Effects of ischemic preconditioning on short-duration cycling performance

Abstract

It has been demonstrated that ischemic preconditioning (IPC) improves endurance performance. However, the potential benefits during anaerobic events and the mechanism(s) underlying these benefits remain unclear. Fifteen recreational cyclists were assessed to evaluate the effects of IPC of the upper thighs on anaerobic performance, skeletal muscle activation, and metabolic responses during a 60-s sprint performance. After an incremental test and a familiarization visit, subjects were randomly submitted in visits 3 and 4 to a performance protocol preceded by intermittent bilateral cuff inflation (4 × (5 min of blood flow restriction + 5 min reperfusion)) at either 220 mm Hg (IPC) or 20 mm Hg (control). To increase data reliability, each intervention was replicated, which was also in a random manner. In addition to the mean power output, the pulmonary oxygen uptake, blood lactate kinetics, and quadriceps electromyograms (EMGs) were analyzed during performance and throughout 45 min of passive recovery. After IPC, performance was improved by 2.1% compared with control (95% confidence intervals of 0.8% to 3.3%, P = 0.001), followed by increases in (i) the accumulated oxygen deficit, (ii) the amplitude of blood lactate kinetics, (iii) the total amount of oxygen consumed during recovery, and (iv) the overall EMG amplitude (P < 0.05). In addition, the ratio between EMG and power output was higher during the final third of performance after IPC (P < 0.05). These results suggest an increased skeletal muscle activation and a higher anaerobic contribution as the ultimate responses of IPC on short-term exercise performance.

The effect of ischaemic preconditioning on central and peripheral fatiguing mechanisms in humans following sustained maximal isometric exercise

“…However, this did not occur in the present study, and as similar reductions in peripheral twitch amplitudes were evident across trials (Table ), no meaningful changes were observed in VA (Figure and Table ). Elevated sEMG activity has also provided indirect evidence that IPC can preserve neural drive (Cruz et al., , ). Again, this increase in muscle recruitment was not observed in the present study (Table ).…”

“…Early findings suggested enhanced oxygen delivery to be the primary mechanistic change induced by IPC; however, recent research has proposed that IPC might also affect neural drive to working skeletal muscle (Barbosa et al., ; Crisafulli et al., ; Cruz, de Aguiar, Turnes, Salvador, & Caputo, ; Cruz, Pereira, Lisboa, & Caputo, ; Paradis‐Deschênes et al., ; Tanaka et al ., ). Barbosa et al.…”

“…() observed an attenuation in the reduction of rates of force development and relaxation times (both contractile characteristics symptomatic of altered neural drive) after IPC, without concomitant changes in haemodynamics or deoxygenation during submaximal handgrip exercise to failure. Amplified surface electromyography (sEMG) at the point of task failure has also been reported after IPC treatment when compared with control conditions (Cruz, de Aguiar, Turnes, Pereira, & Caputo, ; Cruz et al., ). However, the indirect measures used to assess neural drive (Barbosa et al., ) and the multitude of unrelated factors that can influence sEMG measures (Dimitrova & Dimitrov, ; Farina, Holobar, Merletti, & Enoka, ) warrant further investigation with more direct measures capable of profiling muscle activation after IPC.…”

“…Specifically, the primary objective was to determine whether IPC could preserve voluntary activation after a sustained, maximal effort exercise task whilst controlling for any humoral effects through the use of the isometric modality. Given recent evidence (Cruz et al., , ), it was hypothesized that IPC would attenuate any declines in voluntary activation induced by the 2 min fatiguing protocol.…”

Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men

“…It has been suggested that IPC may attenuate group III/IV muscle afferent feedback through the activation of opioid receptors (Cruz et al. , ; Salvador et al. ).…”