by the continuous measurement of relative humidity of air in a ventilated capsule placed on the chest, converted to absolute pressure (PH₂O_chest). Gain for sweating was calculated as a ratio of increase inPH₂O_chest to the appropriate increase inT _re for the whole period of sweating (G) and for unsteady-state (G_u) separately. The did not differ either between the groups of subjects or between the phases of the menstrual cycle. In P, rectal temperature threshold for sweating (T _{re, td}) was 37.85° C in q-L and 37.60° C in q-F (P < 0.01) and corresponded to a significant difference fromT _re at rest. TheT _re, andf _c increased similarly during exercise in q-F and q-L. No menstrual phase-related differences were observed either in the dynamics of sweating or in G. In NP,T _{re, td} was shorter in L than in F (37.70 vs 37.47° C,P<0.02) with a significantly greater value fromT _re at rest. The dynamics and G for sweating were also greater in L than in F. The G_u was 36.8 versus 16.6 kPa · ° C^–1 (P<0.01) while G was 6.4 versus 3.8 kPa · ° C^–1 (P<0.05), respectively. TheT _re, andf _c increased significantly more in phase F than in phase L. It was concluded that in these women performing moderate exercise, there was a greater temperature threshold and larger gains for sweating in phase L than in phase F. Intake of oral contraceptives reduced the differences in the gains for sweating making the thermoregulatory responses to exercise more uniform.     

Cutaneous blood flow and local sweating after systemic atropine administration

Localized cutaneous vasodilation (flush) is seen following systemic atropine administration. To verify calculated enhanced dry heat loss with actual changes in cutaneous blood flow, four men were studied in both control and atropine (0.025 mg·kg^–1;im) experiments (T _a=30°C,T _dp=7°C) during moderate exercise (55% O₂ peak). Esophageal temperature (T _es) and arm sweating ( ) by local dewpoint were measured continously. Skin (forearm) blood flow (FBF) was measured twice each minute by venous occlusion plethysmography. Injection of atropine (2 mg) caused an increased sensitivity (+85%,p<0.01) in FBF toT _es with no change in the vasodilator threshold. An elevatedT _es onset (0.3°C,p<0.05) for sweating occurred with no change in the sensitivity of toT _es (–27%,p<0.20). No elevation in either forearm or occurred before the onset of vasodilation, however, both mean skin ( ) and local arm temperatures were higher in the atropine experiments after 15 min of exercise. Systemic atropine resulted in higher cutaneous vasodilation at the same core temperature with the local skin temperature following passively. The effect of systemic atropine in stimulation of increased cutaneous vasodilation is suggested to result by a combination of central and local responses which may be mediated through the release of vasoactive sustances.     

The relationship between exercise-induced oxidative stress and the menstrual cycle

The purpose of this study was to investigate the relationship between exercise-induced oxidative stress and the menstrual cycle in healthy sedentary woman. Eighteen women with regular menstrual cycles participated in this research. The subjects monitored their basal body temperature (BBT) and carried out a urinary ovulation test (twice) for 2 months prior to the study to determine their menstrual cycle. The subjects performed bicycle ergometer exercise (for 30 min at 60% O_2max) in each phase (menses, follicular and luteal phases) of the menstrual cycle. Serum estradiol and progesterone concentrations were determined from blood that was collected at rest. Serum thiobarbituric acid reactive substances (TBARS), total superoxide dismutase (T-SOD) and extracellular superoxide dismutase (EC-SOD) were determined as markers of oxidative stress in blood samples collected at rest and after exercise. TBARS was significantly lower after exercise [2.4 (0.5) nmol/ml] in the follicular phase, and T-SOD was significantly lower after exercise [3.2 (1.2) U/ml] in the luteal phase. EC-SOD did not show a significant change after exercise during each phase of the menstrual cycle. Furthermore, there was a negative correlation between estradiol and T-SOD (r=–0.46, P<0.05) and between estradiol and EC-SOD (r=–0.55, P<0.05) during the menses. All data are presented as the mean value and its standard deviation.The results of this study suggest that when the estradiol level is high in a menstrual cycle, free radicals produced as a consequence of exercise may be easily eliminated by sedentary women with normal menstrual cycles.     

