Enhanced Local Skeletal Muscle Oxidative Capacity and Microvascular Blood Flow Following 7-Day Ischemic Preconditioning in Healthy Humans.

Ischemic preconditioning (IPC), which involves intermittent periods of ischemia followed by reperfusion, is an effective clinical intervention that reduces the risk of myocardial injury and confers ischemic tolerance to skeletal muscle. Repeated bouts of IPC have been shown to stimulate long-term changes vascular function, however, it is unclear what metabolic adaptations may occur locally in the muscle. Therefore, we investigated 7 days of bilateral lower limb IPC (4 × 5 min) above limb occlusion pressure (220 mmHg; n = 10), or sham (20 mmHg; n = 10), on local muscle oxidative capacity and microvascular blood flow. Oxidative capacity was measured using near-infrared spectroscopy (NIRS) during repeated short duration arterial occlusions (300 mmHg). Microvascular blood flow was assessed during the recovery from submaximal isometric plantar flexion exercises at 40 and 60% of maximal voluntary contraction (MVC). Following the intervention period, beyond the late phase of protection (72 h), muscle oxidative recovery kinetics were speeded by 13% (rate constant pre 2.89 ± 0.47 min-1 vs. post 3.32 ± 0.69 min-1; P < 0.05) and resting muscle oxygen consumption (mO2) was reduced by 16.4% (pre 0.39 ± 0.16%.s-1 vs. post 0.33 ± 0.14%.s-1; P < 0.05). During exercise, changes in deoxygenated hemoglobin (HHb) from rest to steady state were reduced at 40 and 60% MVC (16 and 12%, respectively, P < 0.05) despite similar measures of total hemoglobin (tHb). At the cessation of exercise, the time constant for recovery in oxygenated hemoglobin (O2Hb) was accelerated at 40 and 60% MVC (by 33 and 43%, respectively) suggesting enhanced reoxygenation in the muscle. No changes were reported for systemic measures of resting heart rate or blood pressure. In conclusion, repeated bouts of IPC over 7 consecutive days increased skeletal muscle oxidative capacity and microvascular muscle blood flow. These findings are consistent with enhanced mitochondrial and vascular function following repeated IPC and may be of clinical or sporting interest to enhance or offset reductions in muscle oxidative capacity.

Effects of dietary nitrate, caffeine, and their combination on 20-km cycling time trial performance.

The aim of this study was to examine the acute supplementation effects of dietary nitrate, caffeine, and their combination on 20-km cycling time trial performance. Using a randomized, counterbalanced, double-blind Latin-square design, 14 competitive female cyclists (age: 31 ± 7 years; height: 1.69 ± 0.07 m; body mass: 61.6 ± 6.0 kg) completed four 20-km time trials on a racing bicycle fitted to a turbo trainer. Approximately 2.5 hours before each trial, subjects consumed a 70-ml dose of concentrated beetroot juice containing either 0.45 g of dietary nitrate or with the nitrate content removed (placebo). One hour before each trial, subjects consumed a capsule containing either 5 mg·kg of caffeine or maltodextrin (placebo). There was a significant effect of supplementation on power output (p = 0.001), with post hoc tests revealing higher power outputs in caffeine (205 ± 21 W) vs. nitrate (194 ± 22 W) and placebo (194 ± 25 W) trials only. Caffeine-induced improvements in power output corresponded with significantly higher measures of heart rate (caffeine: 166 ± 12 b·min vs. placebo: 159 ± 15 b·min; p = 0.02), blood lactate (caffeine: 6.54 ± 2.40 mmol·L vs. placebo: 4.50 ± 2.11 mmol·L; p < 0.001), and respiratory exchange ratio (caffeine: 0.95 ± 0.04 vs. placebo: 0.91 ± 0.05; p = 0.03). There were no effects (p ≥ 0.05) of supplementation on cycling cadence, rating of perceived exertion, (Equation is included in full-text article.), or integrated electromyographic activity. The results of this study support the well-established beneficial effects of caffeine supplementation on endurance performance. In contrast, acute supplementation with dietary nitrate seems to have no effect on endurance performance and adds nothing to the benefits afforded by caffeine supplementation.

