Voluntary activation of human knee extensors measured using transcranial magnetic stimulation

The aim of this study was to determine the applicability and reliability of a transcranial magnetic stimulation twitch interpolation technique for measuring voluntary activation of a lower limb muscle group. Cortical voluntary activation of the knee extensors was determined in nine healthy men on two separate visits by measuring superimposed twitch torques evoked by transcranial magnetic stimulation during isometric knee extensions of varying intensity. Superimposed twitch amplitude decreased linearly with increasing voluntary torque between 50 and 100% of mean maximal torque, allowing estimation of resting twitch amplitude and subsequent calculation of voluntary activation. There were no systematic differences for maximal voluntary activation within day (mean ± S.D. 90.9 ± 6.2 versus 90.7 ± 5.9%; P = 0.98) or between days (90.8 ± 6.0 versus 91.2 ± 5.7%; P = 0.92). Systematic bias and random error components of the 95% limits of agreement were 0.23 and 9.3% within day versus −0.38 and 7.5% between days. Voluntary activation was also determined immediately after a 2 min maximal voluntary isometric contraction; in four of these subjects, voluntary activation was determined 30 min after the sustained contraction. Immediately after the sustained isometric contraction, maximal voluntary activation was reduced from 91.2 ± 5.7 to 74.2 ± 12.0% (P < 0.001), indicating supraspinal fatigue. After 30 min, voluntary activation had recovered to 85.4 ± 8.8% (P = 0.39 versus baseline). These results demonstrate that transcranial magnetic stimulation enables reliable measurement of maximal voluntary activation and assessment of supraspinal fatigue of the knee extensors

Acute effects of inspiratory pressure threshold loading upon airway resistance in people with asthma

This is the post-print version of the final paper published in Respiratory Physiology & Neurobiology. The published article is available from the link below. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. Copyright @ 2009 Elsevier B.V.Large inspiratory pressures may impart stretch to airway smooth muscle and modify the response to deep inspiration (DI) in asthmatics. Respiratory system resistance (Rrs) was assessed in response to 5 inspiratory manoeuvres using the forced oscillation technique: (a) single unloaded DI; (b) single DI at 25 cmH2O; (c) single DI at 50% maximum inspiratory mouth pressure [MIP]; (d) 30 DIs at 50% MIP; and (e) 30 DIs at 50% MIP with maintenance of normocapnia. Rrs increased after the unloaded DI and the DI at 25 cmH2O but not after a DI at 50% MIP (3.6 ± 1.6 hPa L s−1 vs. 3.6 ± 1.5 hPa L s−1; p = 0.95), 30 DIs at 50% MIP (3.9 ± 1.5 hPa L s−1 vs. 4.2 ± 2.0 hPa L s−1; p = 0.16) or 30 DIs at 50% MIP under normocapnic conditions (3.9 ± 1.5 hPa L s−1 vs. 3.9 ± 1.5 hPa L s−1; p = 0.55). Increases in Rrs in response to DI were attenuated after single and multiple loaded breaths at 50% MIP

Influence of upper-body exercise on the fatigability of human respiratory muscles

PURPOSE: Diaphragm and abdominal muscles are susceptible to contractile fatigue in response to high-intensity, whole-body exercise. This study assessed whether the ventilatory and mechanical loads imposed by high-intensity, upper-body exercise would be sufficient to elicit respiratory muscle fatigue. METHODS: Seven healthy men (mean±SD: age 24±4 y; peak O2 uptake [V[Combining Dot Above]O2 peak] 31.9±5.3 ml/kg/min) performed asynchronous arm-crank exercise to exhaustion at work rates equivalent to 30% (heavy) and 60% (severe) of the difference between gas-exchange threshold and V[Combining Dot Above]O2 peak. Contractile fatigue of the diaphragm and abdominal muscles was assessed by measuring pre- to post-exercise changes in potentiated transdiaphragmatic and gastric twitch pressures (Pdi,tw and Pga,tw) evoked by supramaximal magnetic stimulation of the cervical and thoracic nerves, respectively. RESULTS: Exercise time was 24.5±5.8 min for heavy exercise and 9.8±1.8 min for severe exercise. Ventilation over the final minute of heavy exercise was 73±20 L/min (39±11% maximum voluntary ventilation [MVV]) and 99±19 L/min (53±11% MVV) for severe exercise. Mean Pdi,tw did not differ pre- to post-exercise at either intensity (p>0.05). Immediately (5-15 min) after severe exercise, mean Pga,tw was significantly lower than pre-exercise values (41±13 vs. 53±15 cmH2O, p<0.05), with the difference no longer significant after 25-35 min. Abdominal muscle fatigue (defined as ≥15% reduction in Pga,tw) occurred in 1/7 subjects after heavy exercise and 5/7 subjects after severe exercise. CONCLUSIONS: High-intensity, upper-body exercise elicits significant abdominal, but not diaphragm, muscle fatigue in healthy men. The increased magnitude and prevalence of fatigue during severe-intensity exercise is likely due to additional (non-respiratory) loading of the thorax.This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 American College of Sports Medicin

