Energy Expenditure – Key Concepts

Components of energy expenditure

• Total energy expenditure (TEE) comprises basal/resting expenditure, thermic effect of food, non-exercise activity thermogenesis (NEAT), and exercise energy expenditure.
• Formula: $\text{TEE} = \text{BMR} + \text{TEF} + \text{NEAT} + \text{EEE}$
• Basal Metabolic Rate (BMR) or Resting Energy Expenditure (REE) is the energy at rest to maintain basic cellular and organ function.
• BMR supports ATP synthesis and protein synthesis and maintains function of heart, lungs, brain, kidneys, and liver.
• BMR accounts for roughly $\approx 70\%$ of TEE.

Basal Metabolic Rate (BMR) / Resting Energy Expenditure (REE)

• Energy expended at rest to maintain basic cellular/organ function.
• Major components: ATP synthesis, protein synthesis; function of vital organs.
• BMR ≈ 70% of TEE.
• BMR correlates with lean body mass: $r \approx 0.79\; (P<0.0001)$.
• Sleeping metabolic rate correlates with fat-free mass: $r \approx 0.77\; (P<0.0001)$.

Tissue contributions to REE

• Major contributors: heart, liver, kidneys, brain collectively account for about $60\%$ of REE.
• These organs comprise only a small fraction of body mass (roughly ~6%).
• Skeletal muscle energy expenditure increases dramatically during exercise.
• Adipose tissue and remaining muscle contribute the remainder of REE.

Energy expenditure during exercise

• Exercise is a powerful physiological challenge; metabolic demand of working muscle increases several-fold.
• Increase in metabolism is matched by increased blood flow to working muscles.

Non-exercise adaptive thermogenesis (NEAT)

• Energy used during daily activities that are not deliberate exercise (e.g., walking, talking, fidgeting, posture).

Adaptive thermogenesis

• Specialized cellular heat production in response to environmental cues.
• Occurs via uncoupled oxidative phosphorylation (e.g., UCP1 in brown adipose tissue).

Biochemical processes of uncoupling and thermogenesis

• Coupling vs uncoupling: proton leak via UCPs dissipates energy as heat rather than producing ATP.
• Key components: Electron transport chain, ATP synthase, UCP1, UCP3; mitochondria (inner membrane, matrix).

White vs brown adipose tissue

• White adipocytes: single large lipid droplet; energy storage.
• Brown adipocytes: many mitochondria; high UCP1; thermogenic capacity.
• Beige adipocytes: thermogenic cells that emerge within white adipose tissue during browning.

Brown adipose tissue distribution and activation

• BAT volume increases across puberty; distribution changes with age.
• Thermogenesis is driven by the sympathetic nervous system (SNS).
• Cold or food stimuli raise noradrenaline → cAMP → free fatty acids (FFAs) → activation of UCP1 → heat production.
• β-adrenoceptors modulate BAT function and UCP1 expression (baseline and cold response).

Skeletal muscle thermogenesis

• Shivering (involuntary) and non-shivering (adaptive) thermogenesis contribute to energy expenditure in muscle.

Futile calcium cycling and thermogenesis

• Futile Ca^{2+} cycling via RyR1 and SERCA, with sarcolipin (SLN), increases energy expenditure.

Browning of white adipose tissue

• Beige adipocytes arise within white adipose tissue and resemble brown adipocytes in function (UCP1 expression).

Browning and whitening of adipose tissue

• Precursor cells: PDGFRa+, CD34+, Ly-6A+, Myf5- can give rise to beige adipocytes.
• Browning triggers: Cold exposure, beta-adrenergic agonism; de novo recruitment or transdifferentiation from existing adipocytes.
• High-fat diet (HFD) promotes whitening; cold exposure and adrenergic signals promote browning.

Learning objectives

• To define and describe the major components of energy expenditure.
• To explain cellular processes of thermogenesis in brown adipose tissue, beige adipocytes, and skeletal muscle.
• To describe the primary pathway of BAT activation and the role of the brain and the SNS.