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.

The influence of aerobic fitness on the recovery of peak power output.

PURPOSE: The aims of this study were to evaluate the recovery kinetics of peak power output (PPO) following a maximal sprint, and to evaluate the influence of aerobic fitness on that recovery process. METHODS: On separate occasions, 16 well-trained men (age: 21 ± 3 years; height: 1.84 ± 0.05 m; and body mass: 78.8 ± 7.8 kg) performed a 30 s maximal sprint on a cycle ergometer, followed by a predetermined stationary rest period (5, 10, 20, 40, 80, and 160 s) and a subsequent 5 s sprint to determine PPO recovery kinetics. On another occasion, [Formula: see text] was monitored during recovery from a 30 s sprint to provide a comparison with the recovery of PPO. Finally, subjects completed a [Formula: see text] test to evaluate the influence of aerobic fitness on the recovery of PPO. RESULTS: Despite following similar time courses (F = 0.36, p = 0.558), and being well described by double-exponential models, the kinetic parameters of PPO and [Formula: see text] in recovery were significantly different (p < 0.05). There was no significant relationship (r = 0.15; p = 0.578) between [Formula: see text] and the time to achieve 50 % recovery of PPO. Moreover, there was no difference (p = 0.61) between the recovery kinetics of participants classified according to their [Formula: see text] (59.4 ± 1.3 vs 48.5 ± 2.2 ml·kg(-1)·min(-1)). CONCLUSION: Despite similar overall recovery kinetics, [Formula: see text] and PPO show differences in key model parameters. Moreover, the recovery of PPO does not appear to be affected by aerobic fitness.

Caffeine and sprinting performance: dose responses and efficacy.

The aims of this study were to evaluate the effects of caffeine supplementation on sprint cycling performance and to determine if there was a dose-response effect. Using a randomized, double-blind, placebo-controlled design, 17 well-trained men (age: 24 ± 6 years, height: 1.82 ± 0.06 m, and body mass(bm): 82.2 ± 6.9 kg) completed 7 maximal 10-second sprint trials on an electromagnetically braked cycle ergometer. Apart from trial 1 (familiarization), all the trials involved subjects ingesting a gelatine capsule containing either caffeine or placebo (maltodextrin) 1 hour before each sprint. To examine dose-response effects, caffeine doses of 2, 4, 6, 8, and 10 mg·kg bm(-1) were used. There were no significant (p ≥ 0.05) differences in baseline measures of plasma caffeine concentration before each trial (grand mean: 0.14 ± 0.28 µg·ml(-1)). There was, however, a significant supplement × time interaction (p < 0.001), with larger caffeine doses producing higher postsupplementation plasma caffeine levels. In comparison with placebo, caffeine had no significant effect on peak power (p = 0.11), mean power (p = 0.55), or time to peak power (p = 0.17). There was also no significant effect of supplementation on pretrial blood lactate (p = 0.58), but there was a significant time effect (p = 0.001), with blood lactate reducing over the 50 minute postsupplementation rest period from 1.29 ± 0.36 to 1.06 ± 0.33 mmol·L(-1). The results of this study show that caffeine supplementation has no effect on short-duration sprint cycling performance, irrespective of the dosage used.

Perceptual and physiological responses to recovery from a maximal 30-second sprint.

