Nutrition

SECTION THREE

Human Performance Optimization

CHAPTER 18 | NUTRITION

Carbohydrates, Lipids, Proteins, Metabolism & Physical Activity Fueling — CAsP Unit 18 Objectives 1–21

Nutrition is the biochemical and physiological foundation of human performance. The macronutrients — carbohydrates, lipids, and proteins — provide the substrates from which ATP (the universal cellular energy currency) is generated, the structural materials from which body tissues are built and repaired, and the regulatory molecules that control every physiological process. In aviation, nutrition knowledge is directly applicable to: optimizing physical readiness and training outcomes, managing energy during sustained operational activity, planning pre-mission fueling strategies, understanding metabolic consequences of dietary extremes, and supporting aircrew in operational environments where food access is limited or nutritional quality is degraded. This chapter covers all 21 CAsP Unit 18 objectives across four topic areas: carbohydrate physiology (18.1–18.8), lipid physiology (18.9–18.13), protein physiology (18.14–18.18), and nutrition for physical activity (18.19–18.21).

SECTION A: CARBOHYDRATES (Objectives 18.1–18.8)

Carbohydrates are organic molecules composed of carbon, hydrogen, and oxygen in the general formula (CH₂O)n. They are classified by the number of sugar units they contain:

Simple Carbohydrates

• Monosaccharides (single sugar units): Glucose (blood sugar; the primary fuel for brain and exercising muscle; direct substrate for glycolysis), Fructose (found in fruit and honey; metabolized primarily in the liver; does not directly enter glycolysis without hepatic conversion), Galactose (found in milk as part of lactose; converted to glucose in the liver).
• Disaccharides (two monosaccharide units linked by a glycosidic bond): Sucrose (glucose + fructose; table sugar; in candy, soft drinks), Lactose (glucose + galactose; milk and dairy products), Maltose (glucose + glucose; malt products; beer; partially digested starch).

Complex Carbohydrates

• Oligosaccharides: 3–10 monosaccharide units. Found in legumes, some vegetables.
• Polysaccharides: Many monosaccharide units (hundreds to thousands). Starch (the main storage form in plants; amylose [linear] + amylopectin [branched]; found in grains, potatoes, legumes, vegetables). Glycogen (the storage form in animals; highly branched; stored in liver and skeletal muscle; see Objective 18.3). Dietary fiber (cellulose, hemicellulose, pectin; indigestible polysaccharides that provide no caloric energy but promote GI health, satiety, and blood glucose regulation).

Major Dietary Carbohydrate Sources

Table 18.1. Major Carbohydrate Types and Primary Dietary Sources

Gluconeogenesis is the synthesis of new glucose from non-carbohydrate precursors. It is the critical metabolic pathway that maintains blood glucose homeostasis when dietary carbohydrate intake is insufficient or when glycogen stores are depleted:

• Primary site: The liver is responsible for approximately 85–90% of gluconeogenesis. The kidney contributes approximately 10–15% during prolonged fasting or acidosis.
• Precursors: Lactate (the Cori cycle: lactate from exercising muscle → liver → glucose → back to muscle), Amino acids (especially alanine from protein catabolism; the glucose-alanine cycle), Glycerol (from triglyceride lipolysis; glycerol backbone → glucose).
• Regulation: Glucagon (from pancreatic α-cells) is the primary stimulator → activates gluconeogenic enzymes (PEPCK, fructose-1,6-bisphosphatase, glucose-6-phosphatase). Insulin inhibits gluconeogenesis. Cortisol stimulates gluconeogenesis by increasing amino acid mobilization from muscle.
• Physiological significance: (1) Maintains blood glucose for obligate glucose users (brain, red blood cells, renal medulla, exercising muscle) during fasting and prolonged exercise; (2) During sustained exercise, gluconeogenesis begins to contribute significantly after ~90 minutes when glycogen stores approach depletion; (3) Prevents hypoglycemia during overnight fasting; (4) Produces glucose from protein during starvation (at the cost of lean muscle mass).
• Cori cycle: Lactate produced by anaerobically exercising muscle → transported to liver via blood → converted to glucose by hepatic gluconeogenesis → glucose released into blood → taken up by muscle. The liver converts anaerobic muscle waste product back into usable fuel. The liver consumes oxygen (aerobic process) to generate glucose from lactate, allowing aerobic metabolism to sustain anaerobic bursts.

