Graham R. Sharpe

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.

Investigations of the Lactate Minimum Test

We evaluated: the agreement between lactate minimum and maximal lactate steady state (MLSS) cycling powers (study 1); whether rates of change of blood lactate concentration during the lactate minimum test reflect that of constant power exercise (study 2); whether the lactate minimum power is influenced by the muscle groups used to elevate blood lactate concentration (study 3). Study 1: 32 subjects performed a lactate minimum test comprising a lactate elevation phase, recovery phase, and incremental phase (five 4 min stages); MLSS was subsequently determined. Study 2: 8 subjects performed a lactate minimum test and five 22 min constant power tests at the incremental phase exercise intensities. Study 3: 10 subjects performed two identical lactate minimum tests, except during the second test the lactate elevation phase comprised arm-cranking. Lactate minimum and MLSS powers demonstrated good agreement (mean bias+/-95% limits of agreement: 2+/-22 W). Rates of change of blood lactate concentration during each incremental phase stage and corresponding constant power test did not correlate. Lactate minimum power was lowered when arm-cranking was used during the lactate elevation phase (157+/-29 vs. 168+/-21 W; p<0.05). The lactate elevation phase modifies blood lactate concentration responses during the incremental phase, thus good agreement between lactate minimum and MLSS powers seems fortuitous.

Locomotor muscle fatigue is not critically regulated after prior upper body exercise

This study examined the effects of prior upper body exercise on subsequent high-intensity cycling exercise tolerance and associated changes in neuromuscular function and perceptual responses. Eight men performed three fixed work-rate (85% peak power) cycling tests: 1) to the limit of tolerance (CYC); 2) to the limit of tolerance after prior high-intensity arm-cranking exercise (ARM-CYC); and 3) without prior exercise and for an equal duration as ARM-CYC (ISOTIME). Peripheral fatigue was assessed via changes in potentiated quadriceps twitch force during supramaximal electrical femoral nerve stimulation. Voluntary activation was assessed using twitch interpolation during maximal voluntary contractions. Cycling time during ARM-CYC and ISOTIME (4.33 ± 1.10 min) was 38% shorter than during CYC (7.46 ± 2.79 min) (P < 0.001). Twitch force decreased more after CYC (-38 ± 13%) than ARM-CYC (-26 ± 10%) (P = 0.004) and ISOTIME (-24 ± 10%) (P = 0.003). Voluntary activation was 94 ± 5% at rest and decreased after CYC (89 ± 9%, P = 0.012) and ARM-CYC (91 ± 8%, P = 0.047). Rating of perceived exertion for limb discomfort increased more quickly during cycling in ARM-CYC [1.83 ± 0.46 arbitrary units (AU)/min] than CYC (1.10 ± 0.38 AU/min, P = 0.003) and ISOTIME (1.05 ± 0.43 AU/min, P = 0.002), and this was correlated with the reduced cycling time in ARM-CYC (r = -0.72, P = 0.045). In conclusion, cycling exercise tolerance after prior upper body exercise is potentially mediated by central fatigue and intolerable levels of sensory perception rather than a critical peripheral fatigue limit.

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 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.

Effects of Protocol Design on Lactate Minimum Power

The aim of this investigation was to use a validated lactate minimum test protocol and evaluate whether blood lactate responses and the lactate minimum power are influenced by the starting power (study 1) and 1 min inter-stage rest intervals (study 2) during the incremental phase. Study 1: 8 subjects performed a lactate minimum test comprising a lactate elevation phase, recovery phase, and incremental phase comprising 5 continuous 4 min stages with starting power being 40% or 45% of the maximum power achieved during the lactate elevation phase, and with power increments of 5% maximum power. Study 2: 8 subjects performed 2 identical lactate minimum tests except that during one of the tests the incremental phase included 1 min inter-stage rest intervals. The lactate minimum power was lower when the incremental phase commenced at 40% (175±29 W) compared to 45% (184±30 W) maximum power (p<0.01), and was increased when 1 min inter-stage rest intervals were included during the incremental phase (192±25 vs. 200±26 W, p<0.01). In conclusion, changes in lactate minimum power were small and thus unlikely to compromise test validity and therefore training status evaluation and exercise prescription.