The aims of this study were to evaluate perceptions of postexercise recovery and to compare patterns of perceived recovery with those of several potential mediating physiological variables. Seventeen well-trained men (age: 22 ± 4 years; height: 1.83 ± 0.05 m; body mass: 78.9 ± 7.6 kg; and body fat: 11.1 ± 2.2%) completed 10 sprint trials on an electromagnetically braked cycle ergometer. Trial 1 evaluated peak power via a 5-second sprint. The remaining trials evaluated (a) the recovery of peak power after a maximal 30-second sprint using rest intervals of 5, 10, 20, 40, 80, and 160 seconds; (b) perceived recovery via visual analog scales; and (c) physiological responses during recovery. The time point in recovery at which individuals perceived they had fully recovered was 163.3 ± 57.5 seconds. Power output at that same time point was 83.6 ± 5.2% of peak power. There were no significant differences between perceived recovery and the recovery processes of VO2 or minute ventilation (V(E)). Despite differences in the time courses of perceived recovery and the recovery of power output, individuals were able to closely predict full recovery without the need for external timepieces. Moreover, the time course of perceived recovery is similar to that of VO2 and V(E).

The reliability and validity of fatigue measures during multiple-sprint work: an issue revisited.

The ability to repeatedly produce a high-power output or sprint speed is a key fitness component of most field and court sports. The aim of this study was to evaluate the validity and reliability of eight different approaches to quantify this parameter in tests of multiple-sprint performance. Ten physically active men completed two trials of each of two multiple-sprint running protocols with contrasting recovery periods. Protocol 1 consisted of 12 x 30-m sprints repeated every 35 seconds; protocol 2 consisted of 12 x 30-m sprints repeated every 65 seconds. All testing was performed in an indoor sports facility, and sprint times were recorded using twin-beam photocells. All but one of the formulae showed good construct validity, as evidenced by similar within-protocol fatigue scores. However, the assumptions on which many of the formulae were based, combined with poor or inconsistent test-retest reliability (coefficient of variation range: 0.8-145.7%; intraclass correlation coefficient range: 0.09-0.75), suggested many problems regarding logical validity. In line with previous research, the results support the percentage decrement calculation as the most valid and reliable method of quantifying fatigue in tests of multiple-sprint performance.

Glomerulonephritis after human parvovirus infection in homozygous sickle-cell disease

Glomerulonephritis with proteinuria of sufficient degree to manifest the nephrotic syndrome followed aplastic crises induced by human parvovirus (B19) in seven patients with homozygous sickle-cell disease, within 7 days in five patients and 6-7 weeks in two. Segmental proliferative glomerulonephritis was found in all four patients who underwent acute renal biopsies and focal segmental glomerulosclerosis was found in the fifth patient who had a biopsy 4 months later. One patient recovered completely, one died in chronic renal failure after 3 months, and the others had impaired creatinine clearance, four with continuing proteinuria (AU)

Nephrotic syndrome and human parvovirus infection in homozygous sickle-cell disease: a temporal association - abstract

Proteinuria of sufficient severity to manifest the nephrotic syndrome and renal impairment has been associated with human parvovirus (B19) infection in 7 patients with homozygous sickle-cell (SS) disease. In most patients, the proteinuria resolved but renal impairment remained. The glomerular histology showed evidence of segmental proliferative glomerulonephritis in 4 out of 5 biopsies. Most events occurred within 2 weeks of B19 associated aplastic crisis, and the mechanism is at present unknown. This association may add to the pathogenic significance of B19 infection in SS disease (AU)

Human parvovirus infection in homozygous sickle cell disease

We studied the epidemiology of human parvovirus B19 infection in 308 children with homozygous sickle cell (SS) disease and 239 controls with a normal haemoglobin (AA) genotype followed from birth in a cohort study. Annual serum samples identified the time and frequency of B19 infection, which did not differ between SS and AA children, about 40 percent of each age group developing specific IgG by age 15. B19 infection followed an epidemic pattern similar to that observed for aplastic crises; accounted for all 91 aplastic crises that occurred; and was found in an additional 23 SS patients, of whom 10 showed mild haematological changes and 13 no changes. The magnitude or duration of IgG response did not differ between these groups. No patient had 2 attacks of aplasia and no patient nor control had 2 attacks of B19 infection. Following B19 infection, serial specific IgG concentrations remained high after 5 years in only 45 percent of SS patients, although the rarity of recurrent aplasia suggests lifelong immunity. B19 infection accounts for most if not all aplastic crises in SS disease, but at least 20 percent of infections do not result in aplasia. An effective vaccine against B19 might make an important contribution to the management of sickle cell disease (AU)

