53030403
Effect of Ischemic Preconditioning on the Recovery of Cardiac Autonomic Control From Repeated Sprint Exercise
Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i. e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 × 5 min at 220 mmHg) or control (CT; 3 × 5 min at 20 mmHg) 48 h, 24 h, and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180° change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake (V˙O2peak), peak carbon dioxide output (V˙O2peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of V˙O2 decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: P = 0.03; partial eta square (η2p) = 0.27, i.e., large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.
46793801
A scoping review of the psychological responses to interval exercise: is interval exercise a viable alternative to traditional exercise?
ABSTRACT While considerable evidence suggests that interval exercise confers numerous physiological adaptations linked to improved health, its psychological consequences and behavioural implications are less clear and the subject of intense debate. The purpose of this scoping review was to catalogue studies investigating the psychological responses to interval exercise in order to identify what psychological outcomes have been assessed, the research methods used, and the results. A secondary objective was to identify research issues and gaps. Forty-two published articles met the review inclusion/exclusion criteria. These studies involved 1258 participants drawn from various active/inactive and healthy/unhealthy populations, and 55 interval exercise protocols (69% high-intensity interval training [HIIT], 27% sprint interval training [SIT], and 4% body-weight interval training [BWIT]). Affect and enjoyment were the most frequently studied psychological outcomes. Post-exercise assessments indicate that overall, enjoyment of, and preferences for interval exercise are equal or greater than for continuous exercise, and participants can hold relatively positive social cognitions regarding interval exercise. Although several methodological issues (e.g., inconsistent use of terminology, measures and protocols) and gaps (e.g., data on adherence and real-world protocols) require attention, from a psychological perspective, the emerging data support the viability of interval exercise as an alternative to continuous exercise.
207493075
Sprint Interval Training Effects on Aerobic Capacity: A Systematic Review and Meta-Analysis
BackgroundSprint interval training (SIT) involving repeated 30-s “all out” efforts have resulted in significantly improved skeletal muscle oxidative capacity, maximal oxygen uptake, and endurance performance. The positive impact of SIT on cardiorespiratory fitness has far-reaching health implications.ObjectiveThe objective of this study was to perform a systematic review of the literature and meta-analysis to determine the effects of SIT on aerobic capacity.MethodsA search of the literature was conducted using the key words ‘sprint interval training’, ‘high intensity intermittent training/exercise’, ‘aerobic capacity’, and ‘maximal oxygen uptake’. Seventeen effects were analyzed from 16 randomized controlled trials of 318 participants. The mean ± standard deviation number of participants was 18.7 ± 5.1. Participant age was 23.5 ± 4.3 years.ResultsThe effect size calculated for all studies indicates that supramaximal-intensity SIT has a small-to-moderate effect (Cohen’s d = 0.32, 95 % CI 0.10–0.55; z = 2.79, P < 0.01) on aerobic capacity with an aggregate improvement of ~3.6 mL·kg−1·min−1 (~8 % increase). The effect is moderate to large in comparison with no-exercise control groups (Cohen’s d = 0.69, 95 % CI 0.46–0.93; z = 5.84, P < 0.01) and not different when compared with endurance training control groups (Cohen’s d = 0.04, 95 % CI −0.17 to 0.24; z = 0.36, P = 0.72).ConclusionSIT improves aerobic capacity in healthy, young people. Relative to continuous endurance training of moderate intensity, SIT presents an equally effective alternative with a reduced volume of activity. This evaluation of effects and analysis of moderating variables consolidates the findings of small-sample studies and contributes to the practical application of SIT to improve cardiorespiratory fitness and health.
21950191
Cardiac autonomic responses to repeated shuttle sprints.
Team sport match play requires athletes to perform a number of repeated shuttle sprints. However, the acute effects of these repeated sprint sequences on lactic acidosis and resulting autonomic state perturbation are not known. The aim of this study was to observe and compare the blood lactate and post-exercise cardiac autonomic responses of a repeated shuttle-sprint ability test with the 30-15 Intermittent Fitness Test (30-15 (IFT)); the latter test representing a standard for exhaustive supramaximal effort. Thirteen adult team sport players performed the repeated shuttle-sprint ability test and the 30-15 (IFT) on separate days in a counter-balanced order. The repeated shuttle-sprint ability test consisted of six repetitions of maximal 2x15 m shuttle sprints ( approximately 5 s) departing every 20 s, while the 30-15 (IFT) involved progressive 30 s shuttle runs interspersed with 15 s of passive recovery until exhaustion. Blood lactate was measured before and after the tests, while autonomic responses were assessed using immediate heart rate recovery and heart rate variability indices. Peak blood lactate (10.6+/-2.1 vs. 10.2+/-2.8 mM) and heart beats recovered in one minute after exercise cessation (36.4+/-7.8 vs. 39.3+/-7.9 bpm) were similar after both the repeated shuttle-sprint ability test and the 30-15 (IFT). With the exception of the vagal-related time-varying root mean square of successive R-R interval differences at each 30 s, which recovered earlier after the repeated shuttle-sprint ability test compared with 30-15 (IFT), all heart rate variability indices decreased similarly after both tests in comparison to baseline values. In conclusion, the repeated shuttle-sprint ability test was shown to induce comparable levels of lactic acidosis and post-exercise autonomic state as the 30-15 (IFT). These levels of metabolic and autonomic states are likely to occur during team sport match play.
26409312
Heart rate recovery after aerobic and anaerobic tests: is there an influence of anaerobic speed reserve?
ABSTRACT The present study assessed if differences in the metabolic profile, inferred from the anaerobic speed reserve (ASR), would influence the dynamics of heart rate recovery (HRR) after two modes of exercise. Thirty-nine physical education students (14 females and 25 males) volunteered for this study. Participants carried out three separate testing sessions to assess maximal sprinting speed (MSS, 1st session), repeated sprint ability (RSA, 2nd session) and maximal aerobic speed (MAS) using the Université of Montreal Track Test (UMTT, 3rd session). ASR was defined as the difference between MSS and MAS. Heart rate was continuously registered throughout the tests and during the 5-min post-test recovery. To evaluate the influence of ASR on post-exercise, HRR comparisons between ASR-based groups [high ASR vs. low ASR] and sex groups (males vs. females) were performed. Significant differences (P < 0.05) were found between high ASR and low ASR groups of the same sex for indices of relative HRR after the RSA and UMTT. In addition, after the RSA test, males from the high ASR group had a significantly slower HRR kinetics compared with the males of the low ASR (P < 0.05) and the females of high ASR (P < 0.05); whereas females of the high ASR groups had a faster HRR kinetics compared with the females of low ASR group (P < 0.05). Our results showed that in males, post-exercise HRR could be related to the ASR, whereas in females, the influence of ASR is less clear.
20574577
Heart-rate recovery immediately after exercise as a predictor of mortality.
BACKGROUND
The increase in heart rate that accompanies exercise is due in part to a reduction in vagal tone. Recovery of the heart rate immediately after exercise is a function of vagal reactivation. Because a generalized decrease in vagal activity is known to be a risk factor for death, we hypothesized that a delayed fall in the heart rate after exercise might be an important prognostic marker.


METHODS
For six years we followed 2428 consecutive adults (mean [+/-SD] age, 57+/-12 years; 63 percent men) without a history of heart failure or coronary revascularization and without pacemakers. The patients were undergoing symptom-limited exercise testing and single-photon-emission computed tomography with thallium scintigraphy for diagnostic purposes. The value for the recovery of heart rate was defined as the decrease in the heart rate from peak exercise to one minute after the cessation of exercise. An abnormal value for the recovery of heart rate was defined as a reduction of 12 beats per minute or less from the heart rate at peak exercise.


RESULTS
There were 213 deaths from all causes. A total of 639 patients (26 percent) had abnormal values for heart-rate recovery. In univariate analyses, a low value for the recovery of heart rate was strongly predictive of death (relative risk, 4.0; 95 percent confidence interval, 3.0 to 5.2; P<0.001). After adjustments were made for age, sex, the use or nonuse of medications, the presence or absence of myocardial perfusion defects on thallium scintigraphy, standard cardiac risk factors, the resting heart rate, the change in heart rate during exercise, and workload achieved, a low value for heart-rate recovery remained predictive of death (adjusted relative risk, 2.0; 95 percent confidence interval, 1.5 to 2.7; P<0.001).


