Analysis of the aerobic-anaerobic transition in elite cyclists during incremental exercise with the use of electromyography

To investigate the validity and reliability of surface electromyography (EMG) as a new non-invasive determinant of the metabolic response to incremental exercise in elite cyclists. The relation between EMG activity and other more conventional methods for analysing the aerobic-anaerobic transition such as blood lactate measurements (lactate threshold (LT) and onset of blood lactate accumulation (OBLA)) and ventilatory parameters (ventilatory thresholds 1 and 2 (VT1 and VT2)) was studied.Twenty eight elite road cyclists (age 24 (4) years; VO2MAX 69.9 (6.4) ml/kg/min; values mean (SD)) were selected as subjects. Each of them performed a ramp protocol (starting at 0 W, with increases of 5 W every 12 seconds) on a cycle ergometer (validity study). In addition, 15 of them performed the same test twice (reliability study). During the tests, data on gas exchange and blood lactate levels were collected to determine VT1, VT2, LT, and OBLA. The root mean squares of EMG signals (rms-EMG) were recorded from both the vastus lateralis and the rectus femoris at each intensity using surface electrodes. Results - A two threshold response was detected in the rms-EMG recordings from both muscles in 90% of subjects, with two breakpoints, EMG(T1) and EMG(T2), at around 60-70% and 80-90% of VO2MAX respectively. The results of the reliability study showed no significant differences (p > 0.05) between mean values of EMG(T1) and EMG(T2) obtained in both tests. Furthermore, no significant differences (p > 0.05) existed between mean values of EMG(T1), in the vastus lateralis and rectus femoris, and VT1 and LT (62.8 (14.5) and 69.0 (6.2) and 64.6 (6.4) and 68.7 (8.2)% of VO2MAX respectively), or between mean values of EMG(T2), in the vastus lateralis and rectus femoris, and VT2 and OBLA (86.9 (9.0) and 88.0 (6.2) and 84.6 (6.5) and 87.7 (6.4)% of VO2MAX respectively). Rms-EMG may be a useful complementary non-invasive method for analysing the aerobic-anaerobic transition (ventilatory and lactate thresholds) in elite cyclists.

Flujo sanguíneo cerebral durante el ejercicio de esprint

Se desconocen los efectos del entrenamiento interválico de alta intesidad (HIIT) sobre el flujo sanguíneo cerebral (FSC) y la oxigenación cerebral. Por ello reclutamos a 20 voluntarios que realizaron una sesión de HIIT (4 test de Wingate con recuperaciones de 4 minutos). Se midió la oxigenación del lóbulo frontal (OLF) y el Vastus lateralis (VL) a través de espectrofotometría cercana a los infrarrojos (NIRS). También se registró la velocidad de la sangre en las arterias cerebrales medias (vACM) mediante Doppler. La vACM disminuyó entre un 5 y 10 % en el primer esprint. En los siguientes esprints se redujo aún más. La vACM descendió en cada esprint coincidiendo con la disminución de la presión tele-espiratoria de dióxido de carbono (PETCO2) y con valores superiores de ventilación pulmonar (VE). Al interrumpirse el pedaleo se redujo bruscamente la vACM. Sin embargo, la OLF se mantuvo estable en el primer esprint sólo reduciéndose ligeramente durante el segundo y tercer Wingate (el cuarto fue similar al tercero). Este estudio muestra que la vACM disminuye durante los ejercicios de esprint, posiblemente debido a la hipocapnia. La reducción de la vACM no ejerce efectos funcionales ni relevantes sobre la oxigenación cerebral, gracias al ajuste de la conductancia vascular a través de los mecanismos de autoregulación, sin que parezca afectar negativamente al rendimiento.

Genes and the ageing muscle: a review on genetic association studies

Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensin-converting enzyme (ACE) gene I/D, α-actinin-3 (ACTN3) R577X, and myostatin (MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions.

Muscle function and body composition profile in adolescents withrestrictive anorexia nervosa: Does resistance training help?

The aim of this study was to analyze the effects of short-term resistance training on the body composition profile and muscle function in a group of Anorexia Nervosa restricting type (AN-R) patients. The sample consisted of AN-R female adolescents (12.8 ± 0.6 years) allocated into the control and intervention groups (n¼18 each). Body composition and relative strength were assessed at baseline, after 8 weeks and 4 weeks following the intervention. Body mass index (BMI) increased throughout the study (p = 0.011). Significant skeletal muscle mass (SMM) gains were found in the intervention group (p = 0.045, d = 0.6) that correlated to the change in BMI (r = 0.51, p < 0.031). Meanwhile, fat mass (FM) gains were significant in the control group (p = 0.047, d = 0.6) and correlated (r > 0.60) with change in BMI in both the groups. Significant relative strength increases (p < 0.001) were found in the intervention group and were sustained over time.

Xanthine oxidase pathway and muscle damage: Insights from McArdle disease

The intent of this review is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.

Muscle signaling in exercise intolerance: Insights from the McArdle mouse model

We recently generated a knock-in mouse model (PYGM p.R50X/p.R50X) of McArdle disease (myophosphorylase deficiency). One mechanistic approach to unveil the molecular alterations caused by myophosphorylase deficiency, which is arguably the paradigm of 'exercise intolerance', is to compare the skeletal-muscle tissue of McArdle, heterozygous, and healthy (wild type (wt)) mice. We analyzed in quadriceps muscle of p.R50X/p.R50X (n=4), p.R50X/wt (n=6) and wt/wt mice (n=5) (all male, 8 wk-old) molecular markers of energy-sensing pathways, oxidative phosphorylation (OXPHOS) and autophagy/proteasome systems, oxidative damage and sarcoplamic reticulum (SR) Ca handling. We found a significant group effect for total AMPK (tAMPK) and ratio of phosphorylated (pAMPK)/tAMPK (P=0.012 and 0.033), with higher mean values in p.R50X/p.R50X mice vs. the other two groups. The absence of massive accumulation of ubiquitinated proteins, autophagosomes or lysosomes in p.R50X/p.R50X mice suggested no major alterations in autophagy/proteasome systems. Citrate synthase activity was lower in p.R50X/p.R50X mice vs. the other two groups (P=0.036) but no statistical effect existed for respiratory chain complexes. We found higher levels of 4-hydroxy-2-nonenal-modified proteins in p.R50X/p.R50X and p.R50X/wt mice compared with the wt/wt group (P=0.011). Sarco(endo)plasmic reticulum ATPase 1 (SERCA1) levels detected at 110kDa tended to be higher in p.R50X/p.R50X and p.R50X/wt mice compared with wt/wt animals (P=0.076), but their enzyme activity was normal. We also found an accumulation of phosphorylated SERCA1 in p.R50X/p.R50X animals. Myophosphorylase deficiency causes alterations in sensory energetic pathways together with some evidence of oxidative damage and alterations in Ca handling but with no major alterations in OXPHOS capacity or autophagy/ubiquitination pathways, which suggests that the muscle tissue of patients is likely to adapt overall favorably to exercise training interventions.