The development of hyperthermia has a profound influence on neuromuscular function, with alterations occurring at both the central and the peripheral level. From a central perspective, heat stress can lead to a reduction in voluntary muscle activation (i.e. hyperthermia-induced central fatigue). Voluntary activation is typically quantified by normalizing the amplitude of the force/torque increment induced by percutaneous muscle (PMS), motor nerve (MNS) or transcranial magnetic stimulation (TMS) during a maximal voluntary isometric contraction (MVC), to the force/torque elicited by the same stimulus on the muscle at rest. When additional force/torque is produced via PMS or MNS during an MVC, it indicates incomplete activation of the motor pathway or that the stimulated axons are discharging at subtetanic rates.