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Biomedical subjects

J Stray-Gundersen

Publications and source records attributed to J Stray-Gundersen.

At least 19 recordsLinked to original sources

Hormonal responses in athletes: the use of a two bout exercise protocol to detect subtle differences in (over)training status.

In overtrained athletes, several signs and symptoms have been associated with the imbalance between training and recovery. However, reliable diagnostic markers for distinguishing between well-trained, overreached (OR) and overtrained (OT) athletes are lacking. A hallmark feature of overtraining syndrome (OTS) is the inability to sustain intense exercise and recover for the next training or competition session. We therefore devised a test protocol utilizing two bouts of maximal work. With this test protocol we tried to establish a difference in hormonal responses between the training status of T and OR athletes. Seven well-trained cyclists participated in this study and were tested before and after a training camp. We also present the data of one OT motocross athlete who was clinically diagnosed as overtrained. All athletes performed two maximal exercise tests separated by 4 h. Blood was analyzed for cortisol, adrenocorticotrophic hormone (ACTH), growth hormone and prolactin (PRL). Performance decreased by 6% between the first and the second exercise test in the OR group and by 11% in the OT subject. Moreover, during the second exercise test there were more marked differences between the T and OR athletes; in particular, the OT subject did not show an increase in some of the hormonal responses. PRL increased only by 14% in the OT subject's second test and there was a 7% decrease in ACTH. The two exercise approach enables us to detect subtle performance decrements that will not be identified by one exercise trigger. The hormonal responses to the second exercise test were different between the T and OR athletes (the increase in the T group was higher than in the OR that was higher than in the OT). The results of the case presentation of an overtrained athlete provide evidence of an altered and dysfunctional hypothalamic-pituitary axis response to two bouts of maximal exercise. These findings can be used to develop markers for diagnosis of OTS and to begin to address the pathologic mechanism operative in the syndrome, as well as providing an outcome measure to evaluate possible therapeutic regimes.

Adaptation, Physiological↗

Determinants of erythropoietin release in response to short-term hypobaric hypoxia.

We measured blood erythropoietin (EPO) concentration, arterial O(2) saturation (Sa(O(2))), and urine PO(2) in 48 subjects (32 men and 16 women) at sea level and after 6 and 24 h at simulated altitudes of 1,780, 2,085, 2,454, and 2,800 m. Renal blood flow (Doppler) and Hb were determined at sea level and after 6 h at each altitude (n = 24) to calculate renal O(2) delivery. EPO increased significantly after 6 h at all altitudes and continued to increase after 24 h at 2,454 and 2,800 m, although not at 1,780 or 2,085 m. The increase in EPO varied markedly among individuals, ranging from -41 to 400% after 24 h at 2,800 m. Similar to EPO, urine PO(2) decreased after 6 h at all altitudes and returned to baseline by 24 h at the two lowest altitudes but remained decreased at the two highest altitudes. Urine PO(2) was closely related to EPO via a curvilinear relationship (r(2) = 0.99), although also with prominent individual variability. Renal blood flow remained unchanged at all altitudes. Sa(O(2)) decreased slightly after 6 h at the lowest altitudes but decreased more prominently at the highest altitudes. There were only modest, albeit statistically significant, relationships between EPO and Sa(O(2)) (r = 0.41, P < 0.05) and no significant relationship with renal O(2) delivery. These data suggest that 1) the altitude-induced increase in EPO is "dose" dependent: altitudes > or =2,100-2,500 m appear to be a threshold for stimulating sustained EPO release in most subjects; 2) short-term acclimatization may restore renal tissue oxygenation and restrain the rise in EPO at the lowest altitudes; and 3) there is marked individual variability in the erythropoietic response to altitude that is only partially explained by "upstream" physiological factors such as those reflecting O(2) delivery to EPO-producing tissues.

Acute Disease↗

The effects of altitude training are mediated primarily by acclimatization, rather than by hypoxic exercise.

