Postexercise HR was always higher than at rest in SeEG. However, in SuEG, the HR at rest was lower than at 10 and 20 minutes after the resistance exercises. Also, the HR at 30 minutes was lower than at 10 minutes (Table 3).
The present study investigated the influence of body posture on BP and HR responses to a session of resistance exercises. The results revealed that MAP was lower at rest over 30 minutes after the exercises only in the supine position. In this sense, the major finding of the present study is that the postexercise hypotensive response is affected by posture during BP assessment.
Although few studies have investigated the effects of resistance exercise on BP, there is evidence to suggest that moderate resistance exercise can be part of a nonpharmacologic intervention strategy to prevent and treat high BP (4). However, the PEH clinical significance relies on its duration and magnitude (11), which would enhance the possibility of subacute inhibitory response, leading to a temporal summation able to induce actual adaptations (21).
Studies have reported significant decline in BP after acute resistance exercise applied at different combinations of volume and intensity. These studies reported PEH using seated recovery to assess the BP (1,21,22,28,30,33). However, the cardiovascular responses may be affected by the body posture. For instance, Raine et al. (29) showed that SBP, DBP, MAP, and PP measured in the seated posture did not differ from the supine posture for 30 minutes after a graded, upright cycling protocol to volitional exhaustion, whereas the HR was significantly lower in the latter. Takahashi et al. (34) confirmed these results, showing that, after 15 minutes in a given rest condition, the HR was higher in the seated (81.7 ± 8.6 bpm) than in the supine recovery posture (62.3 ± 6.9 bpm).
In the present study, there were no changes in BP variables in the rest condition. On the other hand, the HR in SuEG was lower (66.8 ± 3.7 bpm), but not significantly, than in SeEG (71.5 ± 2.1 bpm). It is worth mentioning that, in the present study, the subjects remained at rest for 10 minutes before the exercise protocol, whereas Raine et al. (29) asked subjects to rest for 30 minutes. This difference can partially explain the fact that the HR did not decline significantly in SuEG, which would occur if this posture were sustained longer before exercising. However, the SuCG and SeCG values were similar, suggesting body posture does not influence HR response, at least during the investigated term.
One possible explanation for the influence of the body posture upon resting HR relates to blood transfer to the veins, especially in the regions that are below heart level. When the subject is seated or standing, the hydrostatic pressure gradient increases the BP in regions distant from the heart (35). This gravity effect leads to a greater amount of blood shifting into the veins. Because the potential of the muscle pump to stimulate venous return is lower at rest, the cardiac output tends to decrease. Thus, the HR increases to compensate for a lower stroke volume (11), whereas the supine posture tends to transfer blood to the upper body. The enhanced blood and fluid volume centralization increase venous return, which stimulates baroreceptors, increases cardiac filling and stroke volume, and reduces HR reflexively (29).
After exercise, regardless of body posture, the HR values were higher than at rest, even when there was PEH. The mechanism that explains this effect is partially the same as that previously described. In fact, one of the possible causes of PEH is a reduction of peripheral resistance, which can increase blood flow. This enhanced systemic blood flow relates to a higher shunting of blood to the veins, but the venous return decreases because of the absence of muscle contraction. Consequently, the left ventricular end-diastolic volume and the stroke volume decrease, whereas the HR increases to preserve cardiac output (12-14). This HR increase is mediated by cardiac sympathetic activity combined with reduced parasympathetic modulation of sinoatrial nodes (15,30).
Body posture may influence the postexercise BP responses, but research on this matter is controversial. Raine et al. (29) did not find differences between SBP and MAP as assessed during seated and supine recovery after incremental cardiopulmonary exercise testing protocols of approximately 16 minutes. On the other hand, Raine et al. (29) showed that DBP had larger decreases when measured during supine recovery. Takahashi et al. (34) suggested different conclusions when comparing the cardiovascular responses after 5-minute cycle ergometer exercise at 80% of maximal oxygen uptake. There were no differences between SBP and DBP assessed during 10 minutes in the seated and supine recovery, which may be partially explained by the short period of observation.
