Microvascular Capillary and Precapillary Cardiovascular Disturbances Strongly Interact to Severely Affect Tissue Perfusion and Mitochondrial Function in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Evolving from the Post COVID-19 Syndrome.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent, debilitating and still enigmatic disease. There is a broad overlap in the symptomatology of ME/CFS and the Post-COVID-19 Syndrome (PCS). A fraction of the PCS patients develop the full clinical picture of ME/CFS. New observations in microvessels and blood from patients suffering from PCS have appeared and include microclots and malformed pathological blood cells. Capillary blood flow is impaired not only by pathological blood components but also by prothrombotic changes in the vascular wall, endothelial dysfunction, and the expression of adhesion molecules in the capillaries. These disturbances can finally cause a low capillary flow and even capillary stasis. A low cardiac stroke volume due to hypovolemia and the inability of the capacitance vessels to adequately constrict to deliver the necessary cardiac preload generate an unfavorable low precapillary perfusion pressure. Furthermore, a predominance of vasoconstrictor over vasodilator influences exists, in which sympathetic hyperactivity and endothelial dysfunction play a strong role, causing the constriction of resistance vessels and of precapillary sphincters, which leads to a fall in capillary pressure behind the sphincters. The interaction of these two precapillary cardiovascular mechanisms causing a low capillary perfusion pressure is hemodynamically highly unfavorable in the presence of a primary capillary stasis, which is already caused by the pathological blood components and their interaction with the capillary wall, to severely impair organ perfusion. The detrimental coincidence of microcirculatory and precapillary cardiovascular disturbances may constitute the key disturbance of the Post-COVID-19 syndrome and finally lead to ME/CFS in predisposed patients because the interaction causes a particular kind of perfusion disturbance-capillary ischemia/reperfusion-which has a high potential of causing mitochondrial dysfunction by inducing sodium- and calcium-overload in skeletal muscles. The latter, in turn, worsens the vascular situation through the generation of reactive oxygen species to close a vicious cycle from which the patient can hardly escape.

Maximum strength and power as determinants of on-ice sprint performance in elite U16 to adult ice hockey players.

In ice hockey, speed strength is one of the major physical key performance indicators, which is significantly influenced by maximum strength. The objective of this study was to evaluate the age-dependent relationship of off-ice maximum strength and vertical jump performance with on-ice linear sprint performance, considering age and performance level. Ninety-one male youth and adult professional ice hockey players (age: 19.3 ± 5.49 years) were recruited and divided into four age groups: under 16, 18, 21 years old and professional elite players (Pro) (i.e., > 21 years). They were tested in maximal isometric strength, squat jump (loaded and unloaded), countermovement jump and on-ice sprint performance (15 m and 30 m linear sprint; 15 m flying linear sprint). Statistical analysis revealed that on-ice sprint performance correlated with isometric strength performance (r = |0.34|-|0.63|) and with off-ice jump performance (r = |0.61|-|0.77|) without an influence of age group or performance level. However, performance differed between age groups and performance level, the largest differences being found between the youngest age group (U16) and the Pro group (g = 0.966-3.281). The present study shows that maximum strength influences on-ice sprint performances in ice hockey players, as well as performance differences between age groups and professional players. Strength and jumping performance should therefore be included in regular performance testing in ice hockey. Since performance differences are observed for almost all strength and speed-strength performances of the youth teams to the Pros, training of these variables is strongly recommended to improve in the transition phase from junior to elite level.

Comparison of the effects of long-lasting static stretching and hypertrophy training on maximal strength, muscle thickness and flexibility in the plantar flexors.

