Population-based study of the relationship among muscle morphology, insulin action, and hypertension.
To examine whether changes in muscle morphology are linked to the metabolic abnormalities associated with the insulin resistance syndrome, muscle morphology and the metabolic profile were examined in 52 individuals with untreated hypertension (mean arterial pressure [MAP] = 117+/-7 mm Hg) and 38 carefully matched controls (MAP = 89+/-5 mm Hg). Oral glucose tolerance tests and hyperglycemic clamps were performed for measurements of insulin action on glucose disposal and suppression of nonesterified fatty acids (NEFA). Fully automated, computer-aided techniques were used for morphometric measurements of muscle biopsies from m. vastus lateralis. The hypertensive and normotensive groups did not differ in insulin sensitivity to glucose disposal (0.18+/-0.16 v. 0.19+/-0.13 micromol/kg/min/pmol/L; P = .20) and NEFA suppression (87.5+/-7.3 v. 87.2+/-9.4%, P>0.30) during a hyperglycemic clamp. The groups were similar in the proportion of types 1, 2a, and 2b muscle fibers, fiber size, and capillary density. Fiber roundness (ratio of fiber perimeter squared to fiber area) differed in the hypertensive (1.51+/-0.07) and normotensive (1.58+/-0.12, P = .004) groups, showing that the muscle fibers in the hypertensive group were more rounded in shape, a nonspecific change often seen after minimal ischemic lesions. The quotient expressing fiber roundness was associated with systolic (r = -0.29, P = .01) and diastolic (r = -0.32, P = .005) blood pressure. We conclude that persons with mild and moderate hypertension do not have abnormalities in muscle morphology that could explain the impairment of insulin action often observed in this condition. However, hypertensive individuals have increased muscle fiber roundness. It is wondered whether hypertension may be a condition with defects in the regulation of the transmembranous ion transport, leading to raised intracellular sodium concentration, swelling of the cytoplasma, and roundening of the fibers.
Toft
I
I
Institute of Clinical Medicine, University of Tromsø, Department of Pathology, University Hospital, Norway. Ingridt@fagmed.uit.no
Bønaa
K H
KH
Lindal
S
S
Berg
T J
TJ
Jenssen
T
T
D000328:Adult; D000368:Aged; D001706:Biopsy; D001794:Blood Pressure; D015992:Body Mass Index; D002196:Capillaries / Q000473:pathology; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D015309:Glucose Clamp Technique; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000473:pathology*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D011159:Population Surveillance
D005230:Fatty Acids, Nonesterified; D005947:Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin