The control of respiratory pressures and neuromuscular activation to increase force production in trained martial arts practitioners.

PURPOSE: The mechanisms that explain the ability of trained martial arts practitioners to produce and resist greater forces than untrained individuals to aid combat performance are not fully understood. We investigated whether the greater ability of trained martial arts practitioners to produce and resist forces was associated with an enhanced control of respiratory pressures and neuromuscular activation of the respiratory, abdominal, and pelvic floor musculature. METHODS: Nine trained martial arts practitioners and nine untrained controls were instrumented with skin-surface electromyography (EMG) on the sternocleidomastoid, rectus abdominis, and the group formed by the transverse abdominal and internal oblique muscles (EMGtra/io). A multipair oesophageal EMG electrode catheter measured gastric (Pg), transdiaphragmatic (Pdi), and oesophageal (Pe) pressures and EMG of the crural diaphragm (EMGdi). Participants performed Standing Isometric Unilateral Chest Press (1) and Standing Posture Control (2) tasks. RESULTS: The trained group produced higher forces normalised to body mass2/3 (0.033 ± 0.01 vs. 0.025 ± 0.007 N/kg2/3 mean force in Task 1), lower Pe, and higher Pdi in both tasks. Additionally, they produced higher Pg (73 ± 42 vs. 49 ± 19 cmH2O mean Pg) and EMGtra/io in Task 1 and higher EMGdi in Task 2. The onset of Pg with respect to the onset of force production was earlier, and the relative contributions of Pg/Pe and Pdi/Pe were higher in the trained group in both tasks. CONCLUSION: Our findings demonstrate that trained martial arts practitioners utilised a greater contribution of abdominal and diaphragm musculature to chest wall recruitment and higher Pdi to produce and resist higher forces.

Comparable reductions in hyperpnoea-induced bronchoconstriction and markers of airway inflammation after supplementation with 6·2 and 3·1 g/d of long-chain n-3 PUFA in adults with asthma.

Although high dose n-3 PUFA supplementation reduces exercise- and hyperpnoea-induced bronchoconstriction (EIB/HIB), there are concurrent issues with cost, compliance and gastrointestinal discomfort. It is thus pertinent to establish the efficacy of lower n-3 PUFA doses. Eight male adults with asthma and HIB and eight controls without asthma were randomly supplemented with two n-3 PUFA doses (6·2 g/d (3·7 g EPA and 2·5 g DHA) and 3·1 g/d (1·8 g EPA and 1·3 g DHA)) and a placebo, each for 21 d followed by 14 d washout. A eucapnic voluntary hyperpnoea (EVH) challenge was performed before and after treatments. Outcome measures remained unchanged in the control group. In the HIB group, the peak fall in forced expiratory volume in 1 s (FEV1) after EVH at day 0 (-1005 (sd 520) ml, -30 (sd 18) %) was unchanged after placebo. The peak fall in FEV1 was similarly reduced from day 0 to day 21 of 6·2 g/d n-3 PUFA (-1000 (sd 460) ml, -29 (sd 17) % v. -690 (sd 460) ml, -20 (sd 15) %) and 3·1 g/d n-3 PUFA (-970 (sd 480) ml, -28 (sd 18) % v. -700 (sd 420) ml, -21 (sd 15) %) (P<0·001). Baseline fraction of exhaled nitric oxide was reduced by 24 % (P=0·020) and 31 % (P=0·018) after 6·2 and 3·1 g/d n-3 PUFA, respectively. Peak increases in 9α, 11ß PGF2 after EVH were reduced by 65 % (P=0·009) and 56 % (P=0·041) after 6·2 and 3·1 g/d n-3 PUFA, respectively. In conclusion, 3·1 g/d n-3 PUFA supplementation attenuated HIB and markers of airway inflammation to a similar extent as a higher dose. Lower doses of n-3 PUFA thus represent a potentially beneficial adjunct treatment for adults with asthma and EIB.

The effects of inspiratory muscle training in older adults.