Maximal strength measured via maximal voluntary contraction is known as a key factor in competitive sports performance as well as injury risk reduction and rehabilitation. Maximal strength and hypertrophy are commonly trained by performing resistance training programs. However, literature shows that long-term, long-lasting static stretching interventions can also produce significant improvements in maximal voluntary contraction. The aim of this study is to compare increases in maximal voluntary contraction, muscle thickness and flexibility after 6 weeks of stretch training and conventional hypertrophy training. Sixty-nine (69) active participants (f = 30, m = 39; age 27.4 ± 4.4 years, height 175.8 ± 2.1 cm, and weight 79.5 ± 5.9 kg) were divided into three groups: IG1 stretched the plantar flexors continuously for one hour per day, IG2 performed hypertrophy training for the plantar flexors (5 × 10-12 reps, three days per week), while CG did not undergo any intervention. Maximal voluntary contraction, muscle thickness, pennation angle and flexibility were the dependent variables. The results of a series of two-way ANOVAs show significant interaction effects (p < 0.05) for maximal voluntary contraction (ƞ2 = 0.143-0.32, p < 0.006), muscle thickness (ƞ2 = 0.11-0.14, p < 0.021), pennation angle (ƞ2 = 0.002-0.08, p = 0.077-0.625) and flexibility (ƞ2 = 0.089-0.21, p < 0.046) for both the stretch and hypertrophy training group without significant differences (p = 0.37-0.99, d = 0.03-0.4) between both intervention groups. Thus, it can be hypothesized that mechanical tension plays a crucial role in improving maximal voluntary contraction and muscle thickness irrespective whether long-lasting stretching or hypertrophy training is used. Results show that for the calf muscle, the use of long-lasting stretching interventions can be deemed an alternative to conventional resistance training if the aim is to increase maximal voluntary contraction, muscle thickness and flexibility. However, the practical application seems to be strongly limited as a weekly stretching duration of up to 7 h a week is opposed by 3 × 15 min of common resistance training.

Influence of Long-Lasting Static Stretching Intervention on Functional and Morphological Parameters in the Plantar Flexors: A Randomized Controlled Trial.

ABSTRACT: Warneke, K, Keiner, M, Wohlann, T, Lohmann, LH, Schmitt, T, Hillebrecht, M, Brinkmann, A, Hein, A, Wirth, K, and Schiemann, S. Influence of long-lasting static stretching intervention on functional and morphological parameters in the plantar flexors: a randomised controlled trial. J Strength Cond Res 37(10): 1993-2001, 2023-Animal studies show that long-lasting stretching training can lead to significant hypertrophy and increases in maximal strength. Accordingly, previous human studies found significant improvements in maximal voluntary contraction (MVC), flexibility, and muscle thickness (MTh) using constant angle long-lasting stretching. It was hypothesized that long-lasting stretching with high intensity will lead to sufficient mechanical tension to induce muscle hypertrophy and maximal strength gains. This study examined muscle cross-sectional area (MCSA) using magnetic resonance imaging (MRI). Therefore, 45 well-trained subjects (f: 17, m: 28, age: 27.7 ± 3.0 years, height: 180.8 ± 4.9 cm, mass: 80.4 ± 7.2 kg) were assigned to an intervention group (IG) that stretched the plantar flexors 6 × 10 minutes per day for 6 weeks or a control group (CG). Data analysis was performed using 2-way ANOVA. There was a significant Time × Group interaction in MVC ( p < 0.001-0.019, ƞ 2 = 0.158-0.223), flexibility ( p < 0.001, ƞ 2 = 0.338-0.446), MTh ( p = 0.002-0.013, ƞ 2 = 0.125-0.172), and MCSA ( p = 0.003-0.014, ƞ 2 = 0.143-0.197). Post hoc analysis showed significant increases in MVC ( d = 0.64-0.76), flexibility ( d = 0.85-1.12), MTh ( d = 0.53-0.6), and MCSA ( d = 0.16-0.3) in IG compared with CG, thus confirming previous results in well-trained subjects. Furthermore, this study improved the quality for the morphological examination by investigating both heads of the gastrocnemius with MRI and sonography. Because stretching can be used passively, an application in rehabilitation settings seems plausible, especially if no commonly used alternatives such as strength training are applicable.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Comorbidities: Linked by Vascular Pathomechanisms and Vasoactive Mediators?

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is often associated with various other syndromes or conditions including mast cell activation (MCA), dysmenorrhea and endometriosis, postural tachycardia (POTS) and small fiber neuropathy (SFN). The causes of these syndromes and the reason for their frequent association are not yet fully understood. We previously published a comprehensive hypothesis of the ME/CFS pathophysiology that explains the majority of symptoms, findings and chronicity of the disease. We wondered whether some of the identified key pathomechanisms in ME/CFS are also operative in MCA, endometriosis and dysmenorrhea, POTS, decreased cerebral blood flow and SFN, and possibly may provide clues on their causes and frequent co-occurrence. Our analysis indeed provides strong arguments in favor of this assumption, and we conclude that the main pathomechanisms responsible for this association are excessive generation and spillover into the systemic circulation of inflammatory and vasoactive tissue mediators, dysfunctional ß2AdR, and the mutual triggering of symptomatology and disease initiation. Overall, vascular dysfunction appears to be a strong common denominator in these linkages.

