Biomedical subjects

Alison K McConnell

Publications and source records attributed to Alison K McConnell.

13 recordsLinked to original sources

PubMed2006

The influence of inspiratory and expiratory muscle training upon rowing performance.

We investigated the effect of 4 week of inspiratory (IMT) or expiratory muscle training (EMT), as well as the effect of a subsequent 6 week period of combined IMT/EMT on rowing performance in club-level oarsmen. Seventeen male rowers were allocated to either an IMT (n = 10) or EMT (n = 7) group. The groups underwent a 4 week IMT or EMT program; after interim testing, both groups subsequently performed a 6 week program of combined IMT/EMT. Exercise performance and physiological responses to exercise were measured at 4 and 10 week during an incremental rowing ergometer 'step-test' and a 6 min all-out (6MAO) effort. Pressure threshold respiratory muscle training was undertaken at the 30 repetition maximum load (approximately 50% of the peak inspiratory and expiratory mouth pressure, P (Imax) or P (Emax), respectively). P (Imax) increased during the IMT phase of the training in the IMT group (26%, P < 0.001) and was accompanied by an improvement in mean power during the 6MAO (2.7%, P = 0.015). Despite an increase in P (Emax) by the end of the intervention (31%, P = 0.03), the EMT group showed no significant changes in any performance parameters during either the 'step-test' or 6MAO. There were no significant changes in breathing pattern or the metabolic response to the 6MAO test in either group, but the IMT group showed a small decrease in HR (2-5%, P = 0.001). We conclude that there were no significant additional changes following combined IMT/EMT. IMT improved rowing performance, but EMT and subsequent combined IMT/EMT did not.

Adult↗

PubMed2006

The influence of inspiratory muscle work history and specific inspiratory muscle training upon human limb muscle fatigue.

The purpose of this study was to assess the influence of the work history of the inspiratory muscles upon the fatigue characteristics of the plantar flexors (PF). We hypothesized that under conditions where the inspiratory muscle metaboreflex has been elicited, PF fatigue would be hastened due to peripheral vasoconstriction. Eight volunteers undertook seven test conditions, two of which followed 4 week of inspiratory muscle training (IMT). The inspiratory metaboreflex was induced by inspiring against a calibrated flow resistor. We measured torque and EMG during isometric PF exercise at 85% of maximal voluntary contraction (MVC) torque. Supramaximal twitches were superimposed upon MVC efforts at 1 min intervals (MVC(TI)); twitch interpolation assessed the level of central activation. PF was terminated (T(lim)) when MVC(TI) was <50% of baseline MVC. PF T(lim) was significantly shorter than control (9.93 +/- 1.95 min) in the presence of a leg cuff inflated to 140 mmHg (4.89 +/- 1.78 min; P = 0.006), as well as when PF was preceded immediately by fatiguing inspiratory muscle work (6.28 +/- 2.24 min; P = 0.009). Resting the inspiratory muscles for 30 min restored the PF T(lim) to control. After 4 weeks, IMT, inspiratory muscle work at the same absolute intensity did not influence PF T(lim), but T(lim) was significantly shorter at the same relative intensity. The data are the first to provide evidence that the inspiratory muscle metaboreflex accelerates the rate of calf fatigue during PF, and that IMT attenuates this effect.

Adaptation, Physiological↗

PubMed2006

Diaphragm and intercostal surface EMG and muscle performance after acute inspiratory muscle loading.

We examined the effect of an acute bout of submaximal non-fatiguing inspiratory loading (IL) on maximal inspiratory pressure (MIP), and on the activation of the diaphragm (DI) and intercostals (IC) using surface electromyography (sEMG). After baseline measurements, 12 healthy subjects performed two sets of 30 inspiratory efforts at a load equivalent to 40% of their initial MIP. MIP and maximal DI and IC sEMG activity were recorded after the first and second set of IL, and 15 min after task cessation. After IL, MIP reached (+/-S.E.M.) 111+/-4% (P=0.032) of baseline values, and during MIP, DI and IC root mean square (RMS) sEMG amplitude increased significantly above baseline (143+/-21%, P=0.039 and 137+/-33%, P=0.016, respectively). The significant increase in MIP and RMS amplitude after IL suggests that MIP efforts were initially submaximal, and that prior loading enabled full activation. The changes in DI and IC RMS amplitude may also reflect an improvement in the synergy between them during these maximal efforts.

Adult↗

PubMed2006

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise.

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac-]B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207+/-8 W, mean +/- SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20-28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3+/-2.4 and 168.3+/-7.0 l min(-1) (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9+/-6.8 l min(-1)), 3.46+/-0.20 and 3.83 +/- 0.20 l min(-1) (P<0.01), and 158.5+/-2.7 and 166.8+/-2.7 beats min(-1) (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac-]B increased from 3.7+/-0.2 to 4.7+/-0.3 mmol l(-1) (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac-]B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac-]B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.

