Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans

Christian P. Fischer, Natalie J. Hiscock, Samar Basu, Bengt Vessby, Anders Kallner, Mark A. Febbraio, Bente K. Pedersen

Research output: Contribution to journalArticleResearchpeer-review

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Abstract

Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE α), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CE αγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-isoprostaglandin-F (8-PGF ). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF , increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE α. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE α, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE αγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

Original languageEnglish
Pages (from-to)1679-1687
Number of pages9
JournalJournal of Applied Physiology
Volume100
Issue number5
DOIs
Publication statusPublished - 1 May 2006
Externally publishedYes

Keywords

  • α-tocopherol
  • γ-tocopherol
  • Ascorbic acid
  • Serum
  • Skeletal muscle

Cite this

Fischer, Christian P. ; Hiscock, Natalie J. ; Basu, Samar ; Vessby, Bengt ; Kallner, Anders ; Febbraio, Mark A. ; Pedersen, Bente K. / Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans. In: Journal of Applied Physiology. 2006 ; Vol. 100, No. 5. pp. 1679-1687.
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abstract = "Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE α), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CE αγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50{\%} of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-isoprostaglandin-F 2α (8-PGF 2α). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF 2α, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE α. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE α, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE αγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.",
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Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans. / Fischer, Christian P.; Hiscock, Natalie J.; Basu, Samar; Vessby, Bengt; Kallner, Anders; Febbraio, Mark A.; Pedersen, Bente K.

In: Journal of Applied Physiology, Vol. 100, No. 5, 01.05.2006, p. 1679-1687.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans

AU - Fischer, Christian P.

AU - Hiscock, Natalie J.

AU - Basu, Samar

AU - Vessby, Bengt

AU - Kallner, Anders

AU - Febbraio, Mark A.

AU - Pedersen, Bente K.

PY - 2006/5/1

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N2 - Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE α), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CE αγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-isoprostaglandin-F 2α (8-PGF 2α). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF 2α, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE α. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE α, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE αγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

AB - Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE α), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CE αγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-isoprostaglandin-F 2α (8-PGF 2α). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF 2α, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE α. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE α, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE αγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

KW - α-tocopherol

KW - γ-tocopherol

KW - Ascorbic acid

KW - Serum

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