Recomp insulin resistance sensitivity broken down

Recomp is really a goal or outcome of a dietary & training (& drug) regimen, like fat loss or bulking. Whereas fat loss is defined as decreased FM & retention of LBM, Recomp is defined as increased LBM & decreased FM (fat mass).

Partitioning is a concept that serves the goal of all rational dietary interventions. The p-ratio (partitioning ratio) describes protein deposited in LBM tissues relative to energy intake and, conversely, protein lost from LBM tissues relative to energy deficit. The p-ratio encompasses the factors of i) hormone status (i.e., absolute levels of known key hormones), ii) insulin sensitivity, & iii) leptin sensitivity. There is an interplay between i) - iii).

Insulin sensitivity: when dieting (i.e., in a state of energy deficit), Insulin resistance enhances fat loss by limiting the muscle's use of glucose for fuel - sparing glucose
for use by the brain & ↑intramuscular FA utilization . When bulking, insulin sensitivity within muscle is good & in fat cells bad:

For example: individuals with poor skeletal muscle insulin sensitivity overproduce insulin; store more kcal in AT (why they have more trouble getting "the pump").

Factors that affect insulin sensitivity include: i) b.f.% (primary predictor): ↑b.f. ⇒ ↑FA substrates for fuel (sparing glucose & protein) & dictates adipokine signaling (i.e., adipocyte-secreting hormones [Leptin, TNF-α, IL-..., adiponectin, etc.]), ii) diet: HI CHO (especially refined), saturated fat & low fiber ⇒ ↓insulin sensitivity, iii) muscular contraction ⇒ ↑insulin sensitivity (by ↑glucose uptake into muscle cell; GLUT4 translocation), iv) glycogen depletion ⇒ ↑insulin sensitivity (why though?)... this contradicts later passages where glycogen depletion is said to promote insulin resistance, by sparing glucose & promoting FA oxidation by increasing the use of FA substrates as energy to perform work... the resulting increased blood FA concentrations further promote insulin resistance, v) genetic factors (... another day)
Leptin is an adipokine hormone, secreted primarily by adipocytes, correlate with b.f.%, ↑b.f. ⇒ ↑Leptin. (Visceral vs. subcutaneous depots have different relationships to Leptin). At any given b.f.%, women produce ~2-3x Leptin vs. men. Δ with energy restriction & overfeeding. Leptin is a primary energy storage regulatory signal that reflects: i) b.f. % & ii) energy intake

Example 1: Upon initiating a diet, Leptin may decline by 50% within 1 week (or less) - although obviously have not lost 50% b.f. - so acutely, Leptin Δ become unrelated to b.f. (rather signaling energy intake)

After the initial decline, there is a more gradual decline in leptin related to b.f. loss.

Example 2: Upon overfeeding, leptin similarly ↑rapidly (a without a relationship to Δb.f. )

In the short term, leptin secretion primarily determined by glucose availability - such that pulling glucose out of the fat cell (dieting) ⇒ ↓Leptin & vice versa

Leptin hormone's site-specific effects include effects on the pancreas & liver, in skeletal muscle it ↑FA & ↓AA & glucose use as fuel substrates (enhancing fat loss, promoting protein sparing)....

Essentially, partitioning is a concept that couples leptin & insulin sensitvity (as these are principal factors in how changes in caloric intake (and macronutrient content) affect metabolism (influencing body composition profoundly) as well as hormonal status. We can tweak and enhance it.

P-ratio factors into all aspects of dietary interventions and we want to enhance p-ratio whether recomping, bulking, or cutting.