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muscle up.
muscle up.
Ultimo aggiornamento 2016-10-27
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**type i muscle fiber are sometimes broken down into type i and type ic categories, as a result of recent research.
**type i muscle fiber are sometimes broken down into type i and type ic categories, as a result of recent research.
العضلة المعينية الصغيرة (rhomboid minor muscle) هي، في علم تشريح الإنسان، عضلة تصل عظم الكتف بالفقرات.
in human anatomy, the rhomboid minor is a small skeletal muscle on the back that connects the scapula with the vertebrae of the spinal column.
العضلة الزندية الباسطة للرسغ (extensor carpi ulnaris muscle) هي، في علم تشريح الإنسان، أحد عضلات الطرف العلوي.
in human anatomy, the extensor carpi ulnaris is a skeletal muscle located on the ulnar side of the forearm.
have you ever wondered why some people seem to have an unyielding reservoir of willpower while others struggle to resist the simplest temptations is willpower a fixed attribute or can one cultivate and grow it the answer interestingly lies in understanding that willpower much like a muscle can actually be strengthened so how does one go about improving their willpower here are some practical and actionable tips firstly understand the power of small incremental changes start with setting a small goal
have you ever wondered why some people seem to have an unyielding reservoir of willpower while others struggle to resist the simplest temptations is willpower a fixed attribute or can one cultivate and grow it the answer interestingly lies in understanding that willpower much like a muscle can indeed be strengthened so how does one go about improving their willpower here are some practical and actionable tips firstly understand the power of small incremental changes start with setting small goal
العضلة الكعبرية القصيرة الباسطة للرسغ (extensor carpi radialis brevis muscle) هي، في علم تشريح الإنسان، أحد عضلات الطرف العلوي.
in human anatomy, extensor carpi radialis brevis is a muscle in the forearm that acts to extend and abduct the wrist.
metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main
metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main