Glycogen is a highly branched polymer of glucose — the body’s primary storage form of carbohydrate. Its physiological significance lies in its capacity to rapidly mobilize glucose when metabolic demand requires it:

• Structure: A branched polysaccharide with α-1,4 glycosidic bonds along chains and α-1,6 bonds at branch points (approximately every 8–10 glucose residues). The highly branched structure provides multiple non-reducing ends that can simultaneously be cleaved by glycogen phosphorylase, enabling extremely rapid glucose release.
• Storage sites and amounts: Liver glycogen (~100 g; approximately 400 kcal): Released as glucose into the blood to maintain blood glucose homeostasis for the entire body. The liver is the ‘blood glucose buffer.’ Skeletal muscle glycogen (~300–500 g; approximately 1,200–2,000 kcal; more in trained athletes): Used exclusively for local muscle energy production; CANNOT be released as glucose into the blood (muscle lacks glucose-6-phosphatase).
• Exercise depletion: At moderate to high exercise intensities (60–80% VO₂max), muscle glycogen is the primary fuel source. Glycogen depletion (‘hitting the wall’ or ‘bonking’) at approximately 90 minutes of sustained exercise at high intensity is associated with a dramatic reduction in exercise capacity (forced reduction to the pace at which fat oxidation alone can supply energy).
• Glycogen as emergency fuel: Liver glycogen is the primary defense against hypoglycemia during short-term fasting (e.g., overnight) and during the early phase of sustained aerobic exercise. Liver glycogen is typically depleted after approximately 12–18 hours of fasting or after 90–120 minutes of moderate–high intensity exercise.

Glycogenesis is the synthesis (formation) of glycogen from glucose. It occurs primarily in the liver and skeletal muscle after a meal when blood glucose is elevated:

• Process: Glucose → Glucose-6-phosphate (hexokinase/glucokinase) → Glucose-1-phosphate (phosphoglucomutase) → UDP-glucose (UDP-glucose pyrophosphorylase) → Addition to glycogen chain (glycogen synthase; the key regulatory enzyme) + branching enzyme (creates α-1,6 branch points).
• Regulation: Insulin is the primary stimulator of glycogenesis: post-meal hyperglycemia → insulin release → activates glycogen synthase (via dephosphorylation) → glucose stored as glycogen. Glucagon and epinephrine inhibit glycogenesis (promote glycogenolysis instead) via cAMP-mediated phosphorylation and inactivation of glycogen synthase.
• Physiological significance: (1) Stores dietary glucose energy for future use without immediately elevating blood glucose; (2) Reduces postprandial blood glucose (the insulin-mediated glycogenesis is one of the primary mechanisms of glucose disposal after a meal); (3) Replenishes glycogen stores after exercise; (4) In the post-exercise period, muscle glycogen synthesis is accelerated by: elevated glucose transporter (GLUT-4) expression in exercised muscle, enhanced insulin sensitivity of muscle, and potentially insulin-independent glucose uptake.

