The effects of acute and chronic systemic hypoxia on muscle oxygen supply and oxygen consumption in the rat

Janice M. Marshall; William R. Davies

doi:10.1111/j.1469-445X.1999.tb00072.x

The effects of acute and chronic systemic hypoxia on muscle oxygen supply and oxygen consumption in the rat

Janice M. Marshall^*, William R. Davies

^*Corresponding author for this work

Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

21 Citations (Scopus)

Abstract

The aims of the present study were to evaluate how acute systemic hypoxia affects O₂ delivery to skeletal muscle and muscle O₂ consumption (V̇(O₂)) of the rat and to establish how these relationships are altered by chronic systemic hypoxia. Thus, the effects of breathing different concentrations of O₂ (air, 12% and 8% O₂) upon oxygen delivery and V̇(O₂) were studied in hindlimb muscles of control, normoxic (N) rats and of rats that had been made chronically hypoxic in a chamber at 12% O₂ for 3-4 weeks (CH) rats. Under anaesthesia, arterial blood pressure, femoral blood flow (FBF), arterial O₂ content (C(a,O₂)) and venous O₂ content in the efflux from hindlimb were measured. In N rats, changing the inspirate from air to 12% and 8% O₂ for 5 min each, reduced C(a,O₂) from 20 ± 0.3 ml (100 ml)^-1 in air to 13 ± 1.0 ml (100 ml)^-1 in 8% O₂. FBF did not change significantly (1.7 ± 0.1 ml min^-1 in air) so that O₂ delivery to hindlimb muscles fell from 0.28 ± 0.07 to 0.16 ± 0.02 ml min^-1 in 8% O₂. Nevertheless, the V̇(O₂) of hindlimb muscles was well maintained: 0.06 ± 0.02 ml min^-1 in air and 0.08 ± 0.02 ml min^-1 in 8% O₂. In CH rats breathing 12% O₂, C(a,O₂) (23 ± 1.0 ml (100 ml)^-1) was comparable to that of N rats breathing air, due to an increase in haematocrit, as were FBF (1.6 ± 0.2 ml min^-1 and O₂ delivery (0.39 ± 0.05 ml min^-1). However, V̇(O₂) was 2.5-fold greater in CH rats (0.16 ± 0.03 ml min^-1). As in N rats, FBF was well maintained at 1.7 ± 0.2 and 1.6 ± 0.2 ml min^-1 in 8% O₂ and air, respectively. Further, V̇(O₂) was also well maintained, at 0.7 ± 0.02 and 0.12 ± 0.02 ml min^-1 in 8% O₂ and air, respectively. These results suggest that, contrary to previous reports, muscle V̇(O₂) of the rat is independent of O₂ delivery over a wide range of O₂ delivery values. They also suggest that muscle V̇(O₂) of CH rats is similarly independent of O₂ delivery. The novel finding that muscle V̇(O₂) has a greater absolute value in CH rats can, we propose, be explained by an increase in V̇(O₂) of the vasculature rather than of the skeletal muscle fibres and reflects increased biosynthetic activity of the vessel walls and/or vascular remodelling.

Original language	English
Pages (from-to)	57-68
Number of pages	12
Journal	Experimental Physiology
Volume	84
Issue number	1
DOIs	https://doi.org/10.1111/j.1469-445X.1999.tb00072.x
Publication status	Published - Jan 1999

ASJC Scopus subject areas

Physiology
Nutrition and Dietetics
Physiology (medical)