Muscle sodium content in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

BACKGROUND: Muscle fatigue and pain are key symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Although the pathophysiology is not yet fully understood, there is ample evidence for hypoperfusion which may result in electrolyte imbalance and sodium overload in muscles. Therefore, the aim of this study was to assess levels of sodium content in muscles of patients with ME/CFS and to compare these to healthy controls. METHODS: Six female patients with ME/CFS and six age, BMI and sex matched controls underwent 23Na-MRI of the left lower leg using a clinical 3T MR scanner before and after 3 min of plantar flexion exercise. Sodium reference phantoms with solutions of 10, 20, 30 and 40 mmol/L NaCl were used for quantification. Muscle sodium content over 40 min was measured using a dedicated plugin in the open-source DICOM viewer Horos. Handgrip strength was measured and correlated with sodium content. RESULTS: Baseline tissue sodium content was higher in all 5 lower leg muscle compartments in ME/CFS compared to controls. Within the anterior extensor muscle compartment, the highest difference in baseline muscle sodium content between ME/CFS and controls was found (mean ± SD; 12.20 ± 1.66 mM in ME/CFS versus 9.38 ± 0.71 mM in controls, p = 0.0034). Directly after exercise, tissue sodium content increased in gastrocnemius and triceps surae muscles with + 30% in ME/CFS (p = 0.0005) and + 24% in controls (p = 0.0007) in the medial gastrocnemius muscle but not in the extensor muscles which were not exercised. Compared to baseline, the increase of sodium content in medial gastrocnemius muscle was stronger in ME/CFS than in controls with + 30% versus + 17% to baseline at 12 min (p = 0.0326) and + 29% versus + 16% to baseline at 15 min (p = 0.0265). Patients had reduced average handgrip strength which was associated with increased average muscle tissue sodium content (p = 0.0319, R2 = 0.3832). CONCLUSION: Muscle sodium content before and after exercise was higher in ME/CFS than in healthy controls. Furthermore, our findings indicate an inverse correlation between muscle sodium content and handgrip strength. These findings provide evidence that sodium overload may play a role in the pathophysiology of ME/CFS and may allow for potential therapeutic targeting.

Effects of 10 Months of Speed, Functional, and Traditional Strength Training on Strength, Linear Sprint, Change of Direction, and Jump Performance in Trained Adolescent Soccer Players.

ABSTRACT: Keiner, M, Kadlubowski, B, Sander, A, Hartmann, H, and Wirth, K. Effects of 10 months of speed, functional, and traditional strength training on strength, linear sprint, change of direction, and jump performance in trained adolescent soccer players. J Strength Cond Res 36(8): 2236-2246, 2022-The current study aimed to compare the effects of plyometric and sprint vs. functional vs. strength training on linear sprint (LS 20 m), change of direction (COD; i.e., turning right and left), jump (squat jump [SJ]), and maximum strength (1 repetition maximum [1RM] for a squat) performance in elite adolescent soccer players. A longitudinal design was chosen, and 48 elite male youth were recruited. The athletes were divided into 4 groups (a traditional strength training group [STG], a plyometric and sprint training group [PSTG], a functional training group [FTG], and a control group [CG]). The intervention groups trained for 10 months with additional sessions added to their regular soccer training (4-5 sessions per week); the additional training (2 sessions a week [each about 60 minutes]) consisted of plyometric and sprint training, functional training, and traditional strength training for the PSTG, FTG, and STG, respectively. Data were analyzed using analysis of variance with repeated measurements. The effect sizes were calculated using Hedges g . This study showed significantly superior performance increases with traditional strength training compared with sprint and jump training and functional training for maximum strength (compared with all other groups g = 0.98-1.61), SJ ( g = 0.52-0.87 compared with FGT and CG; not significantly different from PSTG), COD (direction of rotation right: compared with all other groups g = 1.58-2.12; direction of rotation left: no significant differences), and 20-m LS (compared with all other groups g = 0.86-1.39) performance over time. Traditional strength training is recommended to increase strength and speed-strength variables and should therefore be given high priority in athletic training programs for elite youth soccer players.