Glycogenolysis is the breakdown (degradation) of glycogen to release glucose. It is the emergency mobilization pathway that rapidly provides glucose when metabolic demand increases:

• Process: Glycogen phosphorylase (the key regulatory enzyme) cleaves α-1,4 bonds, releasing glucose-1-phosphate from glycogen chains. Debranching enzyme removes branch points. Glucose-1-phosphate → glucose-6-phosphate (phosphoglucomutase) → In the LIVER: glucose-6-phosphatase converts to free glucose → released into blood. In MUSCLE: no glucose-6-phosphatase → glucose-6-phosphate enters glycolysis directly.
• Regulation: Glucagon (liver), epinephrine/adrenaline (liver and muscle): activate glycogen phosphorylase via cAMP-PKA cascade. Exercise-induced muscle contraction: Ca²⁺ (from SR release during muscle contraction) directly activates phosphorylase kinase and glycogen phosphorylase in exercising muscle — this is the non-hormonal, direct link between muscle activation and glycogen mobilization. AMP (signals energy depletion when ATP is being consumed rapidly) also activates phosphorylase.
• Physiological significance: (1) Provides rapid glucose for exercising muscle (Ca²⁺-mediated in muscle, matching ATP demand to glycogenolysis rate); (2) Prevents hypoglycemia during the overnight fast and early fasting (hepatic glucagon-stimulated glycogenolysis); (3) Provides fight-or-flight glucose surge (epinephrine-stimulated glycogenolysis in both liver and muscle during acute stress); (4) Supplies glucose for gluconeogenesis precursors in the liver.

Carbohydrates serve multiple essential roles beyond simply providing fuel:

• Primary energy fuel: Glucose is the preferred fuel for most cells and the OBLIGATE fuel for: brain and CNS (approximately 120 g glucose/day for the resting brain; can shift to ketones during prolonged starvation but not immediately), red blood cells (no mitochondria; entirely glycolytic), and renal medulla. During high-intensity exercise (>60–65% VO₂max), carbohydrate is the dominant fuel because it can be oxidized far faster than fat.
• Protein sparing: Adequate dietary carbohydrate prevents catabolism of muscle and other proteins for gluconeogenesis. When carbohydrate intake is insufficient, the body breaks down amino acids to synthesize glucose — at the cost of lean muscle mass.
• Metabolic primer for fat oxidation: 'Fat burns in a carbohydrate flame': Oxaloacetate (a TCA cycle intermediate, derived from glucose metabolism) is required for the complete oxidation of acetyl-CoA from fat. When carbohydrate is severely depleted (as in starvation or very low carbohydrate diets), reduced oxaloacetate availability limits the rate at which acetyl-CoA from fat can enter the TCA cycle, resulting in ketone body production (incomplete fat oxidation products).
• Structural components: Carbohydrates form components of glycoproteins (cell surface recognition, immunological function), glycolipids (cell membrane components, myelin), RNA and DNA (ribose/deoxyribose backbones), ATP, NAD⁺, FAD, and connective tissue (hyaluronic acid, chondroitin sulfate).
• Dietary fiber: Promotes GI transit, supports beneficial gut microbiota, slows glucose absorption (reducing glycemic index of meals), and reduces colon cancer risk.

Carbohydrate requirements vary substantially with physical activity level because carbohydrate is the fuel most depleted during exercise:

Table 18.2. Carbohydrate Intake Recommendations by Activity Level

The minimum of 130 g/day (RDA) reflects the brain’s obligate glucose requirement. Below this threshold, the body must produce glucose from protein (gluconeogenesis) at the cost of lean tissue, or produce ketone bodies as an alternative brain fuel. Very low carbohydrate diets (<50 g/day; ketogenic diets) can sustain brain function via ketosis but at the expense of compromised high-intensity exercise capacity.

The pattern of carbohydrate vs. fat utilization during exercise is regulated by exercise intensity, duration, substrate availability, and training status. This interaction is quantified by the respiratory exchange ratio (RER or RQ):

Effect of Exercise Intensity

• Low intensity (<40–50% VO₂max): Fat oxidation provides the majority of energy. Carbohydrate contribution is modest. Sustainable for very long durations because fat stores are virtually unlimited (100,000+ kcal).
• Moderate intensity (60–70% VO₂max): Both carbohydrate and fat are used in significant proportions. Muscle glycogen is being consumed at a meaningful rate. Sustainable for 90–120 minutes before glycogen depletion limits performance.
• High intensity (>80% VO₂max): Carbohydrate becomes the dominant fuel. At near-maximal intensities (>90% VO₂max), carbohydrate is essentially the sole fuel because fat oxidation cannot supply ATP rapidly enough (fat metabolism is rate-limited by O₂ delivery and enzyme kinetics). Anaerobic glycolysis supplements aerobic metabolism, producing lactate.

