Adaptations to Aerobic, Anaerobic, and Resistance Training

Primary goals of aerobic training adaptations

Increase the ability to deliver and extract oxygen.

Cardiovascular change in heart size with aerobic training

Increased heart mass and left ventricular (LV) volume.

Frank-Starling mechanism

Greater EDV stretches ventricles more, leading to more forceful contraction and increased SV.

Change in resting heart rate after aerobic training

Decreases substantially due to increased parasympathetic and decreased sympathetic activity.

Effect of aerobic training on blood pressure at submaximal intensity

Decreases blood pressure.

Angiogenesis

Formation of new capillaries; improves oxygen delivery and extraction.

Adaptations in Type I muscle fibers with aerobic training

Increased capillary and mitochondrial density, myoglobin, and oxidative enzymes.

Lactate threshold with aerobic training

Increases, allowing exercise at higher VO2max before lactate accumulates.

Metabolic shift in fuel utilization during aerobic training

Decreased RER; increased fat use and glycogen sparing.

Ventilatory threshold

The point at which ventilation increases exponentially with increasing VO2.

Primary adaptation to the ATP-PCr system in anaerobic training

Increased creatine kinase activity and faster energy production.

Enzyme that increases with anaerobic training enhancing glycolysis

Phosphofructokinase (PFK).

Muscle fiber adaptations with sprint training

Increased CSA of Type IIa and IIx fibers; decrease in Type I fibers.

Anaerobic power vs anaerobic capacity

Power = peak output in first 5-10 seconds; Capacity = total work in 30 seconds.

Primary mechanism of early strength gains in resistance training

Neural adaptations, not hypertrophy.

Motor unit synchronous recruitment

MU fire together, increasing force production and steadiness.

Autogenic inhibition and resistance training effect

GTO-mediated inhibition of contraction; RT decreases this inhibition.

Changes at the neuromuscular junction with resistance training

Increased ACh receptors and vesicles, increased branching, and smaller motor end plate.

Transient hypertrophy vs chronic hypertrophy

Transient: fluid accumulation post-exercise; Chronic: structural muscle growth.

Stimulus for muscle hypertrophy post-resistance training

Increased protein synthesis via mTOR pathway (stimulated by IGF-1, Akt).

Hormone initiating the signaling pathway for protein synthesis

Growth Hormone (GH), which stimulates IGF-1 production.

Hyperplasia

Increase in the number of muscle fibers—more evident in animal models than humans.

Effect of aging on resistance training adaptations

Lower mTOR response and protein synthesis; need more dietary protein for same effect.

Repeated bout effect

Reduced muscle damage and soreness with repeated exposure to the same exercise.