Dyspnea in Post-COVID Syndrome following Mild Acute COVID-19 Infections: Potential Causes and Consequences for a Therapeutic Approach.

Dyspnea, shortness of breath, and chest pain are frequent symptoms of post-COVID syndrome (PCS). These symptoms are unrelated to organ damage in most patients after mild acute COVID infection. Hyperventilation has been identified as a cause of exercise-induced dyspnea in PCS. Since there is a broad overlap in symptomatology with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), causes for dyspnea and potential consequences can be deduced by a stringent application of assumptions made for ME/CFS in our recent review papers. One of the first stimuli of respiration in exercise is caused by metabolic feedback via skeletal muscle afferents. Hyperventilation in PCS, which occurs early on during exercise, can arise from a combined disturbance of a poor skeletal muscle energetic situation and autonomic dysfunction (overshooting respiratory response), both found in ME/CFS. The exaggerated respiratory response aggravating dyspnea does not only limit the ability to exercise but further impairs the muscular energetic situation: one of the buffering mechanisms to respiratory alkalosis is a proton shift from intracellular to extracellular space via the sodium-proton-exchanger subtype 1 (NHE1), thereby loading cells with sodium. This adds to two other sodium loading mechanisms already operative, namely glycolytic metabolism (intracellular acidosis) and impaired Na+/K+ATPase activity. High intracellular sodium has unfavorable effects on mitochondrial calcium and metabolism via sodium-calcium-exchangers (NCX). Mitochondrial calcium overload by high intracellular sodium reversing the transport mode of NCX to import calcium is a key driver for fatigue and chronification. Prevention of hyperventilation has a therapeutic potential by keeping intracellular sodium below the threshold where calcium overload occurs.

Orthostatic Intolerance after COVID-19 Infection: Is Disturbed Microcirculation of the Vasa Vasorum of Capacitance Vessels the Primary Defect?

Following COVID-19 infection, a substantial proportion of patients suffer from persistent symptoms known as Long COVID. Among the main symptoms are fatigue, cognitive dysfunction, muscle weakness and orthostatic intolerance (OI). These symptoms also occur in myalgic encephalomyelitis/chronic fatigue (ME/CFS). OI is highly prevalent in ME/CFS and develops early during or after acute COVID-19 infection. The causes for OI are unknown and autonomic dysfunction is hypothetically assumed to be the primary cause, presumably as a consequence of neuroinflammation. Here, we propose an alternative, primary vascular mechanism as the underlying cause of OI in Long COVID. We assume that the capacitance vessel system, which plays a key role in physiologic orthostatic regulation, becomes dysfunctional due to a disturbance of the microvessels and the vasa vasorum, which supply large parts of the wall of those large vessels. We assume that the known microcirculatory disturbance found after COVID-19 infection, resulting from endothelial dysfunction, microthrombus formation and rheological disturbances of blood cells (altered deformability), also affects the vasa vasorum to impair the function of the capacitance vessels. In an attempt to compensate for the vascular deficit, sympathetic activity overshoots to further worsen OI, resulting in a vicious circle that maintains OI. The resulting orthostatic stress, in turn, plays a key role in autonomic dysfunction and the pathophysiology of ME/CFS.

SAR340835, a Novel Selective Na+/Ca2+ Exchanger Inhibitor, Improves Cardiac Function and Restores Sympathovagal Balance in Heart Failure.

