Task Failure during Exercise to Exhaustion in Normoxia and Hypoxia Is Due to Reduced Muscle Activation Caused by Central Mechanisms While Muscle Metaboreflex Does Not Limit Performance

To determine whether task failure during incremental exercise to exhaustion (IE) is principally due to reduced neural drive and increased metaboreflex activation eleven men (22±2 years) performed a 10s control isokinetic sprint (IS; 80 rpm) after a short warm-up. This was immediately followed by an IE in normoxia (Nx, PIO2:143 mmHg) and hypoxia (Hyp, PIO2:73 mmHg) in random order, separated by a 120 min resting period. At exhaustion, the circulation of both legs was occluded instantaneously (300 mmHg) during 10 or 60s to impede recovery and increase metaboreflex activation. This was immediately followed by an IS with open circulation. Electromyographic recordings were obtained from the vastus medialis and lateralis. Muscle biopsies and blood gases were obtained in separate experiments. During the last 10s of the IE, pulmonary ventilation, VO2, power output and muscle activation were lower in hypoxia than in normoxia, while pedaling rate was similar. Compared to the control sprint, performance (IS-Wpeak) was reduced to a greater extent after the IE-Nx (11% lower P<0.05) than IE-Hyp. The root mean square (EMGRMS) was reduced by 38 and 27% during IS performed after IE-Nx and IE-Hyp, respectively (Nx vs. Hyp: P<0.05). Post-ischemia IS-EMGRMS values were higher than during the last 10s of IE. Sprint exercise mean (IS-MPF) and median (IS-MdPF) power frequencies, and burst duration, were more reduced after IE-Nx than IE-Hyp (P<0.05). Despite increased muscle lactate accumulation, acidification, and metaboreflex activation from 10 to 60s of ischemia, IS-Wmean (+23%) and burst duration (+10%) increased, while IS-EMGRMS decreased (-24%, P<0.05), with IS-MPF and IS-MdPF remaining unchanged. In conclusion, close to task failure, muscle activation is lower in hypoxia than in normoxia. Task failure is predominantly caused by central mechanisms, which recover to great extent within one minute even when the legs remain ischemic. There is dissociation between the recovery of EMGRMS and performance. The reduction of surface electromyogram MPF, MdPF and burst duration due to fatigue is associated but not caused by muscle acidification and lactate accumulation. Despite metaboreflex stimulation, muscle activation and power output recovers partly in ischemia indicating metaboreflex activation has a minor impact on sprint performance

Increased PIO2 at exhaustion in hypoxia enhaces muscle activation and swifty relieves fatigue: a placebo or a PIO2 dependent effect?

To determine the level of hypoxia from which muscle activation (MA) is reduced during incremental exercise to exhaustion (IE), and the role played by PIO2 in this process, ten volunteers (21 ± 2 years) performed four IE in severe acute hypoxia (SAH) (PIO2 = 73 mmHg). Upon exhaustion, subjects were asked to continue exercising while the breathing gas mixture was swiftly changed to a placebo (73 mmHg) or to a higher PIO2 (82, 92, 99, and 142 mmHg), and the IE continued until a new exhaustion. At the second exhaustion, the breathing gas was changed to room air (normoxia) and the IE continued until the final exhaustion. MA, as reflected by the vastus medialis (VM) and lateralis (VL) EMG raw and normalized root mean square (RMSraw, and RMSNz, respectively), normalized total activation index (TAINz), and burst duration were 8–20% lower at exhaustion in SAH than in normoxia (P < 0.05). The switch to a placebo or higher PIO2 allowed for the continuation of exercise in all instances. RMSraw, RMSNz, and TAINz were increased by 5–11% when the PIO2 was raised from 73 to 92, or 99 mmHg, and VL and VM averaged RMSraw by 7% when the PIO2 was elevated from 73 to 142 mmHg (P < 0.05). The increase of VM-VL average RMSraw was linearly related to the increase in PIO2, during the transition from SAH to higher PIO2 (R2 = 0.915, P < 0.05). In conclusion, increased PIO2 at exhaustion reduces fatigue and allows for the continuation of exercise in moderate and SAH, regardless of the effects of PIO2 on MA. At task failure, MA is increased during the first 10 s of increased PIO2 when the IE is performed at a PIO2 close to 73 mmHg and the PIO2 is increased to 92 mmHg or higher. Overall, these findings indicate that one of the central mechanisms by which severe hypoxia may cause central fatigue and task failure is by reducing the capacity for reaching the appropriate level of MA to sustain the task. The fact that at exhaustion in severe hypoxia the exercise was continued with the placebo-gas mixture demonstrates that this central mechanism has a cognitive component.This study was supported by a grant from the Ministerio de Educación y Ciencia of Spain (DEP2009-11638 and FEDER)

