INTRODUCTION

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ORTHOSTATIC STRESS RESULTS in adjustments of cardiovascular variables to maintain mean arterial blood pressure (MAP) (4, 7-9). Decreased responsiveness of cardiovascular mechanisms that normally contribute to regulation of arterial pressure and maintenance of cerebral blood flow increase the risk of syncope after exercise (12, 14). Several investigations found that women have a lower tolerance to various orthostatic challenges at rest compared with men (3, 5, 9, 20). Also, some investigations report that women have less responsiveness in mechanisms that regulate arterial pressure compared with men (3, 8). Frey and Hoffler (4) suggest that men may respond to orthostatic challenges with greater sympathetic stimulation to the peripheral vasculature compared with women, whereas women respond with greater vagally mediated increase in heart rate (HR) compared with men (4).

These mechanisms also play an important role in arterial pressure maintenance when exercise is stopped. At exercise termination, the challenge to maintain cerebral perfusion is compounded by peripheral pooling of blood in the previously active muscle. Because women exhibit less orthostatic tolerance than men at rest, women may be more susceptible to postexercise orthostatic hypotension; however, to our knowledge, no studies have investigated the influence of gender on cardiovascular responses during inactive recovery from exercise. Therefore, the purpose of this study was to compare the responses of women and men during recovery from dynamic exercise. We hypothesized that women have greater decreases in arterial pressure during recovery from exercise compared with men.

To test this hypothesis, we compared hemodynamic responses in men and women during two different exercise recovery modes: 1) inactive recovery, in which the subject stopped cycling exercise and sat completely still, and 2) active recovery, during which the subject pedaled against zero resistance after exercise. The principal difference between inactive and active recovery is the presence of skeletal muscle pumping (1); therefore, we attributed any difference in response between these two conditions to the influence of the ongoing skeletal muscle pumping during active recovery.

	METHODS

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Subjects. Nineteen volunteers (11 women and 8 men) between 21 and 40 yr of age were studied. All subjects were free of any known cardiovascular disease. Before the experimental trials, each subject's maximal oxygen consumption was determined by an incremental treadmill test with the treadmill speed set at 3.13 m/s and elevation increased 2.5% every 1.5 min. Smokers were excluded from participating in this study. Female subjects were not tested during menses. All subjects were asked to refrain from exercise and stimulants such as caffeine for 24 h before testing. Subjects were not studied within 2 h after a meal. Body surface area was as estimated by the standard DuBois nomogram (6). All experimental procedures and protocols were approved by the University of North Texas Health Science Center Institutional Review Board, and each subject gave informed, written consent to participate in the study.

Experimental design. On experimental days, each subject repeatedly performed an exercise protocol that consisted of a 1 min warm-up period on a cycle ergometer (standard) with no resistance, followed by 1-3 min of increased workload to elicit ~60% of their individual predicted maximal HR with a constant pedal rate of 70 rpm. Subjects then sustained exercise at their peak workload for 3 min. We studied two different cycling exercise recovery modes: 1) inactive seated, and 2) active loadless pedaling on the ergometer (70 rpm). The two conditions were performed in random order. In every case, recovery was studied for 5 min. The two recovery modes included one mode that did not engage the skeletal muscle pump (inactive, seated) and one that engaged the skeletal muscle pump (active, loadless pedaling). Ambient temperatures during the studies averaged 24 ± 1°C.

Hemodynamic measurements. Pulsed Doppler ultrasound was used to measure beat-to-beat stroke volume (SV) at the aortic root during rest, exercise, and recovery periods. Doppler-shifted waveforms were obtained with an L-shaped crystal transducer (crystal diameter = 1 cm) with a focal range of 2-8 cm (InterSpec XL, Conshohocken, PA, presently owned by ATL, Bothell, WA). It operated at 3.0 MHz with a pulse repetition frequency of 12.6 kHz. This allowed frequency shifts of 6.3 kHz and a maximum velocity detection of 96 cm/s at the assumed Doppler angle of zero. A 400-Hz high-pass filter was used to eliminate low-frequency noise caused by wall motion. Axial resolution (dB) was ~0.5 mm. The Doppler transducer was positioned in the suprasternal notch, and the ultrasonic beam was directed inferiorly and posteriorly along the flow stream in the ascending aorta. A measurement of aortic diameter at the aortic root was taken from a two-dimensional parasternal long-axis view of the heart with the subject in the supine or left lateral recumbent position before experimentation. SV was calculated from the measurements of aortic diameter and the flow velocity of the blood leaving the heart via the aortic root.

Data analyses. Comparisons of responses during the different exercise recovery modes were performed with repeated-measures analyses of variance. The main effect factors were exercise recovery mode, gender, and time. When significant main effects were observed, a post hoc analysis was performed using Student-Newman-Keuls multiple-comparison test. Statistical significance was set at an  level of 0.05. Data are presented as means ± SE.