For training at altitude to be effective, it must provide some advantage above and beyond similar training at sea level. This advantage could be provided by: 1) acclimatization to altitude which improves oxygen transport and/or utilization; 2) hypoxic exercise which "intensifies" the training stimulus; or 3) some combination of both. Controlled studies of "typical" altitude training, involving both altitude acclimatization and hypoxic exercise have never been shown to improve sea level performance. This failure has been attributed to reduced training loads at altitude. One approach developed by Levine and Stray-Gundersen, called "living high-training low" has been shown to improve sea level performance over events lasting 8-20 minutes. This strategy combines altitude acclimatization (2,500 m) with low altitude training to get the optimal effect. The opposite strategy, "living low-training high" is proposed by Dr. Hoppeler in this debate. In defense of the primacy of the altitude acclimatization effect, data will be presented to support the following: 1). Living high-training low clearly improves performance in athletes of all abilities; 2). The mechanism of this improvement is primarily an increase in erythropoietin leading to increased red cell mass, VO2max, and running performance; 3). Rather than intensifying the training stimulus, training at altitude leads to the opposite effect--reduced speeds, reduced power output, reduced oxygen flux--and, following the principal of symmorphosis, is not likely to provide any advantage for a well trained athlete; 4). At the moderate altitudes used by most athletes, resting oxygen delivery to skeletal muscle is well preserved, arguing against any detrimental effect on "protein synthesis"; 5). It is possible however, that at significantly higher altitudes, acclimatization leads to appetite suppression, inhibition of protein synthesis, muscle wasting, excessive ventilatory work, and metabolic compensation that is NOT advantageous for a competitive athlete.

Acclimatization↗

"Living high-training low" altitude training improves sea level performance in male and female elite runners.

Acclimatization to moderate high altitude accompanied by training at low altitude (living high-training low) has been shown to improve sea level endurance performance in accomplished, but not elite, runners. Whether elite athletes, who may be closer to the maximal structural and functional adaptive capacity of the respiratory (i.e., oxygen transport from environment to mitochondria) system, may achieve similar performance gains is unclear. To answer this question, we studied 14 elite men and 8 elite women before and after 27 days of living at 2,500 m while performing high-intensity training at 1,250 m. The altitude sojourn began 1 wk after the USA Track and Field National Championships, when the athletes were close to their season's fitness peak. Sea level 3,000-m time trial performance was significantly improved by 1.1% (95% confidence limits 0.3-1.9%). One-third of the athletes achieved personal best times for the distance after the altitude training camp. The improvement in running performance was accompanied by a 3% improvement in maximal oxygen uptake (72.1 +/- 1.5 to 74.4 +/- 1.5 ml x kg(-1) x min(-1)). Circulating erythropoietin levels were near double initial sea level values 20 h after ascent (8.5 +/- 0.5 to 16.2 +/- 1.0 IU/ml). Soluble transferrin receptor levels were significantly elevated on the 19th day at altitude, confirming a stimulation of erythropoiesis (2.1 +/- 0.7 to 2.5 +/- 0.6 microg/ml). Hb concentration measured at sea level increased 1 g/dl over the course of the camp (13.3 +/- 0.2 to 14.3 +/- 0.2 g/dl). We conclude that 4 wk of acclimatization to moderate altitude, accompanied by high-intensity training at low altitude, improves sea level endurance performance even in elite runners. Both the mechanism and magnitude of the effect appear similar to that observed in less accomplished runners, even for athletes who may have achieved near maximal oxygen transport capacity for humans.

Acclimatization↗

Changes in hemoglobin values in elite cross-country skiers from 1987-1999.

Hemoglobin data have been available from ski teams beginning from 1987, and from 1989 to 1999 we have followed hemoglobin values in elite cross-country skiers in international competitions. The mean values at the 1989 World Nordic Ski Championships were lower than population reference values, as would be expected from plasma volume expansion associated with endurance training. However, an increase, particularly in the maximal values, became obvious in 1994 and rose further in 1996. These extreme values provide both a health risk to the individual athlete and unfair competition. After a rule limiting hemoglobin values was introduced, the drop of the highest values was remarkable: among men 15 g/l (0.23 mmol/l) and among women 42 g/l (0.65 mmol/l). It would appear that the rule had achieved its goal of limiting extreme hemoglobin values. Yet the mean hemoglobin concentrations in men and women have continued to rise, suggesting the continued use of artificial methods to increase total hemoglobin mass.

Acclimatization↗

Effect of rhEPO administration on serum levels of sTfR and cycling performance.