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@article{a12ce5d4ba754d4cad1169b65a80cca8,

title = "The effects of acute and chronic systemic hypoxia on muscle oxygen supply and oxygen consumption in the rat",

abstract = "The aims of the present study were to evaluate how acute systemic hypoxia affects O2 delivery to skeletal muscle and muscle O2 consumption ({\.V}(O2)) of the rat and to establish how these relationships are altered by chronic systemic hypoxia. Thus, the effects of breathing different concentrations of O2 (air, 12% and 8% O2) upon oxygen delivery and {\.V}(O2) were studied in hindlimb muscles of control, normoxic (N) rats and of rats that had been made chronically hypoxic in a chamber at 12% O2 for 3-4 weeks (CH) rats. Under anaesthesia, arterial blood pressure, femoral blood flow (FBF), arterial O2 content (C(a,O2)) and venous O2 content in the efflux from hindlimb were measured. In N rats, changing the inspirate from air to 12% and 8% O2 for 5 min each, reduced C(a,O2) from 20 ± 0.3 ml (100 ml)-1 in air to 13 ± 1.0 ml (100 ml)-1 in 8% O2. FBF did not change significantly (1.7 ± 0.1 ml min-1 in air) so that O2 delivery to hindlimb muscles fell from 0.28 ± 0.07 to 0.16 ± 0.02 ml min-1 in 8% O2. Nevertheless, the {\.V}(O2) of hindlimb muscles was well maintained: 0.06 ± 0.02 ml min-1 in air and 0.08 ± 0.02 ml min-1 in 8% O2. In CH rats breathing 12% O2, C(a,O2) (23 ± 1.0 ml (100 ml)-1) was comparable to that of N rats breathing air, due to an increase in haematocrit, as were FBF (1.6 ± 0.2 ml min-1 and O2 delivery (0.39 ± 0.05 ml min-1). However, {\.V}(O2) was 2.5-fold greater in CH rats (0.16 ± 0.03 ml min-1). As in N rats, FBF was well maintained at 1.7 ± 0.2 and 1.6 ± 0.2 ml min-1 in 8% O2 and air, respectively. Further, {\.V}(O2) was also well maintained, at 0.7 ± 0.02 and 0.12 ± 0.02 ml min-1 in 8% O2 and air, respectively. These results suggest that, contrary to previous reports, muscle {\.V}(O2) of the rat is independent of O2 delivery over a wide range of O2 delivery values. They also suggest that muscle {\.V}(O2) of CH rats is similarly independent of O2 delivery. The novel finding that muscle {\.V}(O2) has a greater absolute value in CH rats can, we propose, be explained by an increase in {\.V}(O2) of the vasculature rather than of the skeletal muscle fibres and reflects increased biosynthetic activity of the vessel walls and/or vascular remodelling.",

author = "Marshall, {Janice M.} and Davies, {William R.}",

year = "1999",

month = jan,

doi = "10.1111/j.1469-445X.1999.tb00072.x",

language = "English",

volume = "84",

pages = "57--68",

journal = "Experimental Physiology",

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TY - JOUR

T1 - The effects of acute and chronic systemic hypoxia on muscle oxygen supply and oxygen consumption in the rat

AU - Marshall, Janice M.

AU - Davies, William R.