CONCLUSIONS
A delayed decrease in the heart rate during the first minute after graded exercise, which may be a reflection of decreased vagal activity, is a powerful predictor of overall mortality, independent of workload, the presence or absence of myocardial perfusion defects, and changes in heart rate during exercise.
2985789
Assessment of parasympathetic reactivation after exercise.
The objective of this study was to evaluate whether heart rate variability (HRV) can be used as an index of parasympathetic reactivation after exercise. Heart rate recovery after exercise has recently been shown to have prognostic significance and has been postulated to be related to abnormal recovery of parasympathetic tone. Ten normal subjects [5 men and 5 women; age 33 +/- 5 yr (mean +/- SE)] exercised to their maximum capacity, and 12 subjects (10 men and 2 women; age 61 +/- 10 yr) with coronary artery disease exercised for 16 min on two separate occasions, once in the absence of atropine and once with atropine (0.04 mg/kg) administered during exercise. The root mean square residual (RMS), which measures the deviation of the R-R intervals from a straight line, as well as the standard deviation (SD) and the root mean square successive difference of the R-R intervals (MSSD), were measured on successive 15-, 30-, and 60-s segments of a 5-min ECG obtained immediately after exercise. In recovery, the R-R interval was shorter with atropine (P < 0.0001). Without atropine, HRV, as measured by the MSSD and RMS, increased early in recovery from 4.1 +/- 0.4 and 3.7 +/- 0.4 ms in the first 15 s to 7.2 +/- 1.0 and 7.4 +/- 0.9 ms after 1 min, respectively (P < 0.0001). RMS (range 1.7-2.1 ms) and MSSD were less with atropine (P < 0.0001). RMS remained flat throughout recovery, whereas MSSD showed some decline over time from 3.0 to 2.2 ms (P < 0.002). RMS and MSSD were both directly related (r(2) = 0.47 and 0.56, respectively; P < 0.0001) to parasympathetic effect, defined as the difference in R-R interval without and with atropine. In conclusion, RMS and MSSD are parameters of HRV that can be used in the postexercise recovery period as indexes of parasympathetic reactivation after exercise. These tools may improve our understanding of parasympathetic reactivation after exercise and the prognostic significance of heart rate recovery.
41559485
Recovery of heart rate following intense dynamic exercise
The Olympic biathlon is a very demanding physical event that requires high oxygen delivery, good cross‐country skiing skills and skilful use of a rifle. Like all high‐performance endurance athletes, high cardiac vagal tone is a characteristic and extends the range over which cardiac output can increase. In the biathlete, however, the enhanced vagal control of the heart also allows a strategy for better control of stability needed for accurately firing a rifle at the end of each lap of the race. The role of endurance training, central command, reflexes from muscle, and of the carotid–cardiac baroreceptor reflex in changing vagal tone during intense exercise and recovery is discussed.
41239788
Heart rate recovery: autonomic determinants, methods of assessment and association with mortality and cardiovascular diseases
Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise – known as heart rate recovery (HRR) – is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR.
52802644
Transient Limb Ischemia Induces Remote Ischemic Preconditioning In Vivo
Background—Ischemic preconditioning reduces local tissue injury caused by subsequent ischemia-reperfusion (IR), but may also have a salutary effect on IR injury of tissues remote from those undergoing preconditioning. We tested the hypothesis that limb ischemia induces remote preconditioning, reduces endothelial IR injury in humans, and reduces experimental myocardial infarct size. Methods and Results—Endothelial IR injury of the human forearm was induced by 20 minutes of upper limb ischemia (inflation of a blood pressure cuff to 200 mm Hg) followed by reperfusion. Remote preconditioning was induced by three 5-minute cycles of ischemia of the contralateral limb. Venous occlusion plethysmography was used to assess forearm blood flow in response to acetylcholine at baseline and 15 minutes after reperfusion. Experimental myocardial infarction was achieved by 40 minutes of balloon occlusion of the left anterior descending artery in 15-kg pigs. Remote preconditioning was induced by four 5-minute cycles of lower limb ischemia. Triphenyltetrazolium staining was used to assess the extent of myocardial infarction. In the human study, the response to acetylcholine was significantly attenuated in the control group after 15 minutes’ reperfusion, but remote preconditioning prevented this reduction. Limb ischemia caused a significant reduction in the extent of myocardial infarction relative to the area at risk compared with control (26±9% versus 53±8%, P <0.05). Conclusion—Remote ischemic preconditioning prevents IR-induced endothelial dysfunction in humans and reduces the extent of myocardial infarction in experimental animals. Transient limb ischemia is a simple preconditioning stimulus with important potential clinical applications.
13958167
Remote ischaemic pre- and delayed postconditioning – similar degree of cardioprotection but distinct mechanisms
Myocardial ischaemia–reperfusion injury can be significantly reduced by an episode(s) of ischaemia–reperfusion applied prior to or during myocardial ischaemia (MI) to peripheral tissue located at a distance from the heart; this phenomenon is called remote ischaemic conditioning (RIc). Here, we compared the efficacy of RIc in protecting the heart when the RIc stimulus is applied prior to, during and at different time points after MI. A rat model of myocardial ischaemia–reperfusion injury involved 30 min of left coronary artery occlusion followed by 120 min of reperfusion. Remote ischaemic conditioning was induced by 15 min occlusion of femoral arteries and conferred a similar degree of cardioprotection when applied 25 min prior to MI, 10 or 25 min after the onset of MI, or starting 10 min after the onset of reperfusion. These RIc stimuli reduced infarct size by 54, 56, 56 and 48% (all P < 0.001), respectively. Remote ischaemic conditioning applied 30 min into the reperfusion period was ineffective. Activation of sensory nerves by application of capsaicin was effective in establishing cardioprotection only when elicited prior to MI. Vagotomy or denervation of the peripheral ischaemic tissue both completely abolished cardioprotection induced by RIc applied prior to MI. Cardioprotection conferred by delayed remote postconditioning was not affected by either vagotomy or peripheral denervation. These results indicate that RIc confers potent cardioprotection even if applied with a significant delay after the onset of myocardial reperfusion. Cardioprotection by remote preconditioning is critically dependent on afferent innervation of the remote organ and intact parasympathetic activity, while delayed remote postconditioning appears to rely on a different signalling pathway(s).
6389898
Intermittent arm ischemia induces vasodilatation of the contralateral upper limb
Intermittent arm ischemia before percutaneous coronary intervention induces remote ischemic preconditioning (RIPC) and attenuates myocardial injury in patients with myocardial infarction. Several studies have shown that intermittent arm ischemia increases coronary flow and is related to autonomic nerve system. The aim of this study was to determine whether intermittent arm ischemia induces vasodilatation of other arteries and to assess changes in the autonomic nerve system during intermittent arm ischemia in humans. We measured change in the right brachial artery diameter during intermittent left arm ischemia through three cycles of 5-min inflation (200 mmHg) and 5-min deflation of a blood-pressure cuff using a 10-MHz linear array transducer probe in 20 healthy volunteers. We simultaneously performed power spectral analysis of heart rate. Ischemia-reperfusion of the left arm significantly dilated the right brachial artery time-dependently, resulting in a 3.2 ± 0.4% increase after the 3rd cycle. In the power spectral analysis of heart rate, the high-frequency domain (HF), which is a marker of parasympathetic activity, was significantly higher after the 3rd cycle of ischemia-reperfusion than baseline HF (P = 0.02). Intermittent arm ischemia was accompanied by vasodilatation of another artery and enhancement of parasympathetic activity. Those effects may play an important role in the mechanism of RIPC.
37766900
Neural Mechanisms of Cardioprotection
This review highlights the importance of neural mechanisms capable of protecting the heart against lethal ischemia/reperfusion injury. Increased parasympathetic (vagal) activity limits myocardial infarction, and recent data suggest that activation of autonomic reflex pathways contributes to powerful innate mechanisms of cardioprotection underlying the remote ischemic conditioning phenomena.
23987090
Acute ischaemic preconditioning protects against skeletal muscle infarction in the pig.
OBJECTIVE
The aims were to investigate the efficacy of acute ischaemic preconditioning for protection of skeletal muscles against infarction and its effect on muscle blood flow and ischaemic muscle metabolism.


METHODS
The efficacy of preconditioning was tested by subjecting pig latissimus dorsi and gracilis muscles to different numbers and durations of ischaemia/reperfusion cycles before 4 h of global ischaemia. Infarction was assessed at 48 h of reperfusion, using nitroblue tetrazolium dye. Blood flow in the latissimus dorsi was measured at the end of preconditioning and 1.5 and 3.0 h of reperfusion, using the radioactive microsphere (15 microns) technique. Muscle biopsies were taken from the latissimus dorsi before ischaemia, at the end of 2 and 4 h of ischaemia, and 1.5 h of reperfusion.


RESULTS
At least three cycles of 10 min ischaemia and 10 min reperfusion were required for preconditioning of latissimus dorsi and gracilis muscles for protection against infarction. Preconditioning reduced the total infarct size by 44% and 62% in latissimus dorsi and gracilis muscles, respectively. Preconditioning did not affect preischaemia muscle blood flow but it reduced the muscle content (preischaemia reserve) of phosphocreatine and ATP and the muscle energy charge potential (ECP) by 13.5%*, 27.5%*, and 8%* (*P < 0.05), respectively. In spite of a lower preischaemia reserve of phosphocreatine and ATP, the muscle contents of phosphocreatine and ATP and muscle ECP were maintained higher and the lactate lower (*P < or = 0.05) in the preconditioned than in the non-preconditioned (control) muscles at the end of 4 h of ischaemia [phosphocreatine 8.0(SEM 0.4) v 3.2(0.3)*; ATP 9.8(0.7) v 7.8(0.3); ECP 0.72(0.02) v 0.66(0.01)*; lactate 115.4(8.6) v 160.5(11.8)* mumol.g-1 dry muscle]. The level of ATP and ECP also remained significantly higher and the level of lactate significantly lower in the preconditioned than in the non-preconditioned latissimus dorsi muscles at 1.5 h of reperfusion. Hyperaemia was seen in the preconditioned latissimus dorsi muscles at 1.5 h of reperfusion and it subsided by the end of 3h of reperfusion.


CONCLUSIONS
The protective effect of preconditioning can be induced in pig skeletal muscle but at a higher threshold than reported previously in pig cardiac muscle (one cycle). Preconditioning of pig skeletal muscle is associated with a lower energy metabolism during sustained ischaemia. At the present time, it is not known if this energy sparing effect is a major mechanism of ischaemic preconditioning against infarction in skeletal muscles.
24229511
Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection.
Coronary artery disease and its sequelae-ischemia, myocardial infarction, and heart failure-are leading causes of morbidity and mortality in man. Considerable effort has been devoted toward improving functional recovery and reducing the extent of infarction after ischemic episodes. As a step in this direction, it was found that the heart was significantly protected against ischemia-reperfusion injury if it was first preconditioned by brief ischemia or by administering a potassium channel opener. Both of these preconditioning strategies were found to require opening of a K(ATP) channel, and in 1997 we showed that this pivotal role was mediated by the mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)). This paper will review the evidence showing that opening mitoK(ATP) is cardioprotective against ischemia-reperfusion injury and, moreover, that mitoK(ATP) plays this role during all three phases of the natural history of ischemia-reperfusion injury preconditioning, ischemia, and reperfusion. We discuss two distinct mechanisms by which mitoK(ATP) opening protects the heart-increased mitochondrial production of reactive oxygen species (ROS) during the preconditioning phase and regulation of intermembrane space (IMS) volume during the ischemic and reperfusion phases. It is likely that cardioprotection by ischemic preconditioning (IPC) and K(ATP) channel openers (KCOs) arises from utilization of normal physiological processes. Accordingly, we summarize the results of new studies that focus on the role of mitoK(ATP) in normal cardiomyocyte physiology. Here, we observe the same two mechanisms at work. In low-energy states, mitoK(ATP) opening triggers increased mitochondrial ROS production, thereby amplifying a cell signaling pathway leading to gene transcription and cell growth. In high-energy states, mitoK(ATP) opening prevents the matrix contraction that would otherwise occur during high rates of electron transport. MitoK(ATP)-mediated volume regulation, in turn, prevents disruption of the structure-function of the IMS and facilitates efficient energy transfers between mitochondria and myofibrillar ATPases.
20771519
Altered expression of mitochondrial electron transport chain proteins and improved myocardial energetic state during late ischemic preconditioning.
Altered expression of mitochondrial electron transport proteins has been shown in early preconditioned myocardial tissue. We wished to determine whether these alterations persist in the Second Window of Protection (SWOP) and if so, whether a favorable energetic state is facilitated during subsequent ischemia. Fourteen pigs underwent a SWOP protocol with ten 2-minute balloon inflations in the LAD artery, each separated by 2 minutes reperfusion. Twenty-four hours later, mitochondria were isolated from SWOP and SHAM pig hearts and analyzed for uncoupling protein (UCP)-2 content by western blot analysis, proteomic changes by iTRAQ(®) and respiration by an oxygen electrode. In parallel in vivo studies, high-energy nucleotides were obtained by transmural biopsy from anesthetized SWOP and SHAM pigs at baseline and during sustained low-flow ischemia. Compared with SHAM mitochondria, ex vivo SWOP heart tissue demonstrated increased expression of UCP-2, Complex IV (cytochrome c oxidase) and Complex V (ATPase) proteins. In comparison with SHAM pigs during in vivo conditions, transmural energetics in SWOP hearts, as estimated by the free energy of ATP hydrolysis (ΔG(0)), were similar at baseline but had decreased by the end of low-flow ischemia (-57.0 ± 2.1 versus -51.1 ± 1.4 kJ/mol; P < 0.05). In conclusion, within isolated mitochondria from preconditioned SWOP hearts, UCP-2 is increased and in concert with enhanced Complex IV and V proteins, imparts a favorable energetic state during low-flow ischemia. These data support the notion that mitochondrial adaptations that may reduce oxidant damage do not reduce the overall efficiency of energetics during sustained oxygen deprivation.
9728917
Ischemic preconditioning improves maximal performance in humans
Repeated episodes of ischemia followed by reperfusion, commonly referred to as ischemic preconditioning (IPC), represent an endogenous protective mechanism that delays cell injury. IPC also increases blood flow and improves endothelial function. We hypothesize that IPC will improve physical exercise performance and maximal oxygen consumption. The purpose of the study was to examine the effect of ischemic preconditioning in leg skeletal muscles on cycling exercise performance in healthy individuals. Fifteen healthy, well-trained subjects performed two incremental maximal exercise tests on a bicycle ergometer. Power output, oxygen consumption, ventilation, respiratory quotient, and heart rate were measured continuously. Blood pressure and blood lactate were measured before and after the test. One exercise test was performed after the application of ischemic preconditioning, using a protocol of three series of 5-min ischemia at both legs with resting periods of 5 min in between. The other maximal cycling test served as a control. Tests were conducted in counterbalanced order, at least 1 week apart, at the same time of the day. The repeated ischemic periods significantly increased maximal oxygen consumption from 56.8 to 58.4 ml/min per kg (P = 0.003). Maximal power output increased significantly from 366 to 372 W (P = 0.05). Ischemic preconditioning had no effect on ventilation, respiratory quotient, maximal heart rate, blood pressure or on blood lactate. Repeated short-term leg ischemia prior to an incremental bicycle exercise test improves maximal oxygen consumption by 3% and power output by 1.6%. This protocol, which is suggested to mimic the effects of ischemic preconditioning, may have important implications for exercise performance.
975542
Effects of ischemic preconditioning on maximal constant-load cycling performance.
This study investigated the effects of ischemic preconditioning (IPC) on the ratings of perceived exertion (RPE), surface electromyography, and pulmonary oxygen uptake (V̇o2) onset kinetics during cycling until exhaustion at the peak power output attained during an incremental test. A group of 12 recreationally trained cyclists volunteered for this study. After determination of peak power output during an incremental test, they were randomly subjected on different days to a performance protocol preceded by intermittent bilateral cuff pressure inflation to 220 mmHg (IPC) or 20 mmHg (control). To increase data reliability, the performance visits were replicated, also in a random manner. There was an 8.0% improvement in performance after IPC (control: 303 s, IPC 327 s, factor SDs of ×/÷1.13, P = 0.01). This change was followed by a 2.9% increase in peak V̇o2 (control: 3.95 l/min, IPC: 4.06 l/min, factor SDs of ×/÷1.15, P = 0.04), owing to a higher amplitude of the slow component of the V̇o2 kinetics (control: 0.45 l/min, IPC: 0.63 l/min, factor SDs of ×/÷2.21, P = 0.05). There was also an attenuation in the rate of increase in RPE (P = 0.01) and a progressive increase in the myoelectrical activity of the vastus lateralis muscle (P = 0.04). Furthermore, the changes in peak V̇o2 (r = 0.73, P = 0.007) and the amplitude of the slow component (r = 0.79, P = 0.002) largely correlated with performance improvement. These findings provide a link between improved aerobic metabolism and enhanced severe-intensity cycling performance after IPC. Furthermore, the delayed exhaustion after IPC under lower RPE and higher skeletal muscle activation suggest they have a role on the ergogenic effects of IPC on endurance performance.
38047072
Effect of ischemic preconditioning on lactate accumulation and running performance.
PURPOSE
Repeated bouts of ischemia followed by reperfusion (i.e., ischemic preconditioning (IPC)) protect against damage after a myocardial infarction. Recent observational data indicate that IPC improves exercise performance. However, no previous study has examined potential underlying mechanisms for this effect of IPC. Therefore, we examined the potential of IPC to improve 5-km running time trial performance and reduce lactate accumulation during an incremental exercise test.


