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Department of Human Physiology, University of Oregon, Eugene, Oregon
Submitted 26 October 2004 ; accepted in final form 12 December 2004
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ABSTRACT |
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O2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, O2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, O2 remained elevated by 4 ± 2% (P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena. metabolism; hemodynamics; skeletal muscle; recovery
O2 peak)] exercise, whereas shorter or less vigorous exercise elicits inconsistent changes in arterial pressure in normotensive subjects (13, 21). In most subjects, postexercise hypotension is due to a persistent rise in systemic vascular conductance that is not completely offset by increases in cardiac output (21, 23–25), although some exceptions exist [e.g., endurance-trained men (36)]. Whereas sustained vasodilation has been partially linked to a reduced sympathetic neural outflow to skeletal muscle vascular beds and reduced vascular responsiveness to a given sympathetic outflow (15, 22, 24), additional factors appear to mediate the persistent vasodilation during postexercise hypotension (21, 23, 29).
Skeletal muscle blood flow increases with exercise because of local events in the muscle that continually regulate blood flow to meet the changing metabolic demands (37). Immediately after the cessation of intense muscle activity, skeletal muscle blood flow may be as high as 10–15 times the resting value (37), revealing the high flow capacity of active human muscles (33). A single bout of dynamic exercise also generates an elevated postexercise oxygen uptake (O2) (2, 3, 16, 26, 30). This increase in postexercise O2 is commonly referred to as excess postexercise O2 (EPOC) and is described as the excess O2 above that required to support resting metabolic processes after exercise (16). Several factors have been implicated in the generation of EPOC, including, the metabolism of lactate and replenishment of creatine phosphate (5, 7, 8, 14, 16, 19, 26, 30, 35), muscle glycogen resynthesis (8), increased body temperature (6, 9, 12, 20), increased heart rate (12), increased ventilatory rate (19), increased circulating concentrations of catecholamine hormones (4, 10, 11, 17), and replenishing the body's resting oxygen levels (18, 39).
Skeletal muscle blood flow remains elevated several hours postexercise, for reasons that remain unidentified and via an unknown mechanism. It is possible that this elevation is related to meeting the metabolic demands associated with EPOC. Along these lines, regional oxygen delivery and utilization are the product of blood flow and the arteriovenous oxygen difference (i.e., the Fick equation) (33). Muscular exercise is accompanied by increases in skeletal muscle blood flow from 
1.2 l/min at rest to 20–25 l/min during maximal exercise (37). However, the exact vasodilator mechanism or mechanisms underlying exercise hyperemia remain elusive. It is likely that vasodilator metabolites formed by active skeletal muscles act on the resistance vessels in their vicinity to raise local blood flow to match metabolic demands (34). It seems plausible that the sustained elevation of skeletal muscle blood flow after exercise may similarly subserve a continued elevation in skeletal muscle O2. If so, then elevated oxidative metabolism may be one of the causes of the sustained vasodilation in skeletal muscle vascular beds that underlies postexercise hypotension.
Therefore, this study was undertaken to examine the potential association between EPOC and the sustained increase in skeletal muscle blood flow during postexercise hypotension. Specifically, we tested the hypothesis that EPOC would correlate closely with the changes in leg blood flow during recovery from a single bout of dynamic exercise in humans.
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METHODS |
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Subjects
A total of 16 healthy, moderately active, nonsmoking, normotensive subjects between the ages of 20 and 31 yr participated in this study (7 men, 9 women). None of the subjects was taking medications other than oral contraceptives. All female subjects had a negative serum pregnancy test on the screening day. Because the effects of the menstrual cycle on postexercise hypotension are unknown, female subjects were studied during the early follicular phase (1–4 days after the onset of menstruation) or during the placebo phase of oral contraceptives to control for this potential influence.
