7) Muscle soreness and muscle cramps Flashcards
What is Acute Muscle Soreness?
Acute Muscle soreness = Soreness that occurs during or immediately after physical activity
* Can occur in any muscle placed under stress
* Subsides within a few minutes to a few hours
* May be due to tissue edema or accumulation of end products of exercise (ie. H+)
- Not due to muscle damage
Acute Muscle soreness May be due to ? or ?
Acute Muscle soreness May be due to tissue edema or accumulation of end products of exercise (ie. H+)
What is Delayed onset muscle soreness (DOMS)
Delayed onset muscle soreness (DOMS)
- Pain that starts 24-72 hours after intense exercise
* Disappears in 5 – 7 days post-exercise
- Symptoms: Mild muscle soreness to inability to perform certain activities
- Impaired muscular force capacities and increased soreness, pain, stiffness, swelling and altered biomechanics to the adjacent joints
What are symptoms of Delayed Onset Muscle Soreness (DOMS)?
Symptoms: Ranges from Mild muscle soreness to inability to perform certain activities
Impaired muscular force capacities and increased:
* soreness,
* pain,
* stiffness,
* swelling and
* altered biomechanics to the adjacent joints
Delayed onset muscle soreness (DOMS)
- Pain that starts 24-72 hours after intense exercise
* Disappears in 5 – 7 days post-exercise
What causes DOMS?
- Ultrastructural damage of muscle cells (Z-band streaming and broadening which destroys sarcomeres) leads to apoptosis and local inflammatory response
- Biopsy analysis of eccentric strained muscle tissue has proved a loss of myofibrillar integrity with Z-band streaming and a disruption of sarcomeres in the myofibrils
Causes of DOMS
* Ultrastructural damage of muscle cells (? and ? which destroys ?) leads to ? and local ? response
* Biopsy analysis of eccentric strained muscle tissue has proved a loss of ? integrity with ? streaming and a disruption of ? in the myofibrils
- Ultrastructural damage of muscle cells (Z-band streaming and broadening which destroys sarcomeres) leads to apoptosis and local inflammatory response
- Biopsy analysis of eccentric strained muscle tissue has proved a loss of myofibrillar integrity with Z-band streaming and a disruption of sarcomeres in the myofibrils
What types of exercise most often results in DOMS?
- Unaccustomed strenuous exercise, especially exercise focusing on eccentric contractions (lengthening contraction);
- exercise focusing on concentric and isometric contractions see less DOMS
Why does DOMS most often follow eccentric-focused exercise?
Eccentric MM contractions have a greater disruption to the structural elements of muscle and connective tissue than concentric/isometric exercise
Eccentric = More damage
What is Mechanical Hyperalgesia?
Tenderness and movement related pain
- typical sign of DOMS
DOMS = delayed onset muscle soreness
What two things happen in the muscle to cause DOMS?
1) Structural Damage (microtrauma)
2) Inflammation
(1) Structural Damage (microtrauma)
- Muscle specific enzymes in blood suggest damage to MM membranes
- Muscle cell membranes (sarcolemma) rupture or Z-disk streaming (Streaming or smearing of the Z band, which is then no longer confined to a narrow zone which bisects the I band)
- Muscle Pain, tenderness, swelling
(2) Inflammation
- Substances (eg neutrophils, macrophages) released from injured muscle initiate inflammatory process
What two things happen (within muscle) in association with DOMS?
1) Structural Damage (microtrauma)
2) Inflammation
(1) Structural Damage (microtrauma)
- Muscle specific enzymes in blood suggest damage to MM membranes
- Muscle cell membranes (sarcolemma) rupture or Z-disk streaming (Streaming or smearing of the Z band, which is then no longer confined to a narrow zone which bisects the I band)
- Muscle Pain, tenderness, swelling
(2) Inflammation
- Substances (eg neutrophils, macrophages) released from injured muscle initiate inflammatory process
DOMS
(1) Structural Damage (microtrauma)
- ? in blood suggest damage to MM membranes
- ? rupture or ? streaming
- Resulting in: ?, ?, ?
(2) Inflammation
- Substances (eg ?, ?) released from ? initiate inflammatory process
(1) Structural Damage (microtrauma)
- Muscle specific enzymes (eg high creatine kinase) in blood suggest damage to MM membranes
- sarcolemma rupture or Z-disk streaming
- Resulting in: Muscle Pain, tenderness, swelling
(2) Inflammation
- Substances (eg neutrophils, macrophages) released from injured muscle initiate inflammatory process
Sarcolemma = Muscle cell membranes
Z-disc streaming = Streaming or smearingof the Z band - no longer confined to a narrow zone bisecting the I band
Sequence of Events in DOMS
(1) High ? in contractile-elastic system in muscle causes structural damage to muscle and cell membrane
Excessive strain on ?
