Chapter 6: Fatigue, Critical Power, Muscle Soreness, and Muscle Cramps

Flashcards covering fatigue causes, energy system depletion, metabolic by-products, neural factors, critical power, acute muscle soreness, DOMS, and exercise-induced muscle cramps.

What are the two definitions of fatigue provided in the lecture?

1. Decrements in muscular performance with continued effort, accompanied by sensations of tiredness.
2. Inability to maintain required power output to continue muscular work at a given intensity.

What characteristic distinguishes fatigue from muscle weakness or muscle damage?

Fatigue is reversible by rest.

What are the four major causes of fatigue?

1. Decreased rate of energy delivery.
2. Accumulation of metabolic by-products (such as lactate and hydrogen).
3. Failure of the muscle contractile mechanism.
4. Altered neural control of muscle contraction.

How does phosphocreatine ($\text{PCr}$) depletion contribute to fatigue during short-term, high-intensity exercise?

$\text{PCr}$ is depleted more quickly than total $\text{ATP}$, limiting the ability to replace $\text{ATP}$ and leading to a decrease in $\text{ATP}$ concentration.

How does glycogen depletion correlate with fatigue in terms of rate versus total depletion?

Fatigue is related to total glycogen depletion and is unrelated to the rate of glycogen depletion.

In what order are muscle fiber types recruited as exercise intensity increases?

First: type I fibers (light/moderate intensity) Next: type IIa fibers (moderate/high intensity) Last: type IIx fibers (maximal intensity)

How do muscle glycogen depletion and blood glucose interact to cause fatigue during prolonged exercise?

Muscle glycogen is insufficient for prolonged exercise, requiring liver glycogenolysis to release glucose into the blood. As muscle glycogen decreases, liver glycogenolysis increases, and the combination of muscle glycogen depletion plus hypoglycemia results in fatigue.

What inhibitory effects occur when muscle $\text{pH}$ drops below $6.9$ and reaches $6.4$?

At $\text{pH} < 6.9$, glycolytic enzymes are inhibited and $\text{ATP}$ synthesis slows. At $\text{pH} = 6.4$, further glycogen breakdown is prevented, resulting in a rapid decrease in $\text{ATP}$.

What are the consequences of reactive oxygen species accumulation in muscle?

Impaired mitochondrial function, a slower rate of $\text{PCr}$ recovery, and a reduction in oxidative $\text{ATP}$ production.

What possible mechanisms can cause neural transmission failure at the neuromuscular junction?

Reduced acetylcholine ($\text{ACh}$) synthesis and release, altered $\text{ACh}$ breakdown in the synapse, an increase in muscle fiber stimulus threshold, and an altered muscle resting membrane potential.

At what ambient temperatures is the time to exhaustion longest versus shortest?

Time to exhaustion is longest at $11\,^\circ\text{C}$ and shortest at $31\,^\circ\text{C}$.

What is critical power, and what event durations does it correlate with?

The tolerable duration of high-intensity exercise and the highest metabolic rate that can be maintained entirely by oxidative metabolism; it correlates with performance in events lasting from $2\,\text{min}$ to $2\,\text{h}$.

What causes acute muscle soreness, and over what timeframe does it disappear?

It is caused by the accumulation of metabolic by-products ($H^+$) and tissue edema (plasma fluid shifting into the interstitial space, causing swelling); it disappears within minutes to hours.

What is delayed-onset muscle soreness (DOMS), and what is its primary mechanical cause?

Soreness appearing $1$ to $2$ days after an exercise bout, ranging from stiffness to severe pain; its major cause is eccentric contractions.

What blood markers indicate structural muscle damage after heavy training, and what sarcomere structures show damage?

Concentrations of muscle enzymes in the blood increase by $2$ to $10$ times, paralleling the onset of DOMS; structural damage occurs in sarcomere Z-disks and myofilaments.

What is the five-step sequence of events in DOMS?

1. High tension causes structural damage to the muscle and cell membrane.
2. Membrane damage disturbs $Ca^{2+}$ homeostasis, inhibiting cellular respiration and activating enzymes that degrade Z-disks.
3. After a few hours, circulating neutrophils increase.
4. Products of macrophage activity and intracellular contents (histamine, kinins, $K^+$) accumulate, stimulating pain in free nerve endings.
5. Fluid and electrolytes shift into the area, creating edema.

Which factor is identified as apparently the most important contributor to strength loss from DOMS?

Failure in excitation–contraction coupling.

What strategies can be used to minimize DOMS?

Minimizing eccentric work early in training, starting with low intensity and increasing gradually, starting with high-intensity exhaustive training (intense soreness at first, but less later), and performing gentle stretching or repeated bouts of exercise.

According to the neuromuscular control theory, what causes exercise-associated muscle cramps (EAMC)?

Altered control between the motor neuron and muscle, characterized by central hyperexcitable motor neurons and peripheral spontaneous discharges of motor nerves.

According to the electrolyte depletion theory, what is the primary cause of heat cramps?

Large sweat and electrolyte losses, especially sodium and chloride.