28/11/2025
The Effects on Fascia, Muscle, and Nerves: Why Vitamin E Deficiency Is More Common This Time of Year and Why It’s More Common in TBs
Vitamin E is an antioxidant essential for:
• muscle health
• nervous system function
• immune support
• recovery and performance
• preventing muscle soreness (tying up, fasciculations, stiffness)
Horses cannot synthesize vitamin E. They get it only from fresh forage—especially green, growing pasture.
Before exploring the seasonal causes, it’s important to understand how low vitamin E affects the body’s most sensitive systems:
The Effects on Fascia, Muscle, and Nerves
Effects on Muscle
Vitamin E deficiency can lead to:
• increased muscle cell damage from oxidative stress
• slower repair of micro-tears
• reduced ability to clear metabolic waste
• greater post-exercise soreness
• stiffness, cramping, or tying up (especially in TBs)
• difficulty developing or maintaining topline
• delayed recovery after normal work
Muscles fatigue faster, repair slower, and hurt more when vitamin E is low.
Effects on Fascia
The fascial system depends heavily on antioxidants for glide, hydration, and elasticity. Low vitamin E contributes to:
• reduced fascial glide
• thickened or “sticky” fascial planes
• increased whole-body stiffness
• compensatory tension patterns
• slower response to bodywork
• decreased force transmission through myofascial lines
Fascia becomes less elastic and more reactive, creating the tight, rigid feeling many owners notice.
Effects on the Nervous System
Vitamin E is crucial for nerve health—especially long peripheral nerves in the limbs, back, and hindquarters.
Deficiency may cause:
• increased nerve irritability
• muscle fasciculations (twitching)
• poor proprioception
• stumbling or uncoordinated movement
• hypersensitivity to pressure or touch
• vague neurologic signs that mimic weakness
• difficulty maintaining coordination under saddle
Even mild deficiency can make a horse feel shaky, twitchy, weak, or unbalanced.
Horses Without Pasture Access (Year-Round Risk)
Some horses receive little or no access to fresh pasture at any time of year, including:
• metabolic horses on dry lots
• rehab horses on restricted turnout
• horses in desert or arid regions
• horses boarded in facilities with limited grazing
• horses kept in sand pens or small paddocks
These horses are at constant risk of low vitamin E and often require year-round supplementation, not just seasonal support.
Why Vitamin E Deficiency Becomes More Common This Time of Year
1. Pasture Quality Drops Dramatically
In late fall–winter–early spring:
• grass goes dormant
• green content drops
• vitamin E content plunges
• horses graze less
• many move to dry lots or sacrifice paddocks
Fresh grass is the #1 natural source of vitamin E. When it disappears, intake drops sharply.
2. Hay Contains Very Little Vitamin E
Even high-quality hay loses up to 80% of vitamin E within:
• 6–8 weeks after cutting
• and continues degrading during storage
By winter or early spring, most hay contains:
👉 virtually no vitamin E
Even alfalfa loses its vitamin E during curing.
3. Horses Often Work More or Differently in Winter
Changing workload can increase oxidative stress, raising the horse’s vitamin E requirement:
• exercise
• training changes
• trailering
• indoor arena footing
• cold-weather stiffness
This creates a “higher need, lower intake” imbalance.
4. Confinement + Less Movement = Higher Oxidative Stress
More time in:
• stalls
• dry lots
• small paddocks
…reduces muscle circulation and increases oxidative load, raising antioxidant needs.
5. Not All Feeds Provide Enough Vitamin E
Many horses rely on:
• ration balancers
• basic grain mixes
• senior feeds
Even fortified feeds often fail to meet vitamin E needs unless the horse eats the full recommended serving.
Most horses need 1,000–2,000 IU/day, while performance horses may need 2,000–5,000 IU/day.
Why Thoroughbreds May Be More Prone to Vitamin E Deficiency
This is something many professionals observe, and several valid reasons explain why.
1. Higher Metabolic Rate
Thoroughbreds have:
• higher metabolic demand
• faster oxidative turnover
• naturally stronger stress responses
They burn through antioxidants—including vitamin E—much faster.