Screening Visit
Subjects reported to the laboratory for a screening day scheduled at least 2 days before the study day. Subjects reported for this visit at least 2 h postprandial and abstained from caffeine, alcohol, and exercise for 24 h before this visit. Subjects performed an incremental bicycle exercise test (Lode Excaliber, Groningen, The Netherlands) comprised of 1-min workload increments to determine O2 peak. Specifically, after a 2 min warm-up period of easy cycling (20–30 W), workload increased at 20, 25, or 30 W every minute. Selection of the workload increment was subjective, with the goal of producing exhaustion within 8–12 min. Whole body O2 uptake was measured via a mixing chamber (Parvomedics, Sandy, UT) integrated with a mass spectrometry system (Marquette MGA 1100, MA Tech Services, St. Louis, MO). All subjects reached subjective exhaustion (rating of perceived exertion = 19–20) within 12–16 min. After the subjects rested for 15–20 min, they returned to the cycle ergometer for assessment of the workload corresponding to a steady-state O2 of 60% of O2 peak. This workload was used on the study day for the 60-min exercise bout. Subjects self-reported activity levels on two questionnaires (1, 27). Finally, subjects were instructed to ingest the temperature sensing pill the night before reporting to the laboratory for the study day visit. Subject characteristics are presented in Table 1.
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Subjects reported for the study between 6 and 10 AM at least 8 h postprandial. Subjects abstained from caffeine at least 8 h and from alcohol and exercise 24 h before the study. Ingestion of a temperature-sensing pill (HQInc, Palmetto, FL) the evening before the study was used to assess internal temperature as an index of core body temperature. After visiting the restroom, subjects were instrumented on a table for measurement of heart rate via a five-lead electrocardiogram (model Q710, Quinton Instruments Bothell, WA) and arterial pressure via an automated blood pressure monitor (Dinamap Pro100 vital signs monitor, Critikon, Tampa, FL).
Measurements. Preexercise and postexercise measurements were made with subjects in the supine position and consisted of consecutive recordings of heart rate, arterial pressure, internal temperature, and leg blood flow every 15 min for 60 min preexercise and 135 min postexercise.
O2 was measured continuously using a custom-built dilution hood and mass spectrometer-based metabolic system (Parvomedics, Sandy, UT). Ambient air was drawn through a loosely fitting hood past the subject's nose and mouth at a rate sufficient to prevent escape of expired gas (i.e., up to 60 l/min). The rate was adjusted to maintain flow-through carbon dioxide concentrations between 1 and 1.5%.
Femoral artery diameter and velocity were measured by using an ultrasound probe (10-MHz linear vascular probe, GE Vingmed System 5, Horton, Norway). The entire width of the artery was insonated with an angle of 60°. Velocity measurements were taken immediately after diameter measurements and were corrected for the angle of insonation. Leg blood flow was calculated as artery cross-sectional area multiplied by femoral mean blood velocity, doubled to represent both legs, and reported as milliliters per minute. Leg vascular conductance was calculated as flow for both legs divided by mean arterial pressure and expressed as milliliters per minute per millimeters of mercury.
Exercise.
Subjects exercised upright on a stationary cycle at 60% of O2 peak for 60 min. Exercise of this intensity and duration consistently produces a sustained (2 h) postexercise hypotension in healthy normotensive subjects (21). Heart rate, arterial pressure, and internal temperature were recorded every 15 min throughout the exercise period. During exercise, subjects drank 15 ml of water/kg of initial body weight to offset volume loss.
Statistics
The results were analyzed with repeated-measures ANOVA. Significant effects were further tested with Fisher's least significant difference test, and differences were considered significant when P < 0.05. All values are reported as means ± SE.