Excessive gas exchange impairment during exercise in a subject with a history of bronchopulmonary dysplasia and high altitude pulmonary edema

A 27-year-old male subject (V(O2 max)), 92% predicted) with a history of bronchopulmonary dysplasia (BPD) and a clinically documented case of high altitude pulmonary edema (HAPE) was examined at rest and during exercise. Pulmonary function testing revealed a normal forced vital capacity (FVC, 98.1% predicted) and diffusion capacity for carbon monoxide (D(L(CO)), 91.2% predicted), but significant airway obstruction at rest [forced expiratory volume in 1 sec (FEV(1)), 66.5% predicted; forced expiratory flow at 50% of vital capacity (FEF(50)), 34.3% predicted; and FEV(1) /FVC 56.5%] that was not reversible with an inhaled bronchodilator. Gas exchange worsened from rest to exercise, with the alveolar to arterial P(O2) difference (AaD(O2)) increasing from 0 at rest to 41 mmHg at maximal normoxic exercise (VO(2) = 41.4 mL/kg/min) and from 11 to 31 mmHg at maximal hypoxic exercise (VO(2) = 21.9 mL/kg/min). Arterial P(O2) decreased to 67.8 and 29.9 mmHg at maximal normoxic and hypoxic exercise, respectively. These data indicate that our subject with a history of BPD is prone to a greater degree of exercise-induced arterial hypoxemia for a given VO(2) and F(I(O2)) than healthy age-matched controls, which may increase the subject's susceptibility to high altitude illness

Effect of abdominal binding on respiratory mechanics during exercise in athletes with cervical spinal cord injury

West CR, Goosey-Tolfrey VL, Campbell IG, Romer LM. Effect of abdominal binding on respiratory mechanics during exercise in athletes with cervical spinal cord injury. J Appl Physiol 117: 36–45, 2014. First published May 22, 2014; doi:10.1152/japplphysiol.00218.2014.—We asked whether elastic binding of the abdomen influences respiratory mechanics during wheelchair propulsion in athletes with cervical spinal cord injury (SCI). Eight Paralympic wheelchair rugby players with motor-complete SCI (C5-C7) performed submaximal and maximal incremental exercise tests on a treadmill, both with and without abdominal binding. Measurements included pulmonary function, pressure-derived indices of respiratory mechanics, operating lung volumes, tidal flow-volume data, gas exchange, blood lactate, and symptoms. Residual volume and functional residual capacity were reduced with binding (77 18 and 81 11% of unbound, P 0.05), vital capacity was increased (114 9%, P 0.05), whereas total lung capacity was relatively well preserved (99 5%). During exercise, binding introduced a passive increase in transdiaphragmatic pressure, due primarily to an increase in gastric pressure. Active pressures during inspiration were similar across conditions. A sudden, sustained rise in operating lung volumes was evident in the unbound condition, and these volumes were shifted downward with binding. Expiratory flow limitation did not occur in any subject and there was substantial reserve to increase flow and volume in both conditions. V ˙ O2 was elevated with binding during the final stages of exercise (8 –12%, P 0.05), whereas blood lactate concentration was reduced (16 –19%, P 0.05). V ˙ O2/heart rate slopes were less steep with binding (62 35 vs. 47 24 ml/beat, P 0.05). Ventilation, symptoms, and work rates were similar across conditions. The results suggest that abdominal binding shifts tidal breathing to lower lung volumes without influencing flow limitation, symptoms, or exercise tolerance. Changes in respiratory mechanics with binding may benefit O2 transport capacity by an improvement in central circulatory function.This article has been made available through the Brunel Open Access Publishing Fund

No effect of arm exercise on diaphragmatic fatigue or ventilatory constraint in Paralympic athletes with cervical spinal cord injury