PURPOSE: Declining inspiratory muscle function and structure and systemic low-level inflammation and oxidative stress may contribute to morbidity and mortality during normal ageing. Therefore, we examined the effects of inspiratory muscle training (IMT) in older adults on inspiratory muscle function and structure and systemic inflammation and oxidative stress, and reexamined the reported positive effects of IMT on respiratory muscle strength, inspiratory muscle endurance, spirometry, exercise performance, physical activity levels (PAL), and quality of life (QoL). METHODS: Thirty-four healthy older adults (68 ± 3 yr) with normal spirometry, respiratory muscle strength, and physical fitness were divided equally into a pressure-threshold IMT or sham-hypoxic placebo group. Before and after an 8-wk intervention, measurements were taken for dynamic inspiratory muscle function and inspiratory muscle endurance using a weighted plunger pressure-threshold loading device; diaphragm thickness by using B-mode ultrasonography; plasma cytokine concentrations by using immunoassays; DNA damage levels in peripheral blood mononuclear cells by using comet assays; spirometry, maximal mouth pressures, and exercise performance by using a 6-min walk test; PAL by using a questionnaire and accelerometry; and QoL using a questionnaire. RESULTS: Compared with placebo, IMT increased maximal inspiratory pressure (+34% ± 43%, P = 0.008), diaphragm thickness at residual volume (+38% ± 39%, P = 0.03), and peak inspiratory flow (+35% ± 42%, P = 0.049) but did not change other spirometry measures, plasma cytokine concentrations, DNA damage levels in peripheral blood mononuclear cells, dynamic inspiratory muscle function, inspiratory muscle endurance, exercise performance, PAL, or QoL. CONCLUSION: These novel data indicate that in healthy older adults, IMT elicits some positive changes in inspiratory muscle function and structure but neither attenuates systemic inflammation and oxidative stress nor improves exercise performance, PAL, or QoL.

Determinants of inspiratory muscle strength in healthy humans.

We investigated (1) the relationship between the baseline and inspiratory muscle training (IMT) induced increase in maximal inspiratory pressure (P(I,max)) and (2) the relative contributions of the inspiratory chest wall muscles and the diaphragm (P(oes)/P(di)) to P(I,max) prior to and following-IMT. Experiment 1: P(I,max) was assessed during a Müeller manoeuvre before and after 4-wk IMT (n=30). Experiment 2: P(I,max) and the relative contribution of the inspiratory chest wall muscles to the diaphragm (P(oes)/P(di)) were assessed during a Müeller manoeuvre before and after 4-wk IMT (n=20). Experiment 1: P(I,max) increased 19% (P<0.01) post-IMT and was correlated with baseline P(I,max) (r=-0.373, P<0.05). Experiment 2: baseline P(I,max) was correlated with P(oe)/P(di) (r=0.582, P<0.05) and after IMT PI,max increased 22% and Poe/Pdi increased 5% (P<0.05). In conclusion, baseline P(I,max) and the contribution of the chest wall inspiratory muscles relative to the diaphragm affect, in part, baseline and IMT-induced P(I,max). Great care should be taken when designing future IMT studies to ensure parity in the between-subject baseline P(I,max).

Influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training on the plasma cytokine response to maximum sustainable voluntary ventilation.

The influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training (IMT) on the cytokine response to maximum sustainable voluntary ventilation (MSVV) is unknown. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1 h of (1) passive rest and (2) MSVV, whereby participants undertook volitional hyperpnea at rest that mimicked the breathing and respiratory muscle recruitment patterns commensurate with heavy cycling exercise. Plasma cytokines remained unchanged during passive rest. There was a main effect of time (P < 0.01) for plasma interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) concentrations and a strong trend (P = 0.067) for plasma interleukin-1 receptor antagonist concentration during MSVV. Plasma IL-6 concentration was reduced after IMT by 27 ± 18% (main effect of intervention, P = 0.029), whereas there was no change after PLA (P = 0.753). There was no increase in a systemic marker of oxidative stress [DNA damage in peripheral blood mononuclear cells (PBMC)], and diaphragm fatigue was not related to the increases in plasma IL-1ß and IL-6 concentrations. A dose-response relationship was observed between respiratory muscle work and minute ventilation and increases in plasma IL-6 concentration. In conclusion, increases in plasma IL-1ß and IL-6 concentrations during MSVV were not due to diaphragm fatigue or DNA damage in PBMC. Increases in plasma IL-6 concentration during MSVV are attenuated following IMT, and the plasma IL-6 response is dependent upon the level of respiratory muscle work and minute ventilation.