Tratamiento del pie plano flexible infantil con la técnica de calcáneo-stop

Presentamos los resultados obtenidos en los pacientes intervenidos por pie plano flexible infantil con la técnica de calcáneo-stopen nuestro servicio.Estudiamos 47 pacientes y 82 pies intervenidos entre los años 1992 y 2004. Tras las pérdidas por diversos motivos en la revisiónde los casos, valoramos clínicamente 64 pies mediante la escala de Smith y Millar y radiológicamente 49 pies con la medición deuna serie de ángulos en carga pre y postoperatoriamente.Obtenemos resultados clínicos excelentes en 41 pies (64,1%), buenos en 22 (34,4%) y malos en 1 caso (1,5%). Radiológicamente,encontramos una mejoría con significación estadística en la valoración de los ángulos de Costa-Bartani, Meary y flexión plantardel astrágalo; una modificación del ángulo de Giannestras no significativa y no encontramos cambios en la medición del ánguloastrágalo-calcáneo en AP.Realizamos una descripción de nuestra serie y una discusión acerca de la técnica y de la indicación actual de la cirugía en estapatología

Increased PIO2 at exhaustion in hypoxia enhances muscle activation and swiftly relieves fatigue: a placebo or a PIO2 dependent effect?

To determine the level of hypoxia from which muscle activation (MA) is reduced during incremental exercise to exhaustion (IE), and the role played by PIO2 in this process, ten volunteers (21±2 years) performed four IE in severe acute hypoxia (SAH) (PIO2=73 mmHg). Upon exhaustion, subjects were asked to continue exercising while the breathing gas mixture was swiftly changed to a placebo (73 mmHg) or to a higher PIO2 (82, 92, 99, 142 mmHg), and the IE continued until a new exhaustion. At the second exhaustion, the breathing gas was changed to room air (normoxia) and the IE continued until the final exhaustion. MA, as reflected by the vastus medialis (VM) and lateralis (VL) EMG raw and normalized root mean square (RMSraw, RMSNz, respectively), normalized total activation index (TAINz), and burst duration were 8-20 % lower at exhaustion in SAH than in normoxia (P<0.05). The switch to a placebo or higher PIO2 allowed for the continuation of exercise in all instances. RMSraw, RMSNz and TAINz were increased by 5-11% when the PIO2 was raised from 73 to 92 or 99 mmHg, and VL and VM averaged RMSraw by 7% when the PIO2 was elevated from 73 to 142 mmHg (P<0.05). The increase of VM-VL average RMSraw was linearly related to the increase in PIO2, during the transition from SAH to higher PIO2 (R2=0.99, P<0.5). In conclusion, increased PIO2 at exhaustion reduces fatigue and allows for the continuation of exercise in moderate and SAH, regardless of the effects of PIO2 on MA. At task failure, MA is increased during the first 10 s of increased PIO2 when the IE is performed at a PIO2 close to 73 mmHg and the PIO2 is increased to 92 mmHg or higher. Overall, these findings indicate that one of the central mechanisms by which severe hypoxia may cause central fatigue and task failure is by reducing the capacity for reaching the appropriate level of muscle activation to sustain the task. The fact that at exhaustion in severe hypoxia the exercise was continued with the placebo-gas mixture demonstrates that this central mechanism has a cognitive component