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RESULTS |
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During exercise, heart rate increased from 55.0 ± 2.2 to 139.3 ± 4.0 beats/min (average over 60 min; P < 0.05). The goal was to have each subject exercise for 60 min at 60% O2 peak. The percentage of heart rate reserve (heart rate reserve is defined as maximal heart rate achieved during O2 peak testing minus the resting supine heart rate) reached during exercise (64.9 ± 3.5%) was consistent with the target workload. Systolic blood pressure increased from 108.0 ± 2.8 mmHg during supine rest to 141.3 ± 4.4 mmHg (P < 0.05), whereas diastolic blood pressure was unchanged (60.8 ± 1.6 vs. 64.3 ± 2.2 mmHg) over the 60-min bout of exercise. Therefore, mean arterial pressure increased from 77.4 ± 1.5 mmHg during supine rest to 90.7 ± 8.2 mmHg during exercise (P < 0.05). Internal body temperature increased from 36.7 ± 0.1°C during supine rest to 37.9 ± 0.1°C by the final min of exercise (P < 0.05).
Postexercise
Figure 1 shows mean arterial pressure, whole body O2, and leg blood flow preexercise and through 135 min postexercise. Notably, whole body O2 was increased by 11% during the first hour postexercise compared with preexercise (P < 0.05). This elevated O2 was maintained throughout the study protocol, such that O2 at the end of the protocol remained 4% greater than preexercise values (P < 0.05). Leg blood flow increased from 207 ± 30 ml/min before exercise to 280 ± 39 ml/min during the first hour postexercise (P < 0.05). By 105 min postexercise, leg blood flow decreased to within preexercise levels (P = 0.82).
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O2 vs. leg blood flow throughout the protocol. At 15 min postexercise, both leg blood flow and O2 exhibited high values. However, by 30 min postexercise, there was a substantial decline in O2 with little change in leg blood flow. Through the remainder of the protocol, leg blood flow progressively returned to resting preexercise levels, but O2 remained elevated.
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O2 across individuals for the representative time point of 45 min postexercise. Individual responses were variable. The change in mean arterial pressure ranged from –11.4 to +3.7 mmHg, the change in leg vascular conductance ranged from –27.2 to +209.4%, and the change in O2 ranged from –18.0 to +26.1% at this time point. There did not appear to be an association between the degree of pressure reductions and elevations in O2 (r = 0.40, P = 0.13). Similarly, there did not appear to be an association between the degree of leg vasodilation and elevations in O2 (r = 0.37, P = 0.16).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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We assessed changes in metabolism via changes in O2. These data indicate that the preceding exercise caused a modest but prolonged increase in metabolism, requiring an additional 2.86 ± 0.93 liters of oxygen through 135 min of recovery. This observation is consistent with prior reports on EPOC (2, 3, 16, 26, 30). Several factors have been implicated in the generation of EPOC, including the metabolism of lactate and replenishment of creatine phosphate (5, 7, 8, 14, 16, 19, 26, 30, 35), muscle glycogen resynthesis (8), increased body temperature (6, 9, 12, 20), increased heart rate (12), increased ventilatory rate (19), increased circulating concentrations of catecholamine hormones (4, 10, 11, 17), and replenishing the body's resting oxygen levels (18, 39). Some of the metabolic products created during exercise whose oxidation may contribute to the EPOC may also stimulate increases in blood flow to previously active skeletal muscle (38), creating a "postexercise hyperemia."
Our subjects demonstrated a reduction in blood pressure through 60 min after the cessation of exercise consistent with prior reports on postexercise hypotension (21–25). Underlying this postexercise hypotension, we observed an elevated leg blood flow through 90 min postexercise. This rise in skeletal muscle blood flow after exercise is well documented but poorly understood. Although there is clear evidence of reduced sympathetic outflow to skeletal muscle vascular beds in humans (15, 24) and rats (28) during postexercise hypotension, blockade of 
-adrenergic receptors is unable to reproduce the magnitude of postexercise vasodilation in skeletal muscle. There is evidence of vascular -adrenergic hyporesponsiveness in rats (32), but 1- and 2-adrenergic vascular responsiveness is intact in humans (22). Finally, although nitric oxide contributes to postexercise vasodilation in rats (31), independent inhibition of either nitric oxide synthase (23) or cyclooxygenase (29) does not reduce the postexercise vasodilation in humans. Thus additional factors appear to mediate the persistent vasodilation during postexercise hypotension and could be related to ongoing release of metabolic signals from the previously exercised muscle.
