Primary care physicians frequently encourage patients to lead a more active, healthy lifestyle. The rise in popularity of endurance events, yoga, and organized gym-based fitness classes has, no doubt, improved the health of those who participate. But what happens when an individual moves too quickly from a sedentary existence to a more physically active one?
In this article we describe 2 clinical cases of rhabdomyolysis that occurred after healthy individuals participated for the first time in a class involving high-intensity stationary cycling, known as “spinning.” This exercise activity originated in California around 1989 when a competitive cyclist introduced variable resistance and speed training to stationary cycle workouts.1 Over the last 10 years, spinning has gained a worldwide following as a means of building cardiovascular endurance while achieving a significant calorie burn.
CASE 1: Lack of conditioning, improper hydration spell trouble
A previously healthy 38-year-old white man presented with left lower extremity pain and dark urine. Three days earlier, he had participated in a spin class for the first time. Despite a sedentary lifestyle, he had no difficulty completing the session and felt fine during the class. He did feel mildly fatigued afterward. The next day, he played 18 holes of golf in hot, humid weather. He admitted to poor fluid intake, stating he “drank a few beers” during the round. The next day, he began noticing discomfort and swelling in his left knee, which progressed to his anterior thigh. That evening, he became concerned because of a dark red tint to his urine. He was not taking any medications.
The physical exam was unremarkable except for a moderately swollen, tender knee with reduced range of motion. An x-ray of the knee showed a moderate suprapatellar effusion, but no fracture or dislocation. Urinalysis was remarkable for blood and myoglobin. The CPK value was 149,985 U/L (normal, 24-170 U/L), AST was 2234 U/L (normal, 9-25 U/L), ALT was 570 U/L (normal, 7-30 U/L), and BMI was 26.6 kg/m2. Renal function was normal, as evidenced by a BUN of 17 mg/dL and a creatinine level of 1.0 mg/dL. He was afebrile and his WBC count was 9.6 x 103/mm3.
We hospitalized the patient with a diagnosis of rhabdomyolysis and started him on aggressive intravenous (IV) hydration. The patient’s CPK and transaminase levels started trending down the next day, urine output (UOP) remained at goal, and renal function remained stable. Pain and swelling diminished over the next 3 days. He was discharged home on Day 4. At discharge, his CPK level was 26,180 U/L, BUN 10 mg/dL, and creatinine 0.8 mg/dL. At 1 month follow-up, his CPK was within normal limits.
CASE 2: Even those who exercise regularly can overdo it
A previously healthy 26-year-old white woman sought care at our clinic complaining of bilateral leg pain and dark urine. Despite being overweight, she regularly engaged in moderate exercise, and 2 days prior had participated in her first spin class. She felt some discomfort 30 minutes into the class, and the next day noted discomfort in her anterior thighs, which progressively worsened. Two days after the workout, her pain was worse and her urine became reddish-brown. She was not taking any medications.
The physical exam was unremarkable except for antalgic gait and tenderness of the anterior thighs, which were also moderately firm and warm to the touch. Urinalysis showed a large blood concentration and was positive for myoglobin. ALT was 366 U/L, AST was 1383 U/L, CPK was 86,592 U/L, and BMI was 33.36 kg/m2. A BUN level of 11 mg/dL and creatinine level of 0.8 mg/dL suggested normal renal function. Her WBC count was 12.2 x 103/mm3.
We hospitalized the patient for a presumptive diagnosis of rhabdomyolysis, and initiated aggressive IV hydration to achieve a UOP of at least 200 mL/h. CPK levels and renal and liver function were closely monitored. On hospital Day 2, the patient’s thighs were tender and tight, so we consulted orthopedics about possible compartment syndrome. The consultant believed that intervention was unwarranted.
By Day 3, the swelling and pain began to resolve. UOP remained at target, and CPK and transaminase levels continued to trend down. Renal function remained stable. The patient was discharged home on Day 4 with a CPK of 11,388 U/L, BUN of 8 mg/dL, and creatinine of 0.7 mg/dL. At her 2-week follow-up, CPK was down to 772 U/L, and transaminases were within normal limits.
Rhabdomyolysis occurs as a result of damage to the striated muscle cell membranes. Such injury releases into the systemic circulation calcium, potassium, phosphate, urate myoglobin, CPK, aldolase, lactate dehydrogenase, AST, and ALT. In the presence of excess calcium, further muscle fiber necrosis occurs and can lead to acute renal failure.2,3 Serum haptoglobin binding capacity becomes overly saturated. This results in free myoglobin, causing renal tubular obstruction. Myoglobin then dissociates into ferrihemate and globulin. Ferrihemate further exacerbates failure of the renal tubular transport system, eventually resulting in cell death and renal failure.2