The ability to correct an on-going action : accuracy and correction time in elite fencing

Background and Study Aim: Performing an attack in fencing takes fractions of a second implying that there is little time to correct an on-going movement to anticipate the opponent's action. Studies in the lab evaluated correction times in artificial tasks but stand in shrill contrast to elite sports where via extensive training, motor programs are mastered and perfected. This study aim was to expand the knowledge on the capability of elite fencers to correct an on-going attack on a central target when the target suddenly changes position at random time intervals. Material and Methods: Eight elite fencers ( 7 males, 18.3 +/- 4.66 years) performed a fente at a target as fast and accurate as possible. In 80% of the trials, a new target light was lit during the fente, and the fencers had to adjust their movement to hit the new illuminated target. Correction times were set at 100ms, 170ms, 240ms, 310ms or 380ms before the estimated epee-target contact. The number of successful adjustments and the radial error was reported. Results: With increasing correction times (p<0.01), radial error decreased. Based on the correction times, the inflexion point was determined at 277ms. It was demonstrated that correction time influenced the number of adjusted trials (p<0.01). Fencers were able to adjust more trials when correction times were set at 310ms and 380ms (p<0.01). Conclusions: Correction times in humans, which are often measured in laboratory settings, appear to apply for sports situations as well. A quarter of a second is sufficient to correct an on-going movement in which the whole body is involved subtle but effectively when the target unexpectedly changes position

Inflammatory markers are associated with quality of life, physical activity, and gait speed but not sarcopenia in aged men (40-79 years)

Background: Age-related chronic low-grade inflammation (inflammaging) is one of the proposed mechanisms behind sarcopenia. However, findings regarding inflammatory markers in sarcopenic older adults are conflicting. This study aimed to determine the association between inflammatory markers, prevalent as well as incident sarcopenia, sarcopenia-defining parameters, quality of life (QoL), and physical activity in middle-aged and older men. Methods: Men aged 40–79 years (mean 59.66 ± 11.00y) were recruited from population registers in eight European centres for participation in the European Male Aging study (EMAS). Subjects were assessed at baseline (2003–2005) and again after a median follow-up of 4.29 years. In 2577 participants, associations between baseline inflammatory markers [high-sensitive C-reactive protein (hs-CRP), white blood cell count (WBC), albumin] and baseline physical activity (PASE) and QoL (SF-36) were analysed. In the Leuven and Manchester cohort (n = 447), data were available on muscle mass (whole-body dual X-ray absorptiometry) and strength. In this subgroup, cross-sectional associations between baseline inflammatory markers and sarcopenia-defining parameters (handgrip strength, chair stand test, appendicular lean mass, and gait speed) and prevalent sarcopenia were examined. In a further subgroup (n = 277), associations with knee extensor strength were explored. Longitudinally, predictive value of baseline inflammation on functional decline, physical activity, QoL, and incident sarcopenia was examined. Subgroup analyses were performed in subgroups with chronic inflammation and stratified by age. Linear and logistic regressions were used, adjusted for age, body mass index, centre, and smoking. Results: At baseline, hs-CRP and WBC were negatively associated with PASE score (hs-CRP: β = −7.920, P < 0.001; and WBC: β = −4.552, P < 0.001) and the physical component score of SF-36 (hs-CRP: β = −1.025, P < 0.001; and WBC: β = −0.364, P < 0.001). Baseline WBC levels were negatively associated with gait speed (β = −0.013; P = 0.025), quadriceps isometric 90° (β = −5.983; P = 0.035) and isokinetic 60°/s peak torque/body weight (β = −5.532; P = 0.027). The prevalence of sarcopenia at baseline was 18.1% (n = 81). Of those without sarcopenia at baseline, 64 (18.6%) satisfied criteria for sarcopenia at follow-up. There were no significant associations between baseline inflammatory markers and either prevalent or incident sarcopenia, or change in level of sarcopenia-defining parameters between baseline and follow-up. Conclusions: In middle-aged and older men, hs-CRP and WBC were negatively associated with QoL and PASE scores, while WBC was negatively associated with gait speed and knee strength. Associations with hs-CRP remained significant in all ages, whereas WBC levels were only associated with PASE, gait speed and knee strength in older adults (60–79 years). Baseline inflammatory markers (hs-CRP, WBC and albumin) did not predict functional decline, decline in physical activity, decreased QoL or incident sarcopenia

