JEPonline
Journal of 
Exercise Physiologyonline

ISSN 1097-9751

An International Electronic
Journal for Exercise Physiologists

Vol 1 No 1 April 1998


Systems Physiology: Cardiopulmonary

Central and peripheral circulatory responses during four different recovery positions immediately following submaximal exercise

DIEGO R. REDONDO and TOMMY BOONE


REDONDO, D.R. and BOONE, T.  Central and peripheral circulatory responses during four different recovery positions immediately following submaximal exercise. JEPonline, Vol. 1 No. 1, 1998. This study compared central and peripheral circulatory responses in 10 untrained males during the second minute of four different recovery positions. Prior to each recovery, subjects exercised at 75% heart rate (HR) intensity on the treadmill. The Beckman Metabolic Measurement Cart (MMC) and the CO2 rebreathing procedure were used to measure oxygen consumption (VO2) and cardiac output (Q), respectively. Analysis of variance (ANOVA) with repeated measures was followed by the Tukey's multiple comparison test to determine statistically significant differences among means (p<0.05). When compared to sitting, standing, and supine recoveries, the walking recovery resulted in significantly higher stroke volume (SV), VO2, double product (DP), and estimated myocardial oxygen consumption (MVO2). These data indicate that the walking recovery kept the subjects' cardiac effort elevated above the physiological responses of the passive recoveries. When compared to sitting and standing recoveries, the supine recovery demonstrated significantly higher SV and responses and significantly lower arteriovenous oxygen difference (a-vO2 diff) and systemic vascular resistance (SVR) responses. However, since the VO2, DP, and MVO2 data were not significantly different during the three passive recoveries, the statistical decision is that the non-active recoveries are cardiovascularly similar. That is, whether the subject is sitting, standing, or in the supine position immediate post- exercise, the physiological responses are the same but only at 2 minutes of recovery.

Key Words: CARDIAC OUTPUT, STROKE VOLUME, CO2 REBREATHING




Introduction
While it is common to study the cardiovascular system during exercise (1), it is less common to do so during the recovery period (2). In fact, about all that is known is that light exercise should be performed during the recovery to enhance lactate removal and normalize blood and muscle acid-base balance (3,4). The recommendation presupposes that the normalization of acid-base balance is more important than the normalization of other physiologic responses. However, a recovery method that minimizes the work of the heart may be more desirable than one that alters acid-base. To evaluate this point, the CO2 rebreathing procedure was used to study the central and peripheral adjustments of the cardiovascular system during four different recovery positions 2 min into recovery following submaximal treadmill exercise.

Methods
Ten healthy males (age 18-25 years) volunteered to participate in this study. All subjects signed informed consent statements. Data were collected during five sessions. During the first session, the subjects were familiarized with the data gathering procedures including treadmill running and the CO2 rebreathing protocol. The data gathered during this session were used to determine the treadmill speed to elicit 75% of the subjects' age-determined maximal heart rate (HR).

The subjects were then scheduled for additional data collection on separate days at approximately the same time each day. All subjects were treated as their own controls, and participated in four submaximal exercise bouts at 75% HR intensity. During each testing session, the subjects were connected to a Cal Med Electrocardiograph (lead III) monitor and the Beckman Metabolic Measurement Cart (that was calibrated prior to each session). The subjects walked on the treadmill at a pace equal to one half of their predetermined running speed. At the end of a three minute warmup, the treadmill speed was increased to elicit the subjects' 75% HR intensity. The subjects ran for seven minutes. Heart rate and oxygen consumption (VO2) were monitored each minute to ensure that the subjects remained at the desired intensity. During the tenth minute of exercise, cardiac output (Q) and blood pressure (BP) were measured.

Following exercise, the subjects recovered in one of the four recovery positions. The walking recovery required the subjects to continue exercising, but at a speed equivalent to the warmup phase. The sitting recovery took place in a chair placed on the treadmill immediately after the completion of the exercise bout. The subjects were asked to sit motionless in the chair with the feet flat on the floor with the hands in their laps. The standing recovery was carried out with the subjects remaining motionless on the treadmill in a relaxed, standing posture with the arms alongside the body. The supine recovery took place on a padded examination table with the legs uncrossed and on the same level as the rest of the body with the arms alongside the body. The order in which the subjects experienced the different recovery positions was determined by a table of random numbers.

