Rate modulation of human anconeus motor units during high-intensity dynamic elbow extensions

Investigations of high-intensity isometric fatiguing protocols report decreases in motor unit firing rates (MUFRs), but little is known regarding changes in MUFRs following fatigue induced by high-intensity dynamic contractions. The purpose was to evaluate MUFRs of the anconeus (an accessory elbow extensor), and elbow extension power production as a function of time to task failure (TTF) during high velocity fatiguing concentric contractions against a moderately heavy resistance. Fine-wire intramuscular electrode pairs were inserted into the anconeus to record MUs in 12 male participants (25±3y), over repeated sessions on separate days. MUs were tracked throughout a three-stage, varying-load, dynamic elbow extension protocol designed to extend the task duration for >1 minute thereby inducing substantial fatigue. Mean MUFRs and peak power were calculated for three relative time ranges: 0-15% TTF (beginning), 45-60% TTF (middle) and 85-100% TTF (end). Mean duration of the overall fatigue protocol was ~80 seconds. Following the protocol, isometric MVC, highest velocity at 35% MVC load, and peak power decreased 37%, 60%, and 64% compared to baseline, respectively. Data from 20 anconeus MUs tracked successfully throughout the protocol indicated a reduction in MUFRs in relation to power loss from 36 Hz/160W (0-15% TTF) to 28 Hz/97W (45-60% TTF) to 23 Hz/43W (85-100% TTF). During these high-intensity maximal effort concentric contractions, anconeus MUFRs decreased substantially (> 35%). Although the absolute MUFRs were higher in the present study than those reported previously for other muscles during sustained high-intensity isometric tasks, the relative decrease in MUFRs was similar between the two tasks.

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Airway mechanics and lung tissue viscoelasticity: effects of altered blood hematocrit in the pulmonary circulation

The contribution of the hematocrit (Hct) of the blood in the pulmonary vasculature to the overall lung mechanics has not been characterized. We therefore set out to establish how changes of the Hct level in the pulmonary circulation affect the airway and lung tissue viscoelastic properties. The Hct level of the blood in an isolated perfused rat lung model was randomly altered. Intermediate (26.5%), followed by low (6.6%) or normal Hct (43.7%) were set in 2 consecutive sequences. The pulmonary capillary pressure was maintained constant throughout the experiment and the pulmonary hemodynamic parameters were monitored continuously. The airway resistance (Raw), the viscous (G) and elastic (H) parameters and the hysteresivity (=G/H) of the lung tissues were obtained from measurements of forced oscillatory input impedance data. Raw was not affected by the alterations of the Hct levels. As concerns the lung tissues, the decrease of Hct to intermediate or low levels resulted in close to proportional decreases in the viscoelastic parameters G (16.5±7.7%, 12.1±9.5%, p<0.005) and H (13.2±8.6%, 10.8±4.7%, p<0.001). No significant changes in were detected in a wide range of Hct, which indicates that coupled processes cause alterations in the resistive and elastic properties of the lungs following Hct changes in the pulmonary circulation. The diminishment of the viscous and elastic parameters of the pulmonary parenchyma following a reduction of blood Hct demonstrate the significant contribution of the red blood cells to the overall lung viscoelasticity.

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Faster and stronger manifestation of mitochondrial diseases in skeletal muscle than in heart related to cytosolic inorganic phosphate (Pi) accumulation

A model of the cell bioenergetic system was used to compare the effect of oxidative phosphorylation (OXPHOS) deficiencies in a broad range of moderate ATP demand in skeletal muscle and heart. Computer simulations revealed that kinetic properties of the system are similar in both cases despite the much higher mitochondria content and 'basic' OXPHOS activity in heart than in skeletal muscle, because of a much higher each-step activation (ESA) of OXPHOS in skeletal muscle than in heart. Large OXPHOS deficiencies lead in both tissues to a significant decrease in VO₂ and PCr and increase in cytosolic ADP, P_i and H⁺. The main difference between skeletal muscle and heart is a much higher cytosolic P_i concentration in healthy tissue and much higher cytosolic P_i accumulation (level) at low OXPHOS activities in the former, caused by a higher PCr level in healthy tissue (and higher total phosphate pool) and smaller P_i redistribution between cytosol and mitochondria at OXPHOS deficiency. This difference does not depend on ATP demand in a broad range. A much greater P_i increase and PCr decrease during rest-to-moderate-work transition in skeletal muscle at OXPHOS deficiencies than at normal OXPHOS activity significantly slows down the VO₂ on-kinetics. Because high cytosolic P_i concentrations cause fatigue in skeletal muscle and can compromise force generation in skeletal muscle and heart, this system property can contribute to the faster and stronger manifestation of mitochondrial diseases in skeletal muscle than in heart. Shortly, skeletal muscle with large OXPHOS deficiencies becomes fatigued already during low/moderate exercise.