Velocity at V̇O2 max and peak treadmill velocity are not influenced within or across the phases of the menstrual cycle

Velocity at VO_{2 max} (vO_{2 max}) and peak treadmill velocity (PTV) are variables highly predictive of endurance performance. However, how these variables are affected by the menstrual cycle is unknown. The aim of this study was to assess the effect of the menstrual cycle on vO_{2 max} and PTV. Ten, female runners were studied across three menstrual cycles. Training, menstrual history and mood states were assessed for 2 months, with daily salivary samples taken to detect menstrual phases. During the third menstrual cycle, participants completed a maximal test to determine O_{2 max}, vO_{2 max} and PTV in the early follicular phase, late follicular phase, early luteal phase, late luteal phase and menses. Progesterone increased at the onset of the luteal phase [mean (SEM); 490 (73.6) pmol l^–1] compared to the follicular phase [344.6 (59.7) pmol l^–1). No significant differences in the psychological mood states between the phases of the menstrual cycle were found (P>0.05). No significant differences in vO_{2 max} (P=0.611), or PTV (P=0.472) were found between the phases of the menstrual cycle. Thus, vO_{2 max} and PTV are not affected by the monthly menstrual cycle in female endurance runners.     

A comparison of human thermoregulatory response following dynamic exercise and warm-water immersion

We tested the hypothesis that the prolonged elevated plateau of esophageal temperature (T _es) following moderate exercise is a function of some exercise-related factors and not the increase in heat content andT _es during exercise, by comparing the response to increaseT _es during exercise (endogenous heating) and warm-water immersion (exogenous heating). Nine healthy, young [24.0 (1.9) years] subjects performed two separate experiments: (1) 15 min of treadmill exercise at 70% and 15 min rest in a climatic chamber at 29°C, followed by 15 min of immersion in a 42°C water bath and a further 60 min of recovery in the climatic chamber [exercise-water (EW)]; and (2) 15 min of immersion in a 42°C water bath followed by 60 min of recovery in the climatic chamber [water-only (WO)]. Esophageal (T _es) and skin (T _sk) temperatures were recorded at 5-s intervals throughout. TheT _ea at which the forearm to finger temperature gradient (T _fa-T _fi) abruptly decreases was used to identify the threshold for forearm cutaneous vessel dilation (Th_dil) during exercise. Pre-exerciseT _es values were 36.64°C and 36.74°C for EW and WO respectively. The EW post-exerciseT _ea value fell to a stable level of 37.12°C and this value differed by 0.48°C (P < 0.05) from baseline, but was similar to Th_dil (37.09°C). Despite a 1.2°C increase inT _es during the subsequent warm-water immersion,T _es returned to the post-exercise value (37.11°C). The WO post-immersionT _es fell to a stable plateau of 36.9°C, which was not statistically different from the pre-immersion T_es. The data for both warm-water treatments support the hypothesis that increases inT _es and heat content alone are not the primary mechanisms for the post-exercise elevation inT _es and Th_dil. These data also support our previous observation that the exercise-induced elevation in Th_dil persists into recovery.     

No effect of menstrual cycle phase on fuel oxidation during exercise in rowers

The aim of this investigation was to examine the effects of menstrual cycle phase on substrate oxidation and lactate concentration during exercise. Eleven eumenorrheic female rowers (18.4 ± 1.9 years; 172.0 ± 4.0 cm; 67.2 ± 8.4 kg; 27.7 ± 4.8% body fat) completed 1 h rowing ergometer exercise at 70% of maximal oxygen consumption (VO_2max) during two different phases of the menstrual cycle: the follicular phase (FP) and the luteal phase (LP). Resting and exercise measurements of the whole body energy expenditure, oxygen consumption (VO₂), respiratory exchange ratio (RER), substrate oxidation and lactate blood levels were made. Energy expenditure, VO₂ and heart rate during the 1-h exercise were not significantly different (P > 0.05) among menstrual cycle phases. Resting RER and RER during the entire 1 h exercise period were not significantly different among menstrual cycle phases. There was an increase (P < 0.05) in RER in the transition between rest and exercise and a further increase in RER occurred after the first 30 min of exercise at both menstrual cycle phases. Blood lactate concentrations significantly increased in the transition between rest and exercise and remained relatively constant during the whole 1 h of exercise in both menstrual cycle phases. No menstrual cycle phase effect (P > 0.05) was observed for blood lactate concentrations. In conclusion, our results demonstrated no effect of menstrual cycle phase on substrate oxidation and blood lactate concentration during rowing exercise at 70% of VO_2max in athletes. Normally menstruating female rowers should not be concerned about their menstrual cycle phase with regard to substrate oxidation in everyday training.     

