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 (F₆,₂₄ = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F₆,₂₄ = 10.1, P < .001) and 5 mm Hg (F₆,₂₄ = 5.4, P < .001), respectively. Norepinephrine (F₁,₁₂ = 12.1, P = .004) and prolactin (F₁,₁₂ = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F₁,₁₂ = 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.
RCT Entities:
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 (F₆,₂₄ = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F₆,₂₄ = 10.1, P < .001) and 5 mm Hg (F₆,₂₄ = 5.4, P < .001), respectively. Norepinephrine (F₁,₁₂ = 12.1, P = .004) and prolactin (F₁,₁₂ = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F₁,₁₂ = 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.
Authors: R J Gibbons; G J Balady; J W Beasley; J T Bricker; W F Duvernoy; V F Froelicher; D B Mark; T H Marwick; B D McCallister; P D Thompson; W L Winters; F G Yanowitz; J L Ritchie; R J Gibbons; M D Cheitlin; K A Eagle; T J Gardner; A Garson; R P Lewis; R A O'Rourke; T J Ryan Journal: J Am Coll Cardiol Date: 1997-07 Impact factor: 24.094
Authors: Harm H Kampinga; Jurre Hageman; Michel J Vos; Hiroshi Kubota; Robert M Tanguay; Elspeth A Bruford; Michael E Cheetham; Bin Chen; Lawrence E Hightower Journal: Cell Stress Chaperones Date: 2008-07-29 Impact factor: 3.667
Authors: Oliver R Gibson; Alex Dennis; Tony Parfitt; Lee Taylor; Peter W Watt; Neil S Maxwell Journal: Cell Stress Chaperones Date: 2013-10-02 Impact factor: 3.667
Authors: Rebecca M Swanson; Richard G Tait; Beth M Galles; Erin M Duffy; Ty B Schmidt; Jessica L Petersen; Dustin T Yates Journal: J Anim Sci Date: 2020-06-01 Impact factor: 3.159
Authors: Crystal M Roach; Katie L Bidne; Matthew R Romoser; Jason W Ross; Lance H Baumgard; Aileen F Keating Journal: J Anim Sci Date: 2022-07-01 Impact factor: 3.338
Authors: Víctor Toro; Jesús Siquier-Coll; Ignacio Bartolomé; Mario Pérez-Quintero; Armando Raimundo; Diego Muñoz; Marcos Maynar-Mariño Journal: Int J Environ Res Public Health Date: 2021-04-22 Impact factor: 3.390
Authors: M Victoria Sanz Fernandez; Jay S Johnson; Mohannad Abuajamieh; Sara K Stoakes; Jacob T Seibert; Lindsay Cox; Stanislaw Kahl; Theodore H Elsasser; Jason W Ross; S Clay Isom; Robert P Rhoads; Lance H Baumgard Journal: Physiol Rep Date: 2015-02-25