Exercise in Multiple Sclerosis

Multiple sclerosis is an immune-mediated demyelinating disease of the central nervous system. Demyelination slows and disrupts conduction, so the functional consequences depend on lesion location rather than following a single pattern. The features that most affect exercise are muscle weakness and reduced central drive, spasticity, ataxia and impaired balance, sensory loss, visual disturbance, heat sensitivity, bladder urgency, cognitive slowing, and fatigue.

Fatigue deserves separate treatment because it is the commonest and most disabling symptom and it is not ordinary tiredness. It is disproportionate to activity, often present on waking, worsens through the day, and is aggravated by heat. Deconditioning compounds it, which creates the trap the whole topic turns on: fatigue discourages activity, inactivity worsens deconditioning, and deconditioning worsens fatigue. Adapted aerobic, resistance and balance exercise may improve MS-related fatigue, so resting more is rarely the whole answer. Management should also address sleep, pain, spasticity, mood, infection, medication effects and appropriate pacing, and current UK guidance specifically warns against assuming that all fatigue in a person with MS is caused by the MS itself.

Disease course also matters for expectations. In relapsing-remitting disease the aim is to maintain and build capacity between relapses, with activity reduced during an acute relapse and rebuilt afterwards. In progressive disease the goals commonly prioritise maintaining or improving transfers, mobility, function, participation and independence according to current capacity, and that reframing helps patients judge the programme as successful when it is.

Uhthoff's phenomenon is the transient worsening of neurological symptoms when body temperature rises, described originally as deterioration of visual acuity during exertion. It can be triggered by exercise, hot weather, a hot bath or shower, a sauna or a fever.

The principal mechanism is temperature-dependent conduction impairment: in a demyelinated axon, only a small rise in temperature is enough to block conduction that was already marginal. Abnormal sweating, thermosensory processing and other autonomic factors are also thought to contribute, so no single mechanism should be presented as completely established. Three consequences follow and each is examinable. First, it is a pseudo-relapse, not a relapse: it does not indicate new lesions, new damage or disease progression. Second, symptoms usually improve once the heat stress is removed or active cooling is applied. Persistence beyond that short-lived pattern, and particularly beyond 24 hours, requires assessment for relapse, infection or another cause. Third, and most importantly, it is not a reason to avoid exercise; it is a reason to manage temperature.

Practical management is straightforward. Exercise in a cool environment and at cooler times of day, use fans, and wear loose light clothing. Cooling strategies are an option for selected heat-sensitive patients rather than a universal protocol, and include cooling garments, neck wraps, cool drinks, fans, environmental cooling and pre-cooling before activity. The supporting evidence is favourable but the studies are relatively small and heterogeneous. Hydrotherapy suits many people well, with water temperature set to what the individual tolerates, since both heat sensitivity and cold-related discomfort or spasticity can affect participation. Not everyone with MS is heat sensitive, so this is a matter for individual assessment rather than universal restriction.

Aerobic, resistance and balance work all have evidence in MS, and a combined programme is usually the right starting point. Aerobic activity improves cardiorespiratory fitness and fatigue, and modalities that reduce balance demand, such as a recumbent stepper, cycle ergometer or arm ergometer, are often better tolerated than treadmill walking where balance or foot drop is a problem.

Progressive resistance training improves strength, walking and fatigue, and is safe. Balance and gait training addresses the ataxia and postural instability that drive falls, which are common in MS and often under-reported.

Several practical points recur. Perceived exertion or the talk test is particularly useful where autonomic dysfunction, medication or an abnormal chronotropic response makes heart rate unreliable, though heart rate is not unusable in everyone with MS. A reasonable starting dose for mild to moderate disability is aerobic and resistance training two to three times weekly at moderate intensity with gradual progression, plus balance or gait work according to impairment. Sessions should be scheduled at the individual's best-functioning time of day, and shorter more frequent sessions are often better tolerated than long ones. Building in rest intervals and accepting day-to-day variability is not a concession but part of the design, since a rigid programme fails on the first bad week. Bladder urgency needs planning around, spasticity may improve with stretching and with avoiding sudden cold, and cognitive fatigue means instructions should be simple and written down. During an acute relapse, activity should be individually modified according to symptoms, safety and specialist rehabilitation advice rather than pushed through or stopped by blanket rule.

The distinction that matters clinically is between a pseudo-relapse and a true relapse. A pseudo-relapse is a temporary worsening of existing symptoms provoked by heat, infection, fever, stress or fatigue, and it settles once the provoking factor is treated or removed. It is not limited to heat, and the underlying cause still needs assessment and treatment in its own right. A true relapse involves new or worsened neurological symptoms lasting more than 24 hours, after a stable period of at least one month, in the absence of infection or another cause.

Two practical rules follow. Any worsening in the context of fever or possible infection should prompt a search for that infection, urinary infection being particularly common in MS, rather than being attributed to the disease. And symptoms that persist beyond a day after cooling and rest warrant assessment by the person's MS team rather than being managed as exercise-related. Beyond this, the same secondary prevention applies as in any long term condition, and bone health deserves specific attention because reduced mobility, falls risk and corticosteroid courses for relapses combine to raise fracture risk.

• •Exercise does not cause relapses or accelerate progression, and improves fitness, strength, mobility, fatigue and mood.
• •Uhthoff's phenomenon is temperature-dependent conduction block in demyelinated axons, producing a pseudo-relapse.
• •Symptoms usually settle on cooling; persistence beyond 24 hours needs assessment for relapse or infection.
• •Pre-cooling, cool environments, cooling garments and cool drinks all improve exercise tolerance.
• •Use perceived exertion where autonomic dysfunction, medication or chronotropic abnormality makes heart rate unreliable.
• •A relapse is new or worsened symptoms over 24 hours, after a stable month, without infection or another cause.