Adult↗

PubMed2005

The role of inspiratory muscle function and training in the genesis of dyspnoea in asthma and COPD.

The cardinal symptom of both asthma and COPD is dyspnoea, and from a patient perspective, the most troublesome. There are a multitude of inputs to the sensation of dyspnoea, few of which are readily modifiable. The level of inspiratory muscle work contributes to the sense of respiratory muscle effort and thence dyspnoea. Inspiratory muscle work is elevated in patients with COPD and asthma due to hyperinflation and an increased ventilatory requirement for exercise. Treatment tends to concentrate on reducing the load upon the inspiratory muscles induced by hyperinflation. Bronchodilators are the mainstay of treatment for COPD and asthma; they reduce hyperinflation, inspiratory muscle loading and dyspnoea. In addition, programmes of pulmonary rehabilitation have an excellent evidence base for improving dyspnoea, exercise tolerance and quality of life. However, provision within the NHS is limited and not all patients are suitable. One component of pulmonary rehabilitation that can be implemented safely in a home-based setting is specific inspiratory muscle training (IMT). There is a strong theoretical rationale for IMT in patients with airway obstruction, which is also supported by empirical evidence. IMT offers a relatively accessible non-pharmacological treatment for dyspnoea that also improves exercise tolerance and quality of life.

Journal Article↗

PubMed2005

The effect of inspiratory muscle training upon maximum lactate steady-state and blood lactate concentration.

Several studies have reported that improvements in endurance performance following respiratory muscle training (RMT) are associated with a decrease in blood lactate concentration ([Lac](B)). The present study examined whether pressure threshold inspiratory muscle training (IMT) elicits an increase in the cycling power output corresponding to the maximum lactate steady state (MLSS). Using a double-blind, placebo-controlled design, 12 healthy, non-endurance-trained male participants were assigned in equal numbers to an experimental (IMT) or sham training control (placebo) group. Cycling power output at MLSS was initially identified using a lactate minimum protocol followed by a series of constant power output rides (2.5% increments) of 29.5 min duration; MLSS was reassessed following six weeks of IMT or sham IMT. Maximum inspiratory mouth pressure increased significantly (26%) in the IMT group, but remained unchanged in the placebo group. The cycling power output corresponding to MLSS remained unchanged in both groups after the intervention. After IMT, [Lac](B) decreased significantly at MLSS power in the IMT group [-1.17 (1.01) mmol l(-1) after 29.5 min of cycling; mean (SD)], but remained unchanged in the placebo group [+0.37 (1.66) mmol l(-1)]. These data support previous observations that IMT results in a decrease in [Lac](B )at a given intensity of exercise. That such a decrease in [Lac](B) was not associated with a substantial (>2.5%) increase in MLSS power is a new finding suggesting that RMT-induced increases in exercise tolerance and reductions in [Lac](B) are not ascribable to a substantial increase in the 'lactate threshold'.

Adult↗

PubMed2004

Dyspnoea in health and obstructive pulmonary disease : the role of respiratory muscle function and training.

A consistent finding of recent research on respiratory muscle training (RMT) in healthy humans has been an attenuation of respiratory discomfort (dyspnoea) during exercise. We argue that the neurophysiology of dyspnoea can be explained in terms of Cambell's paradigm of length-tension inappropriateness. In the context of this paradigm, changes in the contractile properties of the respiratory muscles modify the intensity of dyspnoea predominantly by changing the required level of motor outflow to these respiratory muscles. Thus, factors that impair the contractile properties of the respiratory muscles (e.g. the pattern of tension development, functional weakening and fatigue) have the potential to increase the intensity of dyspnoea, while factors that improve the contractile properties of these respiratory muscles (e.g. RMT) have the potential to reduce the intensity of dyspnoea. In patients with obstructive pulmonary disease, functional weakening of the inspiratory muscles in response to dynamic lung hyperinflation appears to be a central component of dyspnoea. A decrease in the intensity of respiratory effort sensation (during exercise and loaded breathing) has been observed in both healthy individuals and patients with obstructive pulmonary disease after RMT. We conclude that RMT has the potential to reduce the severity of dyspnoea in healthy individuals and in patients with obstructive pulmonary disease, and that this probably occurs via a reduction in the level of motor outflow. Further work is required to clarify the role of RMT in the management of other disease conditions in which the function of the respiratory muscles is impaired, or the loads that they must overcome are elevated (e.g. cardiorespiratory and neuromuscular disorders).

Asthma↗

PubMed2003

Influence of environmental temperature on exercise-induced inspiratory muscle fatigue.