	RESULTS

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The results are for 19 subjects (11 women and 8 men). No significant differences existed between women and men for age, resting HR, maximal oxygen consumption (Table 1), and DAP. However, significant differences existed in height, weight, SAP, and body surface area (Table 1). In addition, baseline and SV was greater in the men, whereas baseline TPR was greater in the women (Table 2).

MAP. At baseline and during exercise, there were no differences in MAP between women and men. All subjects demonstrated an immediate decrease in MAP after exercise during both the inactive and active recovery modes (Fig. 1). When measured 1 min after exercise, MAP decreased less (P < 0.05) during inactive recovery from exercise in men (18 ± 2 mmHg) compared with women (30 ± 2 mmHg). In men, MAP returned to preexercise levels at minutes 2-5 during the inactive recovery. In women, MAP fell to below preexercise levels at 1-5 min of inactive recovery (P < 0.05). Women and men both demonstrated ~10 mmHg less of a decrease in MAP during the active recovery.

View larger version (21K): [in this window] [in a new window]   Fig. 1.   Mean arterial pressure during submaximal cycling exercise and 5 min of recovery from exercise. The 2 recovery modes were inactive (exercise was stopped completely) and active (subjects continued loadless pedaling after exercise). Values are means ± SE; n = 19 (11 women and 8 men). *Significant gender differences during active recovery, P < 0.05. # Significant gender differences during inactive recovery, P < 0.05.

. Increases in during exercise were greater in men than in women (P < 0.01). During inactive recovery from exercise, returned to preexercise baseline levels faster in women compared with men (Fig. 2). Furthermore, relative to preexercise baseline values, the decrease in was significantly greater during inactive recovery compared with active recovery in both women and men.

View larger version (24K): [in this window] [in a new window]   Fig. 2.   Cardiac output during submaximal cycling exercise and 5 min of recovery from exercise. The 2 recovery modes were inactive (exercise was stopped completely) and active (subjects continued loadless pedaling after exercise). Values are means ± SE; n = 19 (11 women and 8 men). *Significant gender differences during active recovery, P < 0.05. # Significant gender difference during inactive recovery, P < 0.05.

SV. The increase in SV during exercise was greater in men than in women (P < 0.01). Both men and women demonstrated rapid reductions in SV during the first minute of inactive recovery that were followed by gradual reductions thereafter. Like , SV returned to preexercise baseline levels in women and actually fell below preexercise baseline levels during inactive recovery in the women (Fig. 3). In men, SV returned to baseline values at 5 min of inactive recovery. SV was significantly less in women than in men throughout inactive recovery from exercise (Fig. 3). SV was significantly greater during active recovery than inactive recovery in both women and men.

View larger version (23K): [in this window] [in a new window]   Fig. 3.   Stroke volume during submaximal cycling exercise and 5 min of recovery from exercise. Values are means ± SE; n = 19 (11 women and 8 men). *Significant gender differences during active recovery; # significant gender differences during inactive recovery, (P < 0.05).

HR. During exercise, men exhibited lower peak exercise HR compared with women (P < 0.05). Women demonstrated similar decreases in HR during 5 min of inactive recovery from exercise compared with men (Table 2). Furthermore, no gender differences in HR existed during 5 min of active recovery. As expected, during active recovery, HR decreased less compared with inactive recovery for both genders.

TPR. TPR in women was greater than that in men at rest, during exercise, and during both recovery modes (Table 2). Relative to baseline levels, TPR decreased similarly during exercise in women and men (Fig. 4). After exercise, men and women showed increased TPR in response to inactive and active recovery modes, and this increase was greater during inactive recovery. However, relative to peak exercise values, when measured at min 5 of inactive recovery, TPR increased significantly less in women compared with men (Fig. 5). In women and men, TPR remained below baseline values during both inactive and active recovery.

View larger version (21K): [in this window] [in a new window]   Fig. 4.   Total peripheral resistance (TPR) during submaximal cycling exercise and 5 min of recovery from exercise. Values are means ± SE; n = 19 (11 women and 8 men). *Significant gender differences during active recovery, P < 0.05. # Significant gender differences during inactive recovery, P < 0.05.

View larger version (15K): [in this window] [in a new window]   Fig. 5.   TPR expressed as percent changes () from peak exercise (Ex) to minute 5 of inactive recovery from exercise. Values are means ± SE; n = 19 (11 women and 8 men). # Significant gender differences during inactive recovery, P < 0.05.

	DISCUSSION

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These results support the hypothesis that the reduction of MAP during recovery from dynamic exercise is greater in women compared with that shown in men. Furthermore, the physiological difference that explains the greater postexercise decrease in MAP in women compared with men is that women had relatively greater reductions in and less of an increase in TPR after exercise. During active recovery from exercise, skeletal muscle pumping was similarly effective in maintenance of MAP in women and men.