The effects of inspiratory muscle training on plasma interleukin-6 concentration during cycling exercise and a volitional mimic of the exercise hyperpnea.

It is unknown whether the respiratory muscles contribute to exercise-induced increases in plasma interleukin-6 (IL-6) concentration, if this is related to diaphragm fatigue, and whether inspiratory muscle training (IMT) attenuates the plasma IL-6 response to whole body exercise and/or a volitional mimic of the exercise hyperpnea. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1 h of 1) passive rest, 2) cycling exercise at estimated maximal lactate steady state power (EX), and 3) volitional hyperpnea at rest, which mimicked the breathing and respiratory muscle recruitment patterns achieved during EX (HYPEX). Plasma IL-6 concentration remained unchanged during passive rest. The plasma IL-6 response to EX was reduced following IMT (main effect of intervention, P = 0.039) but not PLA (P = 0.272). Plasma IL-6 concentration increased during HYPEX (main effect of time, P < 0.01) and was unchanged postintervention. There was no evidence of diaphragm fatigue (measured by phrenic nerve stimulation) following each trial. In conclusion, plasma IL-6 concentration is increased during EX and HYPEX and this occurred in the absence of diaphragm fatigue. Furthermore, IMT reduced the plasma IL-6 response to EX but not HYPEX. These findings suggest that the respiratory muscles contribute to exercise-induced increases in plasma IL-6 concentration in the absence of diaphragm fatigue and that IMT can reduce the magnitude of the response to exercise but not a volitional mimic of the exercise hyperpnea.

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise.

We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac(-)](B)) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation ([Formula: see text]). Prior to the intervention, the MLSS [lac(-)](B) was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L(-1) in the IMT and control groups, respectively. During volitional hyperpnoea, [Formula: see text] increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min(-1) at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min(-1) in IMT and control groups, respectively; [lac(-)](B) concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L(-1) (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac(-)](B) during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (-28%) and phase II oxygen uptake (-31%) kinetics time constants at the onset of exercise and the MLSS [lac(-)](B) (-15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.

Inspiratory loading intensity does not influence lactate clearance during recovery.

PURPOSE: This study examined the effects of different pressure threshold inspiratory loads on lactate clearance and plasma acid-base balance during recovery from maximal exercise. METHODS: Eight moderately trained males (V˙O(2peak) = 4.29 ± 0.46 L·min⁻¹) performed, on different days, four maximal incremental cycling tests (power started at 0 W and increased by 20 W·min⁻¹) of identical duration (exercise time during the first trial was 16.32 ± 1.12 min). During 20-min recovery, subjects either rested passively or breathed through a constant pressure threshold inspiratory load of 10 (ITL10), 15 (ITL15), or 20 (ITL20) cm H2O. Plasma lactate concentration ([La⁻]) was measured, and acid-base balance was quantified using the physicochemical approach, which describes the dependency of [H⁺] on the three independent variables: strong ion difference ([Na⁺] + [K⁺] - [Cl⁻] + [La⁻]), the total concentration of weak acids, and the partial pressure of carbon dioxide. RESULTS: Peak exercise responses were not significantly different between trials. During recovery, the area under the plasma [La] curve was not different between trials (pooled mean = 261 ± 60 mEq) and the [La] measured at the end of the 20-min recovery was also similar (passive recovery = 9.2 ± 3.1 mEq·L⁻¹, ITL10 = 9.3 ± 3.1 mEq·L⁻¹, ITL15 = 8.7 ± 2.8 mEq·L⁻¹, ITL20 = 8.7 ± 3.2 mEq·L⁻¹). Similarly, changes in other strong ions contributing to strong ion difference and total concentration of weak acids, partial pressure of carbon dioxide, and, therefore, [H⁺] were not different between trials. CONCLUSIONS: These data suggest that, in individuals of moderate endurance training status, inspiratory loading at the intensities used in the present study does not accelerate lactate clearance or modify plasma acid-base balance during recovery from maximal exercise.

