Rafael Torres-Peralta

What limits performance during whole-body incremental exercise to exhaustion in humans?

At the end of an incremental exercise to exhaustion a large functional reserve remains in the muscles to generate power, even at levels far above the power output at which task failure occurs, regardless of the inspiratory O2 pressure during the incremental exercise. Exhaustion (task failure) is not due to lactate accumulation and the associated muscle acidification; neither the aerobic energy pathways nor the glycolysis are blocked at exhaustion. Muscle lactate accumulation may actually facilitate early recovery after exhaustive exercise even under ischaemic conditions. Although the maximal rate of ATP provision is markedly reduced at task failure, the resynthesis capacity remaining exceeds the rate of ATP consumption, indicating that task failure during an incremental exercise to exhaustion depends more on central than peripheral mechanisms.

Limitations to oxygen transport and utilization during sprint exercise in humans: evidence for a functional reserve in muscle O2 diffusing capacity

Severe acute hypoxia reduces sprint performance. Muscle V̇O2 during sprint exercise in normoxia is not limited by O2 delivery, O2 offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle of young healthy men. A large functional reserve in muscle O2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia; this functional reserve is recruited during exercise in hypoxia. During whole‐body incremental exercise to exhaustion in severe hypoxia, leg V̇O2 is primarily dependent on convective O2 delivery and less limited by diffusion constraints than previously thought. The kinetics of O2 offloading from haemoglobin does not limit V̇O2 peak in hypoxia. Our results indicate that the limitation to V̇O2 during short sprints resides in mechanisms regulating mitochondrial respiration.

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 10 s 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 60 s 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 10 s 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 10 s 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 60 s 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 1 min 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 that metaboreflex activation has a minor impact on sprint performance.

Muscle Activation During Exercise in Severe Acute Hypoxia: Role of Absolute and Relative Intensity

The aim of this study was to determine the influence of severe acute hypoxia on muscle activation during whole body dynamic exercise. Eleven young men performed four incremental cycle ergometer tests to exhaustion breathing normoxic (FIO2=0.21, two tests) or hypoxic gas (FIO2=0.108, two tests). Surface electromyography (EMG) activities of rectus femoris (RF), vastus medialis (VL), vastus lateralis (VL), and biceps femoris (BF) were recorded. The two normoxic and the two hypoxic tests were averaged to reduce EMG variability. Peak VO2 was 34% lower in hypoxia than in normoxia (p<0.05). The EMG root mean square (RMS) increased with exercise intensity in all muscles (p<0.05), with greater effect in hypoxia than in normoxia in the RF and VM (p<0.05), and a similar trend in VL (p=0.10). At the same relative intensity, the RMS was greater in normoxia than in hypoxia in RF, VL, and BF (p<0.05), with a similar trend in VM (p=0.08). Median frequency increased with exercise intensity (p<0.05), and was higher in hypoxia than in normoxia in VL (p<0.05). Muscle contraction burst duration increased with exercise intensity in VM and VL (p<0.05), without clear effects of FIO2. No significant FIO2 effects on frequency domain indices were observed when compared at the same relative intensity. In conclusion, muscle activation during whole body exercise increases almost linearly with exercise intensity, following a muscle-specific pattern, which is adjusted depending on the FIO2 and the relative intensity of exercise. Both VL and VM are increasingly involved in power output generation with the increase of intensity and the reduction in FIO2.

Cerebral blood flow, frontal lobe oxygenation and intra-arterial blood pressure during sprint exercise in normoxia and severe acute hypoxia in humans

Cerebral blood flow (CBF) is regulated to secure brain O2 delivery while simultaneously avoiding hyperperfusion; however, both requisites may conflict during sprint exercise. To determine whether brain O2 delivery or CBF is prioritized, young men performed sprint exercise in normoxia and hypoxia (PIO2 = 73 mmHg). During the sprints, cardiac output increased to ∼22 L min−1, mean arterial pressure to ∼131 mmHg and peak systolic blood pressure ranged between 200 and 304 mmHg. Middle-cerebral artery velocity (MCAv) increased to peak values (∼16%) after 7.5 s and decreased to pre-exercise values towards the end of the sprint. When the sprints in normoxia were preceded by a reduced PETCO2, CBF and frontal lobe oxygenation decreased in parallel (r = 0.93, P < 0.01). In hypoxia, MCAv was increased by 25%, due to a 26% greater vascular conductance, despite 4–6 mmHg lower PaCO2 in hypoxia than normoxia. This vasodilation fully accounted for the 22 % lower CaO2 in hypoxia, leading to a similar brain O2 delivery during the sprints regardless of PIO2. In conclusion, when a conflict exists between preserving brain O2 delivery or restraining CBF to avoid potential damage by an elevated perfusion pressure, the priority is given to brain O2 delivery.

A new equation to estimate temperature-corrected PaCO2 from PET CO2 during exercise in normoxia and hypoxia.

