Blood Lactate Concentrations With and Without Exercise in Parkinson's Disease and Multiple Sclerosis Patients
Condition: Parkinson's Disease; Multiple Sclerosis
MeSH terms: Parkinson Disease; Multiple Sclerosis; Sclerosis
Study type: Interventional

Summary: 
      Fatigue is one of the most common and debilitating symptoms experienced in Parkinson's
      Disease (PD) and Multiple Sclerosis (MS). There are multiple proposed mechanisms of
      disorder-related fatigue, however, it is unknown whether PD or MS patients experience
      compromised blood lactate responses to an acute bout of exercise, subjecting them to
      exercise-related fatigue. These populations may experience higher energy expenditure at rest
      due to increased rigidity, however, limited data exists investigating resting energy
      expenditure in these populations.

      Researchers hypothesize that PD and MS patients will display higher resting energy
      expenditure than healthy age-matched controls, and that level of energy expenditure will
      correlate with amount of rigidity or spasticity. Also, we hypothesize that baseline levels of
      lactate will not be different between PD/MS and control groups, but post-exercise blood
      lactate levels will be significantly higher in the PD/MS groups.
    

Detailed description: 
      Patients diagnosed with Parkinson's Disease (PD) and Multiple Sclerosis (MS) frequently
      experience increased levels of muscle weakness and fatigue; This impairment is exacerbated
      with onset of exercise and alleviated with rest or sleep . Importantly, in about 1/3 of PD
      patients, fatigue is considered debilitating , and even further, there is inconclusive
      evidence suggesting that anti-PD and anti-MS drugs improve fatigue. The precise mechanisms
      and pathogenesis of the disorder-specific fatigue in PD and MS remain elusive.

      Both peripheral and central cholinergic systems are affected in PD , however, it has been
      shown that peripheral cholinergic neurons at the neuromuscular junction are normal
      functioning . Even so, recruitment of necessary motor units may be greatly affected due to
      peripheral neuropathy common in both PD and MS . Following repetitive nerve stimulation in PD
      and MS, there is consistent evidence of a decrease in the number of functioning motor units
      and decrements in muscle responses. This promotes progressive fatigue with decrements in the
      amplitude of movement. Therefore, recruitment of motor units may be a major cause of rapid
      fatigue in repetitive movement with PD and MS patients, even though peripheral neuromuscular
      junctions do not seem to be affected. In addition to skeletal muscle inefficiency, work rate
      and efficiency of breathing using respiratory muscles is significantly lower in a PD
      population during repetitive stimulation, used to simulate exercise-induced repetitive
      contractions. Respiratory inefficiencies in MS include, but are not limited to reduced forced
      vital capacity, hypoxemia, and respiratory muscle weakness.

      In addition to possible neurological mechanisms of PD- and MS-related fatigue, rigidity,
      defined as involuntary state of continuous muscle tension in PD, and spasticity and rigidity
      in MS may also have a profound effect on fatigue outcomes . Adequate muscle length is
      required for effective muscle contraction. Rigidity likely changes the length of the muscle
      at rest, and therefore contributes to ineffective muscle contraction when active. In addition
      to inefficient muscle contraction, the increased continuous active contraction, or tone, of
      the muscle results in an increase in resting energy expenditure compared to healthy
      individuals, even in pharmacologically treated PD patients. Interestingly, resting energy
      expenditure in MS patients was shown to be comparable to age-matched healthy controls;
      however, it is important to note that these MS patients remained medicated during the study.
      In addition, rigidity and spasticity, common in PD and MS, respectively may provide varying
      levels of resting energy expenditure; however, no research to date has examined these
      differences. In total, if more energy is being expended at rest, hypothetically, PD and MS
      patients will have inadequate energy stores to exercise to their respective full capacity.
      This could potentiate early onset of lactic acid and hydrogen accumulation in active muscle,
      decrease the pH of the active muscle, and contribute to early fatigue in repetitive tasks.

      Purportedly, the combination of early onset of skeletal and respiratory muscle fatigue, in
      addition to muscle rigidity would create an environment similar to that of high intensity
      exercise, even at low intensities or rest. The ensuing result may likely be an accumulation
      of lactic acid and hydrogen ions, making the muscle environment very acidic. However, changes
      in the levels of resting and post-exercise blood lactate levels have not been elucidated.
      Therefore, we are planning to measure resting energy expenditure using a ventilation face
      mask and a noseclip. Blood lactate will be sampled at rest, after simulated high-intensity
      exercise, and ten minutes after rest (when lactate significantly increases). The exercise
      will consist of performing 5 sets of static, shallow 120 degree squats for 1 minute, with 1
      minute of seated rest between each squat. Sustained isometric contraction at 2/3 of the
      maximal voluntary contractile force for 2 to 3 minutes was found to occlude local blood flow
      enough that local oxygen stores were depleted . Muscle lactate is also increased 12-fold upon
      fatigue of isometric holds such as squats. This same environment of lactic acid buildup can
      be simulated by circulatory occlusion as well as 60-second isometric quadricep contractions .
      Isometric squats will be employed to observe differences in blood response in PD compared to
      healthy individuals.

      Therefore, the purpose of this study is to analyze the differences in resting energy
      expenditure and exercise-induced lactate production in PD and MS compared to healthy,
      age-matched controls.
    

Intervention name(s): pro5 AIRdaptive Power Plate (Badhoevedorp, The Netherlands)
Intervention type(s): Device
Intervention description(s): Subjects will be exposed to vertical vibration with a frequency and peak-to-peak displacement of 30 Hz and 1 mm, respectively, which provides a peak-to-peak acceleration of about 4.16 G.
Whole Body Vibration
Allocation: Non-Randomized
Intervention model: Parallel Assignment
Masking: None (Open Label)
Primary purpose: Treatment
Keywords: Parkinson's Disease; Multiple Sclerosis; Fatigue; Resting Energy Expenditure; Whole Body Vibration; Exercise; Blood Lactate