PURPOSE: We assessed the possibility of using soluble transferrin receptor (sTfR) as an indicator of doping with recombinant erythropoietin (rhEPO). METHODS: A double-blind, placebo-controlled study was conducted with the administration of 5,000 U of rhEPO (N = 10) or placebo (N = 10) three times weekly (181-232 U x kg(-1) x wk-1) for 4 wk to male athletes. We measured hematocrit and the concentration of hemoglobin, sTfR, ferritin, EPO, and quantified the effects on performance by measuring time to exhaustion and maximal oxygen uptake (VO2max) on a cycle ergometer. RESULTS: Hematocrit increased from 42.7 +/- 1.6% to 50.8 +/- 2.0% in the EPO group, and peaked 1 d after treatment was stopped. In the EPO group, there was an increase in sTfR (from 3.1 +/- 0.9 to 6.3 +/- 2.3 mg x L(-1) , P < 0.001) and in the ratio between sTfR and ferritin (sTfR-ferritin(-1)) (from 3.2 +/- 1.6 to 11.8 +/- 5.1, P < 0.001). The sTfR increase was significant after 1 wk of treatment and remained so for 1 wk posttreatment. Individual values for sTfR throughout the study period showed that 8 of 10 subjects receiving rhEPO, but none receiving placebo, had sTfR levels that exceeded the 95% confidence interval for all subjects at baseline (= 4.6 mg x L(-1)). VO2max increased from 63.6 +/- 4.5 mL x kg(-1) x min(-1) before to 68.1 +/- 5.4 mL x kg(-1) x min(-1) 2 d post rhEPO administration (7% increase, P = 0.001) in the EPO group. Hematocrit, sTfR, sTfR-ferritin(-1), and VO2max did not change in the placebo group. CONCLUSION: Serum levels of sTfR may be used as an indirect marker of supranormal erythropoiesis up to 1 wk after the administration of rhEPO, but the effects on endurance performance outlast the increase in sTfR.

Adult↗

Skeletal muscle morphology and exercise response in congenital generalized lipodystrophy.

OBJECTIVE: Congenital generalized lipodystrophy (CGL) is an autosomal recessive genetic disorder characterized by almost complete absence of adipose tissue, muscular appearance, and severe insulin resistance since birth. We investigated whether insulin resistance in CGL patients is associated with abnormal muscle morphology and whether increased muscularity imparts increased muscle strength and exercise capacity RESEARCH DESIGN AND METHODS: We obtained quadriceps muscle biopsies to study muscle fiber types and capillary density in three African-American women (aged 17-20 years) with CGL. We also assessed quadriceps muscle strength, muscle metabolism, and maximal O2 consumption in the patients. RESULTS: Quadriceps muscle biopsies revealed a markedly higher percentage of type II (fast-twitch glycolytic) muscle fibers in patients with CGL versus sedentary young women (75-78 vs. 47-57%, respectively). The capillary-to-fiber ratio (2.7-3.0), however, was normal. Cross-sectional areas of type I (slow-twitch oxidative) (1,262-2,685 microm2) and type II (2,304-3,594 microm2) fibers were far below the normal values (3,811-4,310 and 3,115-4,193 microm2, respectively), suggesting muscle hyperplasia but not hypertrophy The quadriceps muscle strength, as measured by Cybex, was below average; the maximal O2 consumption (23-32 ml x kg(-1) x min(-1)) was also below average. 31P nuclear magnetic resonance spectroscopy of the forearm muscles revealed normal pH and metabolic responses to static and dynamic exercises. CONCLUSIONS: We conclude that insulin resistance in patients with CGL is associated with an increased proportion of type II muscle fibers but not reduced capillary density. Increased muscularity in CGL is due to muscle hyperplasia and is not associated with increased muscle strength.

Adipose Tissue↗

Evidence for restricted muscle blood flow during speed skating.

INTRODUCTION: We have previously hypothesized restricted muscle blood flow during speed skating, secondary to the high intramuscular forces intrinsic to the unique posture assumed by speed skaters and to the prolonged duty cycle of the skating stroke. METHODS: To test this hypothesis, we studied speed skaters (N = 10) during submaximal and maximal cycling and in-line skating, in both low (knee angle = 107 degrees) and high (knee angle = 112 degrees) skating positions (CE vs SkL vs SkH). Supportive experiments evaluated muscle desaturation and lactate accumulation during on-ice speed skating and muscle desaturation during static exercise at different joint positions. RESULTS: Consistent with the hypothesis were reductions during skating in VO2peak (4.28 vs 3.83 vs 4.26 L x min(-1)), the VO2 at 4 mmol x L(-1) blood lactate (3.38 vs 1.93 vs 3.31 L x min(-1)), and cardiac output during maximal exercise (33.2 vs 25.3 vs 25.6 L x min(-1)). The reduction in maximal cardiac output was not attributable to differences in HRmax (197 vs 192 vs 193 b x min(-1)) but to a reduction in SVmax (172 vs 135 vs 134 mL x beat(-1)). The reduction in SV appeared to be related to an increased calculated systemic vascular resistance (354 vs 483 vs 453 dynes x s(-1) x cm(-1)). During maximal skating there was also a greater % O2 desaturation of the vastus lateralis based on near infrared spectrophotometry (50.3 vs 74.9 vs 60.4% of maximal desaturation during cuff ischemia). The results were supported by greater desaturation with smaller knee angles during static exercise and by greater desaturation and accelerated blood lactate accumulation during on-ice speed skating in the low vs high position. The results of this study support the hypothesis that physiological responses during speed skating are dominated by restriction of blood flow, attributable either to high intramuscular forces, the long duty cycle of the skating stroke, or both.

