Response of human skeletal muscle to chronic and acute exercise and ischemia : muscle dimensions, tissue water and blood flow as measured by magnetic resonance imaging and comparative methods
Author: Nygren, Anders T
Date: 2001-06-08
Location: Föreläsningssal M63, Medicingatan 6, Huddinge Universitetssjukhus
Time: 9.00
Department: Institutionen för medicinsk laboratorievetenskap och teknik / Department of Laboratory Sciences and Technology
Abstract
The aim of this study was to investigate the response of human skeletal
muscle to exercise, training and ischemi and to evaluate if magnetic
resonance imaging (MRI) could be used to measure regional muscle
cross-sectional area, muscle perfusion and detect muscle ischemia in
patients with intermittent claudication.
For this purpose studies were performed on 29 healthy young volunteers and 7 patients with intermittent claudication. To study the effect of training under induced ischemia on healthy skeletal muscles, a local external pressure of 50 mmHg was applied in a pressure chamber. To study normally perfused and ischemic muscles during dynamic exercise by MRI, a specially designed foot ergometer was used for graded supine plantar flexion exercise.
- Ischemic training enhanced the adaptation to endurance training with an increased aerobic metabolic capacity, as shown previously. Ischemic training also increased the muscle bulk and fiber cross-sectional areas probably, at least partly, related to an increased glycogen content in the trained muscle. In non-exercising muscles a decreased cross-sectional area was found, suggesting a transfer effect possibly related to neuro-humoral influence by the strenuous ischemic exercise.
- The increased cross-sectional area during high intensity dynamic exercise could to - 50% be related to increased tissue water content, and the remaining 50% to increased blood volume related to increased blood flow.
- MRI, using iv Gd-DTPA bolus injection could not quantitatively assess perfusion as estimated by duplex ultrasonography but was shown to have a linear relationship to mean blood flow velocity within a limited range of 15 - 60 ml * s-1 corresponding to - 35 - 90 ml * 100 g-1 min'.
- Semi -quantitative signal intensity time curve analysis using Gd-DTPA bolus detection is not a solid marker of exercise induced skeletal muscle ischemia. The most usable parameters were the time of Gd-contrast appearance and upslope, but they were also dependent of blood flow kinetics and a cut-off value from the normal range is not settled.
- Exercise induced regional ischemia could be detected by a shortened monoexponentiell transverse relaxation (T2) or persistently prolonged T2. The altered T2 is indicative of reduced intracellular water content in severe ischemic muscles and in less affected muscles an accumulation of intracellular osmoles. This suggests moreover that a highly ischemic muscle is severely disturbed metabolically and that even glycolysis may be highly reduced or even nonexistent.
The mechanism for reduced intracellular water in severe hypoxia are probably multifactorial, and factors involved could be decreased intracellular osmolarity, increased osmolarity in the cellular surroundings and a highly reduced regional capillary pressure gradient. It should be emphasised that muscles with different fiber type distribution act differently to exercise as well as to exercise induced ischemia. The reason for the suspect metabolic failure could be a protective mechanism to cell death, but could induce irreversible cellular injury.
For this purpose studies were performed on 29 healthy young volunteers and 7 patients with intermittent claudication. To study the effect of training under induced ischemia on healthy skeletal muscles, a local external pressure of 50 mmHg was applied in a pressure chamber. To study normally perfused and ischemic muscles during dynamic exercise by MRI, a specially designed foot ergometer was used for graded supine plantar flexion exercise.
- Ischemic training enhanced the adaptation to endurance training with an increased aerobic metabolic capacity, as shown previously. Ischemic training also increased the muscle bulk and fiber cross-sectional areas probably, at least partly, related to an increased glycogen content in the trained muscle. In non-exercising muscles a decreased cross-sectional area was found, suggesting a transfer effect possibly related to neuro-humoral influence by the strenuous ischemic exercise.
- The increased cross-sectional area during high intensity dynamic exercise could to - 50% be related to increased tissue water content, and the remaining 50% to increased blood volume related to increased blood flow.
