Functional training of the inspiratory muscles improves load carriage performance.

Inspiratory Muscle Training (IMT) whilst adopting body positions that mimic exercise (functional IMT; IMTF) improves running performance above traditional IMT methods in unloaded exercise. We investigated the effect of IMTF during load carriage tasks. Seventeen males completed 60 min walking at 6.5 km·h-1 followed by a 2.4 km load carriage time-trial (LCTT) whilst wearing a 25 kg backpack. Trials were completed at baseline; post 4 weeks IMT (consisting of 30 breaths twice daily at 50% of maximum inspiratory pressure) and again following either 4 weeks IMTF (comprising four inspiratory loaded core exercises) or maintenance IMT (IMTCON). Baseline LCTT was 15.93 ± 2.30 min and was reduced to 14.73 ± 2.40 min (mean reduction 1.19 ± 0.83 min, p < 0.01) after IMT. Following phase two, LCTT increased in IMTF only (13.59 ± 2.33 min, p < 0.05) and was unchanged in post-IMTCON. Performance was increased following IMTF, providing an additional ergogenic effect beyond IMT alone. Practitioner Summary: We confirmed the ergogenic benefit of Inspiratory Muscle Training (IMT) upon load carriage performance. Furthermore, we demonstrate that functional IMT methods provide a greater performance benefit during exercise with thoracic loads. Abbreviations: [Lac-]B: blood lactate; FEV1: forced expiratory volume in one second; FEV1/FVC: forced expiratory volume in one second/forced vital capacity ratio; FVC: forced vital capacity; HR: heart rate; IMT: inspiratory muscle training; IMTCON: inspiratory muscle training maintenance; IMTF: functional inspiratory muscle training; LC: load carriage; LCTT: load carriage time trial; Pdi: transdiaphragmatic pressure; PEF: peak expiratory flow; PEmax: maximum expiratory mouth pressure; PImax: maximum inspiratory mouth pressure; RPE: rating of perceived exertion; RPEbreating: rating of perceived exertion for the breathing; RPEleg: rating of perceived exertion for the legs; SEPT: sport-specific endurance plank test; V̇ O2: oxygen consumption; V̇ O2peak: peak oxygen consumption.

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).

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.

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.