Interrater reliability of a customized submaximal cycle ergometer test.

PURPOSE: Graded exercise testing (GXTs) is used to determine maximum oxygen uptake ([Formula: see text]). Recently, customized submaximal exercise testing (CSET) completed on both treadmill and cycle ergometry were validated. METHODS: Interrater reliability of the CSET for cycle ergometry was examined. Thirteen participants (age 31 ± 10.2 y, weight 77.9 ± 10.5 kg, height 176.2 ± 9.9 cm, body mass index 25.1 ± 2.9) completed the 2-stage × 3-min CSET protocol performed by two separate testers. True [Formula: see text] was determined using the highest value derived by a GXT and verification bout. Skeletal muscle oxygen saturation ([Formula: see text]), measured using near-infrared spectrometry on the medial gastrocnemius muscle, and [Formula: see text] were monitored during each CSET; whereby, [Formula: see text] kinetics were modeled breath-by-breath data for each 3-min stage. Measurement agreement was quantified using intraclass coefficient (ICC), typical error (TE), and coefficient of variation (CV). RESULTS: "True" [Formula: see text] (ml·kg-1·min-1) between the GXT (41.3 ± 10.5) and verification (42.5 ± 11.5) was established (ICC = 0.98, TE: 0.98, CV 2.1%). Estimated [Formula: see text] by tester 1 (42.5 ± 9.8) and tester 2 (42.7 ± 8.9) did not differ from "true" [Formula: see text] (F2,36 = 0.02, p = 0.98, ηp2 = 0.00). The second stage evoked a [Formula: see text] slow component of 194 ± 124 ml·min-1 that corresponded with a time-dependent decline of [Formula: see text]. The mean [Formula: see text] from the two CSET testers were highly correlated (ICC = 0.91, TE: 4.1%, CV = 8.9%). CONCLUSIONS: The CSET is a reliable and valid procedure and [Formula: see text] is a useful tool for corroborating the second stage is in the heavy-intensity domain.

Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training.

High-density lipoprotein (HDL) metabolism was studied in eight sedentary men before and after 14 and 32-48 weeks of exercise training. Subjects rode stationary bicycles 1 hour daily, 5 days each week for 14 weeks (n = 8), and 4 days each week thereafter for a total of 32-48 weeks (n = 7) of training. HDL metabolism was assessed with 125I-radiolabeled autologous HDL while subjects consumed defined diets. Maximal oxygen uptake increased 26 +/- 7% (p less than 0.001) after 14 weeks but did not increase further with more prolonged training. Body weight and estimated body fat did not change. HDL cholesterol increased 5 +/- 3 mg/dl, and triglycerides decreased 19 +/- 23 mg/dl after 14 weeks (p less than 0.025 for both), but there were no additional changes with continued training. Postheparin plasma lipoprotein lipase activity was 22% higher than baseline activity after both 14 (p less than 0.025) and 32 or more weeks of exercise. In contrast, hepatic triglyceride lipase activity was 16 +/- 8% and 15 +/- 8% lower than baseline at each measurement (p less than 0.005 for both). The disappearance rate of triglycerides after an intravenously administered fat solution was 24 +/- 24% higher at 14 weeks and 49 +/- 18% (p less than 0.005) higher after more prolonged training. Total and low-density lipoprotein cholesterol and apolipoprotein A-I and A-II concentrations at the end of study were not different from initial values. Plasma volume was 8% above initial values at both post-training measurements. The biological half-life of apolipoprotein A-I was unchanged at 14 weeks but was 10 +/- 13% longer (p = 0.07) and increased in all but one subject at the end of the study. Half-life for apolipoprotein A-II was 8 +/- 8% (p = 0.031) and 11 +/- 14% (p = 0.06) above baseline at 14 and 32 or more weeks, respectively. The synthetic rates for apolipoproteins A-I and A-II were not different from baseline values at 32-48 weeks. We conclude that 8-11 months of exercise training in previously sedentary men enhances fat tolerance and increases HDL cholesterol concentrations by prolonging HDL survival. The changes in HDL apolipoprotein survival, however, do not approximate the differences previously noted between elite endurance athletes and sedentary men. Changes in HDL cholesterol concentration were not large and suggest that the potential for exercise-related changes in HDL may be modest in many subjects.

Homologues of the human C and A apolipoproteins in the Macaca fascicularis (cynomolgus) monkey.