Exercise in the heat has detrimental effects on circulation that might negatively influence endurance performance. If blood is diverted away from the inspiratory muscles to the skin during exercise in the heat, exercise-induced inspiratory muscle fatigue might be exacerbated. Thus, we hypothesised that prolonged heavy endurance exercise in the heat would impair exercise performance and exacerbate inspiratory muscle fatigue compared to exercise in a thermo-neutral environment. Using a crossover design, seven male endurance trained subjects [mean (SEM) maximum oxygen uptake = 62.2 (1.5) ml x kg(-1) x min(-1)] were assigned at random to either a group that exercised in the heat at an ambient temperature of 35 degrees C (H) or a group that exercised in the cool at 15 degrees C (C). Maximum inspiratory mouth pressure at zero flow (P(0)), pressure normalised maximum relaxation rate (MRR/ P(0)), time constant for the pressure decay (tau), and maximum inspiratory flow at 30% P(0) (V(30)) were assessed immediately before and reassessed within 2, 30, and 60 min of completing a pre-loaded time trial [40 min at 65% peak power, plus approximately 30 min time trial] on a cycle ergometer. Group H completed the time trial 432 (135) s slower than group C [2285 (180) vs 1852 (122) s, respectively; Delta=24 (8)%, P=0.0094]. Repeat measurements within 2 min post-exercise revealed significant declines in P(0), MRR/ P(0), tau, and V(30) from baseline values, but no between-group differences were observed. In conclusion, heavy sustained exercise in the heat impaired subsequent time-trial performance but did not exacerbate inspiratory muscle fatigue in endurance-trained subjects.

Adult↗

PubMed2003

Inter-test reliability for non-invasive measures of respiratory muscle function in healthy humans.

The aims of this study were to quantify the inter-test reliability of several voluntary, non-invasive measures of respiratory muscle function and to determine the implications of these data for studies using a repeated-measures design. Systematic measurement differences were found for 50% of the variables ( P</=0.05, t-tests). Nevertheless, 95% ratio limits of agreement for most measures proved acceptable and similar to those reported elsewhere. The random error component of the agreement ratios ranged from 1.047 to 1.149 for measures of pulmonary function in healthy subjects ( n=46), 1.045 to 1.056 for maximum static respiratory pressures ( n=24), 1.062 to 1.173 for measures relating to the maximum pressure-flow-power relationship ( n=16-22), and 1.036 to 1.071 for measures relating to maximum incremental inspiratory muscle performance ( n=12). The judgement that the limits of agreement were acceptable is supported by the sample-size calculations. Estimated sample sizes based upon an alpha level of 0.05 and a statistical power of 0.9 were mostly </=11 for a repeated-measures experimental design, particularly for the larger effect sizes (>/=5%). However, peak expiratory flow, the maximum rate of pressure development and the time constant of relaxation, require larger sample sizes to detect small within-group changes. In conclusion, the described protocols provide reliable measurements for most parameters of respiratory muscle function in healthy subjects. Furthermore, experiments utilising a within-subjects design lasting up to 3 weeks can be conducted with feasible sample sizes (</=11 per group) where substantial (>/=5%) changes are expected.

Adult↗

PubMed2003

Inspiratory muscle fatigue in swimmers after a single 200 m swim.

Inspiratory muscle fatigue may occur in as little as 6 min during high-intensity spontaneously breathing exercise. The aims of this study were to determine whether inspiratory muscle fatigue occurs during swimming exercise and whether inspiratory muscle strength differs between the supine and standing body positions. Seven competitive swimmers were recruited to perform a single 200 m front-crawl swim, corresponding to 90-95% of race pace. Inspiratory muscle strength was measured at residual volume using a hand-held mouth pressure meter that measured maximal inspiratory pressure in the upright and supine positions. At baseline, maximal inspiratory pressure in the supine position was significantly lower than maximal inspiratory pressure in the upright position (112 +/- 20.4 and 133 +/- 16.7 cmH2O, respectively; P < or = 0.01). Post-exercise maximal inspiratory pressure in the supine position (80 +/- 15.7 cmH2O) was significantly lower than baseline maximal inspiratory pressure in the supine position (P < or = 0.01). The results indicate that a single 200 m front-crawl swim corresponding to 90-95% of race pace was sufficient to induce inspiratory muscle fatigue in less than 2.7 min. Furthermore, although diaphragm muscle length is optimized when supine, our results indicate that the force output of the diaphragm and inspiratory accessory muscles is greater when upright than when supine.

Adult↗

PubMed2003

Specificity and reversibility of inspiratory muscle training.

