Why is body size more variable in stressful conditions: an analysis of a potential proximate mechanism

Patterns of variability in quantitative traits across environmental gradients have received relatively little attention in evolutionary ecology. A recent meta-analysis showed that relative phenotypic variability in body size tends to decrease with improving environmental conditions. This pattern was explained by introducing the concept of upper threshold size to a general optimality model of individual growth but alternative explanations certainly exist. In particular, it is frequently observed in insects that variability in individual growth rates decreases with improving environmental conditions. Here we explore the effect of this phenomenon on environment-specific variability in adult sizes. A quantitative model shows that relative variability in adult sizes is independent of environmental quality if absolute variability in growth rates remains constant across the gradient of environmental quality. Deviations from this borderline case are definitely realistic in both directions. Both negative and positive relationships between relative variability of body size and environmental quality can thus be predicted to arise as a consequence of environment-specific variability in growth rates. The variability itself can be both genetic or environmental in its nature. We present empirical data which support both the assumptions and conclusions of our model-based analysis, as well as emphasize the advantages of controlled experiments for understanding the proximate sources of phenotypic variance.     

Absence of exercise-induced MRI enhancement of skeletal muscle in McArdle's disease.

To assess the role of glycogenolysis in mediating exercise-induced increases in muscle water as monitored by changes in muscle proton relaxation times on magnetic resonance imaging (MRI) and cross-sectional area (CSA), five patients with myophosphorylase deficiency (MPD) were compared with seven controls. Absolute and relative work loads were matched during ischemic handgrip and graded cycling, respectively. Relaxation times of active muscle did not increase after handgrip in MPD (T1: 1 +/- 14%, P greater than 0.1; T2: 4 +/- 4%, P greater than 0.1) but did in controls (T1: 59 +/- 30%, P less than 0.005; T2: 26 +/- 9%, P less than 0.005). The volume of exercised muscles, estimated by CSA, increased in both groups after handgrip (controls: 13.8 +/- 3.5%, n = 7, P less than 0.0001; MPD: 7.5 +/- 1.5%, n = 4, P less than 0.005), but the change was greater in controls (P less than 0.02). Ischemic handgrip in controls resulted in a large increase in finger flexor signal intensity (SI) on short tau-inversion recovery images (25 +/- 7%, n = 3; P less than 0.005 compared with preexercise) and a further increase with subsequent reflow (43 +/- 11%, n = 3; P less than 0.001 compared with rest); in MPD, SI did not increase. The ratio of active to inactive muscle SI did not increase from rest to maximal cycle exercise in MPD (0 +/- 20%, n = 2, P greater than 0.1) but did in normals (73 +/- 36%, n = 3; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)