Seasonal variations in vitamin D do not change the musculoskeletal health of physically active ambulatory men with cerebral palsy: a longitudinal cross-sectional comparison study.

Increased levels of vitamin D in the summer months from natural seasonal variations in sun exposure have been linked to improvements in musculoskeletal health and function in UK populations; however, studies have shown that differences in lifestyles because of disability can inhibit the natural vitamin D increase in these populations. We hypothesized that men with cerebral palsy (CP) will experience smaller increases in 25-hydroxyvitamin D (25(OH)D) from winter to summer and men with CP will not experience any improvements in musculoskeletal health and function during the summer. A longitudinal observational study in 16 ambulant men with CP aged 21.0 ± 1.3 years and 16 healthy, physical activity matched, typically developed controls aged 25.4 ± 2.6 years, completed assessments of serum 25(OH)D and parathyroid hormone during winter and summer. Neuromuscular outcomes included vastus lateralis size, knee extensor strength, 10-m sprint, vertical jumps, and grip strength. Bone ultrasounds were performed to obtain radius and tibia T and Z scores. Men with CP and typically developed controls showed a 70.5% and 85.7% increase in serum 25(OH)D from winter to summer months, respectively. Neither group showed seasonal effect on neuromuscular outcomes muscle strength, size, vertical jump, or tibia and radius T and Z scores. A seasonal interaction effect was seen in the tibia T and Z scores (P < .05). In conclusion, there were similar seasonal increases in 25(OH)D observed in men with CP and typically developed controls, but serum 25(OH)D levels were still considered insufficient to improve bone or neuromuscular outcomes.

Musculoskeletal Health in Active Ambulatory Men with Cerebral Palsy and the Impact of Vitamin D.

PURPOSE: (1) To determine the contribution of diet, time spent outdoors, and habitual physical activity (PA) on vitamin D status in men with cerebral palsy (CP) compared to physical activity matched controls (TDC) without neurological impairment; (2) to determine the role of vitamin D on musculoskeletal health, morphology, and function in men with CP compared to TDC. MATERIALS AND METHODS: A cross-sectional comparison study where 24 active, ambulant men with CP aged 21.0 ± 1.4 years (Gross Motor Function Classification Score (I-II) and 24 healthy TDC aged 25.3 ± 3.1 years completed in vivo assessment of musculoskeletal health, including: vastus lateralis anatomical cross-sectional area (VL ACSA), isometric knee extension maximal voluntary contraction (KE iMVC), 10 m sprint, vertical jumps (VJ), and radius and tibia bone ultrasound (US) Tus and Zus scores. Assessments of vitamin D status through venous samples of serum 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone, dietary vitamin D intake from food diary, and total sun exposure via questionnaire were also taken. RESULTS: Men with CP had 40.5% weaker KE iMVC, 23.7% smaller VL ACSA, 22.2% lower VJ, 14.6% lower KE iMVC/VL ACSA ratio, 22.4% lower KE iMVC/body mass (BM) ratio, and 25.1% lower KE iMVC/lean body mass (LBM) ratio (all p < 0.05). Radius Tus and Zus scores were 1.75 and 1.57 standard deviations lower than TDC, respectively (p < 0.05), whereas neither tibia Tus nor Zus scores showed any difference compared to TDC (p > 0.05). The 25(OH)D was not different between groups, and 90.9% of men with CP and 91.7% of TDC had low 25(OH)D levels when compared to current UK recommendations. The 25(OH)D was positively associated with KE iMVC/LBM ratio in men with CP (r = 0.500, p = 0.020) but not in TDC (r = 0.281, p = 0.104). CONCLUSION: Musculoskeletal outcomes in men with CP were lower than TDC, and despite there being no difference in levels of 25(OH)D between the groups, 25 (OH)D was associated with strength (KE iMVC/LBM) in the CP group but not TDC. The findings suggest that vitamin D deficiency can accentuate some of the condition-specific impairments to musculoskeletal outcomes.

Medial gastrocnemius specific force of adult men with spastic cerebral palsy.

INTRODUCTION: Muscle weakness determines functional impairment in spastic cerebral palsy (SCP). Measurement of specific force (SF) allows for strength comparison with unimpaired populations (controls) accounting for neural (activation and coactivation), architectural (fascicle length and pennation angle), and structural differences (moment arm length). METHODS: Medial gastrocnemius (MG) SF (and its determinants) was assessed in both paretic and non-paretic legs of 11 men with SCP and 11 age-matched controls during plantarflexion maximal voluntary isometric contraction (MVIC). RESULTS: SCP fascicles were 28% longer than control fascicles (P < 0.05). Pennation angle of SCP patients was 41% smaller than in controls. The physiological cross-sectional area of SCP MG patients was 47% smaller than in controls (P < 0.05). There was no difference in SF between controls and SCP patients. CONCLUSIONS: Weakness in SCP is primarily attributable to deficits in agonist activation and muscle size; consequently, SF measured in the MG is similar between SCP and controls. Muscle Nerve 56: 298-306, 2017.

Muscle size, activation, and coactivation in adults with cerebral palsy.

INTRODUCTION: Muscle weakness is present in the paretic limbs of individuals with cerebral palsy (CP). We aimed to determine what neuromuscular factors contribute to weakness in adults with CP during isometric maximal voluntary contractions (iMVCs). METHODS: Gastrocnemius anatomical cross-sectional area (ACSA) and agonist and antagonist activation were measured in 11 CP and 11 control adult men during plantarflexion iMVC. RESULTS: Plantarflexion iMVC torque of the paretic leg was 42% and 52% less than in the non-paretic and control limbs, respectively. The paretic gastrocnemius ACSA was smaller than in the control group only. Paretic agonist activation was less than the non-paretic and control groups, whereas antagonist coactivation was higher. Multiple regression analysis revealed muscle activation accounted for 57% of variation in paretic plantarflexion iMVC torque. CONCLUSIONS: In individuals with CP, muscle weakness in the paretic limb is attributed primarily to impaired neural activation and, to a lesser degree, ACSA.