Unclear outcomes of heart rate variability following a concussion: a systematic review.

PURPOSE: : To systematically regroup articles that were published since the latest systematic search, but with specific inclusion criteria to help comparison that will offer a focused presentation of methods and results. This will offer a full overview of HRV's behavior at rest and during exercise in adults post-concussion. METHODS: : The systematic review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) method. A computer-based systematic search was conducted in December 2019 through the Pubmed, Scopus and SPORTDiscus databases. A manual search was performed through the reference list of all articles retained. The reliability of the systematic search was assured by having the article selection process entirely repeated by a second author. RESULTS: : The systematic search yielded a total of 15 articles to be further analyzed. Results show impairment of HRV during exercise for individuals with concussion, heterogenous studies with lack of control over confounding factors and only less than half of the results showing a significant difference between individuals with concussion and controls. CONCLUSION: : Further research should try standardizing HRV measurement protocols that control confounding factors to allow easier comparison between studies and allows the possibility for an eventual meta-analysis.

Validity and reliability of self-assessment of sexual maturity in elite adolescent athletes.

AIM: The variability along the progression of different stages of maturation during puberty suggests that chronological age is not the best indicator in assessing biological status during adolescence. This is particularly relevant for adolescents involved in high level of sports competitions, which implies greater physiological and biomechanical demands to the body. Therefore, monitoring physical changes during this period may help the coaching and medical staff to construct and adapt on an individual basis, better training programs and, then, improve performance while preventing injuries. Thus, the aim of this study was to evaluate the validity and the reliability of self-assessment of sexual maturity among elite adolescent athletes. METHODS: Using the Tanner sexual maturity method, 24 male and 23 female athletes aged 12 to 17 years, were assessed by a physician, and, then, self-assessed for sexual maturity. RESULTS: Agreement with the physician ratings was high (k coefficients of 0.79 for pubic hair and 0.67 for genital development for boys and 0.75 and 0.85 for pubic hair and breast development for girls, respectively). Spearman correlations ranged from 0.86 to 0.97 (P= or <0.05). CONCLUSION: The self-assessment is a valid and reliable method to assess sexual maturity in elite adolescent athletes.

An on-ice aerobic maximal multistage shuttle skate test for elite adolescent hockey players.

The aim of this study was to design an on-ice test to predict V.O (2max) in ice hockey players. 30 elite hockey players (age 14.7 +/- 1.5 years) participated in this study. The oxygen uptake was assessed at submaximal and maximal velocities during an on-ice intermittent maximal multistage shuttle skate test with a 1-min/0.5-min work/rest ratio. The procedure consisted of skating back and forth on a distance of 45 m (stop and go) while following a pace fixed by an audible signal: initial velocity of 3.5 m . s (-1) with increments of 0.2 m . s (-1) every stage. The skating multistage aerobic test (SMAT) enabled the prediction of the V.O (2max) (ml . kg (-1) . min (-1)) from the maximal velocity (m . s (-1)) by means of the following regression equation: V.O (2max) = 18.07 x (maximal velocity) - 35.596 (r = 0.97, SEE = 3.01). The test-retest correlation was 0.92 and SEE = 0.56 stage (n = 23). Following the SMAT validation, an additional group of 112 elite male (age = 14.2 +/- 1.3 years) and 31 elite female (age = 14.0 +/- 1.2 years) ice hockey players performed both the 20-m shuttle run test and the SMAT, which was more specific and accurate to predict V.O (2max). The overall results suggest that the SMAT is highly specific, valid and reliable for the prediction of V.O (2max) of ice hockey players.

Time-based gene expression programme following diaphragm injury in a rat model.

It was hypothesised that diaphragm injury activates a time-based programme of gene expression in muscle repair. Gene expression of different substances, such as proteases (calpain 94 (p94)), transcription factors (myogenin and cFos), growth factors (both basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF)-II), and structural proteins (myosin heavy chain (MHC) and titin), was quantified by RT-PCR in rat diaphragms exposed to caffeine-induced injury. Injured and noninjured (control) rat hemidiaphragms were excised at different time points (1-240 h). In injured hemidiaphragms, in comparison with control muscles, p94 expression levels peaked at 1 h post-injury (PI), cFos mRNA levels began to rise, after an initial dip, and peaked at 96 h PI, while myogenin mRNA levels started to increase as early as 12 h PI, IGF-II mRNA levels initially decreased until 48 h PI and increased thereafter, peaking at 72 h PI, bFGF mRNA levels rose to a maximum at 96 h PI, and MHC and titin mRNA levels were significantly elevated at 72 h PI. Caffeine-induced diaphragm injury is followed by a time-based expression programme of different genes tailored to meet muscle repair needs.