METHODS
In a randomized, crossover study, 13 healthy men performed running exercise, which was preceded by IPC (4 × 5-min 220 mm Hg bilateral leg occlusion) or a control intervention (C) (4 × 5-min 20 mm Hg bilateral leg occlusion). Participants performed a graded maximal treadmill running test, starting with five 3-min submaximal stages (10-14 km·h), followed by increments of 1 km·h every 2 min to 16 km·h, followed by an incline of the treadmill of 2% every 2 min. Blood lactate was examined at each 3-min stage. After 45 min of rest in the supine position, subjects then performed a 5-km running time trial.


RESULTS
We found similar submaximal gas parameters during running exercise with both interventions. The overall increase in blood lactate during the submaximal stages was 1.07 ± 0.11 mmol·L lower when exercise was preceded with IPC versus C (P = 0.023). The 5-km running time trial was completed in a time that was 34 s faster after IPC versus C (95% confidence interval, 5-64 s; P = 0.027).


CONCLUSION
IPC improves 5-km time trial performance in healthy male individuals. Moreover, we found that IPC is associated with an attenuated rise in blood lactate concentration at submaximal level during an incremental running test. This could indicate that IPC allows for higher work rates and thus improves time trial performance.
31190740
The Effect of Ischemic Preconditioning on Repeated Sprint Cycling Performance.
PURPOSE
Ischemic preconditioning enhances exercise performance. We tested the hypothesis that ischemic preconditioning would improve intermittent exercise in the form of a repeated sprint test during cycling ergometry.


METHODS
In a single-blind, crossover study, 14 recreationally active men (mean ± SD age, 22.9 ± 3.7 yr; height, 1.80 ± 0.07 m; and mass, 77.3 ± 9.2 kg) performed twelve 6-s sprints after four 5-min periods of bilateral limb occlusion at 220 mm Hg (ischemic preconditioning) or 20 mm Hg (placebo).


RESULTS
Ischemic preconditioning resulted in a 2.4% ± 2.2%, 2.6% ± 2.7%, and 3.7% ± 2.4% substantial increase in peak power for sprints 1, 2, and 3, respectively, relative to placebo, with no further changes between trials observed for any other sprint. Similar findings were observed in the first three sprints for mean power output after ischemic preconditioning (2.8% ± 2.5%, 2.6% ± 2.5%, and 3.4% ± 2.1%, for sprints 1, 2, and 3, respectively), relative to placebo. Fatigue index was not substantially different between trials. At rest, tissue saturation index was not different between the trials. During the ischemic preconditioning/placebo stimulus, there was a -19.7% ± 3.6% decrease in tissue saturation index in the ischemic preconditioning trial, relative to placebo. During exercise, there was a 5.4% ± 4.8% greater maintenance of tissue saturation index in the ischemic preconditioning trial, relative to placebo. There were no substantial differences between trials for blood lactate, electromyography (EMG) median frequency, oxygen uptake, or rating of perceived exertion (RPE) at any time points.


CONCLUSION
Ischemic preconditioning improved peak and mean power output during the early stages of repeated sprint cycling and may be beneficial for sprint sports.
24785700
Effects of local versus remote ischemic preconditioning on repeated sprint running performance.
BACKGROUND
The aim of this study was to compare the effect of local and remote ischemic preconditioning (IPC) on repeated sprint exercise.


METHODS
Twelve males (age 22±2 years; stature 1.79±0.07 m; body mass 77.8±8.4 kg; mean±SD) completed four trials consisting of remote (arm) and local (leg) IPC and SHAM interventions prior to repeated sprint exercise (3x[6x15+15-m] shuttle sprints), in a double-blind, randomized, crossover designed study. These tests were immediately preceded by IPC (4x5-minute intervals at 220 mmHg bilateral occlusion) or SHAM treatment (4x5-minute intervals at 20 mmHg bilateral occlusion). Sprint performance and percentage decrement score alongside measurement of Tissue Saturation Index, blood lactate and RPE were measured throughout the intervention.


RESULTS
During the IPC/SHAM intervention there was a large decrease in TSI for IPC-arm in comparison to IPC-leg (P<0.05), however IPC-legs resulted in greater soreness compared with the other three conditions (P<0.05). There was no main effects or interaction effects for sprint performance. There was a significant effect of condition (P=0.047, r=0.56) on percentage decrement score across all 18 sprints with IPC demonstrating less fatigue than SHAM. There were no other effects of IPC during the sprint trials for any other physiological measure.


CONCLUSIONS
In conclusion local IPC resulted in more pain/soreness during the IPC/SHAM intervention but both remote and local IPC reduced the fatigue associated with repeated sprint exercise.
6253363
Ischemic preconditioning of the muscle improves maximal exercise performance but not maximal oxygen uptake in humans.
Brief episodes of nonlethal ischemia, commonly known as "ischemic preconditioning" (IP), are protective against cell injury induced by infarction. Moreover, muscle IP has been found capable of improving exercise performance. The aim of the study was the comparison of standard exercise performances carried out in normal conditions with those carried out following IP, achieved by brief muscle ischemia at rest (RIP) and after exercise (EIP). Seventeen physically active, healthy male subjects performed three incremental, randomly assigned maximal exercise tests on a cycle ergometer up to exhaustion. One was the reference (REF) test, whereas the others were performed after the RIP and EIP sessions. Total exercise time (TET), total work (TW), and maximal power output (W(max)), oxygen uptake (VO(2max)), and pulmonary ventilation (VE(max)) were assessed. Furthermore, impedance cardiography was used to measure maximal heart rate (HR(max)), stroke volume (SV(max)), and cardiac output (CO(max)). A subgroup of volunteers (n = 10) performed all-out tests to assess their anaerobic capacity. We found that both RIP and EIP protocols increased in a similar fashion TET, TW, W(max), VE(max), and HR(max) with respect to the REF test. In particular, W(max) increased by ∼ 4% in both preconditioning procedures. However, preconditioning sessions failed to increase traditionally measured variables such as VO(2max), SV(max,) CO(max), and anaerobic capacity(.) It was concluded that muscle IP improves performance without any difference between RIP and EIP procedures. The mechanism of this effect could be related to changes in fatigue perception.
33603269
Remote ischemic preconditioning delays fatigue development during handgrip exercise
Ischemic preconditioning (IPC) of one or two limbs improves performance of exercise that recruits the same limb(s). However, it is unclear whether IPC application to another limb than that in exercise is also effective and which mechanisms are involved. We investigated the effect of remote IPC (RIPC) on muscle fatigue, time to task failure, forearm hemodynamics, and deoxygenation during handgrip exercise. Thirteen men underwent RIPC in the lower limbs or a control intervention (CON), in random order, and then performed a constant load rhythmic handgrip protocol until task failure. Rates of contraction and relaxation (ΔForce/ΔTime) were used as indices of fatigue. Brachial artery blood flow and conductance, besides forearm microvascular deoxygenation, were assessed during exercise. RIPC attenuated the slowing of contraction and relaxation throughout exercise (P < 0.05 vs CON) and increased time to task failure by 11.2% (95% confidence interval: 0.7–21.7%, P <0.05 vs CON). There was no significant difference in blood flow, conductance, and deoxygenation between conditions throughout exercise (P > 0.05). In conclusion, RIPC applied to the lower limbs delayed the development of fatigue during handgrip exercise, prolonged time to task failure, but was not accompanied by changes in forearm hemodynamics and deoxygenation.
8095662
Ischemic Preconditioning and Repeated Sprint Swimming: A Placebo and Nocebo Study.
PURPOSE
Ischemic preconditioning (IPC) has been shown to improve performance of exercises lasting 10-90 s (anaerobic) and more than 90 s (aerobic). However, its effect on repeated sprint performance has been controversial, placebo effect has not been adequately controlled, and nocebo effect has not been avoided. Thus, the IPC effect on repeated sprint performance was investigated using a swimming task and controlling placebo/nocebo effects.


