COMMENTARIES

The Metabolic Syndrome and the Immediate Antihypertensive Effects of Aerobic Exercise

Linda S. Pescatello, Department of Kinesiology, University of CT, Storrs, CT

Please address correspondence to:
Linda S. Pescatello, Ph.D., FACSM
Professor
University of Connecticut
Department of Kinesiology, U-1110
Human Performance Laboratory
Neag School of Education
Storrs, CT 06269-1110
Tel: (860) 486-0008
Fax: (860) 486-1123
Email: Linda.Pescatello@uconn.edu

Linda S. Pescatello


Background

 

The metabolic syndrome (Msyn) affects about 30% of the general population [1] and 40% of those with hypertension [2]. Middle-aged adults with high BP and the Msyn are at higher cardiovascular disease risk (CVD) than those with high BP {systolic BP (SBP) >115 mmHg} and without the Msyn [3,4]. Participation in habitual physical activity and higher cardiovascular fitness are inversely related to the prevalence of CVD, hypertension, and the Msyn [5-7]. Lifestyle modifications are recommended for the prevention, treatment, and control of hypertension and the Msyn, with exercise being an essential component [5,7,8]. Some of the health benefits ascribed to aerobic exercise training programs are due to the acute or immediate responses from a single exercise session, effects that persist from one to three days depending on the CVD risk factor targeted [5,9]. The immediate antihypertensive effects of aerobic exercise, i.e. postexercise hypotension (PEH), result in BP decreases of 5-7 mm Hg that endure for up to 22 hours after the exercise session [5].

Insulin resistance and hyperinsulinemia are thought to be primary etiologic agents of hypertension and the Msyn [10-12]. Multiple mechanisms have been postulated to explain these associations including activation of the sympathetic nervous system, proliferation of vascular smooth muscle, altered cation transport, and increased sodium reabsorption. These derangements increase peripheral vasculature resistance, impair glucose tolerance, provoke dyslipidemia, and endothelial dysfunction, and elevate BP [11,12-14]. Mancia and colleagues [4] longitudinally assessed the relationship between the Msyn and early death among 2,013 adults from 25-74 years of age. The associations they found among the Msyn and death from CVD and all causes were primarily explained by hypertension and hyperglycemia. Despite a common underlying pathophysiology and the importance of exercise in the treatment, prevention, and control of hypertension and the Msyn, the influence of the Msyn on the immediate antihypertensive effects of aerobic exercise among those high BP is not known.

 

Results

We examined the influence of the Msyn on the BP response immediately following a session of low (LIGHT, 40% peak oxygen consumption, VO2peak) and moderate (MODERATE, 60% VO2peak) intensity, aerobic exercise among 46 overweight (body mass index, 29.5 ± (SEM) 0.7 kg·m-2), middle-aged (44.3 ± 1.3 yr) Caucasian men with pre- to Stage 1 hypertension (145.5 ± 1.6/86.3 mmHg). Of these men, 39.1% had the Msyn. Men with the Msyn had higher fasting insulin [111.8 ± 17.1 versus 59.5 ± 7.0 pmol·L-1], homeostasis model assessment (HOMA) (3.3 ± 0.6 versus 1.7 ± 0.2), total cholesterol/high density lipoprotein-cholesterol ratio 5.4 ± 0.2 versus 4.2 ± 0.2 U), and triglycerides (2.4 ± 0.3 versus 1.1 ± 0.1 mmol·L-1) and lower high density lipoprotein cholesterol (0.93 ± 0.03 versus 1.21 ± 0.04 mmol·L-1) than men without the Msyn (p < 0.05).

We found SBP was reduced 7.5 ± 3.2 mmHg (p < 0.05) and diastolic BP (DBP) 4.9 ± 2.5 mmHg (p = 0.052) after LIGHT compared to non-exercise control over 9 hours among men without versus with Msyn. However, BP was not different after MODERATE versus non-exercise control between Msyn groups (p ≥ 0.05). The cardiometabolic factors accounting for 17% of the SBP response after LIGHT were baseline SBP (β = -0.351, r2 = 0.123, p = 0.020), the Msyn (β = 0.277, r2 = 0.077, p = 0.069), and HOMA (β = -0.124, r2 = 0.015, p = 0.424). The Msyn (r2 = 0.096, p = 0.036) was the only significant correlate of the DBP response after LIGHT. No cardiometabolic factors associated with the BP response after MODERATE.