We used antisera to human A and C apolipoproteins to identify homologues of these proteins among the high-density lipoprotein apoproteins of Macaca fascicularis (cynomolgus) monkeys, and NH2-terminal analysis was used to verify the homology. The NH2-terminal sequence of the M. fascicularis apoA-I is identical with that of another Old World species, Erythrocebus patas, and differs from human apoA-I at only 4 of the first 24 residues. M. fascicularis apoA-II contains a serine for cysteine replacement at position 6 and is therefore monomeric like the apoA-II from all species below apes. Human and monkey apoA-II are not otherwise different through their first 25 residues. About 20% of M. fascicularis apoC-I aligns with human apoC-I through residue 22, and 80% lacks an NH2-terminal dipeptide. Otherwise, the monkey apoC-I differs from the human protein at only 2 of 25 positions. Two forms of M. fascicularis apoC-II were identified. ApoC-II1 is highly homologous with human apoC-II, whereas an NH2-terminal hexapeptide is absent from apoC-II2. ApoC-II2 was the predominant species, and apoC-II1 appears to represent a propeptide from which a hexapeptide prosegment is cleaved at a Gln-Asp bond. Both forms of monkey apoC-II are potent activators of lipoprotein lipase. There are two polymorphic forms of M. fascicularis apoC-III, and their electrophoretic mobilities become identical after treatment with neuraminidase. Except for a glycine for serine substitution at position 10, the first 15 NH2-terminal residues of M. fascicularis and human apoC-III are the same.

Exercise acutely increases high density lipoprotein-cholesterol and lipoprotein lipase activity in trained and untrained men.

We studied the effects of a single exercise session on lipid and lipoprotein concentrations and on postheparin plasma lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase activities (HTGLA) in 11 trained (T) and ten untrained (UT) men. Subjects exercised on a bicycle ergometer at 80% of their maximal heart rate for one (UT) or two hours (T). Blood samples were drawn 24 hours before and at ten minutes and 24, 48, and 72 hours after exercise. Values were analyzed before and after adjustment for estimated changes in plasma volume (PV). High density lipoprotein cholesterol (HDL-C) increased 2 +/- 4 mg/dL in T (P less than 0.05) and 1 +/- 2 mg/dL in UT subjects beginning 48 hours after exercise. This increase was magnified by adjusting for the 5% to 8% postexercise expansion of PV. The increase in HDL in the T subjects was produced by increases in the HDL2-C subfraction (+3 +/- 4 mg/dL, P less than 0.05) whereas HDL3 increased in the UT men (+2 +/- 3 mg/dL, P less than 0.05). LPLA did not change in either subject group when estimated PV changes were ignored but increased 11% (P less than 0.05) at 24 hours after exercise when PV was considered. HTGLA was 11% below baseline in the UT men 24 to 72 hours after exercise (P less than 0.05) but showed no change in either subject group after adjustment for PV. These results demonstrate that exercise acutely increases HDL levels by raising the HDL2 subfraction in T and the HDL3 subfraction in UT men.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolonged exercise augments plasma triglyceride clearance.

We studied ten male distance runners before and after a marathon to determine the effects of prolonged exercise on serum lipoprotein values and the capacity to clear plasma triglycerides. Serum lipid and lipoprotein concentrations, intravenous fat clearance, and postheparin plasma lipolytic activities were measured 24 hours before and 18 hours after the race. The clearance rate of exogenous fat increased 76% +/- 64%, postheparin lipoprotein lipase activity increased 46% +/- 35%, and fasting triglyceride levels decreased 26% +/- 13% after the race. High-density lipoprotein (HDL) cholesterol level increased 10% +/- 8%, primarily due to a 19% +/- 17% increase in the HDL2 subfraction. Changes in the clearance rate of exogenous fat were directly related to changes in HDL cholesterol level and the HDL2 subfraction. Thus, the rise in HDL cholesterol concentrations after prolonged exercise may be a consequence of enhanced fat clearance.

Postheparin plasma lipolytic activities in physically active and sedentary men after varying and repeated doses of intravenous heparin.

We sought to determine the optimal dose of heparin for evaluating the activities of lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase (HTGLA) in postheparin plasma. Nine physically active and ten sedentary men (age 30 +/- 5 yr, mean +/- SD) received 30, 50, 75, and 100 IU/kg of heparin in random order during a 2-week period. Based on all the samples, the average LPLA in the athletes was 43% higher (P less than 0.001) and HTGLA was 19% lower than in the untrained subjects (NS). The greatest LPLA was obtained after a heparin dose of 75 IU/kg, but LPLA after the three highest doses were not significantly different. There was also a dose effect on HTGLA (P less than 0.001) with greatest activities following doses of 75 and 100 IU/kg. Despite these dose effects, subjects maintained their rank order for both postheparin lipase activities regardless of the heparin dose. The only exception was for LPLA in the sedentary men probably because of lower LPLA and a smaller range of values. We also examined the effect of repeated daily injections of 75 IU/kg heparin on LPLA, HTGLA, and serum lipids. Repeated heparin administration on three consecutive days produced no significant effects on the apparent lipase activities. When all subjects were combined, HDL-cholesterol was increased over time (P less than 0.05) due to increases in both the HDL2 (P less than 0.05) and HDL3-cholesterol (NS) subfractions. Infusion of heparin or saline on three consecutive days into 18 additional men, however, had no effect on any lipid parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens reduce HDL2-cholesterol and increase hepatic triglyceride lipase activity.