In failing hearts, Na+/Ca2+ exchanger (NCX) overactivity contributes to Ca2+ depletion, leading to contractile dysfunction. Inhibition of NCX is expected to normalize Ca2+ mishandling, to limit afterdepolarization-related arrhythmias, and to improve cardiac function in heart failure (HF). SAR340835/SAR296968 is a selective NCX inhibitor for all NCX isoforms across species, including human, with no effect on the native voltage-dependent calcium and sodium currents in vitro. Additionally, it showed in vitro and in vivo antiarrhythmic properties in several models of early and delayed afterdepolarization-related arrhythmias. Its effect on cardiac function was studied under intravenous infusion at 250,750 or 1500 µg/kg per hour in dogs, which were either normal or submitted to chronic ventricular pacing at 240 bpm (HF dogs). HF dogs were infused with the reference inotrope dobutamine (10 µg/kg per minute, i.v.). In normal dogs, NCX inhibitor increased cardiac contractility (dP/dtmax) and stroke volume (SV) and tended to reduce heart rate (HR). In HF dogs, NCX inhibitor significantly and dose-dependently increased SV from the first dose (+28.5%, +48.8%, and +62% at 250, 750, and 1500 µg/kg per hour, respectively) while significantly increasing dP/dtmax only at 1500 (+33%). Furthermore, NCX inhibitor significantly restored sympathovagal balance and spontaneous baroreflex sensitivity (BRS) from the first dose and reduced HR at the highest dose. In HF dogs, dobutamine significantly increased dP/dtmax and SV (+68.8%) but did not change HR, sympathovagal balance, or BRS. Overall, SAR340835, a selective potent NCX inhibitor, displayed a unique therapeutic profile, combining antiarrhythmic properties, capacity to restore systolic function, sympathovagal balance, and BRS in HF dogs. NCX inhibitors may offer new therapeutic options for acute HF treatment. SIGNIFICANCE STATEMENT: HF is facing growing health and economic burden. Moreover, patients hospitalized for acute heart failure are at high risk of decompensation recurrence, and no current acute decompensated HF therapy definitively improved outcomes. A new potent, Na+/Ca2+ exchanger inhibitor SAR340835 with antiarrhythmic properties improved systolic function of failing hearts without creating hypotension, while reducing heart rate and restoring sympathovagal balance. SAR340835 may offer a unique and attractive pharmacological profile for patients with acute heart failure as compared with current inotrope, such as dobutamine.

Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Chronic Fatigue Syndrome or Myalgic Encephaloymelitis (ME/CFS) is a frequent debilitating disease with an enigmatic etiology. The finding of autoantibodies against ß2-adrenergic receptors (ß2AdR) prompted us to hypothesize that ß2AdR dysfunction is of critical importance in the pathophysiology of ME/CFS. Our hypothesis published previously considers ME/CFS as a disease caused by a dysfunctional autonomic nervous system (ANS) system: sympathetic overactivity in the presence of vascular dysregulation by ß2AdR dysfunction causes predominance of vasoconstrictor influences in brain and skeletal muscles, which in the latter is opposed by the metabolically stimulated release of endogenous vasodilators (functional sympatholysis). An enigmatic bioenergetic disturbance in skeletal muscle strongly contributes to this release. Excessive generation of these vasodilators with algesic properties and spillover into the systemic circulation could explain hypovolemia, suppression of renin (paradoxon) and the enigmatic symptoms. In this hypothesis paper the mechanisms underlying the energetic disturbance in muscles will be explained and merged with the first hypothesis. The key information is that ß2AdR also stimulates the Na+/K+-ATPase in skeletal muscles. Appropriate muscular perfusion as well as function of the Na+/K+-ATPase determine muscle fatigability. We presume that dysfunction of the ß2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia-reperfusion paradigm. The ensuing calcium overload affects the mitochondria, cytoplasmatic metabolism and the endothelium which further worsens the energetic situation (vicious circle) to explain postexertional malaise, exercise intolerance and chronification. Reduced Na+/K+-ATPase activity is not the only cause for cellular sodium loading. In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle. Finally, sodium overload is due to diminished sodium outward transport and enhanced cellular sodium loading. As soon as this disturbance would have occurred in a severe manner the threshold for re-induction would be strongly lowered, mainly due to an upregulated NHE1, so that it could repeat at low levels of exercise, even by activities of everyday life, re-inducing mitochondrial, metabolic and vascular dysfunction to perpetuate the disease.

An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

There is accumulating evidence of endothelial dysfunction, muscle and cerebral hypoperfusion in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). In this paper we deduce the pathomechanisms resulting in central nervous pathology and the myriad of neurocognitive symptoms. We outline tentative mechanisms of impaired cerebral blood flow, increase in intracranial pressure and central adrenergic hyperactivity and how they can well explain the key symptoms of cognitive impairment, brain fog, headache, hypersensitivity, sleep disturbances and dysautonomia.

Relationship Between Maximal Dynamic Force in the Deep Back Squat and Sprinting Performance in Consecutive Segments Up to 30 m.