In women, recovery from exercise was characterized by greater decreases in MAP compared with that shown in men. Therefore, the question arises: What are the potential mechanisms that contribute to these gender differences in MAP regulation after exercise? The factors that determine MAP are SV, HR, and TPR; therefore, adjustments in these variables solely or collectively must explain the gender difference. Other investigations have demonstrated that orthostatic stress was associated with a greater decline in and SV (3) and greater vasoconstriction in women (11, 20).

Orthostasis and gender differences. Previous studies provided evidence that women have lower tolerance to various orthostatic challenges compared with men (3, 9). Hordinsky and colleagues (10) reported that tolerance to lower body negative pressure was 15% lower in women than in men. Recently, several investigations provided more evidence that women exhibit less tolerance to orthostatic stress compared with men (3, 4, 9). The proposed mechanisms that contribute to these differences include greater venous compliance, lesser blood volume, less responsive cardiovascular function (3), impaired arterial-cardiac baroreflex function (3, 15), and lower resting SV in women (16). However, observations regarding impaired baroreflex function are controversial (19). All of the existing data addressing the issue of gender-dependent responses to orthostatic stress are from studies at rest, using lower body negative pressure, standing tests, and Earth's gravity acceleration. To our knowledge, no studies have determined the potential influence of gender as it relates to postexercise orthostatic stress. It is reasonable to suspect that differences between men and women in orthostatic responses and tolerance at rest and after exercise could be associated with similar cardiovascular mechanisms.

Gender differences during inactive recovery from exercise. Our results indicate that inactive recovery from exercise in women was associated with more rapid return of SV and to preexercise levels compared with men. Furthermore, in women, SV fell to levels significantly below preexercise baseline during inactive recovery from exercise. These data suggest that there was a greater decrease in venous return and thus a possibly greater degree of peripheral pooling during inactive recovery in the women. In addition, relative to peak exercise, TPR increased less in women compared with men during inactive recovery. This was surprising because MAP decreased more in the women than in the men during inactive recovery; this greater decrease in MAP in the women would be expected to produce a greater reflex vasoconstriction. This difference in the MAP-TPR relationship may reflect a less effective arterial-vascular baroreflex response. Therefore, there appeared to be a less effective compensatory vasoconstriction to correct for the fall in and MAP in women as noted in studies during orthostasis alone discussed above.

Active recovery, skeletal muscle pumping, and gender. This study supports previous work from our laboratory indicating that active recovery from exercise profoundly attenuates the initial postexercise decrease in MAP (1). Similarly, Takahashi and Miyamoto (18) suggested that light postexercise physical activity plays an important role in facilitating venous return from muscle. As expected, during active recovery, the postexercise decrease in HR was less than during inactive recovery (18). This is due to positive effects of "central command" on HR during active recovery (2, 17, 21). The better maintenance of MAP during active (vs. inactive) recovery was a function of a better maintenance of SV, HR, and , and this effect was similar in both the women and men. Thus the efficacy of the skeletal muscle pump was similar in the women and men.

Limitations of this investigation. It is difficult to identify the physiological differences between women and men solely on the basis of gender differences. Other gender-related factors such as lean body mass, fitness, lifestyle, weight, and height are only some of the potential variations that may contribute to "gender" differences in physiological responses. However, in our study, the men and women were within a relatively narrow age range and had similar fitness levels. The study of possible menstrual cycle phase effects on cardiovascular control is beyond the scope of this investigation. Therefore, we draw no conclusions concerning menstrual cycle effects. Last, we studied recovery from relatively short-duration, low-intensity exercise; therefore, our results may or may not apply to recovery from longer, more strenuous exercise. Previous studies suggest that short-duration exercise at moderate workloads for <5 min does not cause thermoregulatory reflex-mediated responses such as vasodilation and sweating (13). Therefore, our workload of 60% maximal HR for 3 min probably did not elicit substantial cutaneous vasodilation and sweating, although we did not measure those variables. Recently, our laboratory measured sweat rate and skin blood flow under the same exercise conditions and observed no changes (2).

Conclusions. In summary, this study suggests that women may have increased risk of postexercise orthostatic hypotension, and active recovery from exercise should reduce this risk. This conclusion is based on the observation that women exhibited significantly greater decreases in MAP than men during recovery from dynamic exercise. Women had relatively greater reductions in and did not appear to produce the same degree of compensatory vasoconstriction during inactive recovery as the men in the face of the greater challenge (decrease in ). In addition, the results of the present study confirm previous studies showing that the skeletal muscle pump, i.e., active recovery, is important in the maintenance of MAP during recovery from exercise.