The recovery period was evaluated at two minutes postexercise. Heart rate and VO2 were monitored during each minute of recovery. Blood pressure and Q were recorded during minute two of recovery. Cardiac output was measured non-invasively, as described by Campbell and Howell (5). Although the subjects were technically not at steady state during recovery as is typically required when using the CO2 rebreathing procedure, we felt its use was valid in this case for several reasons. First, the workload was sufficiently low to prevent a shift in the CO2 dissociation curve and thus more rapid changes in PvCO2. Second, all rebreathing periods were less than 10 seconds. Hence, the magnitude of the PvCO2 responses was limited. Also, earlier work (6) utilizing the CO2 rebreathing procedure during non-steady state recovery determined that the maximum overestimate of CO2 output in a similar case would be insignificant relative to the total amount of CO2 in the early recovery.

Stroke volume (SV) was determined using the equation SV = Q/HR (7) at minute two of each recovery as well. The following values were also calculated at minute two: (a) arteriovenous oxygen difference, a- vO2 diff = VO2/Q x 100 (8); (b) systemic vascular resistance, SVR = 80 x [mean arterial pressure in mmHg/Q] (9); (c) myocardial oxygen consumption, MVO2 = (DP x .16 - 6.0) x 3.0; (d) and double product, DP = HR x SBP x .01 (7).

These data were evaluated statistically using an analysis of variance (ANOVA) with repeated measures design at the tenth minute of the four treadmill exercise bouts and at minute two of the four recovery periods. Any indication of significant differences was followed by Tukey's multiple comparison test to locate significant differences. The .05 alpha level was used throughout the study.

Results
Table 1 contains the mean data for the subjects' exercise sessions prior to each recovery position. There were no significant differences in the mean exercise values prior to each recovery position. This finding is important because it demonstrates that the subjects began each recovery period at the same physiologic baseline. 
 

Table 1. Central and peripheral circulatory responses of four treadmill runs at 75% HR maximum prior to four different recovery positions (M ± SD)
Variable Walking Sitting Standing Supine F-ratio & Prob
HR 
ml/min

155 
±8

154 
±8

153 
±10

154 
±13

0.34 
& .7978

SV 
ml

106 
±17

106 
±14

102 
±16

105 
±15

0.39 
& .7622


l/min

16.36 
±2.42

16.34 
±2.32

15.59 
±2.38

16.10 
±2.62

1.00 
& .4075

VO2
ml/min

2301 
±874

2689 
±520

2461 
±382

2502 
±340

1.13 
& .3542

SBP 
mmHg

175 
±9

165 
±17

163 
±18

166 
±13

2.30 
& .0993

DBP 
mmHg

83 
±14

80 
±8

85 
±15

83 
±8

0.76 
& .5293

DP


271 
±17

255 
±33

249 
±37

255 
±40

1.97 
& .1410

SVR 
dyn/s/cm-5

563 
±79

538 
±84

579 
±89

540 
±125

0.79 
& .5100

MVO2
ml/min

112 
±8

104 
±16

102 
±18

104 
±19

1.97 
& .1415

a-vO2 diff 
ml/100 ml

16 
±1.4

17 
±3

16 
±1.37

16 
±1.4

0.61 
& .6209

Table 2 summarizes the results obtained when the means of the dependent variables were analyzed at minute two of the four recoveries. The mean HR of the walking recovery was 120 beats/min. This response was significantly higher than the HRs in the sitting and the supine recoveries, but not significantly different from the HR of the standing recovery. The HR in the standing recovery was significantly higher than that of the supine recovery, but not significantly different from the HR of the sitting recovery. The sitting and supine recovery HRs were also not significantly different from each other. The mean SV values for the walking, sitting, standing, and supine recoveries were 85 ml, 46 ml, 40 ml, and 72 ml, respectively. The subjects' SV during the walking recovery was significantly higher than the SV values during the other recoveries. The supine recovery position resulted in a significantly higher SV value than found in both the sitting and standing positions, which were not significantly different from each other.

