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Biomedical subjects

P Sahgal

Publications and source records attributed to P Sahgal.

4 recordsLinked to original sources
PubMed1996

Relation of systemic and local muscle exercise capacity to skeletal muscle characteristics in men with congestive heart failure.

OBJECTIVES: The present study was undertaken to further characterize changes in skeletal muscle morphology and histochemistry in congestive heart failure and to determine the relation of these changes to abnormalities of systemic and local muscle exercise capacity. BACKGROUND: Abnormalities of skeletal muscle appear to play a role in the limitation of exercise capacity in congestive heart failure, but information on the changes in muscle morphology and biochemistry and their relation to alterations in muscle function is limited. METHODS: Eighteen men with predominantly mild to moderate congestive heart failure (mean +/- SEM New York Heart Association functional class 2.6 +/- 0.2, ejection fraction 24 +/- 2%) and eight age- and gender-matched sedentary control subjects underwent measurements of peak systemic oxygen consumption (VO2) during cycle ergometry, resistance to fatigue of the quadriceps femoris muscle group and biopsy of the vastus lateralis muscle. RESULTS: Peak VO2 and resistance to fatigue were lower in the patients with heart failure than in control subjects (15.7 +/- 1.2 vs. 25.1 +/- 1.5 ml/min-kg and 63 +/- 2% vs. 85 +/- 3%, respectively, both p < 0.001). Patients had a lower proportion of slow twitch, type I fibers than did control subjects (36 +/- 3% vs. 46 +/- 5%, p = 0.048) and a higher proportion of fast twitch, type IIab fibers (18 +/- 3% vs. 7 +/- 2%, p = 0.004). Fiber cross-sectional area was smaller, and single-fiber succinate dehydrogenase activity, a mitochondrial oxidative marker, was lower in patients (both p < or = 0.034). Likewise, the ratio of average fast twitch to slow twitch fiber cross-sectional area was lower in patients (0.780 +/- 0.06 vs. 1.05 +/- 0.08, p = 0.019). Peak VO2 was strongly related to integrated succinate dehydrogenase activity in patients (r = 0.896, p = 0.001). Peak VO2, resistance to fatigue and strength also correlated significantly with several measures of fiber size, especially of fast twitch fibers, in patients. None of the skeletal muscle characteristics examined correlated with exercise capacity in control subjects. CONCLUSIONS: These results indicate that congestive heart failure is associated with changes in the characteristics of skeletal muscle and local as well as systemic exercise performance. There are fewer slow twitch fibers, smaller fast twitch fibers and lower succinate dehydrogenase activity. The latter finding suggests that mitochondrial content of muscle is reduced in heart failure and that impaired aerobic-oxidative capacity may play a role in the limitation of systemic exercise capacity.

Aged↗
PubMed1996

Scombroid poisoning.

Scombroid poisoning is described in the literature as a toxic poisoning caused by ingestion of certain dark meat fish undergoing bacterial decomposition. Poisoning results from the ingestion of a heat-stable toxin. We describe the case of a man who presented to the emergency department several hours after eating tuna steak with evidence of scombroid poisoning that was associated with loss of vision and atrial tachycardia with block. All signs and symptoms resolved after treatment for scombroid poisoning.

Acute Disease↗
PubMed1995

Exercise intolerance in chronic heart failure is not associated with impaired recovery of muscle function or submaximal exercise performance.

OBJECTIVES: This study investigated whether recovery of skeletal muscle function is impaired in patients with heart failure and whether impaired recovery is associated with abnormal submaximal systemic exercise tolerance during repeated testing. BACKGROUND: Patients with heart failure experience fatigue during daily activities. Because abnormalities of skeletal muscle play a role in their exercise intolerance, these symptoms may reflect a delay in muscle recovery and a resulting limitation in submaximal exercise tolerance. METHODS: Two protocols were used. In protocol 1, knee extensor strength and endurance, and their recovery after fatiguing exercise, were evaluated in 11 patients (mean [+/- SEM] age 62 +/- 5 years, New York Heart Association functional class 2.3 +/- 0.2, ejection fraction 24 +/- 5%) and in 10 age-matched sedentary control subjects. Protocol 2 examined the recovery of knee extensor endurance and submaximal exercise tolerance, as quantified on a self-powered treadmill, over 24 h in 18 patients (mean age 65 +/- 3 years, functional class 2.4 +/- 0.2, ejection fraction 23 +/- 3%) and in 10 control subjects. RESULTS: Peak oxygen consumption was reduced in both heart failure groups (15.4 +/- 1.4 and 15.6 +/- 1.0 ml/kg per min) compared with that in the respective control groups (23.1 +/- 2.9 and 25.6 +/- 1.0 ml/kg per min, both p < 0.05), as was muscle endurance but not muscle strength. In protocol 1, knee extensor endurance recovered more slowly in the patients than in control subjects (to 62 +/- 4% and 87 +/- 7% of the baseline value after 5 min, respectively, p < 0.05). In protocol 2, submaximal exercise tolerance was lower in the patients with heart failure than in control subjects (1,075 +/- 116 vs. 1,390 +/- 110 m), but knee extensor endurance and walking distance recovered fully by 10 and 30 min, respectively. CONCLUSIONS: Although these findings confirm earlier studies that demonstrated impaired muscle endurance in patients with heart failure, the results provide no evidence that recovery of either muscle function or submaximal exercise tolerance is delayed beyond the initial 5 to 10 min after exercise.

Aged↗