Abstract
Lower aerobic capacity is a strong and independent predictor of cardiovascular morbidity and mortality in patients with metabolic syndrome (MetS). However, the mechanisms are not fully elucidated. We tested the hypothesis that skeletal muscle dysfunction could contribute to the lower aerobic capacity in MetS patients. The incremental exercise tests with cycle ergometer were performed in 12 male patients with MetS with no habitual exercise and 11 age-, sex-and activity-matched control subjects to assess the aerobic capacity. We performed 31 phosphorus-magnetic resonance spectroscopy (MRS) to assess the high-energy phosphate metabolism in skeletal muscle during aerobic exercise. Proton-MRS was also performed to measure intramyocellular lipid (IMCL) content. Peak oxygen uptake (peak VO 2; 34.1±6.2 vs. 41.4±8.4 ml kg -1 min -1, P<0.05) and anaerobic threshold (AT; 18.0±2.4 vs. 23.1±3.7 ml kg -1 min -1, P<0.01) adjusted by lean body mass were lower in MetS patients than control subjects. Phosphocreatine (PCr) loss during exercise was 1.5-fold greater in MetS, suggesting reduced intramuscular oxidative capacity. PCr loss was inversely correlated with peak VO 2 (r=-0.64) and AT (r=-0.60), respectively. IMCL content was threefold higher in MetS and was inversely correlated with peak VO 2 (r=-0.47) and AT (r=-0.52), respectively. Moreover, there was a positive correlation between IMCL content and PCr loss (r=-0.64). These results suggested that lean-body aerobic capacity in MetS patients was lower compared with activity-matched healthy subjects, which might be due to the reduced intramuscular fatty acid oxidative metabolism.
| Original language | English |
|---|---|
| Pages (from-to) | 1029-1034 |
| Number of pages | 6 |
| Journal | Hypertension Research |
| Volume | 34 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - Sep 1 2011 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Internal Medicine
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
Lower aerobic capacity was associated with abnormal intramuscular energetics in patients with metabolic syndrome. / Yokota, Takashi; Kinugawa, Shintaro; Okita, Koichi; Hirabayashi, Kagami; Suga, Tadashi; Hattori, Masaaki; Nakagawa, Yoshinao; Oyama-Manabe, Noriko; Shirato, Hiroki; Tsutsui, Hiroyuki.
In: Hypertension Research, Vol. 34, No. 9, 01.09.2011, p. 1029-1034.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Lower aerobic capacity was associated with abnormal intramuscular energetics in patients with metabolic syndrome
AU - Yokota, Takashi
AU - Kinugawa, Shintaro
AU - Okita, Koichi
AU - Hirabayashi, Kagami
AU - Suga, Tadashi
AU - Hattori, Masaaki
AU - Nakagawa, Yoshinao
AU - Oyama-Manabe, Noriko
AU - Shirato, Hiroki
AU - Tsutsui, Hiroyuki
PY - 2011/9/1
Y1 - 2011/9/1
N2 - Lower aerobic capacity is a strong and independent predictor of cardiovascular morbidity and mortality in patients with metabolic syndrome (MetS). However, the mechanisms are not fully elucidated. We tested the hypothesis that skeletal muscle dysfunction could contribute to the lower aerobic capacity in MetS patients. The incremental exercise tests with cycle ergometer were performed in 12 male patients with MetS with no habitual exercise and 11 age-, sex-and activity-matched control subjects to assess the aerobic capacity. We performed 31 phosphorus-magnetic resonance spectroscopy (MRS) to assess the high-energy phosphate metabolism in skeletal muscle during aerobic exercise. Proton-MRS was also performed to measure intramyocellular lipid (IMCL) content. Peak oxygen uptake (peak VO 2; 34.1±6.2 vs. 41.4±8.4 ml kg -1 min -1, P<0.05) and anaerobic threshold (AT; 18.0±2.4 vs. 23.1±3.7 ml kg -1 min -1, P<0.01) adjusted by lean body mass were lower in MetS patients than control subjects. Phosphocreatine (PCr) loss during exercise was 1.5-fold greater in MetS, suggesting reduced intramuscular oxidative capacity. PCr loss was inversely correlated with peak VO 2 (r=-0.64) and AT (r=-0.60), respectively. IMCL content was threefold higher in MetS and was inversely correlated with peak VO 2 (r=-0.47) and AT (r=-0.52), respectively. Moreover, there was a positive correlation between IMCL content and PCr loss (r=-0.64). These results suggested that lean-body aerobic capacity in MetS patients was lower compared with activity-matched healthy subjects, which might be due to the reduced intramuscular fatty acid oxidative metabolism.
AB - Lower aerobic capacity is a strong and independent predictor of cardiovascular morbidity and mortality in patients with metabolic syndrome (MetS). However, the mechanisms are not fully elucidated. We tested the hypothesis that skeletal muscle dysfunction could contribute to the lower aerobic capacity in MetS patients. The incremental exercise tests with cycle ergometer were performed in 12 male patients with MetS with no habitual exercise and 11 age-, sex-and activity-matched control subjects to assess the aerobic capacity. We performed 31 phosphorus-magnetic resonance spectroscopy (MRS) to assess the high-energy phosphate metabolism in skeletal muscle during aerobic exercise. Proton-MRS was also performed to measure intramyocellular lipid (IMCL) content. Peak oxygen uptake (peak VO 2; 34.1±6.2 vs. 41.4±8.4 ml kg -1 min -1, P<0.05) and anaerobic threshold (AT; 18.0±2.4 vs. 23.1±3.7 ml kg -1 min -1, P<0.01) adjusted by lean body mass were lower in MetS patients than control subjects. Phosphocreatine (PCr) loss during exercise was 1.5-fold greater in MetS, suggesting reduced intramuscular oxidative capacity. PCr loss was inversely correlated with peak VO 2 (r=-0.64) and AT (r=-0.60), respectively. IMCL content was threefold higher in MetS and was inversely correlated with peak VO 2 (r=-0.47) and AT (r=-0.52), respectively. Moreover, there was a positive correlation between IMCL content and PCr loss (r=-0.64). These results suggested that lean-body aerobic capacity in MetS patients was lower compared with activity-matched healthy subjects, which might be due to the reduced intramuscular fatty acid oxidative metabolism.
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U2 - 10.1038/hr.2011.78
DO - 10.1038/hr.2011.78
M3 - Article
C2 - 21753774
AN - SCOPUS:80052470131
VL - 34
SP - 1029
EP - 1034
JO - Hypertension Research
JF - Hypertension Research
SN - 0916-9636
IS - 9
ER -