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Effects of aging on mitochondrial function in skeletal muscle of Quarter Horses

Skeletal muscle function, aerobic capacity and mitochondrial (Mt) function have been found to decline with age in humans and rodents. However, not much is known about age-related changes in Mt function in equine skeletal muscle. Here, we compared fiber type composition and Mt function in Gluteus medius and Triceps brachii muscle between young (age 1.8±0.1 years, n=24) and aged (age 17-25 years, n=10) Quarter Horses. The percentage of myosin heavy chain (MyHC)-IIX was lower in aged compared to young muscles (Gluteus, P=0.092; Triceps, P=0.012), while the percentages of MyHC-I (Gluteus; P<0.001) and MyHC-IIA (Triceps; P=0.023) were increased. Mass-specific Mt density, indicated by citrate synthase activity, was unaffected by age in Gluteus, but decreased in aged Triceps (P=0.023). Cytochrome c oxidase (COX) activity per mg tissue and per Mt unit decreased with age in Gluteus (P<0.001 for both) and Triceps (P<0.001; P=0.003, respectively). Activity of 3-Hydroxyacyl-CoA dehydrogenase per mg tissue was unaffected by age, but increased per Mt unit in aged Gluteus and Triceps (P=0.023, P<0.001, respectively). Mt respiration of permeabilized muscle fibers per mg tissue was unaffected by age in both muscles. Main effects of age appeared when respiration was normalized to Mt content, with increases in LEAK, OXPHOS capacity and electron transport system capacity (P=0.038; P=0.045; P=0.007, respectively), independent of muscle. In conclusion, equine skeletal muscle aging was accompanied by a shift in fiber type composition, decrease in Mt density and COX activity, but preserved Mt respiratory function.

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The Effects of a Roundtrip Trans-American Jet Travel on Physiological Stress, Neuromuscular Performance and Recovery

The purpose was to examine a round trip trans-American jet travel on performance, hormonal alterations, and recovery. Ten matched pairs of recreationally trained men were randomized to either a compression group (COMP) (n= 10, age: 23.1 ± 2.4 years, height: 174.8 ± 5.3cm, body mass: 84.96 ± 10.16 kg, body fat: 15.3 ± 6.0%) or control group (CONT) (n= 9, age: 23.2 ± 2.3 years, height: 177.5 ± 6.3cm, body mass: 84.35 ± 8.99 kg, body fat: 15.1 ± 6.4%). Subjects flew directly from Hartford, CT to Los Angeles, CA one day prior to a simulated sport competition (SSC) designed to create muscle damage and returned the next night on a overnight flight back home. Both groups demonstrated jet lag symptoms and associated decreases in sleep quality at all time points. Melatonin significantly (P < 0.05) increased over the first two days and then remained constant after the SSC. Epinephrine, testosterone, cortisol values significantly increased above resting values before and after the SSC with norepinephrine increases only after the SSC. Physical performances significantly decreased from control values on each day for the CONT group with COMP group exhaibiting no significant declines. Muscle damage markers were significantly elevated following the SSC with the COMP group having significantly lower values while maintaining neuromuscular performance measures that were not different from baseline testing. Trans-American jet travel significantly impacted parameters related to jet lag, sleep quality, hormonal responses, muscle tissue damage markers, and physical performance with an attenuation observed with extended wear compression garments.

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The relation between cardiac output kinetics and skeletal muscle oxygenation during moderate exercise in moderately impaired patients with chronic heart failure

Oxygen uptake (VO₂) kinetics are prolonged in patients with chronic heart failure (CHF). This may be caused by impaired oxygen delivery or skeletal muscle derangements. We investigated whether impaired cardiac output (Q) kinetics limit skeletal muscle oxygen delivery relative to the metabolic demands at submaximal exercise in CHF patients by evaluating the relation between Q kinetics and skeletal muscle deoxygenation. Forty-three CHF patients, NYHA II-III, performed a constant-load exercise test at 80% of the VAT to assess VO₂ kinetics (VO₂). Q kinetics (Q) were assessed by a radial artery pulse contour analysis method. Skeletal muscle deoxygenation was assessed by near infrared spectroscopy at the m. vastus lateralis, using the minimal value of the tissue saturation index during onset of exercise (TSImin). Patients were categorized in slow and normal Q responders relative to metabolic demands (Q/ VO₂ ≥ 1 and Q/ VO₂ < 1, respectively) Q (62 +/- 29s) and VO₂ (60+/-21s) were significantly related (r=0.66, p= 0.001). There was a significant correlation between Q and TSImin in the slow Q responders (r_s= -0.57, p=0.005, n=22 (51%)) In conclusion, in moderately impaired CHF patients with relatively slow Q kinetics, central hemodynamics may limit skeletal muscle oxygenation during moderate-intensity exercise.

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Feed-forward and Reciprocal Inhibition for Gain and Phase Timing Control in a Computational Model of Repetitive Cough

We investigated the hypothesis, motivated in part by a coordinated computational cough network model, that second-order neurons in the nucleus tractus solitarius (NTS) act as a filter that shapes afferent input to the ventral respiratory network (VRC) during the production of cough. In vivo experiments were conducted on anesthetized spontaneously breathing cats. Cough was elicited by mechanical stimulation of the intrathoracic airways. Electromyograms of the parasternal (inspiratory) and rectus abdominis (expiratory) muscles and esophageal pressure were recorded. In vivo data revealed that expiratory motor drive during bouts of repetitive coughs is nonstationary: peak expulsive amplitude increases from the first cough, peaks about the eighth or ninth cough, and then decreases through the remainder of the bout. Model simulations indicated that feed-forward inhibition of a single second-order neuron population is not sufficient to account for all the dynamic features of a repetitive cough bout. When a single second-order population was split into two sub-populations (inspiratory and expiratory), the resultant model produced simulated expiratory motor bursts that were comparable to in vivo data. However, expiratory phase durations during these simulations of repetitive coughing were more stationary than those in vivo. Simulations in which reciprocal inhibitory processes between inspiratory-decrementing and expiratory-augmenting-late neurons were introduced exhibited nonstationary expiratory phase durations. These results support the prediction that serial and parallel processing of airway afferent signals in the NTS play a role in generation of the motor pattern for cough.

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