Exercise in the Metabolic Syndrome

The metabolic syndrome is a clustering of obesity, diabetes, hyperlipidemia, and hypertension that is occurring in increasing frequency across the global population. Although there is some controversy about its diagnostic criteria, oxidative stress, which is defined as imbalance between the production and inactivation of reactive oxygen species, has a major pathophysiological role in all the components of this disease. Oxidative stress and consequent inflammation induce insulin resistance, which likely links the various components of this disease. We briefly review the role of oxidative stress as a major component of the metabolic syndrome and then discuss the impact of exercise on these pathophysiological pathways. Included in this paper is the effect of exercise in reducing fat-induced inflammation, blood pressure, and improving muscular metabolism.

V˙o 2 kinetics reveal a central limitation at the onset of subthreshold exercise in heart transplant recipients

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O2 uptake (V˙o 2) kinetics at the onset of subthreshold exercise are slowed because of an impaired early “cardiodynamic” phase 1, rather than an abnormal subsequent “metabolic” phase 2. Thus we compared the V˙o 2 kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 ± 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 ± 14 W; C67W group). Time-averaged heart rate, breath-by-breathV˙o 2, and O2pulse (O2p) data yielded monoexponential time constants of the V˙o 2 (s) and O2p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 V˙o 2 time constant ([Formula: see text]). The V˙o 2 time constant was higher in HTR (38.4 ± 7.5) than in C40W (22.9 ± 9.6; P ≤ 0.002) or C67W (30.8 ± 8.2; P ≤ 0.05), as was the O2p time constant, resulting from a lower phase 1V˙o 2 increase (287 ± 59 vs. 349 ± 66 ml/min; P ≤ 0.05), O2p increase (2.8 ± 0.6 vs. 3.6 ± 1.0 ml/beat; P ≤ 0.0001), and a longer phase 1 duration (36.7 ± 12.3 vs. 26.8 ± 6.0 s; P≤ 0.05), whereas the[Formula: see text]was similar in HTR and C (31.4 ± 9.6 vs. 29.9 ± 5.6 s; P = 0.85). Thus the HTR have slower subthresholdV˙o 2 kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster[Formula: see text]in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.