Effect of Duration

• First 15–20 minutes: Muscle glycogen (local) is the primary fuel, supplemented by blood glucose.
• 30–90 minutes: Progressive shift toward greater fat utilization as muscle glycogen stores decrease and fat mobilization (lipolysis) increases.
• >90–120 minutes: Muscle glycogen approaching depletion → forced reduction in exercise intensity to the rate at which fat oxidation + gluconeogenesis can supply ATP. Blood glucose (from liver glycogenolysis + gluconeogenesis) becomes increasingly important.

Carbohydrate and the Cross-Over Concept

The cross-over concept describes the shift in predominant fuel source from fat to carbohydrate as exercise intensity increases. At low intensities, fat predominates; at high intensities, carbohydrate predominates. The ‘cross-over point’ shifts RIGHT (toward higher intensities before carbohydrate predominates) with endurance training, as trained muscles become more efficient at fat oxidation.

SECTION B: LIPIDS (Objectives 18.9–18.13)

Lipids are a diverse class of molecules unified by their solubility in organic solvents (fat solvents) and relative insolubility in water. The major lipid classes and their primary dietary and biological sources:

• Triglycerides (triacylglycerols): The predominant storage form of fat in adipose tissue and in food. A glycerol backbone esterified with three fatty acid chains. Dietary sources: animal fats (butter, lard, meat fat), vegetable oils (olive, canola, sunflower), full-fat dairy, nuts, seeds. The body’s largest energy reservoir (≈100,000 kcal in a 70-kg person with 20% body fat).
• Phospholipids: Glycerol + two fatty acids + a phosphate head group with a polar molecule (choline, ethanolamine, inositol, serine). Amphipathic (hydrophobic tails + hydrophilic head) → form lipid bilayer membranes. Not a significant energy fuel but structurally critical. Source: virtually all cell membranes. Dietary sources: egg yolks, soybeans, liver.
• Cholesterol: A sterol (four-ring steroid backbone). Structural component of all cell membranes (regulates membrane fluidity). Precursor for: steroid hormones (cortisol, testosterone, estrogen, aldosterone), bile acids (required for fat digestion), and Vitamin D. Dietary sources: animal products only (egg yolks, shellfish, organ meats, full-fat dairy). Also synthesized endogenously by the liver (approximately 800–1,000 mg/day).
• Fatty acids: The building blocks and energy-releasing components of triglycerides. Classified by: chain length (short, medium, long, very long chain); saturation (saturated [no double bonds; solid at room temperature; animal fats, coconut/palm oil]; monounsaturated [one double bond; olive oil, avocado, nuts]; polyunsaturated [multiple double bonds; vegetable oils, fish, flaxseed]); omega classification (ω-3 vs. ω-6 PUFAs).
• Fat-soluble vitamins: Vitamins A, D, E, and K are lipid-soluble and are transported with dietary fat. Fat malabsorption syndromes produce deficiencies of these vitamins.

Dietary fat recommendations focus not only on total fat intake but on the TYPES of fats consumed, reflecting the different health effects of different fatty acid categories:

Table 18.3. Daily Lipid Intake Recommendations

For physically active individuals, total fat intake at the lower end of the range (20–25% of calories) allows more dietary carbohydrate for glycogen replenishment, which is the performance-limiting fuel for high-intensity and endurance exercise. However, extremely low fat diets (<15% of calories) can impair hormone production, particularly testosterone and estrogen, with implications for muscle recovery, bone health, and overall health.