2. More Prone to Muscle Disorders
TBs are more susceptible to:
• tying up (RER)
• muscle soreness
• fasciculations
• exercise intolerance
Vitamin E deficiency increases the severity and frequency of these issues.
Why Thoroughbreds Are More Prone to Muscle Disorders
Key contributing factors include:
• Natural Predisposition to RER
Many TBs have a genetic tendency toward Recurrent Exertional Rhabdomyolysis (RER), where:
• muscle cells mismanage calcium
• contractions last too long
• muscles cramp, stiffen, or “tie up”
• Fast-Twitch–Dominant Muscle Fibers
TBs are built for:
• speed
• power
• rapid acceleration
Meaning:
• higher heat production
• greater oxidative stress
• elevated vitamin E needs
• High-Strung, Reactive Nervous System
Thoroughbreds often have:
• a naturally “ready for action” nervous system
• higher sympathetic tone
• elevated baseline muscle tension
This makes their muscles:
• more contracted
• more reactive to stress
• more prone to spasms and soreness
• Common TB Management Patterns
Many TBs experience:
• limited turnout
• increased stall time
• high-starch diets
• inconsistent exercise
• environmental stress
All raise the risk of:
• muscle tightness
• cramping
• tying up
• vitamin E depletion
3. Many TBs Are Coming Off the Track
Ex-racers often have:
• long periods stalled
• hay-based diets
• limited turnout
• high muscular stress
• nutritional gaps from racing environments
They frequently begin their post-track life already low in vitamin E.
4. Stress Sensitivity
TBs tend to be:
• sensitive
• high-alert
• reactive
Chronic stress increases oxidative load → increasing vitamin E requirements.
5. Thin Body Type = Less Antioxidant Reserve
Thoroughbreds typically have:
• lower natural fat stores
• fewer fat-soluble nutrient reserves
• faster depletion of vitamin E
This makes deficiency symptoms appear sooner.
Signs of Low Vitamin E (Common in Winter + TBs)
• muscle twitching
• topline loss despite adequate feed
• poor stamina
• slow recovery after exercise
• weakness or stumbling
• vague hind-end issues
• difficulty holding chiropractic/bodywork results
• nerve hypersensitivity
• lowered immune resilience
TBs often show subtle early signs.
Supplement Tip: Not All Vitamin E Forms Are Equal
Vitamin E supplements vary widely in absorption. In horses:
• Natural d-alpha-tocopherol is better absorbed than synthetic dl-alpha-tocopherol
• Water-dispersible (micellized) forms are ideal for horses on low-fat diets or those showing deficiency
• Powdered synthetic forms may not significantly raise blood levels in some horses
For horses showing symptoms, a high-quality natural, water-dispersible form is often the most effective.
Important Selenium Caution
Vitamin E and selenium are often paired, but:
• many feeds and balancers already contain selenium
• too much selenium can be toxic
• avoid stacking multiple E/Se products without checking totals
Always review total selenium intake with a veterinarian before adding selenium-containing supplements.
When to Involve Your Veterinarian
Consider veterinary testing if you notice:
• persistent muscle twitching
• unexplained weakness, stumbling, or poor coordination
• progressive topline loss
• vague neurologic signs
• chronic soreness or delayed recovery
• sudden behavior changes that feel “neurologic”
A simple serum vitamin E test can confirm deficiency and guide dosage.
Other High-Risk Horses
Beyond Thoroughbreds, vitamin E deficiency may appear sooner in:
• older horses
• horses in intense work
• horses with chronic pain or compensation patterns
• metabolic horses kept off grass
• horses recovering from illness or injury
These horses may benefit from proactive supplementation.
The Bottom Line
Vitamin E deficiency becomes more common this time of year because:
• pasture disappears
• hay contains almost no vitamin E
• work + confinement increase antioxidant demand
Thoroughbreds are more prone to deficiency because of:
• higher metabolic demand
• heightened stress reactivity
• muscle sensitivity and RER tendencies
• feeding and turnout patterns
• lower nutrient reserve capacity
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