ABSTRACT: Möck, S, Hartmann, R, Wirth, K, Rosenkranz, G, and Mickel, C. Relationship between maximal dynamic force in the deep back squat and sprinting performance in consecutive segments up to 30 m. J Strength Cond Res 35(4): 1039-1043, 2021-The sprint (in track and field athletics) is characterized by a fluent transition from predominantly knee extending musculature during the initial acceleration phase toward dominance of the hamstring muscle group thereafter. Because of this change in technique, it can be assumed that there is a decrease of correlation of the maximal dynamic force of the deep back squat and sprinting performance with increasing distance. Therefore, sprinting performance for consecutive intervals (0-5, 5-10, 10-15, 15-20, 20-25, and 25-30 m) as well as the 1 repetition maximum (1RM) were determined. Our results show statistically significant (p < 0.01) correlations for both the relationships with the absolute 1RM (r = -0.614 to -0.808) and the relative 1RM (r = -0.646 to -0.749). However, the expected decrease in correlation over distance was not found. The results show that the maximal dynamic force of hip and knee extensors are a basic performance requirement in short-distance sprinting and should be considered in training recommendations.

The Influence of Upper- and Lower-Body Maximum Strength on Swim Block Start, Turn, and Overall Swim Performance in Sprint Swimming.

ABSTRACT: Keiner, M, Wirth, K, Fuhrmann, S, Kunz, M, Hartmann, H, and Haff, GG. The influence of upper- and lower-body maximum strength on swim block start, turn, and overall swim performance in sprint swimming. J Strength Cond Res 35(10): 2839-2845, 2021-Maximum strength and speed strength are 2 major factors that determine a swimmer's performance, including swim start and turn performance, which directly impacts overall swim sprint performance. Nevertheless, data regarding the relationship between swimming performance and maximum strength are not consistent. Specifically, there are minimal data examining the relationship between maximal strength levels, start and turn performances in the scientific literature. This study was designed to determine the relationship between strength and specific markers of swim performance. Therefore, 14 moderate trained swimmers (male; 17.5 ± 1.6 years; mass: 70.2 ± 4.8 kg; height: 181.9 ± 5.7 cm) were tested for maximum strength in back squat and bench press, squat and countermovement jump performance, tethered swimming and swim performance (50- and 100-m crawl sprint, where start and turn performances were also analyzed). A multiple regression analysis was performed using the maximum strength data as predictors of 15-m start performance and swimming power. Furthermore, bivariate Pearson correlation analyses were used to assess the relationship between the strength and power variables and the swim variables. Maximum strength in the bench press and squat explained 50-65% of the performance variance in swimming power and start performance and 45-62% of the performance variance in 50-/100-m swimming performance. The results of this study demonstrated that maximum strength of the upper and lower limbs and jump height were strongly related to sprint swim performance. Therefore, maximum strength in squat and bench press should be included in strength tests, and that swimmers should incorporate lower- and upper-body strength and power training into their training schedule.

Influence of Maximal Strength on In-Water and Dry-Land Performance in Young Water Polo Players.

Keiner, M, Rähse, H, Wirth, K, Hartmann, H, Fries, K, and Haff, GG. Influence of maximal strength on in-water and dry-land performance in young water polo players. J Strength Cond Res 34(7): 1999-2005, 2020-Water polo is a multifaceted sport that is characterized by explosive actions, including sprint swimming, jumping, throwing, and struggling against opponents. Based on these factors, maximal and speed strength may be important characteristics to develop in-water polo players. However, more research is needed to further understand the relationship between various strength characteristics and water polo performance. Therefore, the primary purpose of this study was to examine the relationships between strength, speed strength, and markers of water polo performance in youth water polo players. Sixty-one male youth water polo players (10-14 years, 11.9 ± 1.3 years) had their 1-repetition maximum (1RM) bench press and squat, dry-land speed-strength performance (squat jump [SJ], countermovement jump [CMJ], and medicine ball throw), in-water performance (sprint swim and water jump), and anthropometric measurements assessed. Fifty to 60% of the variance in sprint performance was explained by the 1RM bench press and arm span. The influence of the bench press 1RM was more than twice that of the anthropometric factors. Maximum strength in the squat and speed-strength (jump height in SJ, CMJ) variables explained 18-25% variance in the eggbeater kick (a leg strike technique to stay above and jump out of water), and the bench press 1RM explained the 42% of the variance in loaded throws without the influence of anthropometric factors. This study suggests that upper- and lower-body maximal strength parameters are important predictors of the performance capacity of water polo players.

