High-intensity intermittent exercise induced significant cardiac, vascular, and autonomic improvements after 12 weeks of training.

One bout of aerobic exercise and regular participation in aerobic exercise has been shown to result in a lowering of office and ambulatory blood pressure of hypertensive individuals. Higher-intensity aerobic exercise, up to 70% of maximal oxygen consumption, does not produce a greater hypotensive effect, compared with moderate-intensity aerobic exercise. Intermittent aerobic and anaerobic exercise, however, performed at an intensity >70% of maximal oxygen uptake has been shown to significantly reduce office and ambulatory blood pressure of hypertensive individuals. Thus, faster, more intense forms of exercise can also bring about blood pressure reduction in the hypertensive population. Compared with continuous moderate-intensity aerobic exercise, high-intensity intermittent exercise typically results in a greater aerobic fitness increase in less time and produces greater changes in arterial stiffness, endothelial function, insulin resistance and mitochondrial biogenesis. One of the characteristics of high-intensity intermittent training is that it typically involves markedly lower training volume compared with traditional aerobic and resistance exercise programmes making it a time-efficient strategy to accrue adaptations and blood pressure benefits. This review briefly summarizes the results of studies that have examined the effects of single and repeated bouts of aerobic and resistance exercise on office and ambulatory blood pressure of hypertensive individuals. Then a more detailed summary of studies examining the effect of high-intensity intermittent exercise and training on hypertension is provided.

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Major individual differences in the maximal oxygen uptake response to aerobic training have been documented. Vagal influence on the heart has been shown to contribute to changes in aerobic fitness. Whether vagal influence on the heart also predicts maximal oxygen uptake response to interval-sprinting training, however, is undetermined. Thus, the relationship between baseline vagal activity and the maximal oxygen uptake response to interval-sprinting training was examined. Exercisers (n = 16) exercised three times a week for 12 weeks, whereas controls did no exercise (n = 16). Interval-sprinting consisted of 20 min of intermittent sprinting on a cycle ergometer (8 s sprint, 12 s recovery). Maximal oxygen uptake was assessed using open-circuit spirometry. Vagal influence was assessed through frequency analysis of heart rate variability. Participants were aged 22 ± 4.5 years and had a body mass of 72.7 ± 18.9 kg, a body mass index of 26.9 ± 3.9 kg · m(-2), and a maximal oxygen uptake of 28 ± 7.4 ml · kg(-1) · min(-1). Overall increase in maximal oxygen uptake after the training programme, despite being anaerobic in nature, was 19 ± 1.2%. Change in maximal oxygen uptake was correlated with initial baseline heart rate variability high-frequency power in normalised units (r = 0.58; P < 0.05). Thus, cardiac vagal modulation of heart rate was associated with the aerobic training response after 12 weeks of high-intensity intermittent-exercise. The mechanisms underlying the relationship between the aerobic training response and resting heart rate variability need to be established before practical implications can be identified.

Fat oxidation has been shown to increase after short term green tea extract (GTE) ingestion and after one bout of intermittent sprinting exercise (ISE). Whether combining the two will result in greater fat oxidation after ISE is undetermined. The aim of the current study was to investigate the combined effect of short term GTE and a single session of ISE upon post-exercise fat oxidation. Fourteen women consumed three GTE or placebo capsules the day before and one capsule 90 min before a 20-min ISE cycling protocol followed by 1 h of resting recovery. Fat oxidation was calculated using indirect calorimetry. There was a significant increase in fat oxidation post-exercise compared to at rest in the placebo condition (p < 0.01). After GTE ingestion, however, at rest and post-exercise, fat oxidation was significantly greater (p < 0.05) than that after placebo. Plasma glycerol levels at rest and 15 min during post-exercise were significantly higher (p < 0.05) after GTE consumption compared to placebo. Compared to placebo, plasma catecholamines increased significantly after GTE consumption and 20 min after ISE (p < 0.05). Acute GTE ingestion significantly increased fat oxidation under resting and post-exercise conditions when compared to placebo.