Parvovirus infection and the aplastic crisis of sickle cell disease - abstract

The aplastic crisis is a temporary self-limited erythropietic maturation arrest which, because of the short red cell survival in homozygous sickle-cell (SS) disease, results in rapid fall in haemoglobin level. These aplastic crises occur in epidemics, predominantly affect children, frequently involve siblings simultaneously, and often follow an upper respiratory tract type of infection. Recent evidence suggests that these events may follow human parvovirus (HPV) infection and the role of HPV infection has been examined in the last three epidemics of aplastic crises observed among SS patients in Jamaica. Eighteen patients were affected in the 1973-1975 epidemics, 45 in the 1979-1981 epidemic, and 41 so far in an epidemic in 1984-1985. Serological studies have been possible in 73 patients and in 69 (95 percent) there was evidence consistent with recent HPV infections. This infection appears to confer long-lasting immunity, and recurrent attacks of aplastic crisis have never been described. These data suggest that a parvovirus vaccine may be beneficial in the prevention of aplastic crises (AU)

The development and use of an antibody capture radioimmunoassay for specific IgM to a human parvovirus-like agent

An IgM-antibody capture radioimmunoassay (MACRIA) was developed for detection of IgM antibody specific for the human parvovirus-like agent B19. Diagnosis of infection with this agent by either antigen detection or antibody seroconversion had been made by counter-current immunoelectrophoresis (CIE) in 18 cases of aplastic crisis occurring in children with homozygous sickle-cell desease. The MACRIA described here gave positive results in 17 of 18 cases; in the remaining case only an acute specimen taken from the patient during viraemia and late convalescent specimens taken 184 and 247 days after onset of illness were avaliable. The test was used to investigate 20 further cases of aplastic crisis in which neither viral antigen nor antibody seroconversion could be detected by CIE. Detection of virus-specific IgM permitted diagnosis of infection with this parvovirus-like agent in 17 of these cases. In the remaining three cases only single serum specimens taken late in convalescence, 82, days or more after the onset of symptoms, were available. In addition to these 34 cases of aplastic crisis in which primary infection with this agent was diagnosed by MACRIA, seven cases of apparent 'silent' infection detected by CIE were investigated. The test permitted the discrimination between primary infection and re-exposure to the virus in six of these patients. The use of this assay has added a considerable weight of evidence implicating primary infection with this parvovirus-like agent as an important cause of aplasic crisis in children with sickle-cell disease. Furthermore, MACRIA permits diagnosis of infection when only single serum specimens taken up to ten weeks after infection are available. Thus the use of this test will significantly facilitate the investigation of other clinical syndromes of presumptive infective infectious aetiology (AU)

Outbreak of aplastic crises in sickle cell anaemia associated with parvovirus-like agent

Since 1952, 112 childen with sickle cell anaemia (SCA) in Jamaica have had an aplastic crisis. Outbreaks occurred in 1956, 1960, 1965-67, 1971-73, and 1979-80. Most cases occurred in children under 10 years of age, and an aplastic crisis in a patient over the age of 15 years is rare. There were 38 cases in 1970-80 and stored serum specimens from 28 of these were available for virus studies. Evidence for infection with a parvovirus-like agent was found in 24 of these 28 cases. Viral antigen was detected in 2 patients, both of whom demonstated seroconversion. Serconversion during 1980 was detected in a further 7, increasing amounts of antibody during the convalescent period were found in 5, antibody was found in 2 of 4 patients from whom only an acute phase specimen was available and the remaining 10 were antibody positive in the only convalescent phase sample available for testing. Antibody was found in 4 of 94 controls with the SS genotype (in retrospect 2 of these may have had an aplastic crisis) and in 17 percent of 48 controls with a normal haemoglobin (AA) genotype. The results accord with the possibility that the parvovirus-like agent is the principal cause of aplastic crisis in SCA (Summary)