• Energy storage and fuel: Triglycerides in adipose tissue represent the body’s largest energy reserve (≈100,000 kcal; enough for weeks of survival). During low-to-moderate intensity exercise and at rest, fat oxidation provides the majority of ATP. Fat yields 9 kcal/g vs. 4 kcal/g for carbohydrate and protein.
• Structural function (cell membranes): Phospholipids form the lipid bilayer of all cell membranes. Cholesterol modulates membrane fluidity and permeability. Sphingolipids are key components of neural myelin sheath, nerve conduction.
• Hormone precursors: Cholesterol is the precursor for all steroid hormones (cortisol, aldosterone, testosterone, estrogen, progesterone) and bile acids. Without adequate dietary fat (or endogenous synthesis), steroid hormone production can be impaired.
• Fat-soluble vitamin absorption and transport: Vitamins A, D, E, and K require dietary fat for intestinal absorption. They are transported in chylomicrons and require adequate fat intake and fat digestion for their absorption.
• Thermal insulation: Subcutaneous fat provides thermal insulation, particularly relevant in cold-water immersion scenarios (see Chapter 14). Also provides mechanical cushioning for organs.
• Prostaglandins and eicosanoids: Polyunsaturated fatty acids (especially ω-3 and ω-6) are precursors for eicosanoids (prostaglandins, thromboxanes, leukotrienes) — regulatory molecules involved in inflammation, platelet aggregation, blood vessel tone, and immune function.

Lipid metabolism during exercise involves two interconnected processes: lipolysis (triglyceride breakdown in adipose tissue to release free fatty acids [FFAs]) and fatty acid oxidation (beta-oxidation in the mitochondria of muscle cells):

• Lipolysis: Triggered by epinephrine, norepinephrine, glucagon, cortisol, and growth hormone acting on adipocytes via hormone-sensitive lipase (HSL): Triglyceride → 3 Fatty acids + Glycerol. Fatty acids enter the blood bound to albumin and are transported to exercising muscle.
• Fatty acid uptake by muscle: FFAs cross the sarcolemma (via fatty acid transporters: FAT/CD36, FABP) and are activated to acyl-CoA in the cytoplasm. Transport across the inner mitochondrial membrane requires the carnitine shuttle (acyl-CoA + carnitine → acylcarnitine, transported by CPT-I and CPT-II). This transport step is rate-limiting for fat oxidation during exercise.
• Beta-oxidation: Acyl-CoA undergoes sequential two-carbon cleavage in the mitochondrial matrix, producing: Acetyl-CoA (enters TCA cycle), NADH, and FADH₂. A 16-carbon palmitic acid yields 7 cycles of β-oxidation, producing 8 Acetyl-CoA + 7 NADH + 7 FADH₂. Net ATP yield from palmitate: approximately 106 ATP.
• Intensity limitation: Fat oxidation rate is limited at high exercise intensities because: (1) Fat metabolism requires more O₂ per unit ATP produced than carbohydrate; (2) The carnitine shuttle and β-oxidation enzymes cannot increase their activity fast enough to meet the rapid ATP demand of high-intensity exercise; (3) Epinephrine at high exercise intensities actually INHIBITS lipolysis temporarily. These limitations mean fat cannot sustain exercise above approximately 60–65% VO₂max without supplementation from carbohydrate.

Endurance exercise training produces significant adaptations that enhance fat oxidation capacity — the metabolic basis for the improved fat-burning efficiency of trained athletes:

• Increased mitochondrial density and size: The primary adaptation. More mitochondria per unit of muscle mass → greater capacity for aerobic metabolism, including β-oxidation. Mitochondrial biogenesis is triggered by exercise-induced AMP kinase (AMPK) and PGC-1α activation.
• Increased fat oxidation enzyme activity: Increased activity of β-oxidation enzymes, CPT-I (the carnitine shuttle rate-limiter), and TCA cycle enzymes → greater capacity to oxidize fatty acids.
• Increased fat transporter expression: More FAT/CD36 and FABP (fatty acid binding proteins) → greater fatty acid uptake per unit time by exercising muscle.
• Greater fat oxidation at any given absolute workload: At the same running speed or power output, a trained individual burns proportionally more fat and less carbohydrate than an untrained individual. This spares glycogen for higher intensities when needed (‘glycogen sparing’).
• Rightward shift in cross-over point: Trained individuals shift to carbohydrate dominance at a higher exercise intensity (higher % VO₂max) before fat predominance is lost. This extends the duration of fat-fueled exercise and delays glycogen depletion.
• Increased lipolysis capacity: Enhanced adipose tissue lipolysis (more HSL activity; greater sensitivity to catecholamines) → more FFA available during prolonged exercise.