We have considered the possibility that this elevation in blood flow to previously active muscles could subserve a continued demand for oxygen delivery and perhaps be linked to EPOC. However, our data appear inconsistent with this model for the following reasons. First, if the elevation in leg blood flow were related to an increase in oxygen utilization in the leg, we would have expected a linear relation between O2 and leg blood flow, which we did not find (Fig. 2). Second, individual differences in the metabolic and hemodynamic responses to exercise exist (Fig. 3), yet we found no association between changes in O2 and changes in either arterial pressure or leg vascular conductance after exercise. In fact, some pairs of subjects had very similar reductions in mean arterial pressure despite dissimilar metabolic responses after the exercise. Some subjects exhibited very high EPOC with virtually no reductions in blood pressure, whereas others had significant blood pressure reductions with no elevation in O2. Taken together, these data suggest that EPOC and the elevation in skeletal muscle blood flow underlying postexercise hypotension are not associated and that it is unlikely there is a causal link between these two postexercise phenomena.
We did not measure the arteriovenous oxygen difference across the leg vascular bed, so we cannot be certain that changes in leg blood flow were not accompanied by simultaneous changes in local O2. On the basis of the Fick equation relating O2, blood flow, and the arteriovenous oxygen difference, and our observation that leg blood flow returns to resting values while O2 remained elevated, the only way the excess oxygen could be utilized by the legs would be if there were a progressive rise in the arteriovenous oxygen difference over the 135-min postexercise period. Because this seems highly unlikely, it would appear that the sustained rise in O2 was the result of an increased oxygen utilization in some other vascular bed and not in the previously exercised skeletal muscles of the leg.
We were able to document vasodilation in terms of leg vascular conductance in this protocol, despite what can be considered only a modest postexercise hypotension. The magnitude of postexercise hypotension is greater in hypertensive individuals than the normotensive subjects we studied, and we note that our conclusions regarding the absence of an association between EPOC and postexercise hypotension may be limited to healthy individuals of average fitness. Thus it could be that in different populations (e.g., older individuals with hypertension), elevated metabolism during recovery from exercise contributes to the vasodilation that underlies postexercise hypotension.
Conclusion
In summary, we assessed the potential relationship between postexercise hypotension and EPOC after a bout of moderate-intensity, dynamic exercise. Our observations suggest that the elevated leg blood flow after exercise is not the result of an increased oxygen utilization in the previously exercised skeletal muscle of the legs. These data also demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.
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GRANTS |
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ACKNOWLEDGMENTS |
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This study was conducted by J. T. Williams in partial fulfillment of the requirements for the degree of Masters of Science at the University of Oregon.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
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-block. J Appl Physiol 30: 838–843, 1971.[Medline]
-block on O2 uptake and blood flow in dog hindlimb. J Appl Physiol 51: 1245–1250, 1981.[Medline]
O2 during recovery. Med Sci Sports Exerc 14: 471–476, 1982.
O2 responses of patients with McArdle's disease. J Appl Physiol 68: 1393–1398, 1990.-Adrenergic vascular responsiveness during postexercise hypotension in humans. J Physiol 550: 279–286, 2003.-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide. Am J Physiol Regul Integr Comp Physiol 282: R960–R968, 2002.
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, Preexercise; 
, measurements every 15 min postexercise. Superimposed arrows indicate the time course of postexercise measurements, moving from 15 to 30 min postexercise and from 30 to 135 min postexercise. Values are means ± SE; n = 16 subjects.
) in mean arterial pressure vs. percent change in oxygen uptake from preexercise to 45 min postexercise. Bottom: individual percent change in leg vascular conductance vs. percent change in oxygen uptake from preexercise to 45 min postexercise. Values are means ± SE; n = 16 subjects.