Cardiac output showed a similar response to SV. The Q response during the walking recovery was significantly higher than the values for the sitting, standing, and supine recovery positions. The Q response during the supine recovery position was significantly higher than Qs during both the sitting and standing recoveries which, again, were not significantly different from each other. The mean VO2 value for the walking recovery position (1179 ml/min) was significantly higher than the VO2 values for sitting, standing, and supine recoveries. None of the latter three values was different from each other. The a-vO2 diff values were 11.70 ml/100 ml, 11.03 ml/100 ml, 11.65 ml/100 ml, and 7.10 ml/100 ml for the walking, sitting, standing, and supine recoveries, respectively. The a-vO2 diff in the supine position was significantly lower than the values of the remaining recoveries. The walking, sitting, and standing recoveries did not demonstrate significant differences in a-vO2 diff.

Table 2. Central and peripheral  circulatory responses to four different recovery positions immediately following submaxmial treadmill exercise (M± SD)
Variable Walking 
(A)
Sitting 
(B)
Standing 
(C)
Supine 
(D)
F-ratio 
& Prob
HR
bts/min


120 ± 10 
A-B** 
A-D**

100 ± 8



110 ± 22
C-D**


91 ± 17



11.89 & .0001*



SV
ml



85 ± 13 
A-B** 
A-C** 
A-D**

46 ± 8 
B-D**



40 ± 12 
C-D**



72 ± 6

 

 

71.57 & .00001*

 

 

Q
l/min



10.17 ± 1.51 
A-B** 
A-C** 
A-D**

4.52 ± .65 
B-D**



4.40 ± 1.74 
C-D**



6.55 ± 1.60
 
 

 

80.96 & .00001*

 

 

VO2
ml/min



1170 ± 99
A-B** 
A-C** 
A-D**

491 ± 98

 

 

493 ± 139

 

 

454 ± 107

 

 

183.97 & .00001*
 
 

 

SBP
mmHg
152 ± 12

137 ± 15

138 ± 13

143 ± 16

2.90 & .0525

DBP
mmHg
79 ± 12

70 ± 17

84 ± 9

79 ± 7

.63 & .6072

DP

 

187 ± 14 
A-B** 
A-C** 
A-D**

136 ± 14
 

 

153 ± 38
 

 

131 ± 38
 

 

13.89 & .00001*
 

 

SVR
dyn/s/cm-5






833 ± 110 
A-B** 
A-C** 
A-D**


1782 ± 418 
B-D**




2048 ± 586 
C-D**




1277 ± 258

 
 

 

25.62 & .00001*


 

 

MVO2
ml/min

 

72 ± 7 
A-B** 
A-C** 
A-D**
47 ± 7
 
 

 

54 ± 21
 
 

 

45 ± 18
 
 

 

11.69 & .00001*
 
 

 

a-vO2 diff
ml/100 ml
11.70 ± .98 
A-D**
11.03 ± 2.52 
B-D**
11.65 ± 1.99
C-D**
7.10 ± 1.73

16.21 & .00001*

      *Statistically significant at 0.05 level of confidence.
    **Statistically significant (Tukey multiple comparison test)


The mean SBP responses during walking, sitting, standing, and supine recoveries were 152 mmHg, 137 mmHg, 138 mmHg, and 143 mmHg, respectively. The means were not significantly different from each other. There were also no significant differences in diastolic blood pressure (DBP) during the different recoveries. The DP value of the walking recovery was 187, which was significantly higher than the DP of the sitting (136), standing (153), and supine (131) recoveries. The latter three recoveries were not significantly different from each other. The SVR value during the walking recovery was significantly lower than the values found during the remaining positions. The supine recovery position had a significantly lower SVR value than both the sitting and standing recoveries, which were not significantly different from each other. The estimated MVO2 values for the walking recovery, sitting recovery, standing recovery and supine recovery were 72 ml/min, 47 ml/min, 54 ml/min, and 45 ml/min, respectively. The walking recovery had a significantly higher MVO2 value than the passive recoveries, which were not significantly different from each other.