SECTION C: PROTEINS AND AMINO ACIDS (Objectives 18.14–18.18)

Amino acids are the structural units (monomers) of proteins. Of the 20 standard amino acids used in human protein synthesis, they are classified based on whether the body can synthesize them in sufficient quantities for normal function:

Table 18.4. Essential, Conditionally Essential, and Non-Essential Amino Acids

High biological value (HBV) protein: A complete protein source that contains all 9 essential amino acids in proportions adequate for human protein synthesis. HBV protein sources: eggs (reference protein; biological value ~100), meat, fish, poultry, milk, and whey protein. Lower biological value (LBV): Most plant proteins are incomplete (deficient in one or more EAAs). Plant-based athletes can achieve complete EAA intake by combining complementary protein sources (e.g., rice + legumes).

Table 18.5. Protein Sources, Content, and Notes

Table 18.6. Protein Intake Recommendations by Population

Beyond total daily quantity, distribution and timing of protein intake matter for muscle protein synthesis (MPS): consuming 20–40 g of high-quality protein at each meal (every 3–4 hours), with an emphasis on leucine-rich sources, maximizes the MPS response compared to infrequent large boluses or frequent very small amounts.

• Structural proteins: Collagen (most abundant protein in the body; tendons, ligaments, cartilage, bone matrix, skin), actin and myosin (contractile proteins in muscle), keratin (hair, nails, skin surface).
• Enzymatic catalysis: Virtually all metabolic reactions are catalyzed by protein enzymes. Without enzymes, metabolic reactions would be too slow to sustain life at body temperature.
• Transport proteins: Hemoglobin (O₂ transport), albumin (fatty acids, drugs, hormones, calcium), transferrin (iron), and carrier proteins in cell membranes.
• Immune function: Antibodies (immunoglobulins) are glycoproteins. Complement proteins. Cytokines (signaling proteins for immune coordination).
• Hormones and signaling: Peptide hormones (insulin, glucagon, growth hormone, ADH, EPO, FSH, LH) are proteins or polypeptides. Many intracellular signaling molecules (G-proteins, kinases) are proteins.
• Acid-base buffering: Plasma proteins (especially albumin) and hemoglobin provide approximately 30–35% of blood buffering capacity, essential for maintaining pH homeostasis during exercise.
• Energy substrate (minor): Amino acids can be catabolized for energy (particularly during prolonged exercise and starvation), but this is not a primary role. Protein contributes approximately 5–10% of total energy during prolonged endurance exercise, increasing toward 10–15% when glycogen is severely depleted.

Exercise has a profound effect on protein metabolism, creating both increased protein breakdown and the stimulus for increased protein synthesis:

