The concentration difference between intracellular Ca²⁺ stored in the sarcoplasmic reticulum  and sarcoplasmic [Ca^2+]  is so small (approx 1 to 1.5 times) that ATP powered Ca²⁺ pumps are required to move Ca²⁺ 

from the SR

into the cytoplasm.

This is possible because Ca²⁺ is released from mitochondrial stores close to the contractile proteins.

The rate of onset of muscle contraction is dependent on the diffusion of intracellular ATP and not the diffusion of Ca²⁺.

The concentration difference between intracellular and extracellular Ca²⁺ is so large (about 1 to 20,000) that the Ca²⁺ diffuses much more rapidly than expected.

Membrane invaginations (t-tubular system) carry the action potential into the middle of the muscle fibre triggering an almost simultaneous release of Ca²⁺ from the SR throughout the fibre.

The question cannot be answered because we cannot measure the fibre type ratios in living athletes.

It is the high density of mitochondria present in both power and endurance athletes which determines their elite performance characteristics.

There is little individual variation in fibre type proportions.

Elite power athletes are

born with muscles which are all fast fibres, whereas elite endurance athletes have all slow fibres.

Elite power athletes like high jumpers are born with a higher

than 50% fast-fibre profile, and marathon runners have a higher than 50% slow fibre

profile in key muscles.

The sarcoplasmic reticulum of cardiac muscle is more extensive than that of skeletal muscle.

Skeletal and

cardiac myocytes have extensive networks of t-tubules lined with voltage

sensors.

Cardiac myocytes

are electrically coupled, whereas skeletal muscle fibres do not communicate via

electrical signals between each other.

Dyads are typical in cardiomyocytes, while triads are typical in skeletal muscle.

Mitochondria are more abundant in cardiac muscle than in skeletal muscle.

The voltage sensor depolarizes the SR membrane which

opens the calcium release channels.

Calcium entering through the voltage

sensor activates the ryanodine receptor via calcium-induced calcium release.

The 

ryanodine receptor is opened

by the voltage sensor.

The 

voltage sensor is located in

the membrane of the sarcoplasmic reticulum.

The voltage sensor is a

voltage-gated sodium channel in the sarcolemma.

Smooth muscle can only be stimulated to contract by the CNS.

In smooth muscle, actin filaments and associated myosin attach to regular Z lines producing a striation pattern.

Calcium-dependent phosphorylation of myosin light chains is responsible for the contraction of smooth muscle.

Smooth muscle cells are multi-nucleated like cardiac and skeletal muscle cells.

Myocytes in single-unit smooth muscle are not electrically coupled to each other.

The set length of the muscle is one factor that determines the level of tension developed.

The muscle contracts at its maximum velocity of shortening.

The tension produced is the same as for a single

twitch but maintained for a longer time.

The muscle shortens under a fixed load.

The muscle shortens but does not generate tension.

The main elastic (spring) component within the sarcomere is the endomysium.

In adult humans, a large muscle fibre (one cell) contains around 20 myofibrils.

Skeletal muscle fibres contain hundreds of nuclei and these are located just below the sarcolemma in healthy cells.

Absence of 

the protein

titin makes skeletal muscle fibres more elastic. 

Within a skeletal muscle fibre, each fibril is enveloped

by a sarcolemma membrane.

During the cross-bridge cycle, ATP is broken down to provide energy for the movement of the myosin heads.

During sliding the A band shortens.

Z-lines are found at each end of the sarcomere.

Sliding is caused by the myosin heads interacting with specific sites on the actin molecule.

Muscle works by the relative sliding of the thin filament (actin) over the thick filament (myosin).

The sarcoplasmic reticulum is responsible for Ca²⁺ uptake.

Excitation-contraction coupling.

An action potential conducted down the t-tubules.

An action potential in the surface membrane.

Increase in the sarcoplasmic concentration of Ca²⁺.

Tropomyosin pulls the myosin filament towards the Z-line.

The actin and myosin filaments are both moving.  

The actin filament moves along the fixed myosin filament.

The titin molecule pulls the actin filaments towards the Z-line.

The thick myosin filament moves over the thin actin filament.