Loading of trained inspiratory muscles speeds lactate recovery kinetics.

PURPOSE: The purpose of this study was to investigate the effects of inspiratory threshold loading (ITL) and inspiratory muscle training (IMT) on blood lactate concentration ([lac(-)]B) and acid-base balance after maximal incremental cycling. METHODS: Eighteen subjects were divided into a control (n = 9) or an IMT group (n = 9). Before and after a 6-wk intervention, subjects completed two maximal incremental cycling tests followed by 20 min of recovery with (ITL) or without (passive recovery (PR)) a constant inspiratory resistance (15 cm H2O). The IMT group performed 6 wk of pressure threshold IMT at 50% maximal inspiratory mouth pressure. Throughout recovery, acid-base balance was quantified using the physicochemical approach by measuring the strong ion difference ([SID] = [Na+] + [K+] - [Cl-] + [lac-]), the total concentration of weak acids ([Atot-]), and the partial pressure of carbon dioxide (PCO2). RESULTS: After the intervention, maximal inspiratory mouth pressure increased in the IMT group only (+34%). No differences in lactate clearance were observed between PR and ITL before the intervention in both groups and after the intervention in the control group. After IMT, relative to PR, [lac-]B was reduced throughout ITL (minutes 2-20) by 0.66 +/- 1.28 mmol x L(-1) (P < 0.05), and both the fast (lactate exchange) and the slow (lactate clearance) velocity constants of the lactate recovery kinetics were increased (P < 0.05). Relative to pre-IMT, ITL reduced plasma [H], which was accounted for by an IMT-mediated increase in [SID] due almost exclusively to a 1.7-mmol x L(-1) reduction in [lac-]B. CONCLUSIONS: After maximal exercise, ITL affected lactate recovery kinetics only after IMT. Our data support the notion that the inspiratory muscles are capable of lactate clearance that increases [SID] and reduces [H+]. These effects may facilitate subsequent bouts of high-intensity exercise.

Inspiratory muscle training reduces blood lactate concentration during volitional hyperpnoea.

Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction. To investigate this, we tested the hypothesis that IMT would attenuate the increase in [lac(-)](B) caused by mimicking, at rest, the breathing pattern observed during high-intensity exercise. Twenty-two physically active males were matched for 85% maximal exercise minute ventilation (.V(E) max) and divided equally into an IMT or a control group. Prior to and following a 6 week intervention, participants performed 10 min of volitional hyperpnoea at the breathing pattern commensurate with 85% .V(E) max. The IMT group performed 6 weeks of pressure-threshold IMT; the control group performed no IMT. Maximal inspiratory mouth pressure increased (mean +/- SD) 31 +/- 22% following IMT and was unchanged in the control group. Prior to the intervention in the control group, [lac(-)](B) increased from 0.76 +/- 0.24 mmol L(-1) at rest to 1.50 +/- 0.60 mmol L(-1) (P < 0.05) following 10 min volitional hyperpnoea. In the IMT group, [lac(-)](B) increased from 0.85 +/- 0.40 mmol L(-1) at rest to 2.02 +/- 0.85 mmol L(-1) following 10 min volitional hyperpnoea (P < 0.05). After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05). In conclusion, increases in [lac(-)](B) during volitional hyperpnoea at 85% .V(E) max were attenuated following IMT. These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.