Discussion
This investigation compared the central and peripheral circulatory responses during four different recovery positions immediately following exercise. The walking (active) recovery demonstrated a significantly higher Q than did the other three (passive) recoveries. This finding is in agreement with other data (7), and is the result of the continued elevation in HR and SV while walking. The HR response is similar to the findings by Katch et al. (10), who reported higher HRs during exercise recovery versus non-exercise recovery on the cycle ergometer. This finding also agrees with Cummings (2) who showed higher HRs during light exercise than during supine recovery, and with deVries (3) who noted significantly lower HRs when the subjects were in the supine position versus the upright position. The lack of a significantly higher HR during the walking recovery versus during the standing recovery appears to be the result of the subjects' compensation for the lower SVs found when standing versus when exercising (11). The significantly higher SV during the walking recovery is also responsible for the sustained Q. This is consistent with other published accounts (12), which indicate that SV is increased during work due to increased venous return brought about by the action of the skeletal muscle pump (7,13).

The supine recovery resulted in the second highest Q response, surpassing both the sitting and standing recovery Qs. In that the supine recovery did not have a significantly higher HR response than the other two passive recovery positions, (and in fact had a significantly lower HR than the standing recovery position), the Q response, therefore, had to be a result of the subjects' increase in SV. In this regard, Falls (14) showed that SV is lower while standing, and Bevegard et al. (15) showed that SV is lower while sitting than in the supine position. The increased SV in the supine position is a result of increased venous return to the heart due to decreased impedance of blood flow by gravity (8); whereas, gravity hinders the return of blood to the heart when in the sitting and standing positions. There were no significant differences in the HR or SV values during either the sitting recovery or the standing recovery, and consequently there were no significant differences in Q.

Oxygen uptake was significantly higher in the walking recovery than in the other recovery positions. This finding is in agreement with Katch and associates (10) and Gisolfi et al. (16) who reported that their active recovery values for VO2 were higher than their passive VO2 recovery values. Given that VO2 is the product of Q and a-vO2 diff (7), then either or both components affect the VO2 response. The walking recovery position showed a significantly higher Q and a significantly higher a-vO2 diff when compared to the supine recovery position. This result is consistent with previous findings (3,17), which indicate higher a-vO2 diff values when upright versus when supine. Hence, both Q and a-vO2 diff accounted for the significantly higher VO2 in the walking recovery versus the supine recovery. But, the significantly higher Q alone accounted for the higher VO2 during walking versus the sitting and standing recovery VO2s. The VO2 values for the sitting, standing, and supine recoveries were not significantly different from each other. Although the supine recovery Q response was significantly higher than the sitting and standing Q responses, a-vO2 diff was significantly lower in the supine position versus the sitting and standing positions. This outcome resulted in the VO2s being equivalent across the three passive recoveries. Thus, the supine recovery maintained VO2 via a central (SV) adjustment as compared to the peripheral adjustments required in the sitting and standing recoveries.

The walking (active) recovery DP response was significantly higher than the DP responses during the three passive recoveries. This finding is expected given the significantly higher HR while walking and the higher (but not significant) SBP response while walking versus sitting, standing, and supine recoveries. The passive recoveries demonstrated no significant differences in DP given the lack of significant differences in HR and SBP. Similarly, MVO2 was the highest during the walking recovery, which is expected since DP is highly correlated with MVO2(18). Systemic vascular resistance was significantly lower in the walking recovery versus the three passive recoveries. This finding is expected given that SVR is decreased during exercise and is increased during non-exercise conditions (8,19). The higher Q is associated with the lower SVR in the walking recovery as can be seen when examining the equation for determining SVR. As expected, the supine recovery had a significantly lower SVR, due to the significantly higher Q response than did the sitting and standing recoveries. This response is considered necessary to prevent inordinately large increases in blood pressure (20) of which the walking and supine recoveries with their higher Qs might otherwise cause.

