Classification of middle- and long-distance runners based upon their performance.

The scientific literature lacks consensus on classification of middle- and long-distance runners. This creates situations where the sample studied may not represent the target population and could produce misleading conclusions. Thus, we present an approach for a data-driven classification of middle- and long-distance runners according to their competition results. The best annual results of middle- and long-distance track runners participating at major (Olympics, World and European Championships) and national championships (Denmark, Sweden, Finland, Norway) were gathered for the 2012-2018 period. Overall, 1920 men's and 1808 women's performance results were gathered. The results were grouped accordingly. Quadratic discriminant analysis was applied to define the limits between the groups. Three basic categories could be proposed for classification: world class, international and national. Classification provides a realistic overview of performance standards and the number of athletes for different categories in middle- and long-distance track running in real-world settings. The performance-based classification provides data-driven and unified criteria for reporting standards on athletes' proficiency levels. It allows for more consistent reporting practices on the target population in research. In addition to scientific research, the classification could also be employed for a variety of practical purposes.

Cardiorespiratory fitness and health-related quality of life in women at risk for gestational diabetes.

This study examined the associations of cardiorespiratory fitness (CRF) and leisure-time physical activity (LTPA) with health-related quality of life (HRQoL) in women at risk for gestational diabetes mellitus (GDM). The participants were 39 women planning pregnancy with a history of GDM and/or BMI >29 kg/m2 . We assessed CRF by measuring maximal oxygen consumption (VO2max ) during incremental cycle ergometer exercise until voluntary fatigue. LTPA was self-reported, and HRQoL assessed with the SF-36 Health Survey (SF-36). The mean (SD) VO2max was 27 (6) mL·kg-1 ·min-1 , and the mean LTPA was 2.6 (1.7) h/wk. After controlling for BMI, VO2max was positively associated with the SF-36 General Health scale (ß 1.27, 95% CI: 0.09, 2.44, P=.035) and the Physical Component Summary (ß 0.48, 95% CI: 0.14, 0.82, P=.007). The General Health scale (P=.023) and the Physical Component Summary (P=.011) differed even between those with very poor and poor CRF. After controlling for BMI, LTPA was positively associated with the SF-36 Physical Functioning scale (rs =.34, P=.039), the General Health scale (ß 3.74, 95% CI: 0.64, 6.84, P=.020), and the Physical Component Summary (ß 1.13 95% CI: 0.19, 2.06, P=.020). To conclude, CRF and LTPA were positively associated with perceived general health and physical well-being in women planning pregnancy and at risk for GDM. Even a slightly better CRF would be beneficial for well-being among women with low levels of CRF.

Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia.

An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed the existence of a 'governor' in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle. In contrast, if the function of the heart or some other oxygen-sensitive organ is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxia compared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia.

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia.

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F(I)O2) has no effect on maximal cardiac output (Qcmax), although maximal oxygen uptake (VO2max) and exercise performance do vary along with F(I)O2. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (FI(O)2 = 0.150), normoxia (F(I)O2 = 0.209) and hyperoxia (F(I)O2=0.320). As expected, VO2max decreased in hypoxia [mean (SD) 3.58 (0.45)l.min(-1), P<0.05] and increased in hyperoxia [5.17 (0.34) l.min(-1), P<0.05] in comparison with normoxia [4.55 (0.32)l.min(-1)]. Similarly, maximal power (Wmax) decreased in hypoxia [334 (41) W, P< 0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, Qcmax was 25.99 (3.37) l.min(-1) in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l.min(-1) in normoxia and 30.13 (2.06)l.min(-1) in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in VO2max in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced Qcmax, (2) reduced Qcmax in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced Qcmax and VO2max in acute hypoxia may be the result rather than the cause of the reduced Wmax and skeletal muscle recruitment, thus supporting the existence of a central governor.

Arterial haemoglobin oxygen saturation is affected by F(I)O2 at submaximal running velocities in elite athletes.