Effects of physical training on heat loss responses of young women to passive heating in relation to menstrual cycle

To examine the effects of physical training on cutaneous vasodilation and sweating responses of young women in the follicular and luteal phase, 11 physically trained (T group) and 13 untrained (U group) women were passively heated by lower-leg immersion into hot water of 42°C (ambient temperature of 30°C and 45%RH) for 60 min in their mid-follicular and mid-luteal phases of the menstrual cycle. Female hormones increased significantly from the mid-follicular to the mid-luteal phase in T and U groups, but the degree of increase was significantly lower in T group. Mean body temperature thresholds for cutaneous vasodilation and sweating responses were significantly lower in T group than in U group, in both the menstrual phases, and the differences between the groups were greatest during the mid-luteal phase. The slope of the relationship between frequency of sweat expulsion (F_sw) and and between local sweating rate and F_sw was significantly greater in T group, although the slope of the relationship between cutaneous blood flow and did not differ between the groups, regardless of body site or menstrual phase. These results suggest that regular physical activity enhanced sweating and cutaneous vasodilation in young women. The enhancement of sweating was due to both central and peripheral mechanisms, and the enhancement of cutaneous vasodilation was possibly due to a central mechanism. Enhancement of heat loss responses via central mechanisms was greater during the mid-luteal phase than in the mid-follicular phase because the elevation of female reproductive hormone levels during the mid-luteal phase was relatively low in T group.     

Influence of the menstrual cycle on the sweating response measured by direct calorimetry in women exposed to warm environmental conditions

Summary The whole body sweating response was measured at rest in eight women during the follicular (F) and the luteal (L) phases of the menstrual cycle. Subjects were exposed for 30-min to neutral (N) environmental conditions [ambient temperature (T _a) 28°C] and then for 90-min to warm (W) environmental conditions (Ta, 35°C) in a direct calorimeter. At the end of the N exposure, tympanic temperature (T _ty) was 0.18 (SEM 0.06)°C higher in the L than in the F phase (P<0.05), whereas mean skin temperature ( ) was unchanged. During W exposure, the time to the onset of sweating as well as the concomitant increase in body heat content were similar in both phases. At the onset of sweating, the tympanic threshold temperature (T _{ty, thresh}) was higher in the L phase [37.18 (SEM 0.08)°C] than in the F phase [36.95 (SEM 0.07)°C;P<0.01]. The magnitude of the shift inT _ty, thresh [0.23 (SEM 0.07)°C] was similar to the L-F difference inT _ty observed at the end of the N exposure. The mean skin threshold temperature was not statistically different between the two phases. The slope of the relationship between sweating rate andT _ty was similar in F and L. It was concluded that the internal set point temperature of resting women exposed to warm environmental conditions shifted to a higher value during the L phase compared to the F phase of the menstrual cycle; and that the magnitude of the shift corresponded to the difference in internal temperature observed in neutral environmental conditions between the two phases.     