Can damage ?
Sarcomere comes apart -> Damage to ?
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma).
Excessive strain on connective tissue
Can damage Sarcoplasmic Reticulum (Ca++ stores)
Sarcomere comes apart -> Damage to PM (Sarcolemma)
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
Sequence of Events in DOMS
(1) Tension -> Damage to Sarcoplasmic Reticulum and Sarcolemma (PM):
(2) disturbs ? homeostasis,
SR damage → ↑? in sarcoplasm
- inhibits proteins involved in ? (ATP production)
- activates proteolytic enzymes that degrade the Z-lines.
(1) Tension -> Damage to Sarcoplasmic Reticulum and Sarcolemma (PM):
(2) disturbs calcium homeostasis,
SR damage → ↑Ca++ in sarcoplasm
- inhibits proteins involved in cellular respiration (ATP production)
- activates proteolytic enzymes that degrade the Z-lines.
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
Sequence of Events in DOMS
What happens when the Sarcoplasmic Reticulum is damaged?
(1) Tension -> Damage to Sarcoplasmic Reticulum and Sarcolemma (PM):
(2) disturbs calcium homeostasis,
SR damage → ↑Ca++ in sarcoplasm
- inhibits proteins involved in cellular respiration (ATP production)
- activates proteolytic enzymes that degrade the Z-lines
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
Sequence of Events in DOMS
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines
(3) Elevation in neutrophils → attract ? // participate in ?
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines
(3) Elevation in neutrophils that attract macrophages and participate in inflammation
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
Sequence of Events in DOMS
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines → ↑neutrophils → ↑macrophages and inflammation
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of ? in muscle. This process is accentuated in ? exercise
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines → ↑neutrophils → ↑macrophages and inflammation
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings (nociceptors) in muscle. This process is accentuated in eccentric exercise
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
Sequence of Events in DOMS
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines → ↑neutrophils → ↑macrophages and inflammation → stimulation of nociceptors (free nerve endings)
(5) Fluid and electrolytes move into the area (?) causing ? and activating ?; ? may occur
Tension → SR damage → ↑Ca++ in sarcoplasm → ↓Cell. Resp // ↑Proteolytic enzymes → ↓ATP production // degradation of Z-lines → ↑neutrophils → ↑macrophages and inflammation → stimulation of nociceptors (free nerve endings)
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur
(1) High (mechanical) tension in contractile-elastic system in muscle causes structural damage to muscle and cell membrane (sarcolemma). Excessive strain on connective tissue.
(2) Cell membrane damage disturbs calcium homeostasis, inhibiting cellular respiration. High calcium activates proteolytic enzymes that degrade the Z-lines.
(3) Elevation in neutrophils that participate in inflammation.
(4) Products of macrophage activity and intracellular contents accumulate outside cells resulting in stimulation of free nerve endings in muscle. This process is accentuated in eccentric exercise.
(5) Fluid and electrolytes move into the area (edema) causing swelling and activating pain receptors; muscle spasms may occur.
DOMS and Performance
What are three causes behind the worsened performance (decreased force-generating capacity) during DOMS?
Reduction in the force-generating capacity of the muscle due to:
(1) Physical disruption of the muscle
(2) Loss of contractile proteins (damaged sarcomere/muscle fibre)
(3) Failure within the excitation-contraction coupling process (Damaged SR → Disruption in Ca++ homeostasis (↑Ca++ in sarcoplasm)
(3) is the primary reason for loss of force
- Even with stimulation of the muscle by alpha motor neuron, because the calcium stores are disrupted, the excitation-contraction coupling process is also disrupted
What is the primary reason for the loss of force generating capacity in the muscle during DOMS?
Loss of excitation-contraction coupling process
From disturbance in Calcium homeostasis:
SR damage → ↑Ca++ in sarcoplasm
Alpha-motor neuron stimulation would normally result in release of Ca++ to allow unblocking of myosin binding site
- Instead high calcium in sarcoplasm activates proteolytic enzymes and disrupts cellular respiration/ATP production
DOMS and performance
Muscle ? resynthesis is impaired as MM undergoes repair
Muscle glycogen resynthesis is impaired as MM undergoes repair
Glycogen = stored glucose
- Source for ATP
- Thus disturbing glycogen resynthesis = disturb ATP production
Rhabdomyolysis
What is Rhabdomyolysis?