PY - 1999/1

Y1 - 1999/1

N2 - The aims of the present study were to evaluate how acute systemic hypoxia affects O2 delivery to skeletal muscle and muscle O2 consumption (V̇(O2)) of the rat and to establish how these relationships are altered by chronic systemic hypoxia. Thus, the effects of breathing different concentrations of O2 (air, 12% and 8% O2) upon oxygen delivery and V̇(O2) were studied in hindlimb muscles of control, normoxic (N) rats and of rats that had been made chronically hypoxic in a chamber at 12% O2 for 3-4 weeks (CH) rats. Under anaesthesia, arterial blood pressure, femoral blood flow (FBF), arterial O2 content (C(a,O2)) and venous O2 content in the efflux from hindlimb were measured. In N rats, changing the inspirate from air to 12% and 8% O2 for 5 min each, reduced C(a,O2) from 20 ± 0.3 ml (100 ml)-1 in air to 13 ± 1.0 ml (100 ml)-1 in 8% O2. FBF did not change significantly (1.7 ± 0.1 ml min-1 in air) so that O2 delivery to hindlimb muscles fell from 0.28 ± 0.07 to 0.16 ± 0.02 ml min-1 in 8% O2. Nevertheless, the V̇(O2) of hindlimb muscles was well maintained: 0.06 ± 0.02 ml min-1 in air and 0.08 ± 0.02 ml min-1 in 8% O2. In CH rats breathing 12% O2, C(a,O2) (23 ± 1.0 ml (100 ml)-1) was comparable to that of N rats breathing air, due to an increase in haematocrit, as were FBF (1.6 ± 0.2 ml min-1 and O2 delivery (0.39 ± 0.05 ml min-1). However, V̇(O2) was 2.5-fold greater in CH rats (0.16 ± 0.03 ml min-1). As in N rats, FBF was well maintained at 1.7 ± 0.2 and 1.6 ± 0.2 ml min-1 in 8% O2 and air, respectively. Further, V̇(O2) was also well maintained, at 0.7 ± 0.02 and 0.12 ± 0.02 ml min-1 in 8% O2 and air, respectively. These results suggest that, contrary to previous reports, muscle V̇(O2) of the rat is independent of O2 delivery over a wide range of O2 delivery values. They also suggest that muscle V̇(O2) of CH rats is similarly independent of O2 delivery. The novel finding that muscle V̇(O2) has a greater absolute value in CH rats can, we propose, be explained by an increase in V̇(O2) of the vasculature rather than of the skeletal muscle fibres and reflects increased biosynthetic activity of the vessel walls and/or vascular remodelling.

AB - The aims of the present study were to evaluate how acute systemic hypoxia affects O2 delivery to skeletal muscle and muscle O2 consumption (V̇(O2)) of the rat and to establish how these relationships are altered by chronic systemic hypoxia. Thus, the effects of breathing different concentrations of O2 (air, 12% and 8% O2) upon oxygen delivery and V̇(O2) were studied in hindlimb muscles of control, normoxic (N) rats and of rats that had been made chronically hypoxic in a chamber at 12% O2 for 3-4 weeks (CH) rats. Under anaesthesia, arterial blood pressure, femoral blood flow (FBF), arterial O2 content (C(a,O2)) and venous O2 content in the efflux from hindlimb were measured. In N rats, changing the inspirate from air to 12% and 8% O2 for 5 min each, reduced C(a,O2) from 20 ± 0.3 ml (100 ml)-1 in air to 13 ± 1.0 ml (100 ml)-1 in 8% O2. FBF did not change significantly (1.7 ± 0.1 ml min-1 in air) so that O2 delivery to hindlimb muscles fell from 0.28 ± 0.07 to 0.16 ± 0.02 ml min-1 in 8% O2. Nevertheless, the V̇(O2) of hindlimb muscles was well maintained: 0.06 ± 0.02 ml min-1 in air and 0.08 ± 0.02 ml min-1 in 8% O2. In CH rats breathing 12% O2, C(a,O2) (23 ± 1.0 ml (100 ml)-1) was comparable to that of N rats breathing air, due to an increase in haematocrit, as were FBF (1.6 ± 0.2 ml min-1 and O2 delivery (0.39 ± 0.05 ml min-1). However, V̇(O2) was 2.5-fold greater in CH rats (0.16 ± 0.03 ml min-1). As in N rats, FBF was well maintained at 1.7 ± 0.2 and 1.6 ± 0.2 ml min-1 in 8% O2 and air, respectively. Further, V̇(O2) was also well maintained, at 0.7 ± 0.02 and 0.12 ± 0.02 ml min-1 in 8% O2 and air, respectively. These results suggest that, contrary to previous reports, muscle V̇(O2) of the rat is independent of O2 delivery over a wide range of O2 delivery values. They also suggest that muscle V̇(O2) of CH rats is similarly independent of O2 delivery. The novel finding that muscle V̇(O2) has a greater absolute value in CH rats can, we propose, be explained by an increase in V̇(O2) of the vasculature rather than of the skeletal muscle fibres and reflects increased biosynthetic activity of the vessel walls and/or vascular remodelling.

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DO - 10.1111/j.1469-445X.1999.tb00072.x

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The effects of acute and chronic systemic hypoxia on muscle oxygen supply and oxygen consumption in the rat

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