This study was conducted to determine whether arterial desaturation would occur at submaximal workloads in highly trained endurance athletes and whether saturation is affected by the fraction of oxygen in inspired air (F(I)O2). Six highly trained endurance athletes (5 women and 1 man, aged 25+/-4 yr, VO2max 71.3+/-5.0 ml x kg(-1) x min(-1)) ran 4x4 min on a treadmill in normoxia (F(I)O2 0.209), hypoxia (F(I)O2 0.155) and hyperoxia (F(I)O2 0.293) in a randomized order. The running velocities corresponded to 50, 60, 70 and 80% of their normoxic maximal oxygen uptake (VO2max). In hypoxia, the arterial haemoglobin oxygen saturation percentage (SpO2%) was significantly lower than in hyperoxia and normoxia throughout the test, and the difference became more evident with increasing running intensity. In hyperoxia, the SpO2% was significantly higher than in normoxia at 70% running intensity as well as during recovery. The lowest values of SpO2% were 94.0+/-3.8% (P<0.05, compared with rest) in hyperoxia, 91.0+/-3.6% (P<0.001) in normoxia and 72.8+/-10.2% (P<0.001) in hypoxia. Although the SpO2% varied with the F(I)O2, the VO2 was very similar between the trials, but the blood lactate concentration was elevated in hypoxia and decreased in hyperoxia at the 70% and 80% workloads. In conclusion, elite endurance athletes may show an F(I)O2-dependent limitation for arterial O2 saturation even at submaximal running intensities. In hyperoxia and normoxia, the desaturation is partly transient, but in hypoxia the desaturation worsens parallel with the increase in exercise intensity.

Back extensor and psoas muscle cross-sectional area, prior physical training, and trunk muscle strength--a longitudinal study in adolescent girls.

The association between physical training, low back extensor (erector spinae plus multifidus muscles) and psoas muscle cross-sectional areas (CSA) and strength characteristics of trunk extension and flexion were studied in adolescent girls. A group of athletes (n = 49) (age range 13.7-16.3 years) consisting of gymnasts, figure skaters and ballet dancers was age-matched with non-athletes (n = 17) who acted as a sedentary control group. The CSA of psoas muscles and multifidus plus erector spinae muscles were measured from lumbar axial images by magnetic resonance imaging. Maximal trunk extension and flexion forces were measured in a standing position using a dynamometer and trunk musculature endurance was evaluated using static holding tests. When CSA were adjusted with body mass, the athletes showed significantly greater CSA in both muscles studied (psoas P < 0.001; erector spinae plus multifidus P < 0.05) than the non-athletes. The athletes also had a greater absolute psoas muscle CSA (P < 0.01) and trunk flexion force (P < 0.01) compared to the controls. When the forces were expressed relative to body mass, the athletes were superior both in trunk flexion (P < 0.001) and extension (P < 0.001). There was a significant correlation between muscle CSA and strength parameters, but the force per muscle CSA did not differ significantly between the athletes and the non-athletes. In addition, the athletes showed a better body mass adjusted muscle endurance in trunk flexion (P < 0.05) than the non-athletes. Our study indicated that regular physical training enhances trunk musculature hypertrophy, force and endurance in adolescent girls, and that there is an association between muscle CSA and strength parameters.

Blood flow, lipid oxidation, and muscle glycogen synthesis after glycogen depletion by strenuous exercise.