Inflammatory markers are associated with quality of life, physical activity, and gait speed but not sarcopenia in aged men (40-79 years)

Background Age-related chronic low-grade inflammation (inflammaging) is one of the proposed mechanisms behind sarcopenia. However, findings regarding inflammatory markers in sarcopenic older adults are conflicting. This study aimed to determine the association between inflammatory markers, prevalent as well as incident sarcopenia, sarcopenia-defining parameters, quality of life (QoL), and physical activity in middle-aged and older men. Methods Men aged 40-79 years (mean 59.66 +/- 11.00y) were recruited from population registers in eight European centres for participation in the European Male Aging study (EMAS). Subjects were assessed at baseline (2003-2005) and again after a median follow-up of 4.29 years. In 2577 participants, associations between baseline inflammatory markers [high-sensitive C-reactive protein (hs-CRP), white blood cell count (WBC), albumin] and baseline physical activity (PASE) and QoL (SF-36) were analysed. In the Leuven and Manchester cohort (n = 447), data were available on muscle mass (whole-body dual X-ray absorptiometry) and strength. In this subgroup, cross-sectional associations between baseline inflammatory markers and sarcopenia-defining parameters (handgrip strength, chair stand test, appendicular lean mass, and gait speed) and prevalent sarcopenia were examined. In a further subgroup (n = 277), associations with knee extensor strength were explored. Longitudinally, predictive value of baseline inflammation on functional decline, physical activity, QoL, and incident sarcopenia was examined. Subgroup analyses were performed in subgroups with chronic inflammation and stratified by age. Linear and logistic regressions were used, adjusted for age, body mass index, centre, and smoking. Results At baseline, hs-CRP and WBC were negatively associated with PASE score (hs-CRP: beta = -7.920, P Conclusions In middle-aged and older men, hs-CRP and WBC were negatively associated with QoL and PASE scores, while WBC was negatively associated with gait speed and knee strength. Associations with hs-CRP remained significant in all ages, whereas WBC levels were only associated with PASE, gait speed and knee strength in older adults (60-79 years). Baseline inflammatory markers (hs-CRP, WBC and albumin) did not predict functional decline, decline in physical activity, decreased QoL or incident sarcopenia.</p

The decrease in the (V) over-dot-O-2 slow component induced by prior exercise does not affect the time to exhaustion

In previous studies decreases in the VO(2) slow component were observed after prior heavy exercise. The observed effects after prior low-intensity exercise were rather controversial. The purpose of the present study was to more thoroughly examine the effects of prior low-intensity exercise on the VO(2) slow component. Furthermore, it has been suggested that the VO(2) slow component may be a determinant of exercise tolerance. Therefore we tested the hypothesis whether an attenuated VO(2) slow component induced by prior exercise could affect the time to exhaustion. Ten subjects performed four exercise protocols consisting of heavy cycling exercise (95 % VO(2)peak) until exhaustion. This constant-load exercise was performed without prior exercise (protocol NPE), or was preceded by 6 min heavy cycling exercise (protocol 6HPE), 12 min low-intensity cycling exercise (protocol 12LPE) or 6 min low-intensity cycling exercise (protocol 6LPE). The VO(2) slow component quantified as Delta VO(2 (end-2)) (669 +/- 90 ml x min (-1) in NPE) was significantly reduced after heavy as well as low-intensity exercise (respectively 47 %, 29 % and 17 % in 6HPE, 12LPE and 6LPE). This reduction lead to a significantly lower end VO(2) in 6HPE and 12LPE. The time to exhaustion (594 +/- 139 s in NPE), however, was unaffected by prior exercise rejecting our hypothesis that the attenuated VO(2) slow component could improve the capability to sustain exercise performance.status: publishe

Prior arm exercise speeds the VO2 kinetics during arm exercise above the heart level