We quantified serum lipids and postheparin plasma lipolytic activities in 5 weightlifters presently self-administering androgenic steroids (users) and an equal number not currently using these drugs (non-users). Mean (+/- SD) age (23 +/- 2 vs 25 +/- 4 yr), body weight (102.7 +/- 11.4 vs 86.8 +/- 13.6 kg), and percent body fat (8.6 +/- 2.5 vs 7.8 +/- 6.0%) were not different in users and non-users, respectively. Similarly, there were no differences in total cholesterol (183 +/- 27 vs 176 +/- 32 mg.dl-1) low-density lipoprotein-cholesterol (138 +/- 25 vs 108 +/- 32 mg.dl-1), or triglyceride (93 +/- 26 vs 93 +/- 41 mg.dl-1) levels in the two groups. High-density lipoprotein (HDL)-cholesterol concentrations, however, were significantly lower in the users (26 +/- 10 vs 50 +/- 13 mg.dl-1; P less than 0.05), and most of the difference was due to lower HDL2-cholesterol concentrations (6 +/- 4 vs 22 +/- 9 mg.dl-1; P less than 0.05). Postheparin plasma lipoprotein lipase activity was only slightly lower in the users (3.49 +/- 2.23 vs 5.36 +/- 1.73 mumol FFA.ml-hr-1; P= NS). but hepatic triglyceride lipase activity was significantly higher in this group (27.99 +/- 6.89 vs 11.15 +/- 2.76, mumol FFA.ml-hr-1: P less than 0.001) and correlated inversely with HDL2-cholesterol concentrations (r = -0.81; P less than 0.01). We conclude that androgenic hormones reduce HDL-cholesterol concentrations and the HDL2-cholesterol subfraction, possibly by enhancing hepatic triglyceride lipase activity.

Training, diet and physical characteristics of distance runners with low or high concentrations of high density lipoprotein cholesterol.

We examined possible determinants of serum high density lipoprotein cholesterol (HDL-C) concentrations in 56 male distance runners (aged 20-56 years) by comparing runners whose HDL-C were either above or below the group median of 63 +/- 13 (+/- SD) mg/dl. HDL-C averaged 53 +/- 7 mg/dl for runners below and 73 +/- 11 mg/dl for runners above the median. Neither exercise training (miles run per week, years of running), physical characteristics (height, weight, adiposity), or dietary factors (total daily caloric intake and daily caloric intake from protein, fat, saturated fat, polyunsaturated fat, carbohydrate, and alcohol) differed between the two groups (P greater than 0.05, MANOVA). Apo A-I (P less than 0.01) was higher and triglyceride concentrations lower (P = 0.07) in the high HDL-C group. The data were also analyzed by comparing runners in the lowest and highest tertiles for HDL-C values and essentially the same results were obtained. When all runners were combined, neither training, physical characteristics nor dietary intake was significantly related to HDL-C (P greater than 0.05). Total cholesterol and apo A-I were directly related (r = 0.35 and r = 0.66, respectively, P less than 0.01) and triglycerides inversely related (r = -0.31, P less than 0.05) to HDL-C. Plasma post-heparin lipoprotein lipase activity (LPLA), hepatic triglyceride lipase activity (HTGLA), and HDL-C subfractions were measured in 22 runners.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of high-carbohydrate and high-fat diets on the serum lipid and lipoprotein concentrations of endurance athletes.