UNLABELLED: We studied the interrelationship between blood flow, glycogen synthesis, and glucose and lipid utilization in 14 healthy men. A 4-h euglycemic insulin clamp with indirect calorimetry and muscle biopsies were done after a glycogen depletion (exercise) and after a resting day (control). In spite of the exercise induced decrease in leg muscle glycogen content (28% in the basal state, 22% after hyperinsulinemia, P < 0.05 in both as compared with the control study), basal or insulin stimulated glycogen synthase activity remained unchanged. In the basal state, glucose oxidation was 54% lower (P < 0.001) and lipid oxidation 108% higher (P < 0.001) after the glycogen depletion as compared with that in the control study. During the post-depletion insulin clamp, the glucose oxidation rate was 17% lower (P < 0.02) and lipid oxidation 169% higher (P < 0.01), while the whole body total glucose disposal was similar in both studies. Baseline forearm blood flow was similar and increased equally by over 40% during both insulin clamp studies (P < 0.05). Basal glucose extraction after glycogen depletion study was one third of that in the control study (P < 0.05). Both basal and insulin stimulated leg muscle glycogen content correlated inversely with basal forearm blood flow (r = -0.69, P < 0.01 and r = -0.82, P < 0.001, respectively) and basal lipid oxidation (r = -0.54, P < 0.05 and r = -0.64, P < 0.01, respectively) after glycogen depletion. Basal glycogen synthase fractional activity correlated positively with forearm blood flow (r = 0.78, P < 0.001) and forearm glucose uptake (r = 0.71, P < 0.05) during the insulin infusion. IN CONCLUSION: 1) the unchanged insulin sensitivity in the face of glycogen depletion is probably a result of increased lipid oxidation, and 2) blood flow is related inversely to muscle glycogen content and directly to glycogen synthase activity.

Effects of oxygen fraction in inspired air on force production and electromyogram activity during ergometer rowing.

Six male rowers rowed maximally for 2500 m in ergometer tests during normoxia (fractional concentration of oxygen in inspired air, F(I)O2 0.209), in hyperoxia (F(I)O2 0.622) and in hypoxia (F(I)O2 0.158) in a randomized single-blind fashion. Oxygen consumption (VO2), force production of strokes as well as integrated electromyographs (iEMG) and mean power frequency (MPF) from seven muscles were measured in 500-m intervals. The iEMG signals from individual muscles were summed to represent overall electrical activity of these muscles (sum-iEMG). Maximal force of a stroke (Fmax) decreased from the 100% pre-exercise maximal value to 67 (SD 12)%, 63 (SD 15)% and 76 (SD 13)% (P < 0.05 to normoxia, ANOVA) and impulse to 78 (SD 4)%, 75 (SD 14)% and 84 (SD 7)% (P < 0.05) in normoxia, hypoxia and hyperoxia, respectively. A strong correlation between Fmax and VO2 was found in normoxia but not in hypoxia and hyperoxia. The mean sum-iEMG tended to be lower (P < 0.05) in hypoxia than in normoxia but hyperoxia had no significant effect on it. In general, F(I)O2 did not affect MPF of individual muscles. In conclusion, it was found that force output during ergometer rowing was impaired during hypoxia and improved during hyperoxia when compared with normoxia. Moreover, the changes in force output were only partly accompanied by changes in muscle electrical activity as sum-iEMG was affected by hypoxic but not by hyperoxic gas. The lack of a significant correlation between Fmax and VO2 during hypoxia and hyperoxia may suggest a partial uncoupling of these processes and the existence of other limiting factors in addition to VO2.

Effects of oxygen fraction in inspired air on rowing performance.

The present study examined the effect of oxygen fraction in inspired air (FIO2) on exercise performance and maximum oxygen consumption (VO2max). Six national level male rowers exercised three 2500-m all-out tests on a Concept II rowing ergometer. Each subject performed one test in normoxia (FIO2 20.9%), one in simulated hyperoxia (FIO2 62.2%) and one in simulated hypoxia (FIO2 15.8%) in a randomized single-blind fashion. The mean final rowing time was 2.3 +/- 0.9% (P < 0.01; 95% CI 1.4-3.2) shorter in hyperoxia and 5.3 +/- 1.8% (P < 0.01; 95% CI 3.1-7.5) longer in hypoxia when compared with normoxia. The effect of FIO2 on VO2max exceeded its effect on exercise performance as VO2max was 11.1 +/- 5.7% greater (P < 0.01; 95% CI 5.1-17.1) in hyperoxia and 15.5 +/- 3.2% smaller in hypoxia (P < 0.01; 95% CI 12.2-19.0) than in normoxia. Blood lactate concentration and O2 consumption per power unit (ml O2.W-1) failed to indicate statistically significant differences in anaerobic metabolism between normoxia and the other two conditions. These data suggest that there are other parameters besides those of energy metabolism that affect exercise performance as FIO2 is modified. These possible mechanisms are discussed in this paper.