METHODS
Short-distance university swimmers were randomized to two groups. One group (n = 15, 24 ± 1 yr [mean ± SEM]) was exposed to IPC (ischemia cycles lasted 5 min) and control (CT) (no ischemia); another (n = 15, 24 ± 1 yr) to a placebo intervention (SHAM) (ischemia cycles lasted 1 min) and CT. Seven subjects crossed over groups. Subjects were informed IPC and SHAM would improve performance compared with CT and would be harmless despite circulatory occlusion sensations. The swimming task consisted of six 50-m all-out efforts repeated every 3 min.


RESULTS
IPC, in contrast with SHAM, reduced worst sprint time (IPC, 35.21 ± 0.73 vs CT, 36.53 ± 0.72 s; P = 0.04) and total sprints time (IPC, 203.7 ± 4.60 vs CT, 206.03 ± 4.57 s; P = 0.02), moreover augmented swimming velocity (IPC, 1.45 ± 0.03 vs CT, 1.44 ± 0.03 m·s; P = 0.049). Six of seven subjects who crossed over groups reduced total sprints time with IPC versus SHAM (delta = -3.95 ± 1.49 s, P = 0.09). Both IPC and SHAM did not change blood lactate concentration (P = 0.20) and perceived effort (P = 0.22).


CONCLUSION
IPC enhanced repeated sprint swimming performance in university swimmers, whereas a placebo intervention did not.
31520687
Seven-day remote ischemic preconditioning improves local and systemic endothelial function and microcirculation in healthy humans.
BACKGROUND
Ischemic preconditioning (IPC) protects tissue against ischemia-induced injury inside and outside ischemic areas. The purpose was to examine the hypothesis that daily IPC leads to improvement in endothelial function and skin microcirculation not only in the arm exposed to IPC but also in the contralateral arm.


METHODS
Thirteen healthy, young, normotensive male individuals (aged 22±2 years) were assigned to 7-day daily exposure of the arm to IPC (4×5 minutes). Assessment of brachial artery endothelial function (using flow-mediated dilation (FMD)) and forearm microcirculation (cutaneous vascular conductance (CVC) at baseline and during local heating) was performed before and after 7 days to examine the local (i.e., intervention arm) and remote (i.e., control arm) effect of IPC. We repeated the assessment tests 8 days after the intervention (Post+8).


RESULTS
FMD increased after repeated IPC (P = 0.03) and remained significantly elevated at Post+8 in the intervention (5.0±2.2%, 6.1±2.2%, and 6.6±2.3%) and contralateral arms (5.4±2.2%, 6.0±2.2%, and 7.5±2.2%). Forearm CVC also increased following repeated IPC (P = 0.006) and remained elevated at Post+8 in both arms (intervention: 0.12±0.03, 0.14±0.04, 0.16±0.04 mV/mm Hg; contralateral: 0.14±0.04, 0.015±0.04, 0.17±0.07). No interaction between IPC arm and time was evident for FMD and CVC (both P > 0.05). IPC intervention did not alter CVC responses to local heating (P > 0.05).


CONCLUSIONS
Daily exposure to IPC for 7 days leads to local and remote improvements in brachial artery FMD and resting skin microcirculation that remain after cessation of the intervention and beyond the late phase of protection. These findings may have clinical relevance for micro- and macrovascular improvements.
34406235
The time dependence of the effect of ischemic preconditioning on successive sprint swimming performance.
OBJECTIVES
The present study aimed to determine the effects of ischemic preconditioning on performance in three successive 50-m swimming trials and to measure stroke rate, stroke length and blood lactate accumulation.


DESIGN
Counterbalanced, repeated-measures cross-over study.


METHODS
On two separate days, eleven competitive male swimmers (20±3 years, 182±5cm, 77±5kg) performed three successive 50-m trials in a 50-m swimming pool, preceded by intermittent bilateral cuff inflation (4× 5-min of blood flow restriction+5-min of cuff deflation) at either 220 for thighs and 180mmHg for arms (ischemic preconditioning) or 20mmHg for both limbs (control-treatment). The 50-m trials were conducted 1-, 2-, and 8-h after the procedure.


RESULTS
While no ergogenic effect of ischemic preconditioning was observed for 1-h (0.4%, 95% confidence limits of ±0.6%, p=0.215), there were clear beneficial effects of ischemic preconditioning on 2- and 8-h (1.0% and 1.2%, respectively; 95% confidence limits of ±0.6% in both cases, p≤0.002). Furthermore, ischemic preconditioning increased blood lactate accumulation in 2-(p<0.001) and 8-h (p=0.010) and stroke rate for 2- and 8-h in specific 10-m segments (p<0.05).


CONCLUSIONS
These findings suggest a time-dependent effect of ischemic preconditioning on 50-m swimming performance for competitive athletes, with the time window of the beneficial effect starting after about 2-h and lasting for at least 8-h after ischemic preconditioning. This change in performance was accompanied by an increase in blood lactate accumulation and faster strokes in front crawl.
45459062
Validity of simple field tests as indicators of match-related physical performance in top-level professional soccer players.
The aim of this study was to examine the construct validity of selected field tests as indicators of match-related physical performance. During the competitive season, eighteen professional soccer players (age 26.2 +/- 4.5 yrs, mass 80.8 +/- 7.8 kg, and height 181.9 +/- 3.7 cm) completed an incremental running field test to exhaustion, a vertical-jump and a repeated-sprint ability (RSA) test. Match physical performance was quantified during official matches using a video-computerized, semi-automatic, match analysis image recognition system, (ProZone, Leeds, UK). The selected measures of match physical performance were: total distance covered (TD), high intensity running (HIR: > 14.4 km . h (-1)), very high intensity running (VHIR:> 19.8 km . h (-1)), sprinting (> 25.2 km . h (-1)) and top running speed. Significant correlations were found between peak speed reached during the incremental field test and TD (r = 0.58, R (2) = 0.34; p < 0.05), HIR (r = 0.65, R (2) = 0.42; p < 0.01) and VHIR (r = 0.64, R (2) = 0.41; p < 0.01). Significant correlations were also found between RSA mean time and VHIR (r = - 0.60, R (2) = 0.36; p < 0.01) and sprinting distance (r = - 0.65, R (2) = 0.42; p < 0.01). Significant differences were found between the best and worst group as defined by the median split technique for peak speed (TD = 12 011 +/- 747 m vs. 10 712 +/- 669, HIR = 3192 +/- 482 m vs. 2314 +/- 347 m, and VHIR = 1014 +/- 120 vs. 779 +/- 122 m, respectively; p < 0.05) and RSA mean time (VHIR = 974 +/- 162 m vs. 819 +/- 144 m, and sprinting = 235 +/- 56 vs. 164 +/- 58 m, respectively; p < 0.05). In conclusion, this study gives empirical support to the construct validity of RSA and incremental running tests as measures of match-related physical performance in top-level professional soccer players.
37402705
Validity of a repeated-sprint test for football.
Three studies involving 108 football players were conducted to examine the reliability of a repeated-shuttle-sprint ability (RSSA) test and its ability to differentiate between players of various competitive levels and playing positions. Study 1: Short-term reliability was determined in 22 professional players completing the RSSA test (6 x 40-m sprints with 20 s of recovery between sprints) on two separate occasions. Study 2: Long-term reliability (seasonal changes) was examined in 31 professional players completing the RSSA test four times (during the preseason period, at the start, middle and end of the competitive season). Study 3: 108 players were divided and compared according to competitive level or playing position. Standard error of measurement values expressed as coefficient of variation for RSSA mean time and best time were 0.8 and 1.3 % (short-term reliability) and 0.9 and 1.2 % (long-term reliability), respectively. The smallest worthwhile changes were 0.5 % for both mean and best time. Professional players showed better RSSA performance than amateur players, and defenders displayed the lowest RSSA performance. In conclusion, the RSSA test showed adequate construct validity but only RSSA mean time showed sufficient reliability to detect large training-induced changes but not small important differences.
9029274
Performance and physiological responses to repeated-sprint exercise: a novel multiple-set approach
We investigated the acute and chronic responses to multiple sets of repeated-sprint exercise (RSE), focusing on changes in acceleration, intermittent running capacity and physiological responses. Ten healthy young adults (7 males, 3 females) performed an incremental test, a Yo-Yo intermittent recovery test level1 (Yo-Yo IR1), and one session of RSE. RSE comprised three sets of 5 × 4-s maximal sprints on a non-motorised treadmill, with 20 s of passive recovery between repetitions and 4.5 min of passive recovery between sets. After ten repeated-sprint training sessions, participants repeated all tests. During RSE, performance was determined by measuring acceleration, mean and peak power/velocity. Recovery heart rate (HR), HR variability, and finger-tip capillary lactate concentration ([Lac−]) were measured. Performance progressively decreased across the three sets of RSE, with the indices of repeated-sprint ability being impaired to a different extent before and after training. Training induced a significant increase (p < 0.05) in all indices of performance, particularly acceleration (21.9, 14.7 and 15.2% during sets 1, 2 and 3, respectively). Training significantly increased Yo-Yo IR1 performance by 8% and decreased Δ[Lac−]/work ratio (−15.2, −15.5, −9.4% during sets 1, 2 and 3, respectively) and recovery HR during RSE. There were strong correlations between Yo-Yo IR1 performance and indices of RSE performance, especially acceleration post-training (r = 0.88, p = 0.004). Repeated-sprint training, comprising only 10 min of exercise overall, effectively improved performance during multiple-set RSE. This exercise model better reflects team-sport activities than single-set RSE. The rapid training-induced improvement in acceleration, quantified here for the first time, has wide applications for professional and recreational sport activities.
7551323
The Cosmed K4 telemetry system as an accurate device for oxygen uptake measurements during exercise.
The purpose of this study was to test the accuracy of oxygen uptake (VO2) measurements using the Cosmed K4 portable telemetry system. This system of higher technology than the original Cosmed K2 device, contains a CO2 electrode allowing measurements alternatively by either the Cosmed K4 system (K4) or the CPX Medical Graphics (CPX) during a maximum oxygen uptake (VO2max) ergocycle test, at rest and during several submaximal exercises (25, 50 and 75% of maximal work rate) in seven subjects. Heart rate values were comparable for exercise at the same work stage during gas collection using the two systems, indicating that the physiological stresses were similar. The VO2 values did not significantly differ at rest (4.40+/-0.83 vs 4.16+/-0.58ml x min(-1) x kg[-1]), at 25% Wmax (20.97+/-1.31 vs 21.32+/-2.54 ml x min(-1) x kg[-1]), at 50% Wmax (33.32+/-3.92 vs 33.50+/-3.51 ml x min(-1) x kg[-1]), at 75% Wmax (47.01+/-7.51 vs 47.49+/-7.11 ml x min(-1) kg[-1]) and at maximal intensities (62.07+/-8.48 vs 62.84+/-11.31 ml x min(-1) kg[-1]) using K4 and CPX devices, respectively. The results of this study indicated that the K4 system was accurate for all oxygen uptake measurements from rest to maximum exercise levels.
8160502
Validity of the polar S810 heart rate monitor to measure R-R intervals at rest.
PURPOSE
This study was conducted to compare R-R intervals and the subsequent analysis of heart rate variability (HRV) obtained from the Polar S810 heart rate monitor (HRM) (Polar Electro Oy) with an electrocardiogram (ECG) (Physiotrace, Estaris, Lille, France) during an orthostatic test.