We examined the effects of high-carbohydrate and high-fat diets on the serum lipid levels of distance runners. For seven days before each study, subjects consumed a diet containing 15% protein, 32% fat, and 53% carbohydrate. During 14-day experimental periods, a control group (n = 10) continued the same diet while two other groups consumed 69% of their calories as either carbohydrate (n = 13) or fat (n = 14). High-density lipoprotein (HDL)-cholesterol decreased 9% during the high-carbohydrate diet because of a 26% fall in the HDL2 fraction (1.063 to 1.125 g/mL). These changes were not accompanied by changes in the levels of apolipoproteins (apo) A-I or A-II. Total and low-density lipoprotein (LDL)-cholesterol initially decreased but subsequently exceeded pre-diet values while triglyceride concentrations increased 30% to 50%. Postheparin lipoprotein lipase activity (LPLA) fell 20%. Despite these dietary effects, HDL and HDL2 cholesterol concentrations in the athletes remained above values typical of sedentary men. The high-fat diet produced different effects on the serum lipids and lipoprotein levels of the athletes. HDL levels changed little during the study although HDL-cholesterol and apo A-I on the last diet day were both slightly above initial values. The high-fat diet provided 111 g of saturated fat per day but had surprisingly little effect on total and LDL-cholesterol whereas serum triglycerides fell by 10% to 20%. Postheparin LPLA increased 30% with fat feeding and the changes in LPLA correlated with alterations in triglyceride levels (r = -0.53, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Food dyes produce minimal effects on locomotor activity and vitamin B-6 levels in postweanling rats.

We investigated the effects of food dye consumption on locomotor activity, brain neurotransmitters, tissue vitamin B-6 levels, and hepatic cytochrome P-450 concentrations in postweanling rats. Animals were individually housed in stabilimeter-type activity cages for 4 1/2 weeks, and fed ad libitum a semipurified basal diet containing graded levels (4, 2, 1, 0.5 or 0%) of a blend of all seven Food, Drug and Cosmetic (FD & C) food dyes. Rats in the 4% dye group were significantly (P less than 0.001) less active during the first 3 weeks of dietary treatment, but no significant differences existed among groups during the final 10 days. Similarly, although dye ingestion depressed food intake (P less than 0.0025) and body weight (P less than 0.05) when averaged for all animals, the differences among groups disappeared by the last week of the experiment. Postmortem tissue analyses revealed no significant effect of dyes on brain tissue levels of serotonin, dopamine, norepinephrine, 5-hydroxyindoleacetic acid or homovanillic acid. Moreover, no significant differences were detected in either plasma and brain tissue levels of pyridoxal phosphate or in hepatic cytochrome P-450 concentrations. These results demonstrate that animals may adapt to the chronic consumption of food dyes and do so with minimal evidence of toxicity. Our data also suggest that previously reported behavioural abnormalities attributed to food dyes are probably unrelated to altered vitamin B-6 metabolism.

High-density lipoprotein metabolism in runners and sedentary men.

We studied the high-density lipoprotein (HDL) metabolism of five trained men who ran 16 km daily and five inactive men. Runners were leaner and their aerobic exercise capacity was much greater. The mean HDL cholesterol level was 65 mg/dL in the runners and 41 mg/dL in the controls. The lipid-rich HDL2 species accounted for a much higher proportion of the HDL in runners (49% v 29%). Tracer studies of radioiodinated autologous HDL demonstrated that runners did not produce more HDL protein but rather catabolized less. The mean biologic half-life of HDL proteins was 6.2 days in the runners compared with 3.8 days in the sedentary men. The activity of lipoprotein lipase was 80% higher in the postheparin plasma of the runners, whereas the activity of hepatic triglyceride hydrolase was 38% lower. Thus, the prolonged survival of plasma HDL proteins in runners may result from augmented lipid transfer to HDL by lipoprotein lipase or diminished HDL clearance by hepatic lipase.

Acute increase in lipoprotein lipase following prolonged exercise.

We investigated the acute effects of prolonged exercise on lipoprotein metabolism. Serum lipid and lipoprotein concentrations and plasma postheparin lipolytic activity were measured in ten well-trained men (ages 21 to 39) the day before and after a 42 km foot race. LDL cholesterol decreased by 10% (113 +/- 31 to 103 +/- 32 mg/dL, P less than 0.01) and total HDL-cholesterol levels increased by 9% (65 +/- 18 to 71 +/- 19 mg/dL, P less than 0.01) the day after the race. No changes in the concentration of apolipoprotein A-I or A-II occurred. Triglyceride levels decreased by 39% (95 +/- 38 to 58 +/- 23 mg/dL, P less than 0.001). Two days after the race, total HDL cholesterol (74 +/- 21 mg/dL, P less than 0.05) and the HDL2 subfraction (37 +/- 19 mg/dL, P less than 0.05) remained significantly elevated compared to pre-race values. Most dramatically, the level of lipoprotein lipase activity measured in postheparin plasma nearly doubled after the race, demonstrating that vigorous exercise acutely increases this enzyme activity. The increase in lipoprotein lipase activity probably mediated the fall in serum triglycerides after exercise and may also account for the increase in HDL cholesterol.