 

Discussion

 

Work from our laboratory has shown those with genetic predispositions to CVD experience greater BP reductions immediately following a session of aerobic exercise than those less predisposed to CVD [15-17]. For these reasons, we hypothesized that men with pre- to Stage 1 hypertension and the Msyn would manifest PEH to a greater degree than men without the Msyn. Contrary to our hypothesis, men with high BP and without the Msyn responded more favorably to the immediate antihypertensive effects of lower intensity, aerobic exercise than men with high BP and the Msyn. Furthermore, the magnitude of the exercise-induced BP differences of 5-8 mmHg that we found between Msyn groups has important clinical and public health considerations for the personalization of exercise prescriptions for those with hypertension many of who have the Msyn [2].

The reasons that the men without the Msyn responded more favorably to the antihypertensive effects of LIGHT than men with the Msyn are unclear. The vasoactive properties of insulin are greater with increasing exercise intensity in order to augment the disposal of glucose into the skeletal muscles [18]. However, insulin’s vasoactive role in skeletal muscle perfusion is paradoxical having both hypotensive, i.e. acutely decreasing vascular resistance and BP, and pro-hypertensive effects, i.e. activation of renal sodium reabsorption and the sympathetic nervous system that serve to elevate BP [10,13]. Work from our laboratory [15-17] supports the notion that the immediate BP lowering effects of aerobic exercise are dependent upon the vasodilator-vasoconstrictor balance imposed on the vasculature by interactions among genetic predispositions, exercise intensity, and the depressor and pressor actions of BP regulatory hormones such as catecholamines, rennin, and insulin.

Rheaume and co-investigators studied the effects of acute moderate intensity (50% VO2peak for 30 minutes) [19] and prolonged, vigorous intensity (70% VO2peak for 90 minutes) [20] aerobic exercise on insulin sensitivity as assessed by an intravenous glucose tolerance test among men with elevated BP for up to 4 hours after exercise. They found that insulin sensitivity was increased after moderate but not vigorous intensity exercise. Rheaume et al. [19,20] partially attributed these differential exercise intensity to a higher adrenergic response and greater vasoconstrictor actions after vigorous than moderate intensity exercise.

The results of Rheaume et al. [19,20] provide insight into why men without the Msyn but not men with the Msyn lowered BP following exercise in our study. Men without the Msyn had increased insulin sensitivity (i.e. lower HOMA) compared to men with the Msyn. Among men without the Msyn, as insulin sensitivity increased, the decreases in SBP from baseline after LIGHT (r = 0.403, r2 = .162, p = 0.019) and MODERATE (r = 0.440, r2 = 0.193, p = 0.033) were greater. Furthermore, in multivariable regression analyses, HOMA remained a significant correlate of the SBP response following LIGHT. In contrast, among men with the Msyn, as insulin sensitivity decreased, the decrease in SBP from baseline after LIGHT (r = -0.464, r2 = 0.215, p = 0.053) tended to be greater but not after MODERATE (r = -0.277, r2 = 0.077, p = 0.266). The antihypertensive benefits of lower intensity, aerobic exercise appeared to result from improved insulin sensitivity and a more favorable vasodilator-vasoconstrictor balance following LIGHT than MODERATE among men without the Msyn compared to men with the Msyn. Future investigation is needed to more precisely establish the mechanisms for our observations.

This study has several limitations. Post-prandial plasma insulin and glucose assessments were measured only in the laboratory and not under ambulatory conditions in an attempt to minimize experimental intrusions that could affect the BP measurements and for reasons of subject convenience. However, we examined the relationships among BP, insulin, and glucose in the laboratory and found the findings to be strikingly similar to those reported in this paper over 9 hours. We did not perform an oral glucose tolerance test to determine insulin sensitivity during and after exercise while subjects were still in the laboratory. It remains possible that a more sensitive measure of insulin sensitivity than HOMA may have shown different associations with post exercise BP. Lastly, we attempted to control for the confounding influence of diet on the baseline plasma insulin and glucose concentrations of our subjects prior to the experiments by instructing them to consume a standard meal 2 hours prior to any testing. However, we relied upon self-report to verify dietary compliance which does not ensure the instructions were followed.

Men without the Msyn appear to respond more favorably to the immediate antihypertensive effects of lower intensity, aerobic exercise than men with the Msyn. Factors accounting for this result were baseline BP, the Msyn, and HOMA, explaining 17% of the variability in the SBP response after LIGHT. Future work is needed to confirm our findings in a larger, more ethnically diverse sample of men and women to elucidate reasons for the differential impact that the Msyn has on the antihypertensive effects of aerobic exercise. Considering the significant public health burden of hypertension and the Msyn and the importance of exercise in their prevention, treatment, and control, results from such studies could yield important new knowledge for the personalization of exercise prescriptions among those with hypertension and the Msyn.

References

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