In the present study, the SBP decrease in SeEG after the resistance exercises was not statistically different from SuEG. However, the absolute values recorded for SeEG were systematic lower, which suggests that BP responses were more sensitive in this body posture. These data support those reported by Raine et al. (29) because the PEH in SBP was slightly higher at seated (11 ± 3 mm Hg) than at supine recovery (8 ± 3 mm Hg). Such SBP response may influence the MAP postexercise values because MAP was significantly lower than at rest for SeEG, but not for SuEG. An effect of the exercise on the baroreflex control (24) and the gravitational stress during the seated recovery (29,32), potentially enhancing the PEH, could explain these findings. It should be noted that prolonged sitting (i.e., without prior exercise) imposes a great orthostatic stress in men, with consequent hemodynamic changes that raise peripheral resistance and MAP (9). This might help to explain why resistance exercises influenced the SeEG response more than the SuEG.
In conclusion, body posture can influence BP after resistance exercises. The present findings suggest that the seated posture was related to a higher hypotensive response compared with the supine posture. Such results should be taken into account in studies that aim to observe the cardiovascular responses after resistance training sessions.
A better understanding of the postexercise cardiovascular responses can be important for some population groups, including those with hypertension or coronary heart disease, as well as among healthy, young subjects, to control long-term resting BP. In this context, the control of body posture during assessment of postexercise cardiovascular responses can be useful for determining the specific influence of resistance exercises on variables such as HR and BP while avoiding misinterpretation bias. The results of the present study indicate that seated recovery is suitable for PEH assessment after resistance exercise because MAP reduction was significant only in this posture, implying that supine recovery may mask the hypotensive response because of reduced orthostatic stress.
1. Brown, SP, Clemons, JM, He, Q, and Liu, S. Effects of resistance exercise and cycling on recovery blood pressure. J Sports Sci
12: 463-468, 1994.
2. Byrne, HK and Wilmore, JH. The effects of resistance training
on resting blood pressure in women. J Strength Cond Res
14: 411-418, 2000.
3. Cleroux, J, Kouame, N, Nadeau, A, Coulombe, D, and Lacourciere, Y. After effects of exercise on regional and systemic hemodynamics in hypertension. Hypertension
19: 183-191, 1992.
4. Cornelissen, VA and Fagard, RH. Effect of resistance training
on resting blood pressure: a meta-analysis of randomized controlled trials. J Hypertens
23: 251-259, 2005.
5. Dujic, Z, Ivancev, V, Valic, Z, Bakovic, D, Marinovic-Terzic, I, Eterovic, D, and Wisloff, U. Postexercise hypotension
in moderately trained athletes after maximal exercise. Med Sci Sports Exerc
38: 318-322, 2006.
6. Fisher, MM. The effect of resistance exercise on recovery blood pressure in normotensive and borderline hypertensive women. J Strength Cond Res
15: 210-216, 2001.
7. Floras, JS, Sinkey, CA, Alyward, PE, Seals, DR, Thoren, PN, and Mark, AL. Postexercise hypotension
and sympathoinhibition in borderline hypertensive men. Hypertension
14: 28-35, 1989.
8. Goto, C, Higashi, Y, Kimura, M, Noma, K, Hara, K, Hakagawa, K, Kawamura, M, Chayama, K, Yoshizumi, M, and Nara, I. Effect of different intensities of exercise on endothelium-dependent vasodilation in humans: role of endothelium-dependent nitric oxide and oxidative stress. Circulation
108: 530-535, 2003.
9. Gotshall, RW, Aten, LA, and Yumikura, S. Difference in the cardiovascular response to prolonged sitting in men and women. Can J Appl Physiol
19: 215-225, 1994.
10. Hagberg, JM, Montain, SJ, and Martin, WH. Blood pressure and hemodynamic responses after exercise in older hypertensives. J Appl Physiol
63: 270-276, 1987.
11. Halliwill, JR. Mechanisms and clinical implications of post-exercise hypotension in humans. Exerc Sport Sci Rev
29: 65-70, 2001.
12. Halliwill, JR, Minson, CT, and Joyner, MJ. Effect of systemic nitric oxide synthase inhibition on postexercise hypotension
in humans. J Appl Physiol
89: 1830-1836, 2000.
13. Halliwill, JR, Taylor, JA, and Eckberg, DL. Impaired sympathetic vascular regulation in humans after acute dynamic exercise. J Physiol
495: 279-288, 1996.
14. Hayes, PM, Lucas, JC, and Shi, X. Importance of post-exercise hypotension in plasma volume restoration. Acta Physiol Scand
169: 115-124, 2000.
15. Heffernan, KS, Kelly, EE, Collier, SR, and Fernhall, B. Cardiac autonomic modulation during recovery from acute endurance versus resistance exercise. Eur J Cardiovasc Prev Rehabil
13: 80-86, 2006.
