Abstract
Introduction: Exercise-induced increases in core and skin temperature are well documented. However, muscle temperatures (Tm) are not. Elevated Tm may underlie metabolic, pathological and adaptive responses to exercise, as evidenced from passive heating studies. Furthermore, no one had yet characterised the muscle temperature responses to the spectrum of aerobically conditioning exercise, nor done so within participants. This project, therefore, sought to characterise Tm responses to the spectrum of such exercise and the feasibility of preventing exercise-induced Tm increases as a means to study the role of temperature in exercise. In this explorative study, we tested the hypothesis that interval exercise comprising of moderate intensities and relatively longer set durations will cause greater increases in muscle temperatures compared with continuous training.
Methods: Six physically active participants (2 females) completed four single-legged cycling exercise sessions in randomised order on different days. Three were work-matched and the other included low-volume maximal sprint intervals. Sessions were: 1 x 15 min at 64% single-leg (SL) V̇O2peak (CONT); 3 x 4 min at 79% SL V̇O2peak (MIIT), with 3 min rest between sets; 10 x 1 min at 95% SL V̇O2peak (HIIT), with 1 min rest; and, 6 x 30-s Wingate’s (SIT), with 4 min rest. All sessions included 15-min supine recovery. Muscle, core (oesophageal) and skin temperature were measured in all sessions. Tm was measured at a known depth when resting, using a needle thermocouple, and at initially known depth throughout contractions, using flexible thermocouples. Three participants completed an additional session of MIIT with sets interspersed with 4.5 min of single-leg immersion in cold water (13 ± 1 °C), with Tm monitored between sets.
Results: Tm (~25 mm depth) increased from baseline (post warm-up) (p < 0.001) across bouts, by 2.3 °C (CI95% = [1.6, 3.4]) for SIT, 2.6 °C [1.8, 3.4] for CONT, 3.4 °C [3.0, 3.7] for HIIT and 3.4 °C [2.8, 4.1] for MIIT. The increase averaged 2.9 °C [2.0, 3.8], and although a condition effect was evident (p = 0.04), post hoc testing did not reveal the source of this. Oesophageal temperature increased by a mean of 0.9 [0.6, 1.2] °C across conditions (p < 0.001; interaction: p = 0.87). For work-matched points at ~33% of total work (~ 33.4 ± 5.3 kJ), the Tm increase was approximately two-thirds (1.9 [1.5, 2.3] °C) of the total increase, independently of condition (p = 0.31). Indwelling thermocouples were largely an unreliable representation of Tm and mostly became uncoupled from the temperature profiles of the needle thermocouple (~ 25 mm depth) measurements, due to the flexible thermocouple changing position usually at the outset of the initial contractions. With reference to the feasibility of cooling quadriceps muscle, we were unable to prevent Tm increasing above baseline, using water immersions, with Tm increasing 2.2 ± 0.8 °C (p = 0.008) despite being immersed for two thirds of total time.
Conclusions: Four vastly dissimilar patterns of aerobic conditioning exercise increased Tm by large (2 – 4 °C) and similar extents; these were measured reliably from spot-sampling with solid needle thermocouples but not from continuous sampling with indwelling flexible thermocouples. If muscle temperature is an important driver of adaptation, several patterns of aerobic conditioning exercise can have a significant effect on this stimulus. These increases are less than in some passive studies examining temperature effects on adaptation; however, exercise is also a multifactorial stressor so temperature may not need to be as high to play a role in adaptation. Finally, preventing increases in Tm proved to be difficult, thus emphasising the robustness of this stressor within exercise.