Summary
The results demonstrate that in terms of cardiac effort, the active (walking) recovery placed more demands on the heart than did the passive (sitting, standing, supine) recoveries. Except for blood pressure, SVR, a-vO2 diff, and HR while standing, the walking recovery had significantly higher physiologic values across the four recovery positions. This is especially important, given the higher DP and MVO2 responses during the walking recovery. Since they are good indicators of myocardial effort, depending on the physiologic condition of the exercising subject, it may be better to avoid an active recovery. In fact, since there were no significant differences in DP or MVO2 across the three passive recoveries, in terms of myocardial effort, the passive recoveries are not only hemodynamically similar but less stressful than the active recovery. As to which passive recovery is the best, it appears that the sitting and standing recovery positions are more physiologically similar than is the supine recovery to either (particularly with respect to SV). In fact, given the significant decrease in SV during the sitting and standing recoveries, which should not go unnoticed, the supine recovery position therefore appears to be physiologically the best of the three passive recoveries immediately after submaximal exercise. 


References
1. Miles D, Sawka M, Hanpeter D, Foster J, Doerr B, Frey A. Central hemodynamics during progressive upper- and lower-body exercise and recovery. J Appl Physiol 1984;57:366-370.
2. Cumming GR. Stroke volume recovery from supine bicycle exercise. J Appl Physiol1972;32:575-578.
3. deVries HA. Physiology of exercise for physical education and athletics. Iowa: Wm C Brown Company, 1980.
4. McArdle WD, Katch VL, Katch FI. Exercise physiology: energy, nutrition, and human performance. Philadelphia: Lea & Febiger, 1996.
5. Campbell EJM, Howell JBL. Rebreathing method for measurement of mixed venous PvCO2. Br Med J 1962;3:630-33.
6. Goldberg D, Shephard R. Stroke volume during recovery from upright bicycle exercise. J Appl Physiol: Respirat Environ Exercise Physiol 1980;48:833-837.
7. Astrand P-O, Rodahl K. Textbook of work physiology, 2nd edition. New York: McGraw-Hill Book Company, 1977.
8. Fox EL, Mathews DK. The physiological basis of physical education and athletics. Philadelphia: Saunders Publishing, 1981.
9. Saksena, F.B. Hemodynamics in cardiology. New York: Praeger Publishers, 1983.
10. Katch VL, Gilliam T, Weltman A. Active vs. passive recovery from short- term supramaximal exercise. Res Q 1978;49:153-161.
11. Fox SI. Human physiology. Iowa: Wm C Brown Company, 1984.
12. Jensen CR, Fisher AG. Scientific basis of athletic conditioning. Philadelphia: Lea & Febiger, 1979.
13. Noble BJ. Physiology of exercise and sport. St. Louis: Mosby College Publishing, 1986.
14. Falls HB. Exercise physiology. New York: Academic Press, Inc., 1968.
15. Bevegard BS, Freyschuss U, Strandell T. Circulatory adaptations to arm and leg exercise in man. J Appl Physiol 1966;21:37.
16. Gisolfi C, Robinson S, Turrell ES. Effects of aerobic work performed during recovery from exhausting work. J Appl Physiol 1966;21:167-172.
17. Reeves JT, Grover RF, Blount SG, Filley GF. Cardiac output response to standing and treadmill walking. J Appl Physiol 1961;16:283- 288.
18. Kitamura K, Jorgensen C, Gobel G, Taylor H, Wang Y. Hemodynamic correlates of myocardial oxygen consumption during upright exercise. J Appl Physiol 1972;32:516-522.
19. Guyton, A.C. Textbook of medical physiology. Philadelphia: W.B. Saunders Publishing, 1986.
20. Strauss RH, Editor. Sports medicine. Philadelphia: W.B. Saunders, 1984.
Return to Contents
Copyright ©1998

American Society of Exercise Physiologists
All Rights Reserved