James Stray-Gundersen

Relationships of generalized and regional adiposity to insulin sensitivity in men.

The relative impacts of regional and generalized adiposity on insulin sensitivity have not been fully defined. Therefore, we investigated the relationship of insulin sensitivity (measured using hyperinsulinemic, euglycemic clamp technique with [3-3H]glucose turnover) to total body adiposity (determined by hydrodensitometry) and regional adiposity. The latter was assessed by determining subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses (using magnetic resonance imaging) and the sum of truncal and peripheral skinfold thicknesses. 39 healthy middle-aged men with a wide range of adiposity were studied. Overall, the intraperitoneal and retroperitoneal fat constituted only 11 and 7% of the total body fat. Glucose disposal rate (Rd) and residual hepatic glucose output (rHGO) values during the 40 mU/m2.min insulin infusion correlated significantly with total body fat (r = -0.61 and 0.50, respectively), subcutaneous abdominal fat (r = -0.62 and 0.50, respectively), sum of truncal skinfold thickness (r = -0.72 and 0.57, respectively), and intraperitoneal fat (r = -0.51 and 0.44, respectively) but not to retroperitoneal fat. After adjusting for total body fat, the Rd and rHGO values showed the highest correlation with the sum of truncal skinfold thickness (partial r = -0.40 and 0.33, respectively). We conclude that subcutaneous truncal fat plays a major role in obesity-related insulin resistance in men, whereas intraperitoneal fat and retroperitoneal fat have a lesser role.

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.

Uremic myopathy limits aerobic capacity in hemodialysis patients

Eleven end-stage renal disease patients trained by stationary cycling during their hemodialysis treatments. After a 6-week control period, 12 weeks of training began and was increased to 30 to 60 minutes at > or = 70% of peak heart rate. Baseline, pretraining and, posttraining exercise tests were performed. Workload (WL), oxygen uptake (VO2peak), cardiac output (Q), heart rate (HR), and arterial oxygen content (CaO2) were measured. Stroke volume (SV), arteriovenous oxygen difference ((a-v)O2), and mixed-venous oxygen content (CvO2) were calculated. Rectus femoris biopsies were obtained pretraining and posttraining. At peak exercise, WL increased from 60 +/- 4 to 70 +/- 6 W (P < 0.05), VO2peak showed an upward trend from 14.8 +/- 0.9 to 16.8 +/- 1.3 mL/kg/min (P < 0.1), and Q, HR, SV, CaO2, CvO2, and (a-v)O2 were unchanged. Ten of the 11 patients increased WL, but only six increased VO2peak (five of 11 patients decreased VO2peak). The difference between groups (P < 0.02) was attributable to (a-v)O2, which increased in those who increased VO2peak (P < 0.02). There was an upward trend for succinate dehydrogenase activity (P < 0.06), and phosphofructokinase activity increased (P < 0.05). However, the rectus femoris capillary to fiber ratio, type I and II fiber areas, and fiber area variability were unchanged, and neither histomorphologic nor enzymatic activity changes were related to change in VO2peak. We conclude that not all dialysis patients increase VO2peak after training, but most can improve exercise capacity. Patients who improved VO2peak widened their (a-v)O2 difference, increasing oxygen extraction and showing that oxygen delivery is not always the limiting factor. Thus, the limitation of VO2peak in dialysis patients is a complex interaction of central and peripheral factors. Muscle therapies, such as exercise training, are needed in addition to increased oxygen delivery in rehabilitation of dialysis patients.

Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes

Although many studies of the effect of dynamic exercise training on left ventricular (LV) mass have been reported, controversy continues to exist. Previous work has been criticized because of the techniques used for measuring LV mass, the variable level of training of the subjects recruited and the methods used to normalize the data. In an attempt to resolve this controversy, LV mass was determined using the very accurate and reproducible technique of magnetic resonance imaging (MRI). Highly trained competitive athletes including cross-country skiers, endurance cyclists and long distance runners (VO2max = 77 +/- 1, 72 +/- 2 and 75 +/- 2 ml (kg X min)-1, respectively) were examined. The data were normalized for body weight, body surface area and lean body mass. LV mass was significantly greater in skiers (239 +/- 9 g), runners (244 +/- 10 g) and cyclists (258 +/- 11 g) when compared with nonathletic control subjects (189 +/- 6 g) (p less than 0.001), which represents percent differences of 26, 29 and 37%, respectively. LV mass remained greater in the athletes, regardless of the method used to normalize the data. In addition, there was a good correlation between LV mass and VO2max (r = 0.80, p less than 0.001). It was concluded that LV mass is significantly greater in highly trained competitive endurance athletes and that normalizing LV mass with respect to body weight, body surface area or lean body mass does not alter this relation.

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.

