Abstract
We investigated whether altered peripheral and/or corticospinal excitatory output and voluntary activation are implicated in hypohydration-induced reductions in muscle isometric and isokinetic (90°.s−1) strength. Nine male athletes completed two trials (hypohydrated, euhydrated) comprising 90 min cycling at 40°C, with body weight losses replaced in euhydrated trial. Peripheral nerve and transcranial magnetic stimulations were applied during voluntary contractions pre- and 40 min post-exercise to quantify voluntary activation and peripheral (M-wave) and corticospinal (motor evoked potential) evoked responses in m. vastus medialis. Both maximum isometric (−15.3±3.1 vs −5.4±3.5%) and isokinetic eccentric (−24.8±4.6 vs −7.3±7.2%) torque decreased to a greater extent in hypohydrated than euhydrated trials (p<0.05). Half relaxation time of the twitch evoked by peripheral nerve stimulation during maximal contractions increased after exercise in the hypohydrated (21.8±9.3%) but stayed constant in the euhydrated (1.6±10.7%; p = 0.017) condition. M-wave amplitude during maximum voluntary contraction increased after exercise in the heat in hypohydrated (10.7±18.0%) but decreased in euhydrated condition (−17.4±16.9%; p = 0.067). Neither peripheral nor cortical voluntary activation were significantly different between conditions. Motor evoked potential amplitude increased similarly in both conditions (hypohydrated: 25.7±28.5%; euhydrated: 52.9±33.5%) and was accompanied by lengthening of the cortical silent period in euhydrated but not hypohydrated condition (p = 0.019). Different neural strategies seem to be adopted to regulate neural drive in the two conditions, with increases in inhibitory input of either intracortical or corticospinal origin during the euhydrated trial. Such changes were absent in the hypohydrated condition, yet voluntary activation was similar to the euhydrated condition, perhaps due to smaller increases in excitatory drive rather than increased inhibition. Despite this maximal isometric and eccentric strength were impaired in the hypohydrated condition. The increase in peripheral muscle excitability evident in the hypohydrated condition was not sufficient to preserve performance in the face of reduced muscle contractility or impaired excitation-contraction coupling.
Highlights
It is well accepted that endurance performance is impaired once body water losses exceed 2% of body weight
The main findings of the study are that isometric and isokinetic maximum force production were impaired after 90 min exercise in the heat, and these performance deficits were exacerbated in the hypohydrated condition with significantly greater reductions in maximum isometric and isokinetic eccentric force
This additional strength deficit occurred despite significant increases in peripheral excitatory output (Msup) in the hypohydrated condition and appears to be primarily a consequence of reduced peripheral contractility as evidenced by the increased half relaxation time and tendency for slower relaxation rate in the hypohydrated condition
Summary
It is well accepted that endurance performance is impaired once body water losses exceed 2% of body weight (for recent review see [1]). The literature is less consistent with regard to the effects of hypohydration on maximal muscle strength and power This is most likely due to the significant variation in: methods employed to induce hypohydration (passive vs active heat exposure, fluid restriction, diuretics), and outcome measures used to assess muscle strength and power (isometric and isokinetic peak torque and vertical jump height). These factors make it difficult to isolate the effects of hypohydration. Hayes and Morse [5]
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