PURPOSE: The purpose of this study was to evaluate the pressure-flow specificity of adaptations to inspiratory muscle training (IMT), in addition to the temporal effects of detraining and reduced frequency of training upon these adaptations. METHODS: Twenty-four healthy subjects were assigned randomly to one of four groups (A: low-flow-high-pressure IMT; B: high-flow-low-pressure IMT; C: intermediate flow-pressure IMT; and D: no IMT). Subjects performed IMT 6 d.wk(-1) for 9 wk, and inspiratory muscle function was evaluated at baseline and every 3 wk. Groups A, B, and C were then assigned randomly to either a maintenance group (M) (IMT 2 d.wk(-1) ) or a detraining group (DT) (no IMT). Inspiratory muscle function was reassessed at 9 and 18 wk post-IMT. RESULTS: At 9 wk, group A exhibited the largest increase in pressure, B a large increase in flow, C more uniform increases in pressure and flow, and D no changes in pressure or flow. Maximum inspiratory muscle power increased in groups A, B, and C by 48 +/- 3%, 25 +/- 3%, and 64 +/- 3%, respectively (mean +/- SEM, P < or = 0.01). Maximum rate of pressure development increased in groups A, B, and C by 59 +/- 1%, 10 +/- 1%, and 29 +/- 1%, respectively ( P < or = 0.01). A decrease in inspiratory muscle function was observed at 9 wk post-IMT in DT. Inspiratory muscle function plateaued between 9 and 18 wk but remained above pre-IMT values. Group M retained the improvements in inspiratory muscle function. CONCLUSION: These data support the notion of pressure-flow specificity of IMT. Detraining resulted in small but significant reductions in inspiratory muscle function. Reducing training frequency by two thirds allowed for the maintenance of inspiratory muscle function up to 18 wk post-IMT.

Adult↗

PubMed2002

Effects of inspiratory muscle training on time-trial performance in trained cyclists.

We evaluated the effects of specific inspiratory muscle training on simulated time-trial performance in trained cyclists. Using a double-blind, placebo-controlled design, 16 male cyclists (VO2max = 64 +/- 2 ml x kg(-1) x min(-1); mean +/- s(x)) were assigned at random to either an experimental (pressure-threshold inspiratory muscle training) or sham-training control (placebo) group. Pulmonary function, maximum dynamic inspiratory muscle function and the physiological and perceptual responses to maximal incremental cycling were assessed. Simulated time-trial performance (20 and 40 km) was quantified as the time to complete pre-set amounts of work. Pulmonary function was unchanged after the intervention, but dynamic inspiratory muscle function improved in the inspiratory muscle training group (P < or = 0.05). After the intervention, the inspiratory muscle training group experienced a reduction in the perception of respiratory and peripheral effort (Borg CR10: 16 +/- 4% and 18 +/- 4% respectively; compared with placebo, P < or = 0.01) and completed the simulated 20 and 40 km time-trials faster than the placebo group [66 +/- 30 and 115 +/- 38 s (3.8 +/- 1.7% and 4.6 +/- 1.9%) faster respectively; P = 0.025 and 0.009]. These results support evidence that specific inspiratory muscle training attenuates the perceptual response to maximal incremental exercise. Furthermore, they provide evidence of performance enhancements in competitive cyclists after inspiratory muscle training.

Adult↗

PubMed2002

Inspiratory muscle fatigue in trained cyclists: effects of inspiratory muscle training.

PURPOSE: This study evaluated the influence of simulated 20- and 40-km time trials upon postexercise inspiratory muscle function of trained competitive cyclists. In addition, we examined the influence of specific inspiratory muscle training (IMT) upon the responses observed. METHODS: Using a double-blind placebo-controlled design, 16 male cyclists (mean +/- SEM VO2max 64 +/- 2 mL.kg-1.min-1) were assigned randomly to either an experimental (IMT) or sham-training control (placebo) group. Maximum static and dynamic inspiratory muscle function was assessed immediately pre- and <2, 10, and 30 min post-simulated 20- and 40-km time trials before and after 6-wk of IMT or sham-IMT. RESULTS: Maximum inspiratory mouth pressure (P0) measured within 2 min of completing the 20- and 40-km time trial rides was reduced by 18% and 13%, respectively, and remained below preexercise values at 30 min. The 20- and 40-km time trials induced a reduction in inspiratory flow rate at 30% P0 by 14% and 6% in the IMT group versus 13% and 7% for the placebo group, and also remained below preexercise values at 30 min. There was also a significant slowing of inspiratory muscle relaxation rate postexercise; these trends were almost completely reversed by 30 min postexercise. Significant improvements in 20- and 40-km time trial performance were seen (3.8 +/- 1.7% and 4.6 +/- 1.9%, respectively; P < 0.05) and postexercise reductions in muscle function were attenuated with IMT. CONCLUSION: These data support existing evidence that there is significant global inspiratory muscle fatigue after sustained heavy endurance exercise. Furthermore, the present study provides new evidence that performance enhancements observed after IMT are accompanied by a decrease in inspiratory muscle fatigue.

Adult↗