Author(s): KOLODZIEJ, F., ROBERTS, L., HALL, S., PAHOFF, C., BELLINGER, P., Institution: GRIFFITH UNIVERSITY, Country: AUSTRALIA, Abstract-ID: 2767

INTRODUCTION:
B2-agonists exert small benefits on strength and sprint performance, but high-intensity endurance effects remain equivocal. Literature hints that benefits extend beyond pulmonary effects. Single-muscle isometric exercise studies suggest improved endurance and preservation of peak torque through modulating contractility, recruitment and metabolism, but little is known about how B2-agonists effect fatiguing dynamic exercise. We investigated if acute B2-agonist use alters muscle contractility, recruitment, metabolic demand and fatigue resistance.
METHODS:
Twenty endurance athletes (3 women) completed a double-blind, randomised crossover study comprising a placebo (PLA) and 54ug inhaled B2-agonist, formoterol (FOR) trial. Participants performed a baseline neuromuscular assessment (NMA) of involuntary unpotentiated (UT), potentiated 10Hz (Db10) and 100Hz (Db100) doublet twitches, maximal voluntary isometric (MVIC) and dynamic (MVDC) contractions. Participants then performed a quadricep intermittent fatigue (QIF) protocol of 100-rep knee extension sets to task failure, each followed by NMA. Set 1 was at 20% of baseline MVDC peak torque, increasing by 10%/set until failure. Endurance performance was measured as torque-time integral normalised to exercised leg lean mass (TTI/LLM), and fatigue resistance by MVIC and MVDC peak torque loss. NMA fatigue was characterised by Db10, Db100, and voluntary activation (%VA). Recruitment and metabolic responses were assessed by EMG and near-infrared spectroscopy.
RESULTS:
FOR did not alter repetitions or TTI/LLM (p>0.05). Baseline MVDC (p=0.11) and MVIC peak torque (p=0.45) did not differ. MVDC peak torque loss was greater with FOR (p<0.05, ES=-0.4). Baseline Db10 was lower with FOR (p<0.05, ES=-0.3), while Db100 was unchanged leading to a lower Db10:Db100 ratio (p<0.05, ES=-0.6). FOR attenuated exercise-induced reductions in Db10 (p<0.05, ES=0.4) and Db10:Db100 ratio (p<0.05, ES=0.5). Baseline UT kinetics showed faster relaxation in FOR (p<0.05). Whilst overall %VA decline did not differ at task failure (p=0.29), larger reductions were seen after the first two QIF sets in FOR vs PLA (p<0.05). FOR reduced EMG amplitude variability and drift (p<0.05) in the initial sets, and reduced low-frequency spectral drift throughout (p<0.05), ensuing in MPF rise contrary to decline in PLA in late QIF stages (p<0.05, ES=1.2). These were supported by lower muscle oxygenation (p<0.05, ES=-0.5) and faster desaturation rate into later stages of QIF (p<0.05, ES=-0.7).
CONCLUSION:
Formoterol did not enhance quadricep endurance performance or peak MVIC or MVDC torque, but it reduced fatigue resistance, seen by impaired dynamic peak torque preservation. This could be from transitioning to more fast-twitch contractile characteristics, reducing neural drive, but increasing metabolic cost at submaximal intensities.