METHODS
A total of 18 healthy men (age: 27.1 +/- 1.9 yr; height: 1.82 +/- 0.06 m; mass 77.1 +/- 7.7 kg) performed an active orthostatic test during which R-R intervals were simultaneously recorded with the HRM and the ECG recorder The two signals were synchronized and corrected before a time domain analysis, the fast Fourier transform (FFT) and a Poincaré plot analysis. Bias and limits of agreement (LoA), effect size (ES), and correlation coefficients were calculated.


RESULTS
R-R intervals were significantly different in the supine and standing position between the ECG and the HRM uncorrected and corrected signal (P < 0.05, ES = 0.000 and 0.006, respectively). The bias +/- LoA, however, were 0.9 +/- 12 ms. HRV parameters derived from both signals in both positions were not different (P > 0.05) and well correlated (r > 0.97, P < 0.05), except root mean square of difference (RMSSD) and SD1 in standing position (P < 0.05, ES = 0.052 and 0.057; r = 0.99 and 0.98, respectively).


CONCLUSION
Narrow LoA, good correlations, and small effect sizes support the validity of the Polar S810 HRM to measure R-R intervals and make the subsequent HRV analysis in supine position. Caution must be taken in standing position for the parameters sensitive to the short-term variability (i.e., RMSSD and SD1).
8180950
Comparison of the Polar S810i monitor and the ECG for the analysis of heart rate variability in the time and frequency domains.
The aim of the present study was to compare heart rate variability (HRV) at rest and during exercise using a temporal series obtained with the Polar S810i monitor and a signal from a LYNX(R) signal conditioner (BIO EMG 1000 model) with a channel configured for the acquisition of ECG signals. Fifteen healthy subjects aged 20.9 +/- 1.4 years were analyzed. The subjects remained at rest for 20 min and performed exercise for another 20 min with the workload selected to achieve 60% of submaximal heart rate. RR series were obtained for each individual with a Polar S810i instrument and with an ECG analyzed with a biological signal conditioner. The HRV indices (rMSSD, pNN50, LFnu, HFnu, and LF/HF) were calculated after signal processing and analysis. The unpaired Student t-test and intraclass correlation coefficient were used for data analysis. No statistically significant differences were observed when comparing the values analyzed by means of the two devices for HRV at rest and during exercise. The intraclass correlation coefficient demonstrated satisfactory correlation between the values obtained by the devices at rest (pNN50 = 0.994; rMSSD = 0.995; LFnu = 0.978; HFnu = 0.978; LF/HF = 0.982) and during exercise (pNN50 = 0.869; rMSSD = 0.929; LFnu = 0.973; HFnu = 0.973; LF/HF = 0.942). The calculation of HRV values by means of temporal series obtained from the Polar S810i instrument appears to be as reliable as those obtained by processing the ECG signal captured with a signal conditioner.
43294804
Comparison of three mobile devices for measuring R–R intervals and heart rate variability: Polar S810i, Suunto t6 and an ambulatory ECG system
The first aim of this study was to compare an ambulatory five-lead ECG system with the commercially available breast belt measuring devices; Polar S810i and Suunto t6, in terms of R–R interval measures and heart rate variability (HRV) indices. The second aim was to compare different HRV spectral analysis methods. Nineteen young males (aged between 22 and 31 years, median 24 years) underwent simultaneous R–R interval recordings with the three instruments during supine and sitting rest, moderate dynamic, and moderate to vigorous static exercise of the upper and lower limb. For each subject, 17 R–R interval series of 3-min length were extracted from the whole recordings and then analyzed in frequency domain using (1) a fast Fourier transform (FFT), (2) an autoregressive model (AR), (3) a Welch periodogram (WP) and (4) a continuous wavelet transform (CWT). Intra-class correlation coefficients (ICC) and Bland–Altman limits of agreement (LoA) method served as criteria for measurement agreement. Regarding the R–R interval recordings, ICC (lower ICC 95% confidence interval >0.99) as well as LoA (maximum LoA: −15.1 to 14.3 ms for ECG vs. Polar) showed an excellent agreement between all devices. Therefore, the three instruments may be used interchangeably in recording and interpolation of R–R intervals. ICCs for HRV frequency parameters were also high, but in most cases LoA analysis revealed unacceptable discrepancies between the instruments. The agreement among the different frequency transform methods can be taken for granted when analyzing the normalized power in low and high frequency ranges; however, not when analyzing the absolute values.
22472623
Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure.
OBJECTIVES
Vagally mediated heart rate recovery after exercise was assessed in patients with chronic heart failure and in well trained athletes by analyzing the postexercise heart rate decay.


BACKGROUND
Vagal reactivation is an important cardiac deceleration mechanism after exercise. However, alterations of this mechanism under pathologic conditions have not been characterized because of the lack of a specific index.


METHODS
To find a vagally mediated component of heart rate recovery, the time constants of the beat-by-beat heart rate decay for the first 30 s (T30) and the first 120 s (T120) after exercise were obtained at six levels of exercise in eight normal volunteers: 1) at maximal exercise, 2) at anaerobic threshold, 3) at anaerobic threshold with propranolol administration, 4) at anaerobic threshold with atropine administration, 5) at anaerobic threshold with concomitant administration of both drugs, and 6) at 50% of anaerobic threshold. To investigate the effects of heart failure and endurance training on vagally mediated heart rate recovery, T30 and T120 at anaerobic threshold were obtained in 20 patients with chronic heart failure and in 9 cross-country skiers.


RESULTS
In normal volunteers, T30 and T120 were markedly prolonged by atropine administration, indicating that both time constants are mediated by vagal reactivation. Moreover, T30 was almost independent of the exercise intensity and sympathetic blockade, whereas T120 was affected by sympathetic nerve activity and exercise work load. These results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes (p < 0.01) and significantly larger in patients with chronic heart failure (p < 0.01) than that in respective age-matched normal control subjects.


