Ischemic Preconditioning: Modulating Pain Sensitivity and Exercise Performance

Purpose The purpose of this study was to examine whether an individual’s IPC-mediated change in cold pain sensitivity is associated with the same individual’s IPC-mediated change in exercise performance.Methods Thirteen individuals (8 males; 5 females, 27 ± 7 years, 55 ± 5 ml.kgs–1.min–1) underwent two separate cold-water immersion tests: with preceding IPC treatment and without. In addition, each participant undertook two separate 5-km cycling time trials: with preceding IPC treatment and without. Pearson correlation coefficients were used to assess the relationship between an individual’s change in cold-water pain sensitivity following IPC with their change in 5-km time trial performance following IPC.Results During the cold-water immersion test, pain intensity increased over time (p < 0.001) but did not change with IPC (p = 0.96). However, IPC significantly reduced the total time spent under pain (−9 ± 7 s; p = 0.001) during the cold-water immersion test. No relationship was found between an individual’s change in time under pain (r = −0.2, p = 0.6) or pain intensity (r = −0.3, p = 0.3) following IPC and their change in performance following IPC.Conclusion These findings suggest that IPC can modulate sensitivity to a painful stimulus, but this altered sensitivity does not explain the ergogenic efficacy of IPC on 5-km cycling performance

Enhanced Metabolic Stress Augments Ischemic Preconditioning for Exercise Performance

Purpose: To identify the combined effect of increasing tissue level oxygen consumption and metabolite accumulation on the ergogenic efficacy of ischemic preconditioning (IPC) during both maximal aerobic and maximal anaerobic exercise.Methods: Twelve healthy males (22 ± 2 years, 179 ± 2 cm, 80 ± 10 kg, 48 ± 4 ml.kg−1.min−1) underwent four experimental conditions: (i) no IPC control, (ii) traditional IPC, (iii) IPC with EMS, and (iv) IPC with treadmill walking. IPC involved bilateral leg occlusion at 220 mmHg for 5 min, repeated three times, separated by 5 min of reperfusion. Within 10 min following the IPC procedures, a 30 s Wingate test and subsequent (after 25 min rest) incremental maximal aerobic test were performed on a cycle ergometer.Results: There was no statistical difference in anaerobic peak power between the no IPC control (1211 ± 290 W), traditional IPC (1209 ± 300 W), IPC + EMS (1206 ± 311 W), and IPC + Walk (1220 ± 288 W; P = 0.7); nor did VO2max change between no IPC control (48 ± 2 ml.kg−1.min−1), traditional IPC (48 ± 6 ml.kg−1.min−1), IPC + EMS (49 ± 4 ml.kg−1.min−1) and IPC + Walk (48 ± 6 ml.kg−1.min−1; P = 0.3). However, the maximal watts during the VO2max increased when IPC was combined with both EMS (304 ± 38 W) and walking (308 ± 40 W) compared to traditional IPC (296 ± 39 W) and no IPC control (293 ± 48 W; P = 0.02).Conclusion: This study shows that in a group of participants for whom a traditional IPC stimulus was not effective, the magnification of the IPC stress through muscle contractions while under occlusion led to a subsequent exercise performance response. These findings support that amplification of the ischemic preconditioning stimulus augments the effect for exercise capacity

Influence of Active Recovery on Cardiovascular Function During Ice Hockey

Background: Ice hockey is a popular sport comprised of high-intensity repeated bouts of activity. Light activity, as opposed to passive rest, has been shown to improve power output in repeated sprinting and could potentially help to offset venous pooling, poor perfusion, and the risk of an ischemic event. The objective of our study was, thus, to examine the efficacy of low-intensity lower body activity following a simulated hockey shift for altering hemodynamic function. Methods: In a cross-over design, 15 healthy hockey players (23 ± 1 years, 54 ± 3 mL/kg/min) performed two simulated hockey shifts. In both conditions, players skated up to 85 % of age-predicted heart rate maximum, followed by either passive recovery or active recovery while hemodynamic measures were tracked for up to 180 s of rest. Results: Light active recovery within the confines of an ice hockey bench, while wearing skates and protective gear, was effective for augmenting cardiac output (an average of 2.5 ± 0.2 L/min, p = 0.03) at 45, 50, and 120 s. These alterations were driven by a sustained elevation in heart rate (12 bpm, p = 0.05) combined with a physiological relevant but non-significant (11.6 mL, p = 0.06) increase in stroke volume. Conclusions: Standing and pacing between shifts offers a realistic in-game solution to help slow the precipitous drop in cardiac output (heart rate and stroke volume) that typically occurs with passive rest. Prolonging the duration of an elevated cardiac output further into recovery may be beneficial for promoting recovery of the working skeletal muscles and also avoiding venous pooling and reduced myocardial perfusion. Key Points: Evidence that light activity in the form of standing/pacing is effective for maintaining cardiac output, and thus venous return Increased cardiac output and venous return may help reduce the chances of poor perfusion (ischemia) and could also promote recovery for performance This is a simple, low-risk, intervention demonstrated for the first time to work within the confines of a player’s bench while wearing hockey gea

Left Ventricular Structure and Function in Elite Swimmers and Runners

Sport-specific differences in the left ventricle (LV) of land-based athletes have been observed; however, comparisons to water-based athletes are sparse. The purpose of this study was to examine differences in LV structure and function in elite swimmers and runners. Sixteen elite swimmers [23 (2) years, 81% male, 69% white] and 16 age, sex, and race matched elite runners participated in the study. All athletes underwent resting echocardiography and indices of LV dimension, global LV systolic and diastolic function, and LV mechanics were determined. All results are presented as swimmers vs. runners. Early diastolic function was lower in swimmers including peak early transmitral filling velocity [76 (13) vs. 87 (11) cm ⋅ s-1, p = 0.02], mean mitral annular peak early velocity [16 (2) vs. 18 (2) cm ⋅ s-1, p = 0.01], and the ratio of peak early to late transmitral filling velocity [2.68 (0.59) vs. 3.29 (0.72), p = 0.005]. The diastolic mechanics index of time to peak untwisting rate also occurred later in diastole in swimmers [12 (10)% diastole vs. 5 (4)% diastole, p = 0.01]. Cardiac output was larger in swimmers [5.8 (1.5) vs. 4.7 (1.2) L ⋅ min-1, p = 0.04], which was attributed to their higher heart rates [56 (6) vs. 49 (6) bpm, p < 0.001] given stroke volumes were similar between groups. All other indices of LV systolic function and dimensions were similar between groups. Our findings suggest enhanced early diastolic function in elite runners relative to swimmers, which may be attributed to faster LV untwisting