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Difference between revisions of "Scalzo 2021 J Physiol"

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{{Publication
{{Publication
|title=Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG (2021) Single-leg exercise training augments in vivo skeletal muscle oxidative flux and vascular content and function in adults with type 2 diabetes. J Physiol [Epub ahead of print].
|title=Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG (2021) Single-leg exercise training augments ''in vivo'' skeletal muscle oxidative flux and vascular content and function in adults with type 2 diabetes. J Physiol [Epub ahead of print].
|info=[https://www.ncbi.nlm.nih.gov/pubmed/33569797 PMID: 33569797]
|info=[https://www.ncbi.nlm.nih.gov/pubmed/33569797 PMID: 33569797]
|authors=Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG
|authors=Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG
|year=2021
|year=2021
|journal=J Physiol
|journal=J Physiol
|abstract=Cardiorespiratory fitness is impaired in type 2 diabetes (T2D) conferring significant cardiovascular risk in this population; interventions are needed. Previously, we reported that a T2D-associated decrement in skeletal muscle oxidative flux is ameliorated with acute use of supplemental oxygen, suggesting that skeletal muscle oxygenation is rate limiting to in vivo mitochondrial oxidative flux during exercise in T2D. We hypothesized that single-leg exercise training (SLET) would improve the T2D-specific impairment in in vivo mitochondrial oxidative flux during exercise. Adults with (n = 19) and without T2D (n = 22) with similar body mass indexes and levels of physical activity participated in two weeks of SLET. Following SLET, in vivo oxidative flux measured by 31 P-MRS increased in participants with T2D, but not people without T2D, measured by the increase in initial phosphocreatine synthesis (P = 0.0455 for the group x exercise interaction) and maximum rate of oxidative ATP synthesis (P = 0.0286 for the interaction). Additionally, oxidative phosphorylation increased in all participants with SLET (P = 0.0209). After SLET, there was no effect of supplemental oxygen on any of the in vivo oxidative flux measurements in either group (P>0.02), consistent with resolution of the T2D-associated oxygen limitation previously observed at baseline in subjects with T2D. State 4 mitochondrial respiration also improved in muscle fibers ex vivo. Skeletal muscle vasculature content and calf blood flow increased in all participants with SLET (P<0.0040); oxygen extraction in the calf increased only in T2D (P = 0.0461). SLET resolves the T2D-associated impairment of skeletal muscle in vivo mitochondrial oxidative flux potentially through improved effective blood flow/oxygen delivery.
|abstract=Cardiorespiratory fitness is impaired in type 2 diabetes (T2D) conferring significant cardiovascular risk in this population; interventions are needed. Previously, we reported that a T2D-associated decrement in skeletal muscle oxidative flux is ameliorated with acute use of supplemental oxygen, suggesting that skeletal muscle oxygenation is rate limiting to ''in vivo'' mitochondrial oxidative flux during exercise in T2D. We hypothesized that single-leg exercise training (SLET) would improve the T2D-specific impairment in ''in vivo'' mitochondrial oxidative flux during exercise. Adults with (n = 19) and without T2D (n = 22) with similar body mass indexes and levels of physical activity participated in two weeks of SLET. Following SLET, ''in vivo'' oxidative flux measured by 31 P-MRS increased in participants with T2D, but not people without T2D, measured by the increase in initial phosphocreatine synthesis (P = 0.0455 for the group x exercise interaction) and maximum rate of oxidative ATP synthesis (P = 0.0286 for the interaction). Additionally, oxidative phosphorylation increased in all participants with SLET (P = 0.0209). After SLET, there was no effect of supplemental oxygen on any of the ''in vivo'' oxidative flux measurements in either group (P>0.02), consistent with resolution of the T2D-associated oxygen limitation previously observed at baseline in subjects with T2D. State 4 mitochondrial respiration also improved in muscle fibers ''ex vivo''. Skeletal muscle vasculature content and calf blood flow increased in all participants with SLET (P<0.0040); oxygen extraction in the calf increased only in T2D (P = 0.0461). SLET resolves the T2D-associated impairment of skeletal muscle ''in vivo'' mitochondrial oxidative flux potentially through improved effective blood flow/oxygen delivery.
|keywords=Blood flow, Diabetes, Exercise, Skeletal muscle
|keywords=Blood flow, Diabetes, Exercise, Skeletal muscle
|editor=[[Plangger M]]
|editor=[[Plangger M]]
|mipnetlab=US CO Denver Schauer I
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration, Exercise physiology;nutrition;life style
|diseases=Diabetes
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=2021-03
|additional=2021-03
}}
}}

Revision as of 17:06, 4 March 2021

Publications in the MiPMap
Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG (2021) Single-leg exercise training augments in vivo skeletal muscle oxidative flux and vascular content and function in adults with type 2 diabetes. J Physiol [Epub ahead of print].

Β» PMID: 33569797

Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG (2021) J Physiol

Abstract: Cardiorespiratory fitness is impaired in type 2 diabetes (T2D) conferring significant cardiovascular risk in this population; interventions are needed. Previously, we reported that a T2D-associated decrement in skeletal muscle oxidative flux is ameliorated with acute use of supplemental oxygen, suggesting that skeletal muscle oxygenation is rate limiting to in vivo mitochondrial oxidative flux during exercise in T2D. We hypothesized that single-leg exercise training (SLET) would improve the T2D-specific impairment in in vivo mitochondrial oxidative flux during exercise. Adults with (n = 19) and without T2D (n = 22) with similar body mass indexes and levels of physical activity participated in two weeks of SLET. Following SLET, in vivo oxidative flux measured by 31 P-MRS increased in participants with T2D, but not people without T2D, measured by the increase in initial phosphocreatine synthesis (P = 0.0455 for the group x exercise interaction) and maximum rate of oxidative ATP synthesis (P = 0.0286 for the interaction). Additionally, oxidative phosphorylation increased in all participants with SLET (P = 0.0209). After SLET, there was no effect of supplemental oxygen on any of the in vivo oxidative flux measurements in either group (P>0.02), consistent with resolution of the T2D-associated oxygen limitation previously observed at baseline in subjects with T2D. State 4 mitochondrial respiration also improved in muscle fibers ex vivo. Skeletal muscle vasculature content and calf blood flow increased in all participants with SLET (P<0.0040); oxygen extraction in the calf increased only in T2D (P = 0.0461). SLET resolves the T2D-associated impairment of skeletal muscle in vivo mitochondrial oxidative flux potentially through improved effective blood flow/oxygen delivery. β€’ Keywords: Blood flow, Diabetes, Exercise, Skeletal muscle β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: US CO Denver Schauer I


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Diabetes 





HRR: Oxygraph-2k 

2021-03