Adult↗

Relationship between generalized and upper body obesity to insulin resistance in Asian Indian men.

It has been proposed that excessive insulin resistance in Asian Indians living in urban areas or migrated to western countries is responsible for the higher incidence of type 2 diabetes and coronary heart disease observed in this population. To evaluate whether Asian Indians are more insulin resistant than Caucasians and to define the role of generalized and truncal adiposity, we performed hydrodensitometry, skinfold measurements, and euglycemic-hyperinsulinemic clamps in 21 healthy Asian Indian men and 23 Caucasian men of similar age and body fat content. The glucose disposal rate (Rd) was significantly lower in the Asian Indians than in the Caucasians (3.7+/-1.3 vs. 5.3+/-2.0 mg/min x kg lean body mass, respectively; P = 0.003). Despite similar total body fat content, Asian Indians had higher truncal adiposity than Caucasians (sum of truncal skinfolds, 117+/-37 and 92.4+/-38 mm, respectively). In both Asian Indians and Caucasians, the insulin sensitivity index (Rd/plasma insulin concentrations) was inversely correlated with both total body fat (r = -0.49; P<0.03 and r = -0.67; P<0.001, respectively) and sum of truncal skinfold thickness (r = -0.55; P<0.001 and r = -0.61; P<0.002, respectively). After adjustment for total body fat and truncal skinfold thickness, Asian Indians still had a significantly lower glucose disposal rate (P = 0.04). These results show that Asian Indian men are more insulin resistant than Caucasian men independently of generalized or truncal adiposity. The excessive insulin resistance in Asian Indians is probably a primary metabolic defect and may account for the excessive morbidity and mortality from diabetes and coronary heart disease in this population.

Adult↗

Cardiovascular response to submaximal stationary cycling during hemodialysis.

Exercise intolerance is a problem in renal failure. Stationary cycle training during hemodialysis treatment is recommended as safe, effective, and practical, but requires compensations for both exercise and acute changes in uremia. Eight patients pedalled for 5 minutes, at 60% of VO2peak, at 0, 1, 2, and 3 hours of a hemodialysis treatment. Fluid removed, blood pressure, cardiac output, heart rate, O2 uptake, hematocrit, and arterial O2 content were measured. Mean arterial blood pressure, systemic vascular resistance, stroke volume, (a-v)O2 difference, and mixed-venous O2 content were calculated. Fluid removed was 1,356 mL/hr (P < 0.002 for each hour), but with no significant cardiovascular effects during the first 2 hours. At 3 hours, decreasing cardiac output, stroke volume, and mean arterial pressure all reached significance at rest (P < 0.05), and five of eight patients could not exercise. We conclude that the cardiovascular exercise response is superimposed on hemodynamic effects of dialysis and is adequately stable during the first 2 hours of treatment. After 2 hours, cardiovascular decompensation may preclude exercise.

Analysis of Variance↗

Individual variation in response to altitude training.

Moderate-altitude living (2,500 m), combined with low-altitude training (1,250 m) (i.e., live high-train low), results in a significantly greater improvement in maximal O2 uptake (V(02)max) and performance over equivalent sea-level training. Although the mean improvement in group response with this "high-low" training model is clear, the individual response displays a wide variability. To determine the factors that contribute to this variability, 39 collegiate runners (27 men, 12 women) were retrospectively divided into responders (n = 17) and nonresponders (n = 15) to altitude training on the basis of the change in sea-level 5,000-m run time determined before and after 28 days of living at moderate altitude and training at either low or moderate altitude. In addition, 22 elite runners were examined prospectively to confirm the significance of these factors in a separate population. In the retrospective analysis, responders displayed a significantly larger increase in erythropoietin (Epo) concentration after 30 h at altitude compared with nonresponders. After 14 days at altitude, Epo was still elevated in responders but was not significantly different from sea-level values in nonresponders. The Epo response led to a significant increase in total red cell volume and V(O2) max in responders; in contrast, nonresponders did not show a difference in total red cell volume or V(O2)max after altitude training. Nonresponders demonstrated a significant slowing of interval-training velocity at altitude and thus achieved a smaller O2 consumption during those intervals, compared with responders. The acute increases in Epo and V(O2)max were significantly higher in the prospective cohort of responders, compared with nonresponders, to altitude training. In conclusion, after a 28-day altitude training camp, a significant improvement in 5,000-m run performance is, in part, dependent on 1) living at a high enough altitude to achieve a large acute increase in Epo, sufficient to increase the total red cell volume and V(O2)max, and 2) training at a low enough altitude to maintain interval training velocity and O2 flux near sea-level values.