End‐tidal PCO2 (PETCO2) has been used to estimate arterial pressure CO2 (PaCO2). However, the influence of blood temperature on the PaCO2 has not been taken into account. Moreover, there is no equation validated to predict PaCO2 during exercise in severe acute hypoxia. To develop a new equation to predict temperature‐corrected PaCO2 values during exercise in normoxia and severe acute hypoxia, 11 volunteers (21.2 ± 2.1 years) performed incremental exercise to exhaustion in normoxia (Nox, PIO2: 143 mmHg) and hypoxia (Hyp, PIO2: 73 mmHg), while arterial blood gases and temperature (ABT) were simultaneously measured together with end‐tidal PCO2 (PETCO2). The Jones et al. equation tended to underestimate the temperature corrected (tc) PaCO2 during exercise in hypoxia, with greater deviation the lower the PaCO2tc (r = 0.39, P < 0.05). The new equation has been developed using a random‐effects regression analysis model, which allows predicting PaCO2tc both in normoxia and hypoxia: PaCO2tc = 8.607 + 0.716 × PETCO2 [R2 = 0.91; intercept SE = 1.022 (P < 0.001) and slope SE = 0.027 (P < 0.001)]. This equation may prove useful in noninvasive studies of brain hemodynamics, where an accurate estimation of PaCO2 is needed to calculate the end‐tidal‐to‐arterial PCO2 difference, which can be used as an index of pulmonary gas exchange efficiency.

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, 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.

Arterial to end-tidal Pco2 difference during exercise in normoxia and severe acute hypoxia: importance of blood temperature correction

Negative arterial to end‐tidal Pco2 differences ((a‐ET)Pco2) have been reported in normoxia. To determine the influence of blood temperature on (a‐ET)Pco2, 11 volunteers (21 ± 2 years) performed incremental exercise to exhaustion in normoxia (Nx, PIo2: 143 mmHg) and hypoxia (Hyp, PIo2: 73 mmHg), while arterial blood gases and temperature (ABT) were simultaneously measured together with end‐tidal Pco2 (PETco2). After accounting for blood temperature, the (a‐ET) Pco2 was reduced (in absolute values) from −4.2 ± 1.6 to −1.1 ± 1.5 mmHg in normoxia and from −1.7 ± 1.6 to 0.9 ± 0.9 mmHg in hypoxia (both P < 0.05). The temperature corrected (a‐ET)Pco2 was linearly related with absolute and relative exercise intensity, VO2, VCO2, and respiratory rate (RR) in normoxia and hypoxia (R2: 0.52–0.59). Exercise CO2 production and PETco2 values were lower in hypoxia than normoxia, likely explaining the greater (less negative) (a‐ET)Pco2 difference in hypoxia than normoxia (P < 0.05). At near‐maximal exercise intensity the (a‐ET)Pco2 lies close to 0 mmHg, that is, the mean Paco2 and the mean PETco2 are similar. The mean exercise (a‐ET)Pco2 difference is closely related to the mean A‐aDO2 difference (r = 0.90, P < 0.001), as would be expected if similar mechanisms perturb the gas exchange of O2 and CO2 during exercise. In summary, most of the negative (a‐ET)Pco2 values observed in previous studies are due to lack of correction of Paco2 for blood temperature. The absolute magnitude of the (a‐ET)Pco2 difference is lower during exercise in hypoxia than normoxia.

Greater basal skeletal muscle AMPKα phosphorylation in men than in women: Associations with anaerobic performance

Abstract Objectives: This study was designed to investigate the association of gender, fibre type composition, and anaerobic performance with the basal skeletal muscle signalling cascades regulating muscle phenotype. Design: Muscle biopsies were obtained from 25 men and 10 women all young and healthy. Methods. Protein phosphorylation of Thr172AMPKα, Ser221ACCβ, Thr286CaMKII as well as total protein abundance of PGC-1α, SIRT1, and CnA were measured by Western blot and anaerobic performance by the Wingate test. Results: Percent type I myosin heavy chain (MHC I) was lower in men (37.1 ± 10.4 vs. 58.5 ± 12.5, P < .01). Total, free testosterone and free androgen index were higher in men (11.5, 36.6 and 40.6 fold, respectively, P < .01). AMPKα phosphorylation was 2.2-fold higher in men compared to women (P < .01). Total Ser221ACCβ and Thr286CaMKII fractional phosphorylation tended to be higher in men (P = .1). PGC1-α and SIRT1 total protein expression was similar in men and women, whereas CnA tended to be higher in men (P = .1). Basal AMPKα phosphorylation was linearly related to the percentage of MHC I in men (r = 0.56; P < .01), but not in women. No association was observed between anaerobic performance and basal phosphorylations in men and women, analysed separately. Conclusion: In summary, skeletal muscle basal AMPKα phosphorylation is higher in men compared to women, with no apparent effect on anaerobic performance.

Myoelectronic signal-based methodology for the analysis of handwritten signatures

With the overall aim of improving the synthesis of handwritten signatures, we have studied how muscle activation depends on handwriting style for both text and flourish. Surface electromyographic (EMG) signals from a set of twelve arm and trunk muscles were recorded in synchronization with handwriting produced on a digital Tablet. Correlations between these EMG signals and handwritten trajectory signals were analyzed so as to define the sequence of muscles activated during the different parts of the signature. Our results establish a correlation between the speed of the movement, stroke size, handwriting style and muscle activation. Muscle activity appeared to be clustered as a function of movement speed and handwriting style, a finding which may be used for filter design in a signature synthesizer.