• During exercise (net protein catabolism): Exercise, particularly prolonged endurance exercise, increases amino acid oxidation for energy (especially the branched-chain amino acids: leucine, isoleucine, and valine). Muscle protein breakdown (MPB) exceeds muscle protein synthesis (MPS) during exercise — net negative protein balance during the exercise bout itself. Protein contributes approximately 5–10% of total energy during exercise, increasing if glycogen is depleted (the body is forced to use more amino acids for gluconeogenesis).
• Immediately post-exercise (anabolic window): The post-exercise period is characterized by: (1) Elevated MPS (stimulated by mechanical loading from resistance exercise and by growth factor signaling); (2) Continued elevated MPB. Net protein balance is still negative until protein (amino acids) are consumed. Consuming protein (20–40 g, leucine-rich) within 1–2 hours post-exercise maximizes MPS and creates net positive protein balance (muscle accretion).
• Branched-chain amino acids (BCAAs): Leucine, Isoleucine, Valine. BCAAs are unique in that they are metabolized primarily in MUSCLE (not the liver), making them directly available as fuel and as anabolic signals. Leucine is the most potent single activator of mTOR complex 1 (mTORC1), the master regulator of MPS. Leucine content of a protein source is the primary determinant of its MPS-stimulating capacity.
• Resistance training + protein: The combination of resistance exercise (creates the anabolic stimulus via mechanical loading and growth factors) + adequate leucine-rich protein (provides the amino acid substrate and the mTOR signal) is required for maximal muscle hypertrophy. Neither alone is as effective as the combination.

SECTION D: NUTRITION FOR PHYSICAL ACTIVITY (Objectives 18.19–18.21)

Physically active individuals have substantially higher energy requirements than sedentary individuals, and the macronutrient composition of their diet affects both training performance and body composition adaptations:

• Total caloric intake: Must match energy expenditure to maintain body weight and support training adaptation. Chronic energy deficit during heavy training (Relative Energy Deficiency in Sport, RED-S; formerly ‘female athlete triad’) impairs performance, hormonal function, bone health, immune function, and recovery. Energy availability = (Energy intake − Exercise energy expenditure) / Fat-free mass. Minimum energy availability for health: approximately 30–45 kcal/kg FFM/day.
• Carbohydrate (dominant training fuel): 5–10 g/kg/day depending on training volume and intensity (see Objective 18.7). Carbohydrate is the most performance-critical macronutrient for high-intensity training. Inadequate carbohydrate intake results in chronic glycogen depletion, impaired high-intensity performance, increased protein catabolism, and impaired immune function.
• Protein (muscle maintenance and repair): 1.2–2.2 g/kg/day depending on training type and intensity (see Objective 18.16). Distribution throughout the day (20–40 g per meal/snack every 3–4 hours) maximizes MPS. Post-exercise protein intake is specifically important for stimulating muscle repair and adaptation.
• Fat (essential functions; secondary fuel): 20–35% of total calories (see Objective 18.10). Provides essential fatty acids, fat-soluble vitamins, and serves as the primary fuel during low-to-moderate intensity exercise. Should not be reduced below 20% as this impairs steroid hormone production.

Table 18.7. Macronutrient Intake Recommendations by Activity Level

The debate over optimal macronutrient composition for athletic performance has intensified with the popularity of ketogenic and low-carbohydrate, high-fat (LCHF) diets:

High Carbohydrate / Low Fat Diet (Traditional Sports Nutrition)

• Advantages: Maximizes glycogen storage (critical for high-intensity and endurance performance); supports high-intensity performance above 60–65% VO₂max; rapid glycogen replenishment between training sessions; well-supported by decades of sports nutrition research.
• Disadvantages: Glycogen stores are limited (90–120 minutes of high-intensity exercise); absolute reliance on glycogen can lead to ‘bonking’ if fueling is inadequate; may not be optimal for fat-adapted athletes in ultra-endurance events.

High Fat / Low Carbohydrate Diet (LCHF / Ketogenic)

• Advantages: Maximizes fat oxidation capacity (theoretically unlimited energy source); reduces reliance on glycogen for low-to-moderate intensity exercise; may benefit ultra-endurance athletes where intensity is consistently low; reduces GI distress from carbohydrate supplements during very long events.
• Disadvantages: Significantly impairs high-intensity exercise performance: LCHF diets impair the capacity to oxidize carbohydrate at high intensities (‘metabolic inflexibility’). The enzymes and transporters for rapid carbohydrate metabolism are downregulated during fat adaptation. At exercise intensities >60–65% VO₂max, LCHF athletes require more oxygen per unit of ATP from fat (fat has a lower P/O ratio than carbohydrate), limiting high-intensity capacity. Multiple controlled studies (Burke et al.) have documented impaired performance in elite race walkers on 3-week LCHF diets despite increased fat oxidation capacity.
• Mixed approach (periodized nutrition): Intentional alternation between LCHF (to enhance fat oxidation capacity) and high-CHO (to maximize glycogen for key performance sessions) is an emerging approach, though the evidence for its benefit over consistent high-CHO remains limited.

