Abstract

Studies found that cardiovascular responses to exercise are enhanced in individuals with obesity and are associated with a greater cardiac output (CO) response compared to normal weight controls. However, the mechanisms underlying these altered responses during dynamic exercise are not clear. We investigated whether the cardiovascular responses mediated by the muscle metaboreflex (MMR) activation are augmented in obese men during both static and dynamic exercise. Twenty males (10 obese (OG) and 10 non-obese (NOG)) were studied. Changes in CO, mean arterial pressure (MAP), and total vascular conductance (TVC) were compared between the two groups during dynamic handgrip exercise (DHE), post-exercise muscular ischemia (PEMI), and dynamic exercise corresponding to 40%, 60% and 80% workloads. Subjects completed 2 min of DHE at 30% of MVC, followed by 2 min of PEMI. MAP, CO, and TVC responses to DHE and dynamic exercise were significantly higher in OG, whereas there were no differences during PEMI. Increases in CO and MAP during mild to heavy dynamic exercise were seen in both groups, but the changes in these variables were greater in the OG. There were no significant differences in TVC between the two groups. Compared to NOG, the augmented blood pressure response to DHE and dynamic exercise in OG was associated with a greater increase in CO. Thus, the augmented CO and MAP responses were not associated with the activation of the MMR. Consequently, additional factors specific to obesity, such as the mechanoreflex, may have been involved.

Highlights

  • As the prevalence of obesity increases dramatically worldwide [1,2,3], it is considered a major public health problem

  • In support of our findings, a previous study found that there were no differences in mean arterial pressure (MAP), cardiac output (CO) and peripheral vasoconstriction responses to the muscle metaboreflex (MMR) activation between metabolically healthy obese individuals and non-obese individuals [48]. These findings suggest that obesity evokes heightened blood pressure (BP) by an increase in CO response to static or rhythmic exercise; yet this alteration is not associated with the MMR

  • This study investigated that the exercise-induced excessive BP response is mainly due to an increase in CO mediated by the MMR activation in OG

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Summary

Introduction

As the prevalence of obesity increases dramatically worldwide [1,2,3], it is considered a major public health problem. Regular exercise has been shown to reduce body fat as well as protect against cardiovascular diseases associated with obesity [6,7,8]. Obesity produces excessive increases in arterial blood pressure (BP) during exercise [9,10]. These augmented BP responses may increase the risk of cardiac events associated with exercise (e.g., stroke, acute myocardial infarction) [11,12,13]. Understanding the mechanism that produces the altered hemodynamic responses during acute bouts of exercise may be important to reduce the future risk of cardiovascular disease

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