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Heat stress produces an early phase of protection against oxidative damage in human muscle
Author(s) -
Naito J.,
Hartung E.,
Schramm E.,
Inselmann G.
Publication year - 1999
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.1999.430116.x
Subject(s) - medicine , oxidative stress , muscle damage , heat stress , phase (matter) , chemistry , organic chemistry , atmospheric sciences , geology
Background: It has been rarely reported that heat stress induces an early phase of protection against oxidative damage, whereas a delayed phase of protection is shown in heat stress. To explore the early effect of heat stress against oxidative damage, we evaluated the changes in contractility, lipid peroxidation, and ultrastructure induced by hydrogen peroxide (H 2 O 2 ) with or without heat stress (HS) in human skeleton muscle. Methods: Thirty‐two muscle samples were obtained from the vastus lateralis muscle of 7 subjects. These specimens were divided into three groups based on form of treatment: HS (n=13), non HS (n=14), and control group (n=5). The control group was performed under identical conditions without H 2 O 2 . Specimens in the HS group were incubated at 42°C for 20 min, while those in the non‐HS and control groups were maintained at 37°C. Results: The control group showed no significant change in contractile force. Although contractile force significantly decreased 30 min after H 2 O 2 administration in both the HS and non‐HS groups, only the HS group showed apparent recovery of contractile force 60 min after H 2 O 2 administration. Lipid peroxidation was lower in the HS group than in the non‐HS group. Ultrastructural examination revealed less mitochondrial damage in the HS group compared with the non‐HS group. Conclusion: We found that human skeleton muscle escaped cellular damage induced by H 2 O 2 in the early phase after heat stress. These data suggest evidence for an early effect of heat stress against ischemia/reperfusion injury in human muscle.