Table 18.8. High Carbohydrate vs. High Fat Diet: Performance Comparison

Carbohydrate timing around exercise is one of the most evidence-supported areas of sports nutrition, with specific recommendations for the pre-exercise, during-exercise, and post-exercise windows:

Pre-Exercise Carbohydrate Feedings

• 3–4 hours before exercise (main pre-exercise meal): 200–300 g of carbohydrate in a mixed meal. Emphasize low-to-moderate glycemic index foods (slower digestion, sustained glucose delivery). Adequate time for gastric emptying reduces GI distress during exercise. Allows insulin to normalize before exercise begins.
• 1–2 hours before exercise: 1–2 g/kg body weight of carbohydrate, choosing easily digestible foods (moderate glycemic index; lower fiber and fat to reduce GI distress). Sports bars, banana, white bread with jam, sports drink.
• 30–60 minutes before exercise: High glycemic index carbohydrate (30–60 g) consumed very close to exercise start can be used if needed, but be aware of the potential for reactive hypoglycemia in sensitive individuals: the carbohydrate stimulates insulin release which, in combination with the glucose-lowering effect of exercise onset, can transiently lower blood glucose in the first 15–20 minutes of exercise. This effect is typically transient and does not impair most individuals, but sensitive individuals may prefer to consume carbohydrate immediately at the start of exercise or avoid this timing.

During-Exercise Carbohydrate Feedings

• Exercise <45 minutes: Carbohydrate supplementation not generally required; adequate glycogen stores sustain performance.
• Exercise 45–75 minutes: Mouth rinsing with a carbohydrate solution (without swallowing) can improve performance via neural mechanisms (carbohydrate oral receptors signal the brain to increase motor output); no metabolic benefit required.
• Exercise 1–2 hours: 30–60 g of carbohydrate per hour improves performance vs. no carbohydrate. Glucose or glucose+fructose mixtures are preferred. Fructose is absorbed via a different intestinal transporter (GLUT5) than glucose (SGLT1), allowing higher combined delivery rates.
• Exercise >2–3 hours: 60–90 g carbohydrate per hour, using multiple transportable carbohydrates (glucose + fructose in a 2:1 ratio) to maximize intestinal absorption and deliver carbohydrate at a higher rate without GI distress. Above 60 g/hr of glucose alone, intestinal glucose transporters become saturated; adding fructose (different transporter) allows total delivery of up to 90 g/hr.

Post-Exercise Carbohydrate Recovery

• Immediate post-exercise (0–2 hours): The glycogen synthesis rate is highest in the first 2 hours after exercise (elevated GLUT-4, high muscle insulin sensitivity, high phosphorylase activity returning toward normal). Recommended: 1.0–1.2 g/kg body weight of high glycemic index carbohydrate consumed immediately post-exercise, and repeated every hour for 2–4 hours if rapid glycogen resynthesis is needed for a second same-day session.
• Co-ingestion with protein: Adding 20–25 g of protein to the post-exercise carbohydrate: (1) stimulates MPS for muscle repair; (2) may slightly enhance glycogen synthesis rate by augmenting the insulin response; (3) provides a complete recovery stimulus for both muscle energy stores (glycogen) and muscle structure (protein synthesis).
• Glycemic index of recovery carbohydrate: High glycemic index carbohydrates (white rice, white bread, sports drinks, bananas, potatoes) produce faster initial glycogen resynthesis compared to low glycemic index carbohydrates in the immediate post-exercise window.

Table 18.9. Carbohydrate Feeding Timing and Dosing Around Physical Activity