PURPOSE: To test the hypothesis that the initial O2 uptake kinetics during exercise where the rise in blood flow (and, by implication, O2 delivery) to the working muscles during an abrupt increase in exercise intensity is reduced (i.e., arm exercise performed above the level of the heart) would be faster when preceded by a bout of high-intensity exercise. METHODS: Eleven physically active males completed two protocols, each consisting of two consecutive bouts of 6 min of high-intensity arm crank exercise separated by 6 min of recovery. In one protocol, the arm crank exercise was performed with the arms below the level of the heart (HL). RESULTS: In the HL protocol, the amplitudes of the VO2 fast and slow component were unaffected by prior exercise, whereas the VO2 fast component time constant was significantly reduced in the second bout (49.8+/-22.1 vs 40.7+/-13.2 s; P<0.05). CONCLUSION: The results of this study demonstrate that prior high-intensity exercise caused a significant speeding of the VO2 fast component response during subsequent high-intensity arm crank exercise performed above, and not below, the level of the heart.status: publishe

The decrease in the (V) over-dot-O-2 slow component induced by prior exercise does not affect the time to exhaustion.

In previous studies decreases in the VO(2) slow component were observed after prior heavy exercise. The observed effects after prior low-intensity exercise were rather controversial. The purpose of the present study was to more thoroughly examine the effects of prior low-intensity exercise on the VO(2) slow component. Furthermore, it has been suggested that the VO(2) slow component may be a determinant of exercise tolerance. Therefore we tested the hypothesis whether an attenuated VO(2) slow component induced by prior exercise could affect the time to exhaustion. Ten subjects performed four exercise protocols consisting of heavy cycling exercise (95 % VO(2)peak) until exhaustion. This constant-load exercise was performed without prior exercise (protocol NPE), or was preceded by 6 min heavy cycling exercise (protocol 6HPE), 12 min low-intensity cycling exercise (protocol 12LPE) or 6 min low-intensity cycling exercise (protocol 6LPE). The VO(2) slow component quantified as Delta VO(2 (end-2)) (669 +/- 90 ml x min (-1) in NPE) was significantly reduced after heavy as well as low-intensity exercise (respectively 47 %, 29 % and 17 % in 6HPE, 12LPE and 6LPE). This reduction lead to a significantly lower end VO(2) in 6HPE and 12LPE. The time to exhaustion (594 +/- 139 s in NPE), however, was unaffected by prior exercise rejecting our hypothesis that the attenuated VO(2) slow component could improve the capability to sustain exercise performance.status: publishe

Chasing the "ghost" of the acetyl group deficit - Response

A

In humans the oxygen uptake slow component is reduced by prior exercise of high as well as low intensity

The aim of the study was to examine to what extent prior high- or low-intensity cycling, yielding the same amount of external work, influenced the oxygen uptake (VO2) slow component of subsequent high-intensity cycling. The 12 subjects cycled in two protocols consisting of an initial 3 min period of unloaded cycling followed by two periods of constant-load exercise separated by 3 min of rest and 3 min of unloaded cycling. In protocol 1 both periods of exercise consisted of 6 min cycling at a work rate corresponding to 90% peak oxygen uptake (VO2peak). Protocol 2 differed from protocol 1 in that the first period of exercise consisted of a mean of 12.1 (SD 0.8) min cycling at a work rate corresponding to 50% VO2peak. The difference between the 3rd min VO2 and the end VO2 (deltaVO2(6-3)) was used as an index of the VO2 slow component. Prior high-intensity exercise significantly reduced deltaVO2(6-3). The deltaVO2(6-3) was also reduced by prior low-intensity exercise despite an unchanged plasma lactate concentration at the start of the second period of exercise. The reduction was more pronounced after prior high- than after prior low-intensity exercise (59% and 28%, respectively). The results of this study show that prior exercise of high as well as low intensity reduces the VO2 slow component and indicate that a metabolic acidosis is not a necessary condition to elicit a reduction in deltaVO2(6-3).status: publishe

The decrease in the (V) over-dot-O-2 slow component induced by prior exercise does not affect the time to exhaustion

status: publishe