We tested the hypothesis that exercise training with maximal eccentric (lengthening) muscle actions results in greater gains in muscle strength and size than training with concentric (shortening) actions. Changes in muscle strength, muscle fiber size, and surface electromyographic (EMG) activity of the quadriceps muscle were compared after 36 sessions of isokinetic concentric (n = 8) or eccentric (n = 7) exercise training over 12 wk with use of a one-leg model. Eccentric training increased eccentric strength 3.5 times more (pre/post 46%, P < 0.05) than concentric training increased concentric strength (pre/post 13%). Eccentric training increased concentric strength and concentric training increased eccentric strength by about the same magnitude (5 and 10%, respectively, P > 0.05). Eccentric training increased EMG activity seven times more during eccentric testing (pre/post 86%, P < 0.05) than concentric training increased EMG activity during concentric testing (pre/post 12%). Eccentric training increased the EMG activity measured during concentric tests and concentric training increased the EMG activity measured during eccentric tests by about the same magnitude (8 and 11%, respectively, P > 0.05). Type I muscle fiber percentages did not change significantly, but type IIa fibers increased and type IIb fibers decreased significantly (P < 0.05) in both training groups. Type I fiber areas did not change significantly (P > 0.05), but type II fiber area increased approximately 10 times more (P < 0.05) in the eccentric than in the concentric group. It is concluded that adaptations to training with maximal eccentric contractions are specific to eccentric muscle actions that are associated with greater neural adaptation and muscle hypertrophy than concentric exercise.

The purpose of this study was to determine if a relationship exists among skeletal muscle fiber composition, adiposity, and in vitro muscle glucose transport rate in humans. Rectus abdominus muscle was obtained during elective abdominal surgery from nonobese control (n = 12), obese (n = 12), and obese non-insulin-dependent diabetes mellitus (NIDDM) patients (n = 10). The obese NIDDM group had a significantly lower percentage of type I muscle fibers (32.2 +/- 1.9%) than the obese group (40.4 +/- 2.7%), and both obese groups were significantly lower than the control group (50.0 +/- 2.6%). Insulin-stimulated glucose transport, determined on 28 subjects, was significantly lower in both the obese (3.83 +/- 0.48 nmol.min-1.mg-1) and NIDDM (3.93 +/- 1.0 nmol.min-1.mg-1) groups vs. the control group (7.35 +/- 1.50 nmol.min-1.mg-1). Body mass index (BMI) was inversely correlated to percent type I fibers (r = -0.50, P < 0.01) and to the insulin-stimulated glucose transport rate (r = -0.53, P < 0.01). The percentage of type I muscle fibers was related to the insulin-stimulated glucose transport rate (r = 0.57, P < 0.01), although this relationship was not significant after adjusting for BMI. Although these data do not support an independent relationship between fiber type and insulin action in obesity, a reduced skeletal muscle type I fiber population may be one component of a multifactorial process involved in the development of insulin resistance.

It is widely believed that people who are congenitally limb-deficient or suffer a limb amputation at an early age do not experience phantom limbs. The present study reports on a sample of 125 people with missing limbs and documents phantom experiences in 41 individuals who were either born limb-deficient (n = 15) or underwent amputation before the age of 6 years (n = 26). These cases provide evidence that phantom limbs are experienced by at least 20% of congenitally limb-deficient subjects and by 50% of subjects who underwent amputations before the age of 6 years. The phantoms are detailed and can be described in terms of size, shape, position, movement and temporal properties. The perceptual qualities of the phantoms can also be described by sensory descriptors and are reported as painful by 20% of subjects with phantoms in the congenital limb deficient group and 42% of young amputees. It is argued that these phantom experiences provide evidence of a distributed neural representation of the body that is in part genetically determined.

Leptin, the product of the ob gene, is elevated in obese humans and appears to be closely related to body fat content. The purpose of the present investigation was to determine the effect of aerobic exercise training on systemic leptin levels in humans. Eighteen sedentary middle-aged men (n = 9) and women (n = 9) who did not differ in aerobic capacity (29.4 +/- 1.2 vs. 27.5 +/- 1.2 ml x kg(-1) x min(-1)) or insulin sensitivity index (3.41 +/- 1.12 vs. 4.88 +/- 0.55) were studied. Fat mass was significantly lower in females vs. males (21.83 +/- 2.25 vs. 26.99 +/- 2.37 kg, P < 0.05). Despite this, fasting serum leptin was significantly higher in the females vs. males (18.27 +/- 2.55 vs. 9.88 +/- 1.26 ng/ml, P < 0.05). Serum leptin concentration decreased 17.5% in females (P < 0.05) after 12 wk of aerobic exercise training (4 day/wk, 30-45 min/day) but was not significantly reduced in males. Fat mass was not altered after training in either group. In contrast, both aerobic capacity (+13% males, +9.1% females) and insulin sensitivity (+35% males, +82% females) were significantly improved subsequent to training. These data suggest that 1) women have higher circulating leptin concentrations despite lower fat mass and 2) exercise training appears to have a greater effect on systemic leptin levels in females than in males.

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