Impact of menstrual cycle phase on the exercise status of young,sedentary women

The purpose of the present study was to compare exercise status during the follicular (FP) and luteal (LP) phases of the menstrual cycle of a single group of young, sedentary women, where the marked differential in the blood concentrations of 17-oestradiol ([E₂]) and progesterone ([P₄]) has the potential to alter the metabolic response to exercise. Fourteen females [21.8 (4.0) years, peak oxygen uptake (V̇O_2peak) <45 ml·kg ^–1·min^–1] performed both incremental exercise to exhaustion and steady-state submaximal cycle ergometer exercise while measurements were made of several metabolic and hormonal variables. With the incremental exercise test, time to exhaustion, maximal power output and total work done were not different between the two phases, nor were the absolute values for V̇O_2peak or the corresponding values for ventilation (V̇E), respiratory frequency (f_R) and heart rate (HR). Resting, end-exercise and peak (post-exercise) plasma lactate concentrations and the lactate threshold were not different between the two phases either. However, as the workloads increased during the incremental protocol, plasma lactate concentration, carbon dioxide output (CO₂) and the respiratory exchange ratio (RER) all were lower during LP, while oxygen uptake (V̇O₂) was higher. With steady-state submaximal exercise, at workloads corresponding to 25% and 75% of menstrual cycle phase-specific O_2peak, V̇O₂ and the oxygen pulse (V̇O₂/HR) were higher and RER and plasma lactate concentration lower during LP. Regardless of phase, [E₂] increased with both incremental and steady-state submaximal exercise, while [P₄] was unchanged. It is concluded that while exercise capacity, as defined by O_2peak and the lactate threshold, is unaffected by cycle phase in young, sedentary women, the metabolic responses in the LP during both incremental and steady-state submaximal exercise suggest a greater dependence on fat as an energy source.     

Natural cooling of the brain during outdoor bicycling?

Tympanic membrane temperature (T_tymp) and deep esophageal temperature (T _es) were measured in 8 subjects during normal outdoor bicycling. Metabolic rate was determined by the Douglas bag method. Heart rate was sampled continuously. Skin surface temperatures were measured at the forehead, chest and shoulder, and core temperatures in the deep esophagus and at the tympanic membrane using a radio telemetry system. For each outdoor experiment an indoor experiment in a climatic chamber, adjusted to the same air temperature but in still air, was performed. The subjects exercised at the same as in the outdoor trial on a stationary bicycle ergometer. Measurements were taken with the same equipment as in the outdoor experiments. O₂-consumption · min^–1) and heart rates (beats·min^–1) were similar during outdoor and indoor bicycling, averaging 2.38±0.018 (SE) and 2.26±0.07, 141±7 and 147±8, respectively. During steady stateT _es was the same during outdoor and indoor bicycling (37.95°C), whileT _tymp was significantly lower during outdoor bicycling. (T _es–T _tymp) was 1.25°C during outdoor and 0.5°C during indoor exercise. It is concluded that, if tympanic temperature is lowered by counter-current cooling of its arterial supply, then cooling of the brain may also take place in humans during physical activity under normal outdoor conditions with convective air movements. But the magnitude of a possible brain cooling cannot be deduced from the fall in tympanic temperature.     

Post-exercise thermal homeostasis as a function of changes in pre-exercise core temperature

We have previously reported that, following continuous exercise, a prolonged elevated plateau of esophageal temperature (T _es) was directly related to the T _es at the time of cutaneous vasodilation (Th_dil) during exercise. In order to investigate the hypothesis that the factors which result in an increase of the post-exercise Thdil and define the post-exercise T _es elevation are related to pre-exercise T _es, nine healthy, young [24.0 (1.9) years], non-training males rested at 29°C, 50% humidity for > 1 h (control). They then completed three successive cycles of 15 min treadmill running at 70% maximal oxygen consumption ( ) followed by 30 min rest. Esophageal, rectal (T _re) and skin (T _sk) temperatures and forearm cutaneous blood flow were recorded at 5-s intervals throughout. Laser-Doppler flowmetry of forearm skin blood flow was used to identify the Thdil during exercise. Pre-exercise T _es was 36.74 (0.25)°C and post-exercise Tes fell to stable and significant (P < 0.05) elevations above pre-exercise values at 37.22(0.27)°C, 37.37(0.27)°C and 37.48(0.26)°C following each successive work bout respectively. Correspondingly, Th_dil during each work bout rose in proportion to, and was not different than, the post-exercise T _es in the following recovery [37.20(0.23)°C, 37.41(0.24)°C and 37.58(0.24)°C]. Although the increases were less with each successive exercise bout, the differences between each exercise bout, in terms of post-exercise Tes and Th_dil values, were significant (P < 0.05). These results reinforce our previous observations of elevations in Th_dil and post-exercise Tes after a single exercise bout and lead to the tentative conclusions that (1) pre-exercise Test has a direct influence on Thdil and post-exercise Test and (2) the exercise-induced increase of Th_dil persists into recovery, influencing post-exercise thermal recovery.     