16. Howard, MG and Dicarlo, SE. Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit. J Appl Physiol
73: 2662-2667, 1992.
17. Lockwood, JM, Pricher, MP, Wilkins, BW, Holowatz, LA, and Hallwill, JR. Postexercise hypotension
is not explained by a prostaglandin-dependent peripheral vasodilation. J Appl Physiol
98: 447-453, 2005.
18. MacDonald, JR, Hogben, CD, Tarnopolsky, MA, and MacDougall, JD. Post exercise hypotension is sustained during subsequent bouts of mild exercise and simulated activities of daily living. J Hum Hypertens
15: 567-571, 2001.
19. MacDonald, JR, MacDougall, J, and Hogben, C. The effects of exercise intensity on post exercise hypotension. J Hum Hypertens
13: 527-531, 1999.
20. MacDonald, JR, MacDougall, JD, and Hougben, CD. The effects of exercise duration on post-exercise hypotension. J Hum Hypertens
14: 125-129, 2000.
21. MacDonald, JR, MacDougall, JD, Interisano, SA, Smith, KM, McCartney, N, Moroz, JS, Younglai, EV, and Tarnopolsky, MA. Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise. Eur J Appl Physiol Occup Physiol
79: 148-154, 1999.
22. Mediano, MFF, Paravidino, V, Simão, R, Pontes, FL, and Polito, MD. Subacute behavior of the blood pressure after power training
in controlled hypertensive individuals. Braz J Sports Med
11: 307-309, 2005.
23. Nobrega, ACL. The subacute effects of exercise: concept, characteristics, and clinical implications. Exerc Sport Sci Rev
33: 84-87, 2005.
24. Norton, KH, Boushel, R, Stange, S, Saltin, B, and Raven, PB. Resetting of the carotid arterial baroreflex during dynamic exercise in humans. J Appl Physiol
87: 332-338, 1999.
25. Pescatello, LS, Fargo, AE, Leach, CN, and Scherzer, HH. Short-term effect of dynamic exercise on arterial blood pressure. Circulation
83: 1557-1561, 1991.
26. Pickering, TG, Hall, JE, Appel, LJ, Falkner, BE, Graves, J, Hill, MN, Jones, DW, Kurtz, T, Sheps, SG, and Rocella, EJ. Recommendations for blood pressure measurement in humans and experimental animals. Part 1: Blood pressure measurement in humans. A statement for professionals from the subcommittee of professional and public education of the American Heart Association council on high blood pressure research. Hypertension
45: 142-161, 2005.
27. Polito, MD, Rosa, CC, and Schardong, P. Acute cardiovascular responses on knee extension at different performance modes. Braz J Sports Med
10: 177-180, 2004.
28. Polito, MD, Simão, R, Senna, GW, and Farinatti, PTV. Hypotensive effects of resistance exercises performed at different intensities and same work volumes. Braz J Sports Med
9: 74-77, 2003.
29. Raine, NM, Cable, NT, George, KP, and Campbell, IG. The influence of recovery posture on post-exercise hypotension in normotensive men. Med Sci Sports Exerc
33: 404-412, 2001.
30. Rezk, CC, Marrache, RCB, Tinucci, T, Mion, D Jr, and Forjaz, CLM. Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity. Eur J Appl Physiol
98: 105-112, 2006.
31. Rondon, MUPB, Alves, MJNN, Braga, ANFW, Teixeira, OTUN, Barreto, ACP, Krieger, EM, and Negrão, CE. Postexercise blood pressure reduction in elderly hypertensive patients. J Am Coll Cardiol
39: 676-682, 2002.
32. Rowell, LB. Human Cardiovascular Control
. New York: Oxford University Press, 1993.
33. Simão, R, Fleck, S, Polito, MD, Monteiro, WD, and Farinatti, PTV. Effects of resistance training
intensity, volume, and session format on the postexercise hypotensive response. J Strength Cond Res
19: 853-858, 2005.
34. Takahashi, T, Havano, J, Okada, A, Saitoh, T, and Kamiva, A. Effects of the muscle pump and body posture on cardiovascular responses during recovery from cycle exercise. Eur J Appl Physiol
94: 576-583, 2005.
35. Vander, A, Sherman, J, and Luciano, D. Human Physiology: The Mechanisms of Body Function. New York: William C Brown, 1997.