Cervical spinal cord injury (CSCI) results in a decrease in the capacity of the lungs and chest wall for pressure, volume, and airflow generation. We asked whether such impairments might increase the potential for exercise-induced diaphragmatic fatigue and mechanical ventilatory constraint in this population. Seven Paralympic wheelchair rugby players (mean ± SD peak oxygen uptake = 16.9 ± 4.9 ml·kg–1·min–1) with traumatic CSCI (C5–C7) performed arm-crank exercise to the limit of tolerance at 90% of their predetermined peak work rate. Diaphragm function was assessed before and 15 and 30 min after exercise by measuring the twitch transdiaphragmatic pressure (Pdi,tw) response to bilateral anterolateral magnetic stimulation of the phrenic nerves. Ventilatory constraint was assessed by measuring the tidal flow volume responses to exercise in relation to the maximal flow volume envelope. Pdi,tw was not different from baseline at any time after exercise (unpotentiated Pdi,tw = 19.3 ± 5.6 cmH2O at baseline, 19.8 ± 5.0 cmH2O at 15 min after exercise, and 19.4 ± 5.7 cmH2O at 30 min after exercise; P = 0.16). During exercise, there was a sudden, sustained rise in operating lung volumes and an eightfold increase in the work of breathing. However, only two subjects showed expiratory flow limitation, and there was substantial capacity to increase both flow and volume (<50% of maximal breathing reserve). In conclusion, highly trained athletes with CSCI do not develop exercise-induced diaphragmatic fatigue and rarely reach mechanical ventilatory constraint

Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men (n = 19; maximal aerobic capacity = 64.0 ± 1.9 ml·kg–1·min–1) and women (n = 19; maximal aerobic capacity = 57.1 ± 1.5 ml·kg–1·min–1). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a 15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men (n = 11) was 30.6 ± 2.3, 20.7 ± 3.2, and 13.3 ± 4.5%, respectively, whereas results in women (n = 8) were 21.0 ± 2.1, 11.6 ± 2.9, and 9.7 ± 4.2%, respectively, with sex differences occurring at 10 and 30 min (P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts

Exercise-induced diaphragm fatigue in a Paralympic champion rower with spinal cord injury

Introduction. The aim of this case report was to determine whether maximal upper-body exercise was sufficient to induce diaphragm fatigue in a Paralympic champion adaptive rower with low-lesion spinal cord injury (SCI). Case Presentation. An elite arms-only oarsman (age 28 y, stature 1.89 m, mass 90.4 kg) with motor-complete SCI (T12) performed a 1000 m time-trial on an adapted rowing ergometer. Exercise measurements comprised pulmonary ventilation and gas exchange, diaphragm EMG-derived indices of neural respiratory drive and intrathoracic pressure-derived indices of respiratory mechanics. Diaphragm fatigue was assessed by measuring pre- to post-exercise changes in the twitch transdiaphragmatic pressure (Pdi,tw) response to anterolateral magnetic stimulation of the phrenic nerves. The time-trial (248 ± 25 W, 3.9 min) elicited a peak O2 uptake of 3.46 L·min−1 and a peak pulmonary ventilation of 150 L·min−1 (57% MVV). Breath-to-stroke ratio was 1:1 during the initial 400 m and 2:1 thereafter. The ratio of inspiratory transdiaphragmatic pressure to diaphragm EMG (neuromuscular efficiency) fell from rest to 600 m (16.0 vs. 3.0). Potentiated Pdi,tw was substantially reduced (−33%) at 15-20 min post-exercise, with only partial recovery (−12%) at 30-35 min. Conclusions. This is the first report of exercise-induced diaphragm fatigue in SCI. The decrease in diaphragm neuromuscular efficiency during exercise suggests that the fatigue was partly due to factors independent of ventilation (e.g., posture and locomotion)

Supraspinal fatigue after normoxic and hypoxic exercise in humans.

Inadequate cerebral O₂ availability has been proposed to be an important contributing factor to the development of central fatigue during strenuous exercise. Here we tested the hypothesis that supraspinal processes of fatigue would be increased after locomotor exercise in acute hypoxia compared to normoxia, and that such change would be related to reductions in cerebral O₂ delivery and tissue oxygenation. Nine endurance-trained cyclists completed three constant-load cycling exercise trials at ∼80% of maximal work rate: (1) to the limit of tolerance in acute hypoxia; (2) for the same duration but in normoxia (control); and (3) to the limit of tolerance in normoxia. Throughout each trial, prefrontal cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assessed using near-infrared spectroscopy and trans-cranial Doppler sonography, respectively. Cerebral O₂ delivery was calculated as the product of arterial O₂ content and MCAV. Before and immediately after each trial, twitch responses to supramaximal femoral nerve stimulation and transcranial magnetic stimulation were obtained to assess neuromuscular and cortical function, respectively. Exercise time was reduced by 54%in hypoxia compared to normoxia (3.6 ± 1.3 vs. 8.1 ± 2.9 min; P0.05). Cortical voluntary activation was also decreased after exercise in all trials, but the decline in hypoxia (Δ18%) was greater than in the normoxic trials (Δ5-9%)(P <0.05). The reductions in cortical voluntary activation were paralleled by reductions in cerebral O₂ delivery. The results suggest that curtailment of exercise performance in acute severe hypoxia is due, in part, to failure of drive from the motor cortex, possibly as a consequence of diminished O₂ availability in the brain