Disturbance of thermal homeostasis during post-exercise hyperthermia

The response of core temperature to exercise was investigated during recovery in order to avoid the antagonistic competition between exercise and thermal reflexes for the same effector systems which control skin blood flow. Five healthy, non-training males [mean (SD) age, 23.8 (2.04) years] were habituated to 29° C at relative 50% humidity for more than 2 h and then exercised by treadmill running at about 75% maximum oxygen uptake for 18 min. They then remained at 29° C for up to 65 min of recovery. Oesophageal (T _es), rectal (T _re) and skin temperatures (T _sk) were recorded at 5-s intervals throughout. The abrupt fall of temperature gradient from the forearm to finger was used to identify the T _es for skin vessel dilatation (T _dil) during exercise. Mean (SE) Ts rose from a resting value of 36.67 (0.15)° C to 38.22 (0.24)° C, mean T _re rose from 37.09 (0.25)° C to 38.23 (0.15)° C, and T _dil occurred at 37.39 (0.32)° C. Within 10 min of recovery mean T _es fell to 37.31 (0.24)° C, where it remained a significant 0.64° C above its pre-exercise (PrEx) level (P0.018) but insignificantly different from T _dil for the remaining 55 min of recovery. Meanwhile, T _re fell gradually throughout recovery to 37.64 (0.18)° C. The T _sk at all non-acral sites except the thigh had recovered to PrEx levels by 20–30 min post-exercise (PoEx). The rapid PoEx fall of T _es to the level of T _dil and the subsequent plateau above PrEx values suggests that heat dissipation during recovery was primarily passive once T _es had fallen to T _dil, even though T _es and T _re were significantly elevated. The relationship of these results to the set-point and load error concepts of thermal control is discussed.These data have been presented at the Canadian Physiological Society Winter meeting, January 1993, but have not been previously published     

Short-term exercise-heat acclimation enhances skin vasodilation but not hyperthermic hyperpnea in humans exercising in a hot environment

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [(V)\dot]_{\textO 2 \textpeak} \dot{V}_{{{\text{O}}_{{ 2 {\text{peak}}}} }} separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T _es), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ( [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} ) during exercise. The training lowered the T _es threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T _es and the peak FVC during exercise. It also lowered minute ventilation ( [(V)\dot]_\textE \dot{V}_{\text{E}} ) during exercise, but this effect disappeared after removing the influence of [(V)\dot]_\textO2 \dot{V}_{{{\text{O}}_{2} }} on [(V)\dot]_\textE \dot{V}_{\text{E}} . The training did not change the slope relating ventilatory variables to T _es. We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.     

Responses of menstrual women,amenorrheal women,and men to exercise in a hot,dry environment

Summary Rectal (T_re) and mean skin temperatures, heart rate (fc) and sweat rate (M_sw) during exercise in a hot, dry environment were compared among four menstrual women (both before and after ovulation), four amenorrheal women and four men, all with similar aerobic capacities. Progesterone and estrogen were compared in a pair of monozygotic twins (one menstrual and one amenorrheal) who participated in the study. Before acclimation, subjects were given a heat-stress test (HST) consisting of treadmill walking at 25%–30% max in a hot, dry environment (T_db/T_wb=48/25 C) until T_re reached 39 C or fc reached 160 beat·min^–1. Subjects were then acclimated to the dry heat with conventional acclimation procedures. After acclimation, subjects were given a HST which continued for 3 h. Before acclimation T_re and fc increased more rapidly in the women, which resulted in significantly shorter HST times for the women as compared with the men. Following acclimation all subjects maintained similar T_re, fc, and sweat rates. There were no differences between the exercise/heat-stress responses of the preovulatory menstrual women, postovulatory menstrual women, and amenorrheal women. Although the estrogen concentrations were normal in the menstrual twin, her progesterone concentrations were significantly depressed. Both hormones were depressed in the amenorrheal twin. Following acclimation thermoregulatory function in dry heat did not differ between the sexes when fitness level was similar. Neither were there any differences in thermoregulation between the pre- and postovulatory phases of the menstrual cycle or between the menstrual and amenorrheal women.     