Acclimatization↗

Relationship of anterior and posterior subcutaneous abdominal fat to insulin sensitivity in nondiabetic men.

Recent studies from our reveal that adipose tissue (AT) in the subcutaneous abdominal region is the most important determinant of peripheral and hepatic insulin sensitivity. Because of different anatomic and physiologic characteristics of anterior and posterior subcutaneous abdominal AT, we investigated the relationship of the masses of each compartment, as determined by magnetic resonance imaging, to insulin sensitivity (using euglycemic hyperinsulinemic glucose clamp technique), and other anthropometric variables. Thirty-four healthy men with varying ranges of obesity were recruited for the study. The mass of posterior subcutaneous abdominal AT was approximately 1.6 times more than that of the anterior compartment, and these masses accounted for 12.9% and 8.2% of the total body fat mass, respectively. All anthropometric variables, including body mass index (BMI), waist-to-hip circumference ratio (WHR), skin-fold thicknesses, and intraperitoneal AT mass were more significantly related to the posterior than the anterior subcutaneous abdominal AT mass. Compared to the anterior compartment mass, the posterior compartment mass displayed stronger relationship with insulin-mediated glucose disposal (Rd) (r = -0.44, p = 0.009, and r = -0.76, p = 0.0001, respectively) as well as with residual hepatic glucose output during the 40 mU.m-2.min-1 insulin infusion (r = 0.39, p = 0.02, and r = 0.53, p = 0.001, respectively). After adjusting for total body fat, the Rd values showed a significant partial correlation with the posterior subcutaneous abdominal AT mass (r = 0.52, p = 0.002). To conclude, posterior subcutaneous abdominal AT mass is more important determinant of peripheral and hepatic insulin sensitivity than the anterior subcutaneous abdominal AT.

Adipose Tissue↗

"Living high-training low": effect of moderate-altitude acclimatization with low-altitude training on performance.

The principal objective of this study was to test the hypothesis that acclimatization to moderate altitude (2,500 m) plus training at low altitude (1,250 m), "living high-training low," improves sea-level performance in well-trained runners more than an equivalent sea-level or altitude control. Thirty-nine competitive runners (27 men, 12 women) completed 1) a 2-wk lead-in phase, followed by 2) 4 wk of supervised training at sea level; and 3) 4 wk of field training camp randomized to three groups: "high-low" (n = 13), living at moderate altitude (2,500 m) and training at low altitude (1,250 m); "high-high" (n = 13), living and training at moderate altitude (2,500 m); or "low-low" (n = 13), living and training in a mountain environment at sea level (150 m). A 5,000-m time trial was the primary measure of performance; laboratory outcomes included maximal O2 uptake (VO2 max), anaerobic capacity (accumulated O2 deficit), maximal steady state (MSS; ventilatory threshold), running economy, velocity at VO2 max, and blood compartment volumes. Both altitude groups significantly increased VO2 max (5%) in direct proportion to an increase in red cell mass volume (9%; r = 0.37, P < 0.05), neither of which changed in the control. Five-kilometer time was improved by the field training camp only in the high-low group (13.4 +/- 10 s), in direct proportion to the increase in VO2 max (r = 0.65, P < 0.01). Velocity at VO2 max and MSS also improved only in the high-low group. Four weeks of living high-training low improves sea-level running performance in trained runners due to altitude acclimatization (increase in red cell mass volume and VO2 max) and maintenance of sea-level training velocities, most likely accounting for the increase in velocity at VO2 max and MSS.

Acclimatization↗

Evidence of a secondary hypervolemia in trained man following acute high intensity exercise.

