Purpose: The overall objective of this thesis was to investigate the role and development of sprinting speed in soccer. Six original studies plus a published review have been completed towards with this objective.Valid and reliable measurement of sprint times is a prerequisite to reliably detect true changes in sprinting performance. Therefore, the purpose of study I was to quantify potential sprint time differences between single beamed (SB) and dual beamed (DB) timing systems. The aim of study II was to compare different sprint start positions and generate correction factors between popular timing triggering methods on 40 m sprint. The results from these two methodological studies secured a fundamental platform for interpretation of further sprint data in the thesis. The purpose of studies III and IV was to use a large database of soccer athlete sprint and countermovement jump (CMJ) tests collected under highly standardized conditions over 15 years to estimate generalizable differences in sprinting speed and jumping height as a function of: 1) athlete playing level, 2) field position, and 3) age. Additionally, we also evaluated the evolution of sprint and CMJ ability among male professionals and female elite players in Norwegian soccer over a 15 year period. The purpose of study VI was to investigate the effect of training at 90% sprint speed on maximal and repeated sprinting performance in soccer. The aim of study VII was two fold: 1) To compare the effects of training at 90 and 100% sprint speed on maximal and repeated sprint performance, and 2) to compare the effects of directly supervised sprint training versus unsupervised training on maximal and repeated sprint performance. Results: Simultaneous measurements with SB and DB timing revealed that coefficient of variation (CV) was 0.4 and 0.7% for 0-20 m and 20-40 m sprint times, respectively, while SEM was 0.01 s for both distances when arm and leg motion was controlled for (study I, phase 1), During normal sprint action (study I, phase 2), CV increased to 1.4 and 1.2% for 0-20 m and 20-40 m splits, respectively, while SEM was 0.02 s for both distances. During normal sprint action, absolute time differences for 0-20 m sprint times ranged from -0.05 to 0.06 s between SB and DB timing. Compared to block starts reacting to gunfire, hand release, standing photo cell start and foot release start yielded 0.17 ±0.09, 0.27 ±0.12 and 0.69 ±0.11 s faster times respectively over 40 m (study II). In study III and IV, data from a large sample of athletes tested under identical conditions demonstrated small to large differences in sprinting times across playing standards. CMJ performance was practically identical among male national teams and 1 st -2 nd division players. Forwards were faster than defenders, midfielders and goalkeepers, respectively. Sprint performance peaked in the age range 20-28 years for male professional players, while no differences in sprinting velocity were observed among female age categories. Furthermore, the data revealed a small but si...

The present study showed that impaired RV systolic function, hypertrophy, and dilation were present even at a slight increase of mPAP, which indicates an early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index, and strain could detect subclinical disease and separate controls from those with no PH.

The purpose of the present study was to investigate muscle hypertrophy, strength, and myonuclear and satellite cell (SC) responses to high-frequency blood flow-restricted resistance exercise (BFRRE). Thirteen individuals [24 ± 2 yr (mean ± SD), 9 men] completed two 5-day blocks of 7 BFRRE sessions, separated by a 10-day rest period. Four sets of unilateral knee extensions to voluntary failure at 20% of one repetition maximum (1RM) were conducted with partial blood flow restriction (90–100 mmHg). Muscle samples obtained before, during, 3 days, and 10 days after training were analyzed for muscle fiber area (MFA), myonuclei, SC, and mRNA and miRNA expression. Muscle size was measured by ultrasonography and magnetic resonance imaging and strength with 1RM knee extension. With the first block of BFRRE, SC number increased in both fiber types (70%–80%, P < 0.05), whereas type I and II MFA decreased by 6 ± 7% and 15 ± 11% ( P < 0.05), respectively. With the second block of training, muscle size increased by 6%–8%, whereas the number of SCs (type I: 80 ± 63%, type II: 147 ± 95%), myonuclei (type I: 30 ± 24%, type II: 31 ± 28%), and MFA (type I: 19 ± 19%, type II: 11 ± 19%) peaked 10 days after the second block of BFRRE, whereas strength peaked after 20 days of detraining (6 ± 6%, P < 0.05). Pax7- and p21 mRNA expression were elevated during the intervention, whereas myostatin, IGF1R, MyoD, myogenin, cyclinD1 and -D2 mRNA did not change until 3–10 days postintervention. High-frequency low-load BFRRE induced robust increases in SC, myonuclei, and muscle size but modest strength gains. Intriguingly, the responses were delayed and peaked 10–20 days after the training intervention, indicating overreaching. NEW & NOTEWORTHY In line with previous studies, we demonstrate that high-frequency low-load blood flow-restricted resistance exercise (HF-BFRRE) can elicit robust increases in satellite cell and myonuclei numbers, along with gains in muscle size and strength. However, our results also suggest that these processes can be delayed and that with very strenuous HF-BFRRE, there may even be transient muscle fiber atrophy, presumably because of accumulated stress responses. Our findings have implications for the prescription of BFR exercise.

The present study aimed to explore the prevalence of pre-capillary pulmonary hypertension (PH) and characterise haemodynamic vascular responses to physical exercise in chronic obstructive pulmonary disease (COPD) outpatients, where left ventricular dysfunction and comorbidities were excluded.98 patients with COPD underwent right heart catheterisation at rest and during supine exercise. Mean pulmonary artery pressure (Ppa), pulmonary capillary wedge pressure (Ppcw) and cardiac output (CO) were measured at rest and during exercise. Exercise-induced increase in mean Ppa was interpreted relative to increase in blood flow, mean Ppa/CO, workload (W) and mean Ppa/W. Pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC) were calculated. PH at rest was defined as mean Ppa at rest o25 mmHg and Ppcw at rest ,15 mmHg.Prevalence of PH was 5%, 27% and 53% in Global Initiative for Chronic Obstructive Lung Disease stages II, III and IV, respectively. The absolute exercise-induced rise in mean Ppa did not differ between subjects with and without PH. Patients without PH showed similar abnormal haemodynamic responses to exercise as the PH group, with increased PVR, reduced PAC and steeper slopes for mean Ppa/CO and mean Ppa/W.Exercise revealed abnormal physiological haemodynamic responses in the majority of the COPD patients. The future definition of PH on exercise in COPD should rely on the slope of mean Ppa related to cardiac output and workload rather than the absolute values of mean Ppa.

A large variability of DeltaPOP and a poor agreement between DeltaPP and DeltaPOP limits DeltaPOP as a tool for evaluation of fluid responsiveness in intensive care unit patients. This is in contrast to DeltaPP, which shows a small variability.