Right atrial pressure and forearm blood flow during prolonged exercise in a hot environment

Right atrial pressure (RAP) at rest is known to be reduced by an increase in skin blood flow (SkBF) in a hot environment. However, there is no clear evidence that this is so during exercise. To clarify the effect of the increase in SkBF on RAP during exercise, we measured forearm blood flow (FBF) (as an index of SkBF) and RAP continuously using a Swan-Ganz catheter in five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min in a hot environment (30°C, relative humidity 20%). Cardiac output increased from 5.5±0.21/min at rest to 17.9±1.21/min (mean±SE, P<0.01) in the first 10 min of exercise and then remained steady until the end of exercise. FBF did not change significantly during the first 5 min, but then increased from 2.7±0.5 ml/100 ml per min at rest to 10.8±1.7 ml/100 ml per min (P<0.001) by 25 min as pulmonary arterial blood temperature (T _b) rose from 37.0±0.1°C to 38.1±0.1°C (P<0.001). FBF then reached a plateau, despite a continuing increase in T _b. RAP increased significantly from 4.3±0.8 to 7.6±1.2 mm Hg (P<0.001) during the first 5 min of exercise and then gradually declined to 6.1±1.0 mm Hg by 25 min (P<0.001 vs. 5 min) and further to 5.7±1.0 mm Hg by 50 min, a value not significantly higher than at rest. This reduction in RAP during exercise was significantly correlated with the increase in FBF (r=–0.97, P<0.001) with a regression equation of RAP=–0.25×FBF+8.8. These results suggest that the decrease in RAP after 5 min exercise was caused by an increase in SkBF during exercise in a hot environment.Part of this work has been published in abstract form [FASEB J 5A1400 (1991)]     

Changes of ventilation and ventilatory response to hypoxia during the menstrual cycle

The relationship between change in hypoxic sensitivity in respiration, defined as increment in ventilation per drop of arterial O₂ saturation , with the phase change from follicular to luteal and those in resting pulmonary ventilation , mean inspiratory flow (V _T/T _I), alveolar partial pressures of CO₂ and O₂ ( and , respectively) and body temperature was studied in 10 women. There was a significant relationship between % increase in hypoxic sensitivity and decrement of resting that occurred in the luteal phase. However, no significant relationships were observed between change in hypoxic sensitivity and those in the remaining parameters studied. The intersubject variation in % increase in resting during the luteal phase was not associated with that in % increase in hypoxic sensitivity. The results indicate that the contribution of increased hypoxic sensitivity to increasing during the luteal phase is variable among subjects. Reasons for the increase in hypoxic sensitivity with hypocapnia are discussed.     

Isometric strength and endurance during the menstrual cycle

Seven healthy young women, 3 of whom had been taking oral contraceptives, were examined during the course of 2 menstrual cycles to assess their isometric strength, their endurance during a series of 5 fatiguing isometric contractions at a tension of 40% MVC, and their blood pressures and heart rates during those fatiguing contractions. Two sets of experiments were performed, one in which the subject's forearm temperature was allowed to vary as a function of T _A , and one with the muscle temperature stabilized by immersion of the forearm in water at 37 C. During exposure to ambient temperatures, isometric strength and both the heart rate and blood pressure responses at rest and at the end of a fatiguing, sustained isometric exercise, were not significantly different during any phase of the menstrual cycle in any subject. In contrast, the isometric endurance in the women not taking oral contraceptives varied sinusoidally in all 5 contractions with a peak endurance midway through the ovulatory phase and the lowest endurance mid-way through the luteal phase of the menstrual cycle. The isometric endurance of the women taking oral contraceptives did not vary during their menstrual cycle. After stabilization of the temperature of the muscles of the forearm in water at 37 C, the isometric endurance of the normal subjects showed a hyperbolic response with the maximal endurance at the beginning and end of their cycles, and the shortest endurance at mid-cycle. Here again, however, the isometric endurance of the women taking oral contraceptives did not vary after immersion of their forearms in the 37 C water.