Abstract
PurposeWe hypothesized that 5 weeks of endurance training with blood flow restriction (R-training), providing relative ischemia and stimulation of the muscle chemoreflex, would decrease the exercise pressor reflex (EPR) when compared to training with the same workload in a free-flow condition (NR-training).Methods10 subjects performed one-leg knee-extension training four times a week during a 5-week period. Both legs were trained with identical workload, with one leg being trained during flow-restriction induced by lower body positive pressure. The EPR was assessed by measuring the increase in heart rate (HR) and mean arterial pressure (MAP) during an isometric knee extension of 35% of max torque for 90 s, this was done before (C), and after training in each leg (R and NR, respectively).ResultsAt the end of isometric contraction, the increase in mean AP (MAP) in the NR-trained leg and in the control condition were 41 ± 4 and 38 ± 4 mmHg, respectively, whereas the increase in the R-trained leg was 30 ± 4 mmHg (p < 0.05 R vs C and NR), corresponding to a decrease of about 25%. A similar patter was observed with respect to responses in HR, where the increase was 28 ± 3 and 28 ± 3 bpm in the NR and C, and 22 ± 4 in the R condition (p < 0.05 R vs C and NR).ConclusionsPeripheral metabolic changes induced by relative ischemia are important in modifying the EPR in response to exercise training.
Highlights
It is generally admitted that the cardiovascular response to physical exercise implies the concerted action of a central command mechanism, and of the exercise pressor reflex (EPR), with influence from the cardiopulmonary reflex (Rowell and O’Leary 1990; Michelini et al 2015; Fadel and Raven 2012)
This study indicates that relative ischemia induced by flow restriction during exercise appear to decrease the exercise pressor reflex
It has previously been shown that endurance training of the forearm reduces the increase in muscle sympathetic nerve activity (MSNA), but not mean arterial pressure (AP) (MAP) or heart rate (HR), during isometric handgrip (Somers et al 1992)
Summary
It is generally admitted that the cardiovascular response to physical exercise implies the concerted action of a central command mechanism, and of the exercise pressor reflex (EPR), with influence from the cardiopulmonary reflex (Rowell and O’Leary 1990; Michelini et al 2015; Fadel and Raven 2012). The EPR implies mechanoand chemo-sensitive receptors that affect afferent nerve traffic in c-fibers, which in turn increase the sympathetic outflow to the heart and resistance vessels (Rowell and O’Leary 1990; Seals et al 1988). This is possibly accompanied by a postulated simultaneous withdrawal of vagal tone to the heart, which occurs in the first seconds of exercise (Fagraeus and Linnarsson 1976; Lador et al 2008). Insight on the role of the EPR may come from endurance training, as long as it was previously shown
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