Left ventricular dimensions and mass using magnetic resonance imaging in female endurance athletes

Few published studies of left ventricular (LV) mass in female endurance athletes have been performed with M-mode echocardiography, which involves assumptions of LV geometry. Therefore, magnetic resonance imaging, a 3-dimensional technique, was used to examine LV mass, LV end-diastolic volume and mean wall thickness in female long distance runners (n = 13; mean age 29 years), cyclists (n = 12; mean age 26 years) and cross-country skiers (n = 11; mean age 24 years), and the findings were compared with sedentary control subjects (n = 10; mean age 27 years) matched for height and body weight. The physical characteristics for all subjects included height (mean 166 cm, and body weight (mean 56 kg). The percent body fat (mean 11.7) and maximal oxygen uptake (VO2max, mean 63 ml.kg-1.min-1) were similar (p greater than 0.05) among all athletic groups, but significantly different from the control group (body fat, mean 22.5%; VO2max, mean 35 ml.kg-1.min-1). LV mass (mean 159 kg), LV end-diastolic volume (mean 122 ml), and mean wall thickness (mean 11.5 mm) were also similar among the athletic groups and significantly larger than the following control values: LV mass (mean 115 g), LV end-diastolic volume (mean 93 ml) and mean wall thickness (mean 9.8 mm). Ratios of LV mass to lean body weight were similar among all athletic groups, although athletic groups had larger ratios (p less than 0.05) than the sedentary control subjects. LV mass/LV end-diastolic volume ratio was similar (p greater than 0.05) among all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of altitude on football performance

Altitude will impact football performance through two separate and parallel pathways related to the hypobaric (physical) and hypoxic (physiological) components of terrestrial altitude: (a) the decrease in partial pressure of oxygen reduces maximal oxygen uptake and impairs “aerobic” performance by reducing maximal aerobic power, increasing the relative intensity of any given absolute level of work, and delaying recovery of high‐energy phosphates between high‐intensity “interval” type efforts; (b) the decrease in air density reduces air resistance which will facilitate high‐velocity running, but will also alter drag and lift thereby impairing sensorimotor skills. These effects appear to have their greatest impact very early in the altitude exposure, and their physiological/neurosensory consequences are ameliorated by acclimatization, though the extent of restoration of sea level type performance depends on the absolute magnitude of the competing and living altitudes.

The effect of body position on the energy cost of cycling

Energy expenditure during bicycling on flat terrain depends predominantly on air resistance, which is a function of total frontal area (bicycle and rider), coefficient of drag, and air speed. Body position on the bicycle may affect energy expenditure by altering either frontal area or coefficient of drag. In this study, oxygen uptake (VO2) was measured for each of four body positions in 10 cyclists (8 males, 2 females, 24 +/- 2 yr, 67.7 +/- 3.3 kg, VO2max = 65.8 +/- 1.5 ml.kg-1.min-1) while each bicycled up a 4% incline on a motor-driven treadmill (19.3 km.h-1), thereby eliminating air resistance. Positions studied included: 1) seated, hands on brake hoods, cadence 80 rev.min-1; 2) seated, hands on dropped bar (drops), 80 rev.min-1; 3) standing, hands on brake hoods, 60 rev.min-1; and 4) seated, hands on brake hoods, 60 rev.min-1. Subjects rode their own bicycles, which were equipped with a common set of racing wheels. Energy expenditure, expressed as VO2 per unit combined weight, was not significantly different between drops and hoods positioning (30.2 +/- 0.6 vs 29.9 +/- 0.9 ml.kg-1.min-1) but was significantly greater for standing compared with seated cycling (31.7 +/- 0.4 vs 28.3 +/- 0.7 ml.kg-1.min.-1, P less than 0.01). These results indicate that body posture can affect energy expenditure during uphill bicycling through factors unrelated to air resistance.

Muscle cross-sectional area and torque in resistance-trained subjects.

SummaryEight elite male bodybuilders (MB), five elite female bodybuilders (FB), eight male control (MC), and eight female control recreational weight-trainers (FC) performed maximal elbow flexions on an isokinetic dynamometer at velocities between 1.02 and 5.24 rad·s−1, from which peak torque (PT) was measured. Elbow flexor cross-sectional area (CSA) was measured by computed tomographic scanning. Flexor CSA·lean body mass−1 ratios were greater in MB than in other subject groups. Correlations of PT were positively related to CSA but negatively to CSA·lean body mass−1 and to PT·CSA−1. PT·CSA−1 at low-velocity contractions were greater in MC and FC than in MB and FB groups, suggesting a training effect. The velocity-associated declines in torque between velocities of 1.02 and 5.24 rad·−1 averaged 28.4 ± 0.9% and were statistically identical in men and women among the subject groups, suggesting that neither gender nor training had affected this variable.

Defining the “dose” of altitude training: how high to live for optimal sea level performance enhancement

Chronic living at altitudes of ∼2,500 m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared with athletes living at lower altitudes. After 4 wk of group sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m). All athletes trained together daily at a common altitude from 1,250-3,000 m following a modified live high-train low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. On return from altitude, 3,000-m time trial performance was significantly improved in groups living at the middle two altitudes (2,085 and 2,454 m), but not in groups living at 1,780 and 2,800 m. EPO was significantly higher in all groups at 24 and 48 h, but returned to sea level baseline after 72 h in the 1,780-m group. Erythrocyte volume was significantly higher within all groups after return from altitude and was not different between groups. These data suggest that, when completing a 4-wk altitude camp following the live high-train low model, there is a target altitude between 2,000 and 2,500 m that produces an optimal acclimatization response for sea level performance.