Rhabdomyolysis = Breakdown (dissolution) of striated muscle
More extreme than doms
Muscle injury → leakage of MM cell contents (electrolytes, myoglobin) and other sarcoplasmic proteins (Creatine phosphokinase (CPK), lactate dehydrogenase) into circulation and extracellular fluid
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Symptoms:
* Muscle swelling
* Weak, tender and sore muscles * Dark tea-coloured urine
* Decreased urination
* Nausea
* Loss of consciousness
Rhabdomyolysis
Rhabdomyolysis:
Muscle injury so severe it leads to: ?
Muscle injury → leakage of MM cell contents (electrolytes, myoglobin) and other sarcoplasmic proteins (Creatine phosphokinase (CPK), lactate dehydrogenase) into circulation and extracellular fluid
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
Rhabdomyolysis = Breakdown (dissolution) of striated muscle
- More extreme than doms
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Symptoms:
* Muscle swelling
* Weak, tender and sore muscles * Dark tea-coloured urine
* Decreased urination
* Nausea
* Loss of consciousness
Rhabdomyolysis
Rhabdomyolysis:
What is important regarding the leakage of muscle cell contents into bloodstream during rhabdomyolysis?
Muscle injury → leakage of MM cell contents (electrolytes, myoglobin) and other sarcoplasmic proteins (Creatine phosphokinase (CPK), lactate dehydrogenase (LDH)) into circulation and extracellular fluid
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Rhabdomyolysis = Breakdown (dissolution) of striated muscle
- More extreme than doms
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Symptoms:
* Muscle swelling
* Weak, tender and sore muscles * Dark tea-coloured urine
* Decreased urination
* Nausea
* Loss of consciousness
Rhabdomyolysis
Rhabdomyolysis:
Skeletal mm damage due to several causes including:
- ?
- ?
- ? injury
- lack of ? (prolonged large reduction)
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Rhabdomyolysis = Breakdown (dissolution) of striated muscle
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Symptoms:
* Muscle swelling
* Weak, tender and sore muscles * Dark tea-coloured urine
* Decreased urination
* Nausea
* Loss of consciousness
Rhabdomyolysis
Rhabdomyolysis:
Symptoms?
* Muscle symptoms?
* Kidney symptoms?
Symptoms:
* Muscle swelling
* Weak, tender and sore muscles
* Dark tea-coloured urine
* Decreased urination
* Nausea
* Loss of consciousness
Rhabdomyolysis = Breakdown (dissolution) of striated muscle → release of mm cell contents (electrolytes, myoglobin, creatine phosphokinase, lactate dehydrogenase) into circulation and ecf
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Rhabdomyolysis
Why is Rhabdomyolysis more severe than DOMS?
Myoglobin damages kidneys in large quatities; if kidneys cannot get rid of myoglobin fast enough, kidney failure and death can occur
Rhabdomyolysis = Breakdown (dissolution) of striated muscle → release of mm cell contents (electrolytes, myoglobin, creatine phosphokinase, lactate dehydrogenase) into circulation and ecf
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Rhabdomyolysis
What is Exertional Rhabdomyolysis?
“Caused by exercise”
- Breakdown and necrosis of striated skeletal muscle after engaging in physical activity
Seen in spin classes/boot camps
- Repetitive use of large mm groups (gluteus maximus and quadriceps muscles)
Risk Factors:
- intensity of exercise
- conditioning of participant
- hydration
- body temperature
Rhabdomyolysis = Breakdown (dissolution) of striated muscle → release of mm cell contents (electrolytes, myoglobin, creatine phosphokinase, lactate dehydrogenase) into circulation and ecf
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Rhabdomyolysis
What is Exertional Rhabdomyolysis?
“Caused by exercise”
- Breakdown and necrosis of striated skeletal muscle after engaging in physical activity
Seen in spin classes/boot camps
- Repetitive use of large mm groups (gluteus maximus and quadriceps muscles)
Risk Factors:
- intensity of exercise
- conditioning of participant
- hydration
- body temperature
Rhabdomyolysis = Breakdown (dissolution) of striated muscle → release of mm cell contents (electrolytes, myoglobin, creatine phosphokinase, lactate dehydrogenase) into circulation and ecf
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Rhabdomyolysis
Exertional Rhabdomyolysis: Breakdown and necrosis of striated skeletal muscle after engaging in physical activity (caused by exercise)
- Most often seen during what types of exercise?