A prebiotic galactooligosaccharide mixture reduces severity of hyperpnoea-induced bronchoconstriction and markers of airway inflammation

Gut microbes have a substantial influence on systemic immune function and allergic sensitisation. Manipulation of the gut microbiome through prebiotics may provide a potential strategy to influence the immunopathology of asthma. This study investigated the effects of prebiotic Bimuno-galactooligosaccharide (B-GOS) supplementation on hyperpnoea-induced bronchoconstriction (HIB), a surrogate for exercise-induced bronchoconstriction, and airway inflammation. A total of ten adults with asthma and HIB and eight controls without asthma were randomised to receive 5·5 g/d of either B-GOS or placebo for 3 weeks separated by a 2-week washout period. The peak fall in forced expiratory volume in 1 s (FEV1) following eucapnic voluntary hyperpnoea (EVH) defined HIB severity. Markers of airway inflammation were measured at baseline and after EVH. Pulmonary function remained unchanged in the control group. In the HIB group, the peak post-EVH fall in FEV1 at day 0 (-880 (sd 480) ml) was unchanged after placebo, but was attenuated by 40 % (-940 (sd 460) v. -570 (sd 310) ml, P=0·004) after B-GOS. In the HIB group, B-GOS reduced baseline chemokine CC ligand 17 (399 (sd 140) v. 323 (sd 144) pg/ml, P=0·005) and TNF-α (2·68 (sd 0·98) v. 2·18 (sd 0·59) pg/ml, P=0·040) and abolished the EVH-induced 29 % increase in TNF-α. Baseline C-reactive protein was reduced following B-GOS in HIB (2·46 (sd 1·14) v. 1·44 (sd 0·41) mg/l, P=0·015) and control (2·16 (sd 1·02) v. 1·47 (sd 0·33) mg/l, P=0·050) groups. Chemokine CC ligand 11 and fraction of exhaled nitric oxide remained unchanged. B-GOS supplementation attenuated airway hyper-responsiveness with concomitant reductions in markers of airway inflammation associated with HIB.

Reproducibility of the bronchoconstrictive response to eucapnic voluntary hyperpnoea

BACKGROUND Eucapnic voluntary hyperpnoea (EVH) is considered an effective bronchoprovocation challenge for identifying exercise-induced bronchoconstriction (EIB). However, the reproducibility of the hyperpnoea-induced bronchoconstriction (HIB) response elicited by EVH remains unknown and was therefore the focus of this study. METHODS Two cohorts of 16 physically active males (each cohort comprised 8 controls and 8 with physician diagnosis of asthma) participated in two studies of the short- and long-term reproducibility of the bronchoconstrictive response to an EVH test with dry air. EVH was performed on days 0, 7, 14, and 21 (short-term study), and 0, 35, and 70 (long-term study). HIB was diagnosed by a ≥10% fall in forced expiratory volume in 1 s (FEV1) after EVH. RESULTS On day 0 of the short-term study, FEV1 fell by 2 ± 1% (P < 0.05) and 27 ± 18% (P < 0.01) from pre-to post-EVH in control and HIB-positive groups respectively. The post-EVH fall in FEV1 did not differ across the short-term study test days. In the HIB-positive group, the day-to-day coefficient of variation, reproducibility, and smallest meaningful change for the fall in FEV1 were 12%, 328 mL, and 164 mL, respectively. On day 0 of the long-term study, FEV1 fell by 2 ± 2% and 25 ± 18% (P < 0.01) after EVH in control and HIB-positive groups respectively. The post-EVH fall in FEV1 did not differ across the long-term study test days. In the HIB-positive group, the day-to-day coefficient of variation, reproducibility, and smallest meaningful change for the fall in FEV1 were 10%, 196 mL, and 98 mL respectively. CONCLUSION The EVH test elicits a reproducible bronchoconstrictive response in physically active males with physician diagnosed asthma. These data thus support the clinical utility of the EVH test for EIB screening and monitoring.

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.

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.