Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases.Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extracellular protein responses of exercise.Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered.Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress.Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F 6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F 6,24 = 10.1, P < .001) and 5 mm Hg (F 6,24 = 5.4, P < .001), respectively. Norepinephrine (F 1,12 = 12.1, P = .004) and prolactin (F 1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F 1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials.Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

Objective The aim of this study was to examine the cortical and segmental excitability changes during fatigue of the soleus muscle. Methods Ten healthy young subjects performed 45 plantar flexion maximal voluntary contractions (MVCs) (7-s on/3-s off) in 9 epochs of five contractions. Motor evoked potentials (MEPs) using transcranial magnetic stimulation and H-reflexes were assessed during the task. Results The torque and the soleus EMG activity both showed the greatest decline during the 1st epoch, followed by a gradual, but significant decrease by the end of the task (~70% pre-fatigue). The H-reflex sampled at rest after each epoch decreased to 66.6 ± 18.3% pre-fatigue after the first epoch, and then showed no further change. The MEP on 10% pre-fatigue MVC after each epoch increased progressively (252.9 ± 124.2% pre-fatigue). There was no change in the MEPs on the 3rd MVC in each epoch. The silent period on the MVC increased (109.0 ± 9.2% pre-fatigue) early with no further changes during the task. Conclusions These findings support that the motor cortex increases excitability during fatigue, but with a concomitant inhibition. Significance These findings are in contrast to upper extremity muscles and may reflect a distinct response specific to postural, fatigue-resistant muscle.

Introduction-Long-lasting alterations in hormones, neurotransmitters and stress proteins after hyperthermia may be responsible for the impairment in motor performance during muscle fatigue.

With long-term electrical stimulation training, paralyzed muscle can serve as an effective load delivery agent for the skeletal system. Muscle adaptations to training, however, will almost certainly outstrip bone adaptations, exposing participants in training protocols to an elevated risk for fracture. Assessing the physiological properties of the chronically paralyzed quadriceps may transmit unacceptably high shear forces to the osteoporotic distal femur. We devised a two-pulse doublet strategy to measure quadriceps physiological properties while minimizing the peak muscle force. The purposes of the study were 1) to determine the repeatability of the doublet stimulation protocol, and 2) to compare this protocol among individuals with and without spinal cord injury (SCI). Eight individuals with SCI and four individuals without SCI underwent testing. The doublet force-frequency relationship shifted to the left after SCI, likely reflecting enhancements in the twitch-to-tetanus ratio known to exist in paralyzed muscle. Posttetanic potentiation occurred to a greater degree in subjects with SCI (20%) than in non-SCI subjects (7%). Potentiation of contractile rate occurred in both subject groups (14% and 23% for SCI and non-SCI, respectively). Normalized contractile speed (rate of force rise, rate of force fall) reflected well-known adaptations of paralyzed muscle toward a fast fatigable muscle. The doublet stimulation strategy provided repeatable and sensitive measurements of muscle force and speed properties that revealed meaningful differences between subjects with and without SCI. Doublet stimulation may offer a unique way to test muscle physiological parameters of the quadriceps in subjects with uncertain musculoskeletal integrity.

Torque steadiness and low-frequency fatigue (LFF) were examined in the human triceps brachii after concentric or eccentric fatigue protocols. Healthy young males (n = 17) performed either concentric or eccentric elbow extensor contractions until the eccentric maximal voluntary torque decreased to 75% of pre-fatigue for both (concentric and eccentric) protocols. The number of concentric contractions was greater than the number of eccentric contractions needed to induce the same 25% decrease in eccentric MVC torque (52.2 ± 2.9 vs. 41.5 ± 2.1 for the concentric and eccentric protocols, respectively, p < .01). The extent of peripheral fatigue was ~ 12% greater after the concentric compared to the eccentric protocol (twitch amplitude), whereas LFF (increase in double pulse torque/ single pulse torque), was similar across protocols. Steadiness, or the ability for a subject to hold a submaximal isometric contraction, was ~ 20 % more impaired during the Ecc protocol (p = .052). Similarly, the EMG activity required to hold the torque steady was nearly 20 %greater after the eccentric compared to concentric protocol. These findings support that task dependent eccentric contractions preferentially alter CNS control during a precision based steadiness task.