- Risk factors (5)
“Caused by exercise”
- Breakdown and necrosis of striated skeletal muscle after engaging in physical activity
Seen in spin classes/boot camps
- Repetitive use of large mm groups (gluteus maximus and quadriceps muscles)
Risk Factors:
- intensity of exercise
- conditioning of participant
- hydration
- body temperature
- drugs such as NSAIDS because of impact on kidneys
Rhabdomyolysis = Breakdown (dissolution) of striated muscle → release of mm cell contents (electrolytes, myoglobin, creatine phosphokinase, lactate dehydrogenase) into circulation and ecf
- More extreme than doms
Myoglobin - processed in kidney
[Myoglobin]+++ → exceeds kidney’s handling capacity → kidney blockage → kidney failure
- Can test blood for muscle contents (high CPK / LDH) to check for mm damage
Skeletal mm damage due to several causes including:
- strenuous exercise
- heat stroke
- crush injury
- lack of blood flow (prolonged large reduction)
Exercise associated muscle cramps (EAMC)
What is the definition of exercise associated muscle cramps (EAMC)?
Exercise associated muscle cramps: a temporary involuntary contraction of skeletal muscle that is intense and painful
- can occur during or immediately after muscular exercise or during sleep
- Most common in endurance events
- Vary in intensity and duration
Hard to study in lab (random == hard to induce)
Exercise associated muscle cramps (EAMC)
Exercise associated muscle cramps (EAMC)
- can occur?
- Most common during what type of exercise?
- Vary in ? and ?
Exercise associated muscle cramps: a temporary involuntary contraction of skeletal muscle that is intense and painful
- can occur during or immediately after muscular exercise or during sleep
- Most common in endurance events
- Vary in intensity and duration
Hard to study in lab (random == hard to induce)
What are two proposed mechanisms of Exercise Associated Muscle Cramps (EAMC)?
Proposed mechanisms of EAMC:
1. Electrolyte depletion theory: disturbance of water and salt balance
2. Altered neuromuscular control theory
Proposed mechanisms of EAMC:
1. Electrolyte depletion theory: disturbance of water and salt balance
* Sweating causes spontaneous muscle contractions due to loss of normal resting membrane potential
* Cramp is often associated with large sweat losses during prolonged exercise in the heat, but can occur in cool environments with little or no sweat loss
* Sweat loss alone and the consequent disturbances of electrolyte balance cannot account for all cramps
- Altered neuromuscular control theory:
* Muscle fatigue causes abnormal activity of the muscle spindle and Golgi tendon organ
* Abnormal discharge of alpha motor neuron drive to the afflicted muscles
* No prevention strategy or treatment is consistently effective
- Altered neuromuscular control theory:
EAMC
What is the electrolyte depletion theory?
- Disturbance of ? balance
- ? causes spontaneous MM contractions due to loss of ?
- Cramp is often associated with large ? losses during prolonged exercise in the heat, but can occur in cool environments with little or no sweat loss
- ? alone and the consequent disturbances of ? balance cannot account for all cramps
One Theory behind exercise associated muscle cramps
- Disturbance of water and salt balance
- Sweating causes spontaneous MM contractions due to loss of normal resting membrane potential
- Cramp is often associated with large sweat losses during prolonged exercise in the heat, but can occur in cool environments with little or no sweat loss
- Sweat loss alone and the consequent disturbances of electrolyte balance cannot account for all cramps
- Altered neuromuscular control theory:
* Muscle fatigue causes abnormal activity of the muscle spindle and Golgi tendon organ
* Abnormal discharge of alpha motor neuron drive to the afflicted muscles
* No prevention strategy or treatment is consistently effective
EAMC
What is the Altered neuromuscular control theory?
* Muscle fatigue causes abnormal activity of the ? and ? (sensory organs)
* Abnormal discharge of ? drive to the afflicted muscles
One Theory behind exercise associated muscle cramps
Altered neuromuscular control theory:
* Muscle fatigue causes abnormal activity of the muscle spindle and Golgi tendon organ (sensory organs)
* Abnormal discharge of alpha motor neuron drive to the afflicted muscles (as mm fatigues, the muscle spindle and golgi tendon organ fall out of sync)
This theory suggests that EAMCs occur when fatigue and other risk factors contribute to a final common pathophysiological pathway to produce an imbalance between excitatory and inhibitory stimuli at the α motor nerve
The muscle spindles and golgi tendon organs are proprioceptive sensory organs:
- muscle spindle: senses the changes in muscle length and the rate of lengthening
- Golgi tendon organ: senses the changes in muscle tension