Correlation of dynamic strength in the standing calf raise with sprinting performance in consecutive sections up to 30 meters.

Sprinting represents a result-relevant task in many sports. The correlation of sprinting performance and one-repetition maximum (1RM) in a squat has been assumed as assured. Results of the correlation with 1RM of the plantar flexors are still pending. Assuming an increasing relevance of the reactive working capacity with increasing distance, a decrease of the influence of maximum strength of the calves is conceivable. We investigated the correlation of 1RM in a calf raise and sprint performance in consecutive sections up to 30 meters. The results showed medium to strong, very significant correlations (p < 0.01) for absolute (r = -0.483 to r = -0.720) and relative (r = -0.460 to -0.577) strength, whereas an increase of the correlation throughout the course is observed. The dynamic maximum strength of the calves is a basic prerequisite for short sprints and should be regarded as a performance reserve.

Validity and Reliability of the Garmin Vector Power Meter in Laboratory and Field Cycling.

To assess the validity and reliability of the Garmin Vector against the SRM power meter, 6 cyclists completed 3 continuous trials at power outputs from 100-300 W at 50-90 rev·min-1 and a 5-min time trial in laboratory and field conditions. In field conditions only, a 30-s sprint was performed. Data were compared with paired samples t-tests, with the 95% limits of agreement (LoA) and the typical error. Reliability was calculated as the coefficient of variation (CV). There was no significant difference between the devices in power output in laboratory (p=0.245) and field conditions (p=0.312). 1-s peak power was significantly different between the devices (p=0.043). The LoA were ~1.0±5.0 W and ~0.5±0.5 rev·min-1 in both conditions. The LoA during the 30-s sprint was 6.3±38.9 W and for 1-s peak power it was 18.8±17.1 W. The typical error for power output was 2.9%, while during sprint cycling it was 7.4% for 30-s and 2.7% for 1-s peak power. For cadence, the typical error was below 1.0%. The mean CVs were ~1.0% and ~3.0% for the SRM and Garmin, respectively. These findings suggest, that the Garmin Vector is a valid alternative for training. However, during sprint cycling there is lower agreement with the SRM power meter. Both devices provide good reliability (CV<3.0%).

Low-Level But Not High-Level Baroreceptor Stimulation Inhibits Atrial Fibrillation in a Pig Model of Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) increases susceptibility to atrial fibrillation (AF) by a combined sympatho-vagal hyperactivation. The purpose of this study was to investigate the effect of autonomic nervous system modulation by low-level baroreceptor stimulation (LL-BRS) compared to high-level BRS (HL-BRS) on atrial arrhythmogenic changes in a pig model of OSA. METHODS AND RESULTS: Sixteen pigs received tracheotomy under general urethane/chloralose anesthesia. Group 1 pigs (n = 8) received LL-BRS (at 80% of that slowing sinus rate) for 3 hours and group 2 pigs (n = 8) received HL-BRS (slowing sinus rate). Changes in atrial effective refractory period (AERP) and AF-inducibility were determined during applied negative thoracic pressure (NTP) for 2 minutes before and at the end of the 3-hour stimulation protocol. Group 1: LL-BRS prolonged AERP from 150 ± 5 to 172 ± 19 milliseconds (P < 0.001). After 3 hours of LL-BRS, NTP-induced AERP-shortening was diminished from -51 ± 10 milliseconds (-34%) to -22 ± 4 milliseconds (-13%) (P < 0.01). AF-inducibility during NTP maneuvers decreased from 90% at baseline to 15% (P < 0.01). Group 2: HL-BRS shortened AERP from 150 ± 17 to 132 ± 8 milliseconds (P = 0.024). After 3 hours of HL-BRS, NTP-induced AERP-shortening was increased from -55 ± 7 milliseconds (-36%) to -72 ± 11 milliseconds (-54%) (P < 0.05) and AF-inducibility was not affected. NTP-induced changes in blood gases and blood pressure were not different between the groups. CONCLUSION: LL-BRS suppressed NTP-induced AERP-shortening and AF-inducibility. By contrast HL-BRS further perpetuated NTP-induced AERP-shortening and increased AF-inducibility. These findings support only the use of LL-BRS as a novel therapeutic modality to treat AF in OSA.