Morphological and functional recovery from diaphragm injury: an in vivo rat diaphragm injury model.

Our objective was to develop an in vivo model to study the timing and mechanisms underlying diaphragm injury and repair. Diaphragm injury was induced in anesthetized rats by the application of a 100 mM caffeine solution for a 10-min period to the right abdominal diaphragm surface. Diaphragms were removed 1, 4, 6, 12, 24, 48, 72, and 96 h and 10 days after the injury, with contractile function being assessed in strips in vitro by force-frequency curves. The extent of caffeine-induced membrane injury was indicated by the percentage of fibers with a fluorescent cytoplasm revealed by inward leakage of the procion orange dye. One hour after caffeine exposure, 32.9 +/- 3.1 (SE) % of fibers showed membrane injury that resulted in 70% loss of muscle force. Within 72-96 h, the percentage of fluorescent cells decreased to control values. Muscle force, however, was still reduced by 30%. Complete muscle strength recovery was observed 10 days after the injury. Whereas diaphragmatic fiber repair occurred within 4 days after injury induction, force recovery took up to 10 days. We suggest that the caffeine-damaged rat diaphragm is a useful model to study the timing and mechanisms of muscle injury and repair.

Lipopolysaccharide-induced diaphragmatic contractile dysfunction and sarcolemmal injury in mice lacking the neuronal nitric oxide synthase.

In this study we evaluated the role of the neuronal nitric oxide synthase (nNOS) in lipopolysaccharide (LPS)-induced diaphragmatic contractile dysfunction and sarcolemmal injury. Wild-type (WT) mice or mice deficient in the nNOS gene (nNOS(-/-)) were injected with either saline (control) or Escherichia coli LPS (LPS groups) and sacrificed 12 h later. The diaphragm was then examined for NOS expression, NOS activity, and in-vitro contractility. We also assessed sarcolemmal injury in isolated muscle strips under resting condition and after 3 min of artificial stimulations. In WT mice, LPS injection reduced maximum force to about 75% of that of control animals and raised total NOS activity significantly due to the induction of the iNOS isoform. Although muscle fiber injury was minimal under resting condition, the percentage of injured fibers in control and LPS-injected mice approached 27% and 40% of total fibers, respectively, in response to artificial stimulation. By comparison, LPS injection in nNOS(-/-) mice elicited a worsening of muscle contractility (maximum force < 60% of control animals) but elicited degrees of sarcolemmal injury similar to those observed in the WT animals. In addition, muscle NOS activity and iNOS protein level in nNOS(-/-) mice injected with LPS reached about 10% and 60% of that of WT animals, respectively (p < 0.05 compared with WT animals). Protein level of endothelial NOS isoform in the diaphragm was not altered by LPS injection in either WT or nNOS(-/-) animals. We conclude that nNOS plays a protective role in attenuating the negative influence of sepsis on diaphragmatic contractility but is not involved in the pathogenesis of sepsis-induced sarcolemmal injury.

Induction of the ATP-sensitive potassium (uK(ATP)-1) channel by endotoxemia.

The effect of sepsis on the ubiquitously expressed ATP-sensitive potassium (uK(ATP)-1) channel expression was measured in Sprague-Dawley rat diaphragms. Rats were treated with either 0.5 ml saline or 20 mg/Kg E. coli lipopolysaccharides and sacrificed at 3, 6, 12, 24, or 48 h later. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that channel mRNA expression was increased at 3 h and continued to rise up to 48 h. Western blotting analysis showed a approximately 9-fold increase in channel protein expression 24 h after sepsis. Our results demonstrate that sepsis upregulates the uK(ATP)-1 channel.

Influence of tension time on muscle fiber sarcolemmal injury in rat diaphragm.

We hypothesized that the amount of sarcolemmal injury is directly related to the total tension time (TT(tot)), calculated as mean tension x total stimulation time. Diaphragm strips from Sprague-Dawley rats were superfused at optimal muscle length with Krebs containing procion orange to identify sarcolemmal injury. TT(tot) was induced by stimulation with 100 Hz for 3 min at duty cycles of 0.02, 0.15, 0.3, and 0.6, or with continuous contractions at 0.2, 0.4, 0.6, and 1.0 of maximal tension. A significant positive correlation between TT(tot) and the percentage of fibers with injured sarcolemma (r(2) = 0.63, P < 0.05) is seen. Stimulation (at 100 Hz, duty cycle = 1) resulted in fast fatigue with low injury, likely caused by altered membrane conductivity. Stimulations inducing the largest injury are those showing progressive force loss and high TT(tot), where injury may be due to activation of membrane degradative enzymes. The maximal tension measured at 20 min poststimulation was inversely related to the number of fibers injured, suggesting loss of force is caused by cellular injury.