CONCLUSIONS
The T30 value could be a specific index for vagally mediated heart rate recovery. Vagally mediated heart rate recovery after exercise is accelerated in well trained athletes but blunted in patients with chronic heart failure.
38608711
Reliability of heart rate measures used to assess post‐exercise parasympathetic reactivation
Postexercise HRR (heart rate recovery) and HRV (heart rate variability) are commonly used to asses non‐invasive cardiac autonomic regulation and more particularly reactivation parasympathetic function. Unfortunately, the reliability of postexercise HRR and HRV remains poorly quantified and is still lacking. The aim of this study was to examine absolute and relative reliability of HRR and HRV indices used to assess postexercise cardiac parasympathetic reactivation.
1372640
Effect of repeated-sprints on the reliability of short-term parasympathetic reactivation
This study determined the reliability of post-exercise heart rate recovery (HRR) and vagal-related HR variability (HRV) after repeated-sprints (RSs), and contrasted it with the smallest worthwhile change (SWC) of these indices. Fourteen healthy male participants performed on four occasions, separated by 7 days, five 30-m sprints interspersed by 25-s of recovery. Post-exercise HR during 10 min of seated rest was measured. HRR during the first 60-s of recovery was computed (HRR60s). HRV indices were calculated in time and frequency domains during the last 5-min of the recovery. Absolute and relative reliability were assessed by typical error of measurement expressed as coefficient of variation (CV) and intraclass correlation coefficients (ICCs), respectively. Sensitivity was assessed comparing SWC to the typical error of measurement. CV ranged from 3.6% to 13.5% and from 6.3% to 109.2% for the HRR and HRV indices, respectively. ICCs were from 0.78 to 0.96 and from 0.76 to 0.92, respectively. HRR and HRV indices showed large discrepancies reliability. HRR60s and the square root of the mean sum of the squared differences between R-R intervals presented the highest levels of both absolute and relative reliability. However, SWC was lower than the typical error of measurement, indicating insufficient sensitivity to confidently detect small, but meaningful, changes in HRR and HRV indices.
33888275
Reliability of resting and postexercise heart rate measures.
In this study, we compared the reliability of short-term resting heart rate (HR) variability (HRV) and postexercise parasympathetic reactivation (i.e., HR recovery (HRR) and HRV) indices following either submaximal or supramaximal exercise. On 4 different occasions, beat-to-beat HR was recorded in 15 healthy males (21.5 ± 1.4 yr) during 5 min of seated rest, followed by submaximal (Sub) and supramaximal (Supra) exercise bouts; both exercise bouts were followed by 5 min of seated recovery. Reliability of all HR-derived indices was assessed by the typical error of measurement expressed as a coefficient of variation (CV,%). CV for HRV indices ranged from 4 to 17%, 7 to 27% and 41 to 82% for time domain, spectral and ratio indices, respectively. The CV for HRR ranged from 15 to 32%. Spectral CVs for HRV were lower at rest compared with Supra (e.g., natural logarithm of the high frequency range (LnHF); 12.6 vs. 26.2%; P=0.02). HRR reliability was not different between Sub and Supra (25 vs. 14%; P=0.10). The present study found discrepancy in the CVs of vagal-related heart rate indices; a finding that should be appreciated when assessing changes in these variables. Further, Supra exercise was shown to worsen the reliability of HRV-spectral indices.
23529241
Dynamic asymmetry of phosphocreatine concentration and O2 uptake between the on‐ and off‐transients of moderate‐ and high‐intensity exercise in humans
The on‐ and off‐transient (i.e. phase II) responses of pulmonary oxygen uptake (V̇O2) to moderate‐intensity exercise (i.e. below the lactate threshold, θL) in humans has been shown to conform to both mono‐exponentiality and ‘on‐off’ symmetry, consistent with a system manifesting linear control dynamics. However above θL the V̇O2 kinetics have been shown to be more complex: during high‐intensity exercise neither mono‐exponentiality nor ‘on‐off’ symmetry have been shown to appropriately characterise the V̇O2 response. Muscle [phosphocreatine] ([PCr]) responses to exercise, however, have been proposed to be dynamically linear with respect to work rate, and to demonstrate ‘on‐off’ symmetry at all work intenisties. We were therefore interested in examining the kinetic characteristics of the V̇O2 and [PCr] responses to moderate‐ and high‐intensity knee‐extensor exercise in order to improve our understanding of the factors involved in the putative phosphate‐linked control of muscle oxygen consumption. We estimated the dynamics of intramuscular [PCr] simultaneously with those of V̇O2 in nine healthy males who performed repeated bouts of both moderate‐ and high‐intensity square‐wave, knee‐extension exercise for 6 min, inside a whole‐body magnetic resonance spectroscopy (MRS) system. A transmit‐receive surface coil placed under the right quadriceps muscle allowed estimation of intramuscular [PCr]; V̇O2 was measured breath‐by‐breath using a custom‐designed turbine and a mass spectrometer system. For moderate exercise, the kinetics were well described by a simple mono‐exponential function (following a short cardiodynamic phase for V̇O2,), with time constants (τ) averaging: τV̇O2,on 35 ± 14 s (±s.d.), τ[PCr]on 33 ± 12 s, τV̇O2,off 50 ± 13 s and τ[PCr]off 51 ± 13 s. The kinetics for both V̇O2 and [PCr] were more complex for high‐intensity exercise. The fundamental phase expressing average τ values of τV̇O2,on 39 ± 4 s, τ[PCr]on 38 ± 11 s, τV̇O2,off 51 ± 6 s and τ[PCr]off 47 ± 11 s. An associated slow component was expressed in the on‐transient only for both V̇O2 and [PCr], and averaged 15.3 ± 5.4 and 13.9 ± 9.1 % of the fundamental amplitudes for V̇O2 and [PCr], respectively. In conclusion, the τ values of the fundamental component of [PCr] and V̇O2 dynamics cohere to within 10 %, during both the on‐ and off‐transients to a constant‐load work rate of both moderate‐ and high‐intensity exercise. On average, ≈90 % of the magnitude of the V̇O2 slow component during high‐intensity exercise is reflected within the exercising muscle by its [PCr] response.
37234682
Parasympathetic Effects on Heart Rate Recovery after Exercise
Background Exercise and its recovery period are associated with increased risk of death relative to sedentary periods. They are also accompanied by dynamic changes in autonomic tone. Little information is available regarding parasympathetic effects during high-intensity exercise and recovery. Methods Ten normal subjects (five women; age 33 ± 2 years) underwent exercise testing on a bicycle ergometer. On day 1, subjects exercised to maximum tolerated workload using a graded protocol with 5 minutes at maximal workload (peak heart rate achieved 174.7 ± 5.4 bpm). On day 2, subjects performed the identical exercise protocol as on day 1; 1 minute into the maximum exercise stage, atropine (0.04 mg/kg) was administered. Heart rate was recorded every minute during exercise, and an electrocardiogram was recorded every minute in recovery for 10 minutes. The parasympathetic effect on heart rate was defined by the difference in heart rate with and without atropine. Results The parasympathetic effect during maximal exercise was 3.4 to 6 bpm (p < .05). During recovery, a large parasympathetic effect on heart rate was noted by 1 minute (22.8 bpm; p < .0002), increased until 4 minutes, and then remained stable until 10 minutes. Despite faster heart rates with parasympathetic blockade, the P-R interval was shorter (p < .002), consistent with a significant parasympathetic effect on the atrioventricular node in recovery. Evaluation of the Q-T-R-R relationship on the 2 days demonstrated significant changes in both the slope (p < .0001) and the intercept (p < .0001), consistent with a modification of ventricular repolarization by parasympathetic tone in recovery. Conclusion These data indicate that in normal subjects, parasympathetic effects persist during high-intensity exercise and are prominent in the early phases of recovery. These parasympathetic effects may play an important role in prevention of sudden cardiac death during these periods of increased risk.
8953487
Monitoring training status with HR measures: do all roads lead to Rome?
Measures of resting, exercise, and recovery heart rate are receiving increasing interest for monitoring fatigue, fitness and endurance performance responses, which has direct implications for adjusting training load (1) daily during specific training blocks and (2) throughout the competitive season. However, these measures are still not widely implemented to monitor athletes' responses to training load, probably because of apparent contradictory findings in the literature. In this review I contend that most of the contradictory findings are related to methodological inconsistencies and/or misinterpretation of the data rather than to limitations of heart rate measures to accurately inform on training status. I also provide evidence that measures derived from 5-min (almost daily) recordings of resting (indices capturing beat-to-beat changes in heart rate, reflecting cardiac parasympathetic activity) and submaximal exercise (30- to 60-s average) heart rate are likely the most useful monitoring tools. For appropriate interpretation at the individual level, changes in a given measure should be interpreted by taking into account the error of measurement and the smallest important change of the measure, as well as the training context (training phase, load, and intensity distribution). The decision to use a given measure should be based upon the level of information that is required by the athlete, the marker's sensitivity to changes in training status and the practical constrains required for the measurements. However, measures of heart rate cannot inform on all aspects of wellness, fatigue, and performance, so their use in combination with daily training logs, psychometric questionnaires and non-invasive, cost-effective performance tests such as a countermovement jump may offer a complete solution to monitor training status in athletes participating in aerobic-oriented sports.
25530315
Changes in heart rate recovery after high-intensity training in well-trained cyclists
Heart rate recovery (HRR) after submaximal exercise improves after training. However, it is unknown if this also occurs in already well-trained cyclists. Therefore, 14 well-trained cyclists (VO2max 60.3 ± 7.2 ml kg−1 min−1; relative peak power output 5.2 ± 0.6 W kg−1) participated in a high-intensity training programme (eight sessions in 4 weeks). Before and after high-intensity training, performance was assessed with a peak power output test including respiratory gas analysis (VO2max) and a 40-km time trial. HRR was measured after every high-intensity training session and 40-km time trial. After the training period peak power output, expressed as W kg−1, improved by 4.7% (P = 0.000010) and 40-km time trial improved by 2.2% (P = 0.000007), whereas there was no change in VO2max (P = 0.066571). Both HRR after the high intensity training sessions (7 ± 6 beats; P = 0.001302) and HRR after the 40-km time trials (6 ± 3 beats; P = 0.023101) improved significantly after the training period. Good relationships were found between improvements in HRR40-km and improvements in peak power output (r = 0.73; P < 0.0001) and 40-km time trial time (r = 0.96; P < 0.0001). In conclusion, HRR is a sensitive marker which tracks changes in training status in already well-trained cyclists and has the potential to have an important role in monitoring and prescribing training.
123217261
Statistical Power Analysis for the Behavioral Sciences
Contents: Prefaces. The Concepts of Power Analysis. The t-Test for Means. The Significance of a Product Moment rs (subscript s). Differences Between Correlation Coefficients. The Test That a Proportion is .50 and the Sign Test. Differences Between Proportions. Chi-Square Tests for Goodness of Fit and Contingency Tables. The Analysis of Variance and Covariance. Multiple Regression and Correlation Analysis. Set Correlation and Multivariate Methods. Some Issues in Power Analysis. Computational Procedures.
4679864
Acute ischemic preconditioning does not influence high-intensity intermittent exercise performance
This study evaluated the acute effect of ischemic preconditioning (IPC) on a high-intensity intermittent exercise performance and physiological indicators in amateur soccer players. Thirteen players (21.5 ± 2 yrs) attended three trials separated by 3–5 days in a counterbalanced randomized cross-over design: IPC (4 × 5-min occlusion 220 mmHg/reperfusion 0 mmHg) in each thigh; SHAM (similar to the IPC protocol but “occlusion” at 20 mmHg) and control (seated during the same time of IPC). After 6-min of each trial (IPC, SHAM or control), the players performed the YoYo Intermittent Endurance Test level 2 (YoYoIE2). The distance covered in the YoYoIE2 (IPC 867 ± 205 m; SHAM 873 ± 212 m; control 921 ± 206 m) was not different among trials (p = 0.10), furthermore, lactate concentration and rate of perceived exertion did not differ (P > 0.05) among protocols. There were also no significant differences in either mean heart rate (HR) or peak HR (p > 0.05) for both IPC and SHAM compared to control. Therefore, we conclude that acute IPC does not influence high-intensity intermittent exercise performance in amateur soccer players and that rate of perceived exertion, heart rate and lactate do not differ between the intervention IPC, SHAM and control.
3626293
Effect of Ischemic Preconditioning on Endurance Performance Does Not Surpass Placebo
Purpose Recent studies have reported ischemic preconditioning (IPC) can acutely improve endurance exercise performance in athletes. However, placebo and nocebo effects have not been sufficiently controlled, and the effect on aerobic metabolism parameters that determine endurance performance (e.g., oxygen cost of running, lactate threshold, and maximal oxygen uptake [V˙O2max]) has been equivocal. Thus, we circumvented limitations from previous studies to test the effect of IPC on aerobic metabolism parameters and endurance performance in well-trained runners. Methods Eighteen runners (14 men/4 women) were submitted to three interventions, in random order: IPC; sham intervention (SHAM); and resting control (CT). Subjects were told both IPC and SHAM would improve performance compared to CT (i.e., similar placebo induction), and IPC would be harmless despite circulatory occlusion sensations (i.e., nocebo avoidance). Next, pulmonary ventilation and gas exchange, blood lactate concentration, and perceived effort were measured during a discontinuous incremental test on a treadmill. Then, a supramaximal test was used to verify the V˙O2max and assess endurance performance (i.e., time to exhaustion). Results Ventilation, oxygen uptake, carbon dioxide output, lactate concentration, and perceived effort were similar among IPC, SHAM, and CT throughout the discontinuous incremental test (P > 0.05). Oxygen cost of running, lactate threshold, and V˙O2max were also similar among interventions (P > 0.05). Time to exhaustion was longer after IPC (mean ± SEM, 165.34 ± 12.34 s) and SHAM (164.38 ± 11.71 s) than CT (143.98 ± 12.09 s; P = 0.02 and 0.03, respectively), but similar between IPC and SHAM (P = 1.00). Conclusions IPC did not change aerobic metabolism parameters, whereas improved endurance performance. The IPC improvement, however, did not surpass the effect of a placebo intervention.
7774168
Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men
Ischemic preconditioning (IPC) has been hypothesized to elicit ergogenic effects by reducing feedback from metabolically sensitive group III/IV muscle afferents during exercise. If so, reflex efferent neural outflow should be attenuated. We investigated the effects of IPC on muscle sympathetic nerve activity (MSNA) during static handgrip (SHG) and used post‐exercise circulatory occlusion (PECO) to isolate for the muscle metaboreflex. Thirty‐seven healthy men (age: 24 ± 5 years [mean ± SD]) were randomized to receive sham (n = 16) or IPC (n = 21) interventions. Blood pressure, heart rate, and MSNA (microneurography; sham n = 11 and IPC n = 18) were collected at rest and during 2 min of SHG (30% maximal voluntary contraction) and 3 min of PECO before (PRE) and after (POST) sham or IPC treatment (3 × 5 min 20 mmHg or 200 mmHg unilateral upper arm cuff inflation). Resting mean arterial pressure was higher following sham (79 ± 7 vs. 83 ± 6 mmHg, P < 0.01) but not IPC (81 ± 6 vs. 82 ± 6 mmHg, P > 0.05), while resting MSNA burst frequency was unchanged (P > 0.05) with sham (18 ± 7 vs. 19 ± 9 bursts/min) or IPC (17 ± 7 vs. 19 ± 7 bursts/min). Mean arterial pressure, heart rate, stroke volume, cardiac output, and total vascular conductance responses during SHG and PECO were comparable PRE and POST following sham and IPC (All P > 0.05). Similarly, MSNA burst frequency, burst incidence, and total MSNA responses during SHG and PECO were comparable PRE and POST with sham and IPC (All P > 0.05). These findings demonstrate that IPC does not reduce hemodynamic responses or central sympathetic outflow directed toward the skeletal muscle during activation of the muscle metaboreflex using static exercise or subsequent PECO.
31020757
Ischemic preconditioning reduces hemodynamic response during metaboreflex activation.
Ischemic preconditioning (IP) has been shown to improve exercise performance and to delay fatigue. However, the precise mechanisms through which IP operates remain elusive. It has been hypothesized that IP lowers the sensation of fatigue by reducing the discharge of group III and IV nerve endings, which also regulate hemodynamics during the metaboreflex. We hypothesized that IP reduces the blood pressure response during the metaboreflex. Fourteen healthy males (age between 25 and 48 yr) participated in this study. They underwent the following randomly assigned protocol: postexercise muscle ischemia (PEMI) test, during which the metaboreflex was elicited after dynamic handgrip; control exercise recovery session (CER) test; and PEMI after IP (IP-PEMI) test. IP was obtained by occluding forearm circulation for three cycles of 5 min spaced by 5 min of reperfusion. Hemodynamics were evaluated by echocardiography and impedance cardiography. The main results were that after IP the mean arterial pressure response was reduced compared with the PEMI test (means ± SD +3.37 ± 6.41 vs. +9.16 ± 7.09 mmHg, respectively). This was the consequence of an impaired venous return that impaired the stroke volume during the IP-PEMI more than during the PEMI test (-1.43 ± 15.35 vs. +10.28 ± 10.479 ml, respectively). It was concluded that during the metaboreflex, IP affects hemodynamics mainly because it impairs the capacity to augment venous return and to recruit the cardiac preload reserve. It was hypothesized that this is the consequence of an increased nitric oxide production, which reduces the possibility to constrict venous capacity vessels.
38488589
Role of muscle mass and mode of contraction in circulatory responses to exercise.
The roles of the mode of contraction (i.e., dynamic or static) and the active muscle mass as determinants of the cardiovascular responses to exercise were studied. Six healthy men performed static handgrip (SHG), dynamic handgrip (DHG), static two-knee extension (SKE), and dynamic two-knee extension (DKE) to local muscular fatigue in approximately 6 min. Increases in mean arterial pressure were similar for each mode of contraction, 29 +/- 5 and 30 +/- 3 mmHg in SHG and DHG and 56 +/- 2 and 48 +/- 2 mmHg in SKE and DKE (P greater than 0.05) but larger for KE than HG (P less than 0.001). Cardiac output increased more for dynamic than for static exercise and for each mode more for KE than HG (P less than 0.001). Systemic resistance was lower for dynamic than static exercise and fell from resting levels by approximately 1/3 during DKE. The magnitude of the pressor response was related to the active muscle mass but independent of the contraction mode. However, the mode of contraction affected the circulatory changes contributing to the pressor response. Equalization of the pressor responses was achieved by proportionately larger increases in cardiac output during dynamic exercise.
8032727
Autonomic control of heart rate by metabolically sensitive skeletal muscle afferents in humans
Isolated activation of metabolically sensitive skeletal muscle afferents (muscle metaboreflex) using post‐exercise ischaemia (PEI) following handgrip partially maintains exercise‐induced increases in arterial blood pressure (BP) and muscle sympathetic nerve activity (SNA), while heart rate (HR) declines towards resting values. Although masking of metaboreflex‐mediated increases in cardiac SNA by parasympathetic reactivation during PEI has been suggested, this has not been directly tested in humans. In nine male subjects (23 ± 5 years) the muscle metaboreflex was activated by PEI following moderate (PEI‐M) and high (PEI‐H) intensity isometric handgrip performed at 25% and 40% maximum voluntary contraction, under control (no drug), parasympathetic blockade (glycopyrrolate) and β‐adrenergic blockade (metoprolol or propranalol) conditions, while beat‐to‐beat HR and BP were continuously measured. During control PEI‐M, HR was slightly elevated from rest (+3 ± 2 beats min−1); however, this HR elevation was abolished with β‐adrenergic blockade (P < 0.05 vs. control) but augmented with parasympathetic blockade (+8 ± 2 beats min−1, P < 0.05 vs. control and β‐adrenergic blockade). The HR elevation during control PEI‐H (+9 ± 3 beats min−1) was greater than with PEI‐M (P < 0.05), and was also attenuated with β‐adrenergic blockade (+4 ± 2 beats min−1, P < 0.05 vs. control), but was unchanged with parasympathetic blockade (+9 ± 2 beats min−1, P > 0.05 vs. control). BP was similarly increased from rest during PEI‐M and further elevated during PEI‐H (P < 0.05) in all conditions. Collectively, these findings suggest that the muscle metaboreflex increases cardiac SNA during PEI in humans; however, it requires a robust muscle metaboreflex activation to offset the influence of cardiac parasympathetic reactivation on heart rate.
25178328
Effect of ischemic preconditioning on repeated sprint ability in team sport athletes
Abstract This study investigated whether ischemic preconditioning (IPC) in a trained population affected repeated sprint performance. A secondary aim was to assess responses according to gender. Sixteen (nine females and seven males) well trained team sport athletes took part in a randomised crossover study design. Participants underwent an IPC and placebo treatment involving three periods of 5 min occlusion applied unilaterally (3 × 5 min occlusion to each leg) at either 220 mmHg or 50 mmHg. Each period of occlusion was followed by 5 min reperfusion. Following treatment 5 × 6 s maximal effort sprints were undertaken on a cycle ergometer against 7.5% body mass, each interspersed by 24 s recovery. Measured parameters included peak power, total power, percentage decrement, post-exercise blood lactate and ratings of perceived exertion. Nor within subject main effect for IPC was observed, neither was there an interaction effect with gender. Effect sizes were trivial (ES < 0.2) with the exception of a moderate (ES < 1.2) change in post-exercise blood lactate in the female cohort (1.6 ± 0.4 mmol−1 lower following IPC). Results suggest no benefit to team sport players in utilising IPC as a means of enhancing repeated sprint performance. A lower blood lactate response in female participants following IPC may suggest improved blood flow through vasodilation.
20274899
Are the Beneficial Effects of Ischemic Preconditioning on Performance Partly a Placebo Effect?
The acute effect of ischemic preconditioning (IPC) on the maximal performance in the 100-m freestyle event was studied in recreational swimmers. 15 swimmers (21.0±3.2 years) participated in a random crossover model on 3 different days (control [CON], IPC or SHAM), separated by 3-5 days. IPC consisted of 4 cycles of 5-min occlusion (220 mmHg)/5-min reperfusion in each arm, and the SHAM protocol was similar to IPC but with only 20 mmHg during the occlusion phase. The subjects were informed that both maneuvers (IPC and SHAM) would improve their performance. After IPC, CON or SHAM, the volunteers performed a maximal 100-m time trial. IPC improved performance (p=0.036) compared to CON. SHAM performance was only better than CON (p=0.059) as a tendency but did not differ from IPC performance. The individual response of the subjects to the different maneuvers was very heterogeneous. We conclude that IPC may improve performance in recreational swimmers, but this improvement could mainly be a placebo effect.
10011182
Ischemic Preconditioning and Placebo Intervention Improves Resistance Exercise Performance
Abstract Marocolo, M, Willardson, JM, Marocolo, IC, da Mota, GR, Simão, R, and Maior, AS. Ischemic preconditioning and PLACEBO intervention improves resistance exercise performance. J Strength Cond Res 30(5): 1462–1469, 2016—This study evaluated the effect of ischemic preconditioning (IPC) on resistance exercise performance in the lower limbs. Thirteen men participated in a randomized crossover design that involved 3 separate sessions (IPC, PLACEBO, and control). A 12-repetition maximum (12RM) load for the leg extension exercise was assessed through test and retest sessions before the first experimental session. The IPC session consisted of 4 cycles of 5 minutes of occlusion at 220 mm Hg of pressure alternated with 5 minutes of reperfusion at 0 mm Hg for a total of 40 minutes. The PLACEBO session consisted of 4 cycles of 5 minutes of cuff administration at 20 mm Hg of pressure alternated with 5 minutes of pseudo-reperfusion at 0 mm Hg for a total of 40 minutes. The occlusion and reperfusion phases were conducted alternately between the thighs, with subjects remaining seated. No ischemic pressure was applied during the control (CON) session and subjects sat passively for 40 minutes. Eight minutes after IPC, PLACEBO, or CON, subjects performed 3 repetition maximum sets of the leg extension (2-minute rest between sets) with the predetermined 12RM load. Four minutes after the third set for each condition, blood lactate was assessed. The results showed that for the first set, the number of repetitions significantly increased for both the IPC (13.08 ± 2.11; p = 0.0036) and PLACEBO (13.15 ± 0.88; p = 0.0016) conditions, but not for the CON (11.88 ± 1.07; p > 0.99) condition. In addition, the IPC and PLACEBO conditions resulted insignificantly greater repetitions vs. the CON condition on the first set (p = 0.015; p = 0.007) and second set (p = 0.011; p = 0.019), but not on the third set (p = 0.68; p > 0.99). No difference (p = 0.465) was found in the fatigue index and lactate concentration between conditions. These results indicate that IPC and PLACEBO IPC may have small beneficial effects on repetition performance over a CON condition. Owing to potential for greater discomfort associated with the IPC condition, it is suggested that ischemic preconditioning might be practiced gradually to assess tolerance and potential enhancements to exercise performance.
44582005
Placebo effect of carbohydrate feedings during a 40-km cycling time trial.
PURPOSE
The placebo effect, a favorable outcome from belief that one has received a beneficial treatment, may be an important phenomenon in athletic performance. We have therefore investigated the placebo effect of a carbohydrate supplement on endurance performance.