Exercise induced hypervolemia is well documented following the initial onset of chronic exercise. In trained man, however, it might be difficult to induce further PV expansion with exercise induced hypervolemia already present. Therefore the primary goal of this study was determine the effect of acute high intensity exercise on plasma volume (PV), cardiac output (CO), stroke volume (SV), heart rate (HR), and oxygen consumption (VO2), in fourteen male competitive runners (VO2max 60.7 +/- 6.4 ml.kg-1.min-1) in the middle of their season. In this well trained state, subjects twice performed three steady state runs at different speeds, and one maximal graded exercise test (baseline). After this baseline evaluation, subjects exercised at a high intensity (approximately 90-95% of VO2max) on 2 consecutive days (short-term high intensity STHI exercise). Subjects then repeated the submaximal runs and maximal exercise test (post high intensity exercise, PHIE). Following the intense exercise period, the subjects experienced an increase in PV of 4.4% (p < 0.05), HR was significantly reduced for any given running speed (p < 0.05) as was blood lactate concentration (p < 0.05), and SV was significantly increased by 4% (p < 0.05). Both CO and VO2 at submaximal running speeds were unaffected by the acute increase in exercise intensity. Maximal HR was also significantly reduced following the intense exercise (p < 0.05), but VO2max was unchanged. These data illustrate that STHI exercise can induce a secondary hypervolemia at a given work rate in trained man. These findings support scientific and anecdotal reports of a reduced HR response at a given work rate PHIE.

Adult↗

Important determinants of anaerobic running performance in male athletes and non-athletes.

The purpose of this study was to investigate the importance of selected metabolic and neuromuscular determinants as predictors of anaerobic running performance. The subjects were male 400-m runners (n = 21), middle- (n = 8) and long-distance runners (n = 11), power athletes (n = 14) and physically active men (n = 34). Maximal power (Pmax), peak blood lactate concentration (peak BLa), power at 10 mM blood lactate level (P10mM), height (CMJrest) and percentage decrease (CMJdecrease) of the counter-movement jump were determined by the maximal anaerobic running test (MART). In addition, maximal oxygen uptake (VO2max) was determined on a treadmill and maximal running velocity (V30m) was measured by the 30-m speed test on a track. Stepwise regression analysis revealed that V30m, P10mM and peak BLa accounted for 92% (P < 0.001) of the variation in Pmax. Regression analysis showed also that V30m, P10mM and delta P (the difference between Pmax and VO2max) were the most important determinants of the 400-m run on a track within a homogeneous group of 400-m runners. The middle-distance and 400-m runners had higher Pmax and P10mM than the long-distance and control group (p < 0.05). The 400-m runners had superior V30m and delta P than the other groups. Furthermore, the 400-m runners and power athletes had higher peak BLa than the long-distance and control group (p < 0.05). The present findings showed that V30m, P10mM and peak BLa determined by the 30-m speed test and the MART were the most important components of anaerobic work capacity. These determinants could be used to explain the differences in anaerobic work capacity between various sport groups as well as between different athletes.

Adult↗

Relationship of generalized and regional adiposity to insulin sensitivity in men with NIDDM.

Abdominal obesity, particularly excess intraperitoneal fat, is considered to play a major role in causing insulin resistance and NIDDM. To determine if NIDDM patients accumulate excess intraperitoneal fat, and whether this contributes significantly to their insulin resistance, 31 men with mild NIDDM with a wide range of adiposity were compared with 39 nondiabetic, control subjects for insulin sensitivity (measured using euglycemic-hyperinsulinemic clamp technique with [3-3H]glucose turnover) and total and regional adiposity (assessed by hydrodensitometry and by measuring subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses using magnetic resonance imaging [MRI], and truncal and peripheral skinfold thicknesses using calipers). MRI analysis revealed that intraperitoneal fat was not increased in NIDDM patients compared with control subjects; in both groups it averaged 11% of total body fat. NIDDM patients, however, had increased truncal-to-peripheral skinfolds thickness ratios. In NIDDM patients, as in control subjects, amounts of truncal subcutaneous fat showed a stronger correlation with glucose disposal rate than intraperitoneal or retroperitoneal fat; however, NIDDM patients were more insulin resistant at every level of total or regional adiposity. Further, no particular influence of excess intraperitoneal fat on hepatic insulin sensitivity was noted. We conclude that NIDDM patients do not have excess intraperitoneal fat, but that their fat distribution favors more truncal and less peripheral subcutaneous fat. Moreover, for each level of total and regional adiposity, NIDDM patients have a heightened state of insulin resistance.

Adipose Tissue↗