Lipopolysaccharide-induced diaphragmatic contractile dysfunction in mice lacking the inducible nitric oxide synthase.

The goal of this study was to evaluate the importance of the inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-induced diaphragmatic contractile dysfunction. Many investigators have proposed that iNOS induction in the ventilatory and limb muscles of animals injected with Escherichia coli LPS leads to impaired muscle contractility and increased fatigability. We tested this proposal by examining wild-type mice and iNOS-deficient (iNOS knockout) mice. Both types of mice were injected with either saline (control) or E. coli LPS and killed after 12 h. Diaphragm nitric oxide synthase (NOS) activity, NOS expression, and muscle contractility were assessed with L-citrulline assay, immunoblotting, and in vitro bath preparation, respectively. LPS injection in wild-type mice induced iNOS protein expression and augmented total diaphragmatic NOS activity, which coincided with impaired muscle force generated at frequencies higher than 30 Hz. In iNOS knockout mice, injection of LPS augmented constitutive muscle NOS activity, upregulated the expression of the neuronal NOS (nNOS), but elicited a significantly greater decline in force generated in response to high frequency of stimulation compared with wild-type animals. We conclude that iNOS may play a protective role in attenuating the inhibitory influence of LPS on muscle contractility.

Influence of the bipolar electrode transfer function on the electromyogram power spectrum.

This study demonstrates the impact of the bipolar electrode transfer function on the canine diaphragm electromyogram (EMG) power spectrum, as evaluated with a new electrode design and implantation technique. The results show that: (a) changes in interelectrode distance transformed single-peaked power spectrums into double-peaked spectrums; (b) the mean action potential conduction velocity (APCV), and power spectrum center frequency (CF) and median frequency (MF), are related for interelectrode distances of 5 and 10 mm, but not for 15 and 20 mm; and (C) CF, MF, -3-dB, and -6-dB bandwith values depend on interelectrode distance. We conclude that bipolar electrodes, with a nonfixed interelectrode distance, cannot be used for physiological interpretations of the EMG power spectrum. Nonetheless, power spectrums obtained with fixed and appropriate interelectrode distances can be trusted, if the electrodes are positioned in the direction of the muscle fibers and in regions with low densities of motor endplates.

The effect of glibenclamide on frog skeletal muscle: evidence for K+ATP channel activation during fatigue.

1. The purpose of this study was to determine whether ATP-sensitive K+ (K+ATP) channels are activated and contribute to the decrease in force during fatigue development in the sartorius muscle of the frog, Rana pipiens. Tetanic force (elicited by field stimulation), action potential and membrane conductance (using conventional microelectrodes), were measured in the presence and absence of glibenclamide, a K+ATP channel antagonist. Experiments were performed in bicarbonate-buffered solutions at pH 7.2. 2. In unfatigued muscle 100 mumol l-1 glibenclamide had no effect on the resting potential, the overshoot, the half-depolarization time or the maximum rate of depolarization of action potentials, while the mean half-repolarization time increased by 19 +/- 4% (+/- S.E.M.) and the maximum rate of repolarization decreased by 17 +/- 5%. 3. Fatigue was elicited using 100 ms tetanic contractions every 1 s for 3 min. In the absence of glibenclamide the mean half-repolarization time increased from 0.57 +/- 0.05 to 0.89 +/- 0.05 ms during fatigue. The mean half-repolarization times after fatigue, when muscle fibres were exposed to 100 mumol l-1 glibenclamide either 60 min prior to fatigue or 60 s before the end of fatigue, were 1.16 +/- 0.08 and 1.17 +/- 0.07 ms respectively. Application of 100 mumol l-1 glibenclamide after 5 min of recovery did not increase the half-repolarization time, but decreased the rate of recovery compared to control values. 4. In unfatigued muscles, 100 mumol l-1 glibenclamide did not affect the tetanic contraction. In the absence of glibenclamide, the mean tetanic force after fatigue was 11.0 +/- 0.9% of prefatigue values. Application of 100 mumol l-1 glibenclamide 60 min before fatigue increased the rate of fatigue development as the mean tetanic force was 4.8 +/- 0.8% after 3 min of stimulation. The addition of 100 mumol l-1 glibenclamide 60 s before the end of fatigue had no effect on tetanic force during this time compared to control. 5. In the absence of glibenclamide, muscles recovered 90.1 +/- 1.6% of their tetanic force after 100 min. Addition of 100 mumol l-1 glibenclamide 60 min prior to fatigue significantly reduced the capacity of muscles to recover their tetanic force: after 100 min of recovery tetanic force was only 47.3 +/- 9.4% of the pre-fatigue value.(ABSTRACT TRUNCATED AT 400 WORDS)