METHODS
Forty-three competitive endurance cyclists (2 female, 41 male) performed two simulated 40-km time trials on an air-braked ergometer. In the first trial they ingested water to establish baseline performance (mean power 265 +/- 46 W for 58 +/- 4 min, mean +/- SD). For the second trial 6-8 d later they were randomized to two groups: one group ingested 16 mL x kg(-1) of a drink containing 7.6 g x 100 mL(-1) carbohydrate; the other ingested an indistinguishable noncaloric placebo drink. Cyclists in each group were further randomized to three subgroups according to whether they were told the drink contained carbohydrate, placebo, or either (not told).


RESULTS
Changes in mean power in the second trial were: told carbohydrate, 4.3 +/- 4.8%; told placebo, 0.5 +/- 5.8%; and not told, -1.1 +/- 8.5%. The difference between the told-carbohydrate and told-placebo groups was 3.8% (95% likely range 7.9 to -0.2%). The change in performance in the not-told group was more variable than that of the told groups by a factor of 1.6 (2.6 to 1.0). The real effect of carbohydrate was a slight reduction in power of 0.3% (4.4 to -3.8%).


CONCLUSIONS
(a) The placebo effect of a potentially ergogenic treatment during unblinded laboratory time trials lasting approximately 1 h is probably a small but worthwhile increase in endurance power. (b) Blinding subjects to the treatment increases individual differences in endurance effort, which may reduce precision of performance outcomes in controlled trials.
12681889
Pharmacological and psychological effects of caffeine ingestion in 40-km cycling performance.
UNLABELLED
The ergogenic effects of caffeine are well documented. Research has yet to examine any psychological contribution to this effect.