- MRI, using iv Gd-DTPA bolus injection could not quantitatively assess perfusion as estimated by duplex ultrasonography but was shown to have a linear relationship to mean blood flow velocity within a limited range of 15 - 60 ml * s-1 corresponding to - 35 - 90 ml * 100 g-1 min'.
- Semi -quantitative signal intensity time curve analysis using Gd-DTPA bolus detection is not a solid marker of exercise induced skeletal muscle ischemia. The most usable parameters were the time of Gd-contrast appearance and upslope, but they were also dependent of blood flow kinetics and a cut-off value from the normal range is not settled.
- Exercise induced regional ischemia could be detected by a shortened monoexponentiell transverse relaxation (T2) or persistently prolonged T2. The altered T2 is indicative of reduced intracellular water content in severe ischemic muscles and in less affected muscles an accumulation of intracellular osmoles. This suggests moreover that a highly ischemic muscle is severely disturbed metabolically and that even glycolysis may be highly reduced or even nonexistent.
The mechanism for reduced intracellular water in severe hypoxia are probably multifactorial, and factors involved could be decreased intracellular osmolarity, increased osmolarity in the cellular surroundings and a highly reduced regional capillary pressure gradient. It should be emphasised that muscles with different fiber type distribution act differently to exercise as well as to exercise induced ischemia. The reason for the suspect metabolic failure could be a protective mechanism to cell death, but could induce irreversible cellular injury.
List of papers:
I. Esbjornsson M, Jansson E, Sundberg CJ, Sylven C, Eiken O, Nygren A, Kaijser L (1993). "Muscle fibre types and enzyme activities after training with local leg ischaemia in man. " Acta Physiol Scand 148(3): 233-41
Pubmed
II. Nygren AT, Sundberg CJ, Goransson H, Esbjornsson-Liljedahl M, Jansson E, Kaijser L (2000). "Effects of dynamic ischaemic training on human skeletal muscle dimensions. " Eur J Appl Physiol 82(1-2): 137-41
Pubmed
III. Nygren AT, Karlsson M, Kaijser L (2001). "Effect of glycogen loading on skeletal muscle cross-sectional area and T2 relaxation." (Submitted)
IV. Nygren AT, Greitz D, Kaijser L (2000). "Changes in cross-sectional area in human exercising and non-exercising skeletal muscles. " Eur J Appl Physiol 81(3): 210-3
Pubmed
V. Nygren AT, Greitz D, Kaijser L (2000). "Skeletal muscle perfusion during exercise using Gd-DTPA bolus detection." J Cardiovasc Magn Reson 2(4): 263-70
VI. Nygren AT, Greitz D, Kaijser L (2001). "Skeletal muscle ischemia evaluated in intermittent claudication with MRI using T2 and Gd-DTPA bolus detection." (Submitted)
I. Esbjornsson M, Jansson E, Sundberg CJ, Sylven C, Eiken O, Nygren A, Kaijser L (1993). "Muscle fibre types and enzyme activities after training with local leg ischaemia in man. " Acta Physiol Scand 148(3): 233-41
Pubmed
II. Nygren AT, Sundberg CJ, Goransson H, Esbjornsson-Liljedahl M, Jansson E, Kaijser L (2000). "Effects of dynamic ischaemic training on human skeletal muscle dimensions. " Eur J Appl Physiol 82(1-2): 137-41
Pubmed
III. Nygren AT, Karlsson M, Kaijser L (2001). "Effect of glycogen loading on skeletal muscle cross-sectional area and T2 relaxation." (Submitted)
IV. Nygren AT, Greitz D, Kaijser L (2000). "Changes in cross-sectional area in human exercising and non-exercising skeletal muscles. " Eur J Appl Physiol 81(3): 210-3
Pubmed
V. Nygren AT, Greitz D, Kaijser L (2000). "Skeletal muscle perfusion during exercise using Gd-DTPA bolus detection." J Cardiovasc Magn Reson 2(4): 263-70
VI. Nygren AT, Greitz D, Kaijser L (2001). "Skeletal muscle ischemia evaluated in intermittent claudication with MRI using T2 and Gd-DTPA bolus detection." (Submitted)
Issue date: 2001-05-18
Publication year: 2001
ISBN: 91-628-4789-9
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