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.

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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.

BackgroundThis study examined the effect of carbohydrate and whey protein supplements on recovery of neuromuscular function after prolonged load carriage.MethodsTen male participants (body mass: 81.5 ± 10.5 kg, age: 28 ± 9 years, O2max: 55.0 ± 5.5 ml·kg-1·min-1) completed three treadmill walking tests (2 hr, 6.5 km·h-1), carrying a 25 kg backpack consuming 500 ml of either: (1) Placebo (flavoured water) [PLA], (2) 6.4% Carbohydrate Solution [CHO] or (3) 7.0% Whey Protein Solution [PRO]. For three days after load carriage, participants consumed two 500 ml supplement boluses. Muscle performance was measured before and at 0, 24, 48 and 72 h after load carriage, during voluntary and electrically stimulated contractions.ResultsIsometric knee extension force decreased immediately after load carriage with no difference between conditions. During recovery, isometric force returned to pre-exercise values at 48 h for CHO and PRO but at 72 h for PLA. Voluntary activation decreased immediately after load carriage and returned to pre-exercise values at 24 h in all conditions (P = 0.086). During recovery, there were no differences between conditions for the change in isokinetic peak torque. Following reductions immediately after load carriage, knee extensor and flexor peak torque (60°·s-1) recovered to pre-exercise values at 72 h. Trunk extensor and flexor peak torque (15°·s-1) recovered to pre-exercise values at 24 h (P = 0.091) and 48 h (P = 0.177), respectively.ConclusionRecovery of neuromuscular function after prolonged load carriage is improved with either carbohydrate or whey protein supplementation for isometric contractions but not for isokinetic contractions.

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 (FEV 1 ) 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 FEV 1 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.