AIM
To explore the psychological and pharmacological effects of caffeine in laboratory cycling performance.


METHOD
Fourteen male competitive cyclists performed 14 40-km time trials (eight experimental interspersed with six baseline). The experimental phase consisted of two trials for each of four experimental conditions: informed caffeine/received caffeine, informed no treatment/received caffeine, informed caffeine/received placebo, and informed no treatment/received no treatment. Conditions were nonrandomized. ANOVA was used to estimate main effects and interactions for mean values of power, heart rate, blood lactate, and maximal oxygen uptake. Probabilistic inferences for mean power were based on a smallest worthwhile change of 1.5%.


RESULTS
Relative to baseline, a very likely beneficial main effect of receiving caffeine (3.5%; 95% confidence interval 1.5 to 5.5%), and a possibly beneficial main effect of being informed of caffeine (0.7%; -0.7 to 2.1%) were observed. A substantial interaction between belief and pharmacology indicated that caffeine exerted a greater effect on performance in conditions when subjects were informed that they had not ingested it, whereas belief exerted a greater influence on performance in the absence of caffeine (2.6%; -0.7 to 5.9%). A possibly harmful negative placebo (nocebo) effect was observed when subjects were correctly informed that they had ingested no caffeine (-1.9%; -4.1 to 0.3%). No clinically significant changes relative to baseline were observed in mean heart rate. Clear and substantial increases in blood lactate were evident after receipt of caffeine. Data for mean oxygen uptake were unclear.


CONCLUSION
Our data support the ergogenic efficacy of caffeine but suggest that both positive and negative expectations impact performance.
205238907
Effects of high-intensity interval versus continuous exercise training on post-exercise heart rate recovery in coronary heart-disease patients.
BACKGROUND
Heart rate recovery (HRR) has been considered a prognostic and mortality indicator in both healthy and coronary patients. Physical exercise prescription has shown improvements in VO2peak and HRR, but most of the studies have been carried out applying continuous training at a moderate intensity, being very limited the use of protocols of high intensity interval training in coronary patients. We aimed to compare the effects of a moderate continuous training (MCT) versus a high intensity interval training (HIIT) programme on VO2peak and HRR.


METHODS
Seventy three coronary patients were assigned to either HIIT or MCT groups for 8weeks. Incremental exercise tests in a cycloergometer were performed to obtain VO2peak data and heart rate was monitored during and after the exercise test to obtain heart rate recovery data.


RESULTS
Both exercise programmes significantly increase VO2peak with a higher increase in the HIIT group (HIIT: 4.5±4.46ml/kg/min vs MCT: 2.46±3.57ml/kg/min; p=0.039). High intensity interval training resulted in a significantly increase in HRR at the first and second minute of the recovery phase (15,44±7,04 vs 21,22±6,62, p<0,0001 and 23,73±9,64 vs 31,52±8,02, p<0,0001, respectively).


CONCLUSIONS
The results of our research show that the application of HIIT to patients with chronic ischemic heart disease of low risk resulted in an improvement in VO2peak, and also improvements in post-exercise heart-rate recovery, compared with continuous training.
25036123
Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction.
The interest for the antifibrillatory effect of vagal stimulation has been largely limited by the fact that this concept seemed restricted to acute experiments in anesthetized animals. To explore the potentially protective role of vagal stimulation in conscious animals we developed a chronically implantable device to be placed around the cervical right vagus. An anterior myocardial infarction was produced in 161 dogs; 1 month later an exercise stress test was performed on the 105 survivors. Toward the end of the test the circumflex coronary artery was occluded for 2 minutes. Fifty-nine (56%) dogs developed ventricular fibrillation and, before this test was repeated, were assigned either to a control group (n = 24) or to be instrumented with the vagal device (n = 35). Five dogs were excluded because of electrode malfunction. Compared with the heart rate level attained after 30 seconds of occlusion during exercise in the control test, vagal stimulation led to a decrease of approximately 75 beats/min (from 255 +/- 33 to 170 +/- 36 beats/min, p less than 0.001). In the control group 22 (92%) of 24 dogs developed ventricular fibrillation during the second exercise and ischemia test. By contrast, during vagal stimulation ventricular fibrillation occurred in only 3 (10%) of the 30 dogs tested and recurred in 26 (87%) during an additional exercise and ischemia test in the control condition (p less than 0.001 versus the vagal stimulation test; internal control analysis). Combined analysis of the tests performed in the control condition showed that ventricular fibrillation was reproducible in 48 (89%) of the 54 dogs tested. The protective effect of vagal stimulation was also significant in the group comparison analysis and even after exclusion of those four dogs in which ventricular fibrillation was not reproducible (92% versus 11.5%, control versus vagal stimulation, p less than 0.001). When heart rate was kept constant by atrial pacing, the vagally mediated protection was still significant (p = 0.015) as five (55%) of nine dogs survived the test. This study shows that vagal stimulation, performed shortly after the onset of an acute ischemic episode in conscious animals with a healed myocardial infarction, can effectively prevent ventricular fibrillation. This striking result seems to depend on multiple mechanisms having a synergistic action. The decrease in heart rate is an important but not always essential protective mechanism. The electrophysiological effects secondary to the vagally mediated antagonism of the sympathetic activity on the heart are likely to play a major role.
14218155
Heart rate recovery after exercise: a predictor of ventricular fibrillation susceptibility after myocardial infarction.
Heart rate recovery after exercise, thought to be related to cardiac parasympathetic tone, has been shown to be a prognostic tool for all-cause mortality. However, the relationship between this variable and confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, myocardial ischemia was induced with a 2-min occlusion of the left circumflex artery during the last minute of exercise in mongrel dogs with myocardial infarction (n = 105 dogs). VF was induced in 66 animals (susceptible), whereas the remaining 39 dogs had no arrhythmias (resistant). On a previous day, ECG was recorded and a time-series analysis of heart rate variability was measured 30, 60, and 120 s after submaximal exercise (treadmill running). The heart rate recovery was significantly greater in resistant dogs than in susceptible dogs at all three times, with the most dramatic difference at the 30-s mark (change from maximum: 48.1 +/- 3.6 beats/min, resistant dogs; 31.0 +/- 2.2 beats/min, susceptible dogs). Correspondingly, indexes of parasympathetic tone increased to a significantly greater extent in resistant dogs at 30 and 60 s after exercise. These differences were eliminated by atropine pretreatment. When considered together, these data suggest that resistant animals exhibit a more rapid recovery of vagal activity after exercise than those susceptible to VF. As such, postexercise heart rate recovery may help identify patients with a high risk for VF following myocardial infarction.
11770726
Changes in heart rate recovery in response to acute changes in training load
Heart rate recovery is an indirect marker of autonomic function and changes therein may offer a practical way of quantifying the physiological effects of training. We assessed whether per cent heart rate recovery (HRr%) after a standardized sub-maximal running (Heart rate Interval Monitoring System: HIMS) test, changed with acute changes in training load. A total of 28 men and women (mean age 30 ± 5 years) trained ad libitum for 2 weeks during which their heart rate (HR) was recorded. Training load was quantified using Training Impulse (TRIMPs). The participants were grouped based on whether they increased (Group I, n = 9), decreased (Group D, n = 8) or kept their training load constant (Group S, n = 11) from week 1 to week 2. Each week, the subjects completed a HIMS test. Changes between weeks in HR at the end of the test and HRr% were compared between groups. Mean per cent change in TRIMPs from week 1 to week 2 was significantly different among the groups (Group I, 55 ± 21% vs Group S, −6 ± 6% vs Group D, −42 ± 16%; P < 0.05). Group I had a slower HRr% and Group D tended to have a slightly faster HRr% after HIMS 2 than after HIMS 1 (mean per cent change 5.6 ± 8.7 vs −2.6 ± 3.9; P = 0.03). Thus a negative effect on HRr was observed with increases in training load. Sub-maximal HR was not affected by acute changes in training load. Whereas HR during exercise measures cardiac load, HRr may reflect the state of the autonomic nervous system, indicating the body’s capacity to respond to exercise.
2121084
Daily exercise prescription on the basis of HR variability among men and women.
PURPOSE
To test the utility of HR variability (HRV) in daily exercise prescription in moderately active (approximately two exercises per week) men and women.


METHODS
A total of 21 men and 32 women were divided into standard training (ST: males = 7 and females = 7), HRV-guided training (HRV-I: males = 7 and females = 7; HRV-II: females = 10), and control (males = 7 and females = 8) groups. The 8-wk aerobic training period included 40-min exercises at moderate and vigorous intensities (70% and 85% of maximal HR). The ST group was instructed to perform two or more sessions at moderate and three or more sessions at vigorous intensity weekly. HRV-I and HRV-II groups trained on the basis of changes in HRV, measured every morning. In the HRV-I group, an increase or no change in HRV resulted in vigorous-intensity training on that day. Moderate-intensity exercise or rest was prescribed if HRV had decreased. The HRV-II group performed a vigorous-intensity exercise only when HRV had increased. Peak oxygen consumption (VO2peak) and maximal workload (Loadmax) were measured by a maximal bicycle ergometer test before and after the intervention.


RESULTS
The changes in VO2peak did not differ between the training groups either in men or in women. In men, the change in Loadmax was higher in the HRV-I group than in the ST group (30 +/- 8 vs 18 +/- 10 W, P = 0.033). In women, no differences were found in the changes in Loadmax between the training groups (18 +/- 10, 15 +/- 11, and 18 +/- 5 W for ST, HRV-I, and HRV-II, respectively). The HRV-II group performed fewer vigorous-intensity exercises than the ST and HRV-I groups (1.8 +/- 0.3 vs 2.8 +/- 0.6 and 3.3 +/- 0.2 times per week, respectively, P < 0.01 for both).


CONCLUSIONS
HRV measurements are beneficial in exercise training prescription in moderately active men and women. Women benefit from HRV guidance by achieving significant improvement in fitness with a lower training load.
30753924
Standardized versus customized high-intensity training: effects on cycling performance.
PURPOSE
To determine whether a submaximal cycling test could be used to monitor and prescribe high-intensity interval training (HIT).


METHODS
Two groups of male cyclists completed 4 HIT sessions over a 2-wk period. The structured-training group (SG; n = 8, VO2max = 58.4 ± 4.2 mL · min-1 · kg-1) followed a predetermined training program while the flexible-training group (FG; n = 7, VO2max = 53.9 ± 5.0 mL · min-1 · kg-1) had the timing of their HIT sessions prescribed based on the data of the Lamberts and Lambert Submaximal Cycle Test (LSCT).


RESULTS
Effect-size calculations showed large differences in the improvements in 40-km time-trial performance after the HIT training between SG (8 ± 45 s) and FG (48 ± 42 s). Heart-rate recovery, monitored during the study, tended to increase in FG and remain unchanged in SG.


CONCLUSIONS
The results